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BANGLADESH
JOURNAL OF CARDIOLOGY
EDITORIALBOARD
CHIEF PATRON
Dr. A. M. Shamim
CHAIRMAN, EDITORIAL COMMITTEE
Dr. Abduz Zaher, FRCP
EDITORIAL BOARD
Dr. A. K. Miah, PhD
Dr. A. P. M. Sohrabuzzaman, FCPS
Dr. Reyan Anis, FRCP
Dr. Arun Kumar Sharma, FACC
Dr. Md. Elias Ali, MD
Dr. Lutfor Rahman, MS
Dr. Md. Lokman Hossain, MS
Dr. Mahbubul Islam, DA
Dr. A. H. M. Abul Monsur, D Card
EDITOR
Dr. Baren Chakraborty, FRCP
ASSISTANT EDITOR
Dr. Mahbubor Rahman, FRCP
Dr. Fahmida Zaman, FACC
CHIEF EXECUTIVE
Dr. (Brig Gen) Manzoor A. Mollah (Retd.)
SECRETARY, PUBLICATION COMMITTEE
Al-Emran Chowdhury
EDITORIAL STAFF
Kuddus Hawladar Nipun
Md. Mizanur Rahman
ADDRESS OF CORRESPONDENCE
Editor, Bangladesh Journal of Cardiology, Labaid Cardiac Hospital, House 1, Road 4, Dhanmondi, Dhaka 1205, Bangladesh
Tel : 88-02-8610793-8, 9670210-3, Fax : 880-02-9615497, Mobile : 01819425302, E-mail : baren_chakraborty@yahoo.com
707-711
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737-741
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Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11
APM Sohrabuzzaman, F Zaman, N Mohammad, M E Ali, H Rahman, M Z Kabir, A Sohel,
S S Pathan, M A Khayer, ASMN Islam, R J Tamanna
Labaid Cardiac Hospital, Dhaka, Bangladesh
Objective
Background
Methods
Results
Conclusion
The objective of this trial was to see level of periprocedural cardiac biomarker as evidence of myocardial
necrosis using Bivaluridin versus Abciximab in patients who were undergoing PCI in a tertiary care
cardiac hospital.
Prevention of hemorrhagic complications has emerged as a priority in patients undergoing PCI in addition
to suppressing periprocedural ischemia. In patients with stable angina and NSTEMI, Bivalirudin has been
shown to result in similar rates of composite ischemia as Heparin plus Abciximab, while significantly
reducing major bleeding. Does Bivalirudin cause less myocardial necrosis as evidenced by Troponin I and
CKMB in patients undergoing PCI is unknown.
A prospective all comers’ intention to treat patients was included in the study. The laboratory was blinded
about the study drugs of the patients. The use of drugs was in the discretion of the operator and was
decided upon the purchasing capacity of the patients. Study period was January 2013 to December 2015.
The patients included with STEMI >20 mins and <24 hours in duration. Patients with NSTEMI, Unstable
angina and chronic stable angina were included. Principal exclusion criteria were any contraindication to
the use of Bivalirudin or Abciximab. The study medications were UFH (5000 unit IV; subsequent boluses
titrated to ACT 200-250secs); Bivalirudin (Bolus 0.75 mg/kg IV, infusion 1.75 mg/kg/h) during and 4 hours
post procedure; or Abciximab (Bolus: 0.25mg/kg and infusion: 0.125 mcg/kg/min) during and 12 hours
post procedure; Antiplatelets: Aspirin 300mg and Clopidogrel 600mg or Prasugrel 60mg preprocedure.
Troponin I & CKMB were measured as a biochemical marker of myocardial necrosis at Pre-procedure
(base line), Just after procedure (0 hours), 8 hours, 16 hours and 24 hours post procedure.
Ninety three patients (male 80, female 13) age ranges from 31 to 80 years (mean ±SD:53.83±11.52)
were enrolled. PCI was done in all cases. All patients got aspirin 300mg and clopidogrel 600mg or
prasugrel 60mg preprocedure and Unfractionated Heparin (5000 unit IV*; subsequent boluses titrated
to ACT 200-250secs) during procedure. Bivalirudin was used in 69 (74.2%) and Abciximab in 24 (25.8%)
of patients. Mean difference of Troponin I in Bivalirudin and Abciximab group at different times did not
reveal statistical significance (Figure 1); but CK-MB level did better outcome (Figure 2).
In this small scale trial of patients undergoing PCI in a single centre compared Abciximab and Bivalirudin
to prevent myocardial necrosis as evidenced by Troponin I & CKMB resulted non-inferior outcome with
Bivalirudin.
Introduction
An invasive strategy of coronary angiography, with
revascularization when appropriate is recommended for
high-risk patient who have an acute coronary syndrome
(ACS).1,2,3 Anti-coagulation is a mainstay of treatment for
patient with ACS and is recommended by international
guidelines.4,5,6 Prevention of hemorrhagic complications has
emerged as a priority in patients undergoing PCI in addition
to suppressing peri-procedural ischemia. Identification of
most appropriate adjunctive antithrombotic therapy before,
APM Sohrabuzzaman, MD, FCPS, Senior Consulatant
Fahmida Zaman, FACC, Consultant
Nur Mohammad, MD, Consultant
Md Elias Ali, MD, Senior Consultant
Habibur Rahman, D Card, Consultant
Mohammad Ziaul Kabir, D Card Consultant
Atiquzzaman Sohel, D Card, Consultant
Shiblee Sadik Pathan, D Card Consultant
Mohammad Abul Khayer, D Card, Consultant
ASM Nazmul Islam, D Card, Consultant
Rownak Jahan Tamanna, MD, Consultant
Correspondence: A P M Sohrabuzzaman, MD, FCPS
Director, Cardiac Cath Lab & Heart Rhythm Services, Labaid Cardiac Hospital,
Professor, School of Health Science, State University of Bangladesh,
Dhaka, Bangladesh. e mail: aicd.pace@yahoo.com
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during, and after percutaneous coronary intervention (PCI)
has been the target of extensive research for the past three
decades.1
Intravenous Heparin is traditionally regarded as the standard
anticoagulant strategy to prevent peri-procedural ischemic
events during PCI. Moreover it has hypersensitivity reaction,
Bleeding complication, Heparin induced thrombocytopenia
(HIT), transient elevation of serum aminotransferase and
hyperkalemia. Because of large intra and interindividual
variability and indirect mechanism of action of Heparin
alternative option have been developed.4,7,8
Abciximab is a glycoprotein IIb/IIIa inhibitor (GPI) with
potent platelet antiaggregative effects.1,9 Although the
administration of Abciximab during PCI was not associated
with a clinical benefit in patient in stable condition who were
given loading dose of clopidogrel before intervention.1,10,11
Howeverpotent antiplatelet effectcausesthrombocytopenia
and increase risk of bleeding, which in turn is strongly
correlated with an unfavorable prognosis.1,12
Bivaluridin is a direct thrombin inhibitor that has increasingly
been used in patient undergoing PCI since the time that
the first study comparing Heparin plus a glycoprotein IIb/
IIIa inhibitor with Bivaluridin the randomized evaluation
in PCI Linking Angiomax to Reduced Clinical Events-2
(REPLACE-2) trial suggest noninferiority of the Bivaluridin
strategy.13 A recent randomized controlled trial (RCT)
comparing Bivaluridin with Heparin alone, however found
a significant increase in the rate of myocardial infarction
(MI) with Bivaluridin and no difference in bleeding events,
suggesting that the diverging result among RCTs might be
influenced by the concomitant administration of a GPI with
Heparin. In patients with stable angina and Non ST Elevation
MI (NSTEMI), Bivalirudin has been shown to result in similar
rates of composite ischemia as Heparin plus Abciximab,
while significantly reducing major bleeding.4,14
Peri-procedural myocardial necrosis causes decrease cardiac
function and has adverse long term clinical outcome. In this
era none of the authors show interest to find out evidence
of myocardial necrosis during and after procedure. All the
authors have interest to see clinical outcome, bleeding
manifestation and thrombotic events in recent past.
Available laboratory evidence of myocardial necrosis in
Bangladesh are raise of creatinine kinase MB (CK-MB) and
troponin-I. Does Bivaluridin cause less myocardial necrosis as
evidenced by Troponin I and CK-MB in patientswho undergone
PCI is unknown? The objective of this trial was to see level of
periprocedural cardiac biomarker as evidence of myocardial
necrosis using Bivaluridin versus Abciximab in patients who
were undergoing PCI in a tertiary care cardiac hospital.
Methods
A prospective all comers intention to treat patients was
included in the study. The laboratory was blinded about the
study drugs. The use of drugs was in the discretion of the
operator and was decided upon the purchasing capacity of
the patients. Study period was January 2013 to December
2015. The patients who got the study drugs were included.
Principal exclusion criteria were any contraindication to PCI
and use of Bivalirudin or Abciximab. Prior thrombolytic,
current use of warfarin, history of bleeding diathesis or
known coagulopathy (including HIT), or will refuse blood
transfusions, history of intracerebral mass, aneurysm, AVM,
or hemorrhagic stroke; stroke or TIA within 6 months or
any permanent neurologic deficit; GI or GU bleed within 2
months, or major surgery within 6 weeks; recent or known
plateletcount<100,000cells/mm3orheamoglobin<10g/dL,
Planned elective surgical procedure that would necessitate
interruption of thienopyridines during the first 6 months
post enrollment. The study was approved by institutional
review board or ethics committee and all patients gave
written informed consent.
Patient was randomly assigned, in an open-lebel fashion
according to the purchasing capacity of the study drugs. The
patients were divided into two groups Bivalirudin versus
Abciximab group. The study medicatons were Antiplatelets:
Aspirin 300mg and Clopidogrel 600mg or Prasugrel 60mg
preprocedure and UFH (5000 unit IV; subsequent boluses
titrated to ACT 200-250secs) during procedure in both
groups. In Bivalirudin group, Bivalirudin (Bolus 0.75 mg/kg
IV, infusion 1.75 mg/kg/h) during and 4 hours post procedure
and in Abciximab group, Abciximab (Bolus: 0.25mg/
kg and infusion: 0.125 mcg/kg/min) during and 12 hours
post procedure. Troponin I & CKMB were measured as a
biochemical marker of myocardial necrosis at Pre-procedure
(base line), just after procedure (0 hours), 8hours, 16 hours
and 24 hours post-procedure.
After collection of laboratory data primary analysis were
performed for all patient who underwent randomization
according to intention to treat principle. We used SPSS
version 15 for statistical analysis. Result was expressed as
mean difference.
Results
Total Ninety three patients (male 80, female 13) age ranges
from 31 to 80 years, Median age 54 years. Patients were
enrolled during the period January 2013 to December 2015.
All patients had PCI as intention treat purpose. All patients
got aspirin 300mg and clopidogrel 600mg or prasugrel
60mg preprocedure and Unfractionated Heparin (5000 unit
IV bolus; subsequent boluses titrated to ACT 200-250 secs)
during procedure. Bivalirudin was used in 69 (74.2%) and
Abciximab in 24 (25.8%) of patients.
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Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11
Among 93 patients 42 (45.2%) had primary PCI, 32(34.4%) had
STEMI, 9(9.7%) had NSTEMI, 6(6.5%) had unstable anigina,
Table-1
Table-3
Table-2
Diagnosis of the study patients (n=93)
Comparison of mean Troponin I (ng/ml) level in
Bivalirudin and Abciximab group at different
times (n=93)
Type of vessels of the study patients (n=93)
4(4.3%) had Chronic stable angina. (Table-1)
Vessels involvement during PCI, single vessel 77 patients,
double vessel 14 patients, and triple vessel 2 patients.
Among the single vessel PCI, LAD were 36(38.7%), RCA were
Diagnosis Number Percentage
Primary 42 45.2
STEMI 32 34.4
NSTEMI 9 9.7
UA 6 6.5
CSA 4 4.3
19.3 28.6 34.6 35.1 31.4
18.7 69.9 40.7 36.8 35.7
Vessel Name of Vessels Number Percentage
Single LAD 36 38.7
RCA 32 34.4
LCX 9 9.7
Double LAD+LCX 4 4.3
LAD+RCA 8 8.6
LCX+RCA 2 2.2
Triple LAD+LCX+RCA 2 2.2
32 (34.4%), LCX were 9 (9.7%) were done (Table-2)
In Bivaluridin vs Abciximab group base line troponin I (mean)
was 19.3 vs 18.7, at 0 hours- 28.6 vs 69.9, at 8hours-34.6
vs 40.7, at 16 hours-35.1 vs 36.8 and after 24 hours-31.4
vs 35.7. (Table-3) Whereas CK-MB (mean) in Bivaluridin vs
Abciximab group at base line 98 vs 77, at 0 hours 135 vs 239,
at 8hours 159 vs 250, at 16 hours-110 vs 148 and after 24
hours-84 vs 112. (Table-4)
In this study we found slightly higher troponin I level in
Abciximab group at different times after PCI within 24 hours
of observation but it was not statistically significant (Figure
1) and much higher in CK-MB level in Abciximab group at
different times but did not reveal statistical significance
(Figure 2). In this small scale study Bivaluridin resulted non
inferior outcome to prevent myocardial necrosis asevidenced
by Troponin I and CKMB with Abciximab.
Discussion
In this small study we had used Bivlirudin in 74% cases and
Abciximab in 26% cases. We found less myocardial necrosis in
CKMB level only in Bivalirudin group than that of Abciximab
Figure-1 Mean difference of Troponin I Status by Bivalirudin and Abciximab used
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Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11
Figure-2 Mean difference of CKMB status by Bivalirudin and Abciximab used
Table-4 Comparison of mean CK-MB (IU/ml) level in Bivalirudin and Abciximab group at different times (n=93)
Group Baseline 0 hours 8 hours 16 hours 24 hours
Bivaluridin(n=69) 98 135 159 110 84
Abciximab(n=24) 77 239 250 148 112
group during PCI for 24hours observation. Bivalirudin is
cheaper than Abciximab in Bangladesh. So patient were
more capable to purchase Bivalirudin than Abciximab.Hence
number of patient were high in Bivaluridin group.
Myocardial infarction resulting elevation of biomarkers at
study entry make it difficult to detect myocardial injury after
the procedure. To diagnose procedure related myocardial
necrosis at least 50% increase above the level of biomarker
recorded before procedure.1 In HORIZONS-AMI study they
found that Bivaluridin was superior to Abciximab and
Heparin in patient undergoing primary PCI for STEMI.1,11
Bivaluridin is also superior in patients with acute NSTEMI
shown in ACUITY clinical trial.1,12
There were no significant differences in the peak creatine
kinase level or creatine kinase MB fraction between the
Bivalirudin group and the group that received Heparin plus
Abciximab.15 In our study Abciximab group had higher
cardiac biomarker level. This was might be due to higher
myocardial necrosis during procedure or acute coronary
events like acute STEMI patients were more in this study.
Before any comment on Abciximab that causes more
periprocedural myocardial necrosis randomization should
be done in 1:1 fashion and preprocedure diagnosis should
be same in both groups.
Treatment with Abciximab may decrease the short and
long term risk of death 15,16,17 and these agents are used
in more than 90% of patient who undergo primary PCI in
the United States and in the majority of such patients in
Europe.15,18,19
But in this subcontinent specially South Asian countries
Bivalirudin is more costeffective than Abciximab.In our study
we found that Bivalirudin is non-inferior than Abciximab in
periprocedural myocardial necrosis.
There were several strength of this study including there
was no sponsor of this study and laboratory was completely
blind about patient’s diagnosis and medications used. On
the other hand few limitation also we advocate these were;
randomization was not 1:1 fashion, baseline diagnosis were
not unique, base line cardiac biomarker were not same in all
cases. Moreover we did not focus on bleeding menifestation,
stent thrombosis, periprocedural cardiac events.
In conclusion this small scale, prospective all comers
intention to treat trial of patients undergoing PCI in a single
centre showed that Bivalirudin was non-inferior to that of
Abciximab to prevent periprocedural myocardial necrosis as
evidenced by Troponin I and CKMB.
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Reference
1. Kastrati A, Neumann F J, Schuiz S, Massberg S, Byrne
R A, Ferenc M et al. Abciximab and Heparin versus
Bivalirudin for non-ST-Elevation Myocardial Infarction.
N Engl J Med 2011; 365:1980-89
2. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA
focused update of the guidelines for the management
of patients with unstable angina/non-ST-elevation
myocardial infarction (updating the 2007 guideline):
a report of the American College of Cardiology
Foundation/American Heart Association Task Force on
Practice Guidelines. Circulation 2011;123:2022-2060
3. Bassand JP, Hamm CW, Ardissino D, et al. Guidelines
for the diagnosis and treatment of non-ST-segment
elevation acute coronary syndromes. Eur Heart J 2007;
28:1598-1660
4. Navarese EP, Schulze V, Andreotti F, Kowalewski M,
Kołodziejczak M, Kandzari DE, et al Comprehensive
meta-analysis of safety and efficacy of bivalirudin versus
heparin with or without routine glycoprotein IIb/IIIa
inhibitors in patients with acute coronary syndrome.
JACC Cardiovasc Interv. 2015;8(1 ):201-213.
5. O’Gara P T, Kushner FG, Ascheim DD, et al. 2013 ACCF/
AHA guideline for the management of ST-elevation
myocardial infarction: a report of the American College
of Cardiology Foundation/American Heart Association
Task Force on Practice Guidelines. J Am Coll Cardiol
61:e78–e140
6. Hamm C W, Bassand JP, Agewall S et al.(2011) ESC
Guidelines for the management of acute coronary
syndromes in patients presenting without persistent ST-
segment elevation: The Task Force for the management
of acute coronary syndromes (ACS) in patients
presenting without persistent ST-segment elevation of
the European Society of Cardiology (ESC). Eur Heart J
32:2999–3054
7. Steinberg DH, Shah P, Kinnaird T et al.(2008) Bleeding
risk and outcomes of Bivalirudin versus Glycoprotein
IIb/IIIa inhibitors with targeted low-dose unfractionated
Heparin in patients having percutaneous coronary
intervention for either stable or unstable angina
pectoris. Am J Cardiol 2008;( 102):160–164
8. Navarese EP, De Luca G, Castriota F, et al. Low-
molecular-weight heparins vs. unfractionated heparin
in the setting of percutaneous coronary intervention
for ST-elevation myocardial infarction: a meta-analysis.
J Thromb Haemost 2011; 9:1902–1915.
9. Neumann FJ, Hochholzer W, Pogatsa-Murray G, Schomig
A, Gawaz M. Antiplatelet effects of abciximab, tirofiban
and eptifibatide in patients undergoing coronary
stenting. J Am Coll Cardiol 2001;37:1323-1328
10. Kastrati A, Mehilli J, Schuhlen H, et al. A clinical trial
of abciximab in elective percutaneous coronary
intervention after pretreatment with clopidogrel. N Engl
J Med 2004;350:232-238
11. Mehilli J, Kastrati A, Schuhlen H, et al. Randomized
clinical trial of abciximab in diabetic patients undergoing
elective percutaneous coronary interventions after
treatment with a high loading dose of clopidogrel.
Circulation 2004;110:3627-3635
12. Ndrepepa G, Berger PB, Mehilli J, et al. Periprocedural
bleeding and 1-year outcome after percutaneous
coronary interventions: appropriateness of including
bleeding as a component of a quadruple end point. J Am
Coll Cardiol 2008;51:690-697
13. Lincoff AM, Bittl JA, Harrington RA, et al. Bivalirudin
and provisional glycoprotein IIb/IIIa blockade compared
with heparin and planned glycoprotein IIb/IIIa blockade
during percutaneous coronary intervention: REPLACE-2
randomized trial. JAMA 2003;289:853-863.
14. Shahzad A, Kemp I, Mars C, et al. Unfractionated heparin
versus bivalirudin in primary percutaneous coronary
intervention (HEAT-PPCI): an open-label, single centre,
randomised controlled trial. Lancet 2014;384:1849–
1858.
15. Gregg WS, Bernhard W, Giulio G, Jan ZP, Bruce RB,
Dariusz D et al Bivelirudin during Primary PCI IN Acute
Myocardial Infarction. N Engl J Med 2008; 358:2218-
2230.
16. De Luca G, Suryapranata H, Stone GW, et al. Abciximab
as adjunctive therapy to reperfusion in acute ST-segment
elevation myocardial infarction: a meta-analysis of
randomized trials. JAMA 2005;293:1759-1765
17. Kandzari DE, Hasselblad V, Tcheng JE, et al. Improved
clinical outcomes with abciximab therapy in acute
myocardial infarction: a systematic overview of
randomized clinical trials. Am Heart J 2004;147:457-
462
18. Dauerman HL, Frederick PD, Miller D, French WJ.
Current incidence and clinical outcomes of bivalirudin
administration among patients undergoing primary
coronary intervention for stent thrombosis elevation
acute myocardial infarction. Coron Artery Dis
2007;18:141-148
19. Fox KA, Steg PG, Eagle KA, et al. Decline in rates of
death and heart failure in acute coronary syndromes,
1999-2006. JAMA 2007;297:1892-1900
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Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15
1M Rahman, 1M E Ali, 1S Nazneen, 1S S Pathan, 1M A Khayer, 2M A Hossain, 3S M D Hossain, 4R Islam
1. Labaid Cardiac Hospital, Dhaka
2. Bangladesh Medical College, Dhaka
3. Khulna Medical College, Khulna
4. Uttara Adhunik Medical College, Dhaka
Objective
Background
Methods
Results
Conclusion
The aim of this study is to evaluate the feasibility, efficacy and outcomes of primary percutaneous
coronary intervention (PPCI) done in Labaid Cardiac Hospital (LCH) from 2004 to 2017.
Primary PCI is the preferred method of treatment of Acute ST segment Elevation Myocardial Infarction
(STEMI) in a PCI-capable hospital within 12 hours of onset of ischemic type chest discomfort. A full-
time dedicated heart team is required to accomplish this goal.
Since the inception of LCH in 2004 only one patient underwent PPCI in first year. Since then, the
number of patients has been increasing significantly. Total 697 patients underwent PPCI upto August,
2017. Most of them were followed up clinically and a few angiographically.
25 patients (3.58%) died during the index hospitalization, 19 patients (2.72%) developed stent
thrombosis of whom acute stent thrombosis occurred in 7 patients, subacute thrombosis occurred in
8 patients and remaining 4 patients developed late stent thrombosis. Major bleeding occurred in 30
patients (4.30%) required blood transfusions. All of them had femoral artery puncture approach. Only
2 patients (0.28%) developed intracranial hemorrhage which was managed conservatively.
Primary PCI is a very effective, life-saving method of treatment of acute STEMI, reduces overall major
adverse cardiovascular events (MACE). Labaid Cardiac Hospital is a major center in the country as a
round the clock PCI-capable superspeciality hospital.
Introduction
Acute myocardial infarction is the leading cause of sudden
cardiac death, cardiogenic shock, ischemic cardiomyopathy,
congestive heart failure and arrhythmias. It poses a great
threat to modern medicine after invention of antibiotics and
reasonable control of communicable diseases. Increasing
incidence of diabetes mellitus, hypertension, dyslipidemias
and consumption of tobacco are the major risk factors
for ischemic heart disease. Sedentary modern urban life
style, air and sound pollutions, food adulteration, excess
social and family stress contribute to the development
of cardiovascular diseases. On top of these global factors,
South Asian population are facing a different genetic/
Mahbubor Rahman, FRCP, Senior Consultant and CCU Incharge
Md Elias Ali, MD, Senior Consultant
Shaheena Nazneen, D Card, Consultant
Shiblee Sadik Pathan, D Card, Consultant
Mohammad Abul Khayer, D Card, Consultant
Md Amir Hossain, FCPS, Associate Professor of Cardiology
S M Delwar Hossain, D Card, Assisstant Professor of Cardiology
Rakibul Islam, FACC, Professor of Cardiology
Correspondence: Mahbubor Rahman, FRCP
Labaid Cardiac Hospital Room 313, House 1, Road 4
Dhanmondi R/A, Dhaka 1205, Bangladesh.
Phone: +8801716914634, email: mahbubordr@gmail.com
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Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15
geographical pattern of narrow, diffuse coronary artery
diseases. After introduction of PPCI, the outcomes of STEMI
have been improved a lot. The mortality and morbidity have
been decreased significantly. There are many obstacles in
widespread use of PPCI in Bangladesh including poor public
hospital facilities, higher cost in private hospitals, lack of
insurance coverage, less number of PCI capable hospitals,
lack of infrastructures at peripheral cities, lack of trained
manpower, lack of public awareness, unbearable traffic
congestions in the capital city and many more. Despite
these hurdles, LCH introduced PPCI in 2004 when it started
it’s journey. Since then, number of PPCI has been increasing
steadily.
Methods
We started PPCI in 2004 and did only one case in that year. In
the year of 2016 we did PPCI on 162 patients. Upto August
2017, total number of PPCI has reached to 697. Of them 520
(74.60%) were male, age difference between 21 years and 91
years (Mean age 58.5 years, SD 6.7), 230 (32.99%) patients
had diabetic, 354 (50.78%) patients were hypertensive, 380
(54.51%) patients were current male smokers, 321 (46.05%)
were dyslipidemic. Average duration of ischemic type chest
pain before reaching the emergency department was 6.5
hours, mean door to balloon time was 62 minutes, SD 9.
Upto 2011 (total 95 patients, 13.62%) GP IIb/IIIa inhibitors
(abciximab and Eptifibatide) were used as adjunctive anti-
platelet agents. After the publication of results of HORIZON
AMI trial, the scenario was dramatically changed. Since then,
most of our patients (602 patients, among them 500 patients
(83.05%) received bivalirudin.
Results
We have followed up 615 patients (88.23%) mostly clinically
and a few angiographically. Clinical follow up includes
telephonic communication and out patient basis ECG,
Echocardiographic assessment, biochemical evaluation,
nuclear imaging of ischemia and viability of myocardium.
Among 697 patients, 352 (50.50%) had infarct related single
vessel disease (SVD), 190 (27.85%) patients had double vessel
disease (DVD) and 132 patients (18.93%) had triple vessel
disease (TVD). Only 23 patients (3.29%) had severe left main
disease, 58 patients (8.32%) presented with cardiogenic
shock of whom 12 patients (20.68%) died during the index
hospitalization.
Left anterior descending (LAD) artery was involved in 56%
cases, Right Coronary Artery (RCA) was involved in 30% cases
and in 10.61% cases left circumflex artery (LCX) was involved.
Initial success rate of opening the infarct related artery was
96%.
Total 25 patients (3.58%) died (of which 12 patients were
in cardiogenic shock) during the index hospitalization. Ten
patients died on the Cathlab table from cardiac arrest, mostly
due to ventricular asystole. Only ten patients received intra-
aortic balloon pump (IABP). All of them were in cardiogenic
shock. Two patients survived who received IABP support.
Nineteen patients (2.72%) developed stent thrombosis within
5 years, of whom 7 patients had acute stent thrombosis
(within 24 hours), 8 patients had subacute stent thrombosis
(within 30 days) and 4 patients had late and very late stent
thrombosis. Upto 2012, 53% patients received bare metal
stent (BMS) and 47% patients received drug eluting stent
(DES) mostly of which were first generation DES. After
that trend had changed, new generation DES with better
outcomes facilitated their use. After 2015, 90% patients
undergoing PPCI received DES.
Slow flow/no flow phenomenon is a great challenge for
interventional cardiologists. Apparent successful opening of
the occluded artery doesn’t ensure the microcirculation and
functionalrescueofischemicmyocardium.Latepresentations,
huge thrombus burden, excessive manipulation of the lesion,
use of thrombus aspiration catheter, predilatation with a
big/used balloon, mismatch between artery and stent sizes,
underapposed or edge dissections are the principal causes
of slow/no flow phenomenon. Intracoronary administration
of adenosine, diltiazem, nitroprusside, trinitrate, and
adjunctive bivalirudin are the pharmacotherapies that help
to overcome this problem in most cases. Auto reperfusion
is an old method to deal with the problem but there is no
substantial evidence to support its regular use.
Major bleeding occurred in 30 patients (4.30%) required
blood transfusions. Most of them received GP IIb/IIIa
inhibitors. After the growing use of Bivalirudin incidence
of major bleeding has significantly reduced. Only 2 patients
(0.28%) developed intracranial hemorrhage, both of them
received abciximab.
Discussion
Acute STEMI is the leading cause of death in coronary care
units throughout the world. It has a tremendous impact on
short and long term mortality and morbidity. With the new
development of techniques and adjunctive anti-thrombotic
agents, it’s outcomes have been improving rapidly and new
trials have been directing the clinicians to a deeper insight
of the disease and its management.
Acute myocardial infarction is classified on the basis of the
presence or absence of ST-Segment Elevation on the ECG and
is further classified into six typesof infarctionsdue to coronary
atherothrombosis (type 1), infarction due to a supply demand
mismatchthatisnottheresultofacuteatherothrombosis(type
2), infarction causing sudden death without the opportunity
for biomarker or ECG confirmation (type 3), infarction related
to a PCI (type 4a), infarction related to thrombosis of a
coronary stent (type 4b), and infarction related to coronary
artery bypass grafting (CABG) surgery (type 5)1.
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For patients with STEMI, urgent reperfusion of the culprit
occluded artery often achieved via PPCI, reduces mortality
and other MACE. Adjunctive antithrombotic antiplatelet
therapies are used during PPCI to reduce MACE rates. The
most commonly used agents include unfractionated heparin
(UFH) or low molecular weight heparin (LMWH) plus/minus
glycoprotein IIb/IIIa inhibitors (GPI). These agents reduce
the rates of pre-procedural ischemic and thrombotic events,
thoughthese benefitscomeat thecost ofincrease in bleeding
complications. Bivalirudin is a direct thrombin inhibitor with
a short half-life and linear pharmacokinetics, which results in
a predictable serum concentrations and anticoagulant effect.
Bivalirudin has emerged as an efficacious and safe alternative
to heparin plus GPI both in stable coronary artery disease
and acute coronary syndrome patients.2
In our practice, we usually load the patient with 3000 units
IV UFH before the procedure. After getting the angiographic
views of the culprit lesion, we give the initial 0.75mg/
kg bolus dose of Bivalirudin followed by an infusion at a
rate of 1.75mg/kg/hr for two hours after the completion
of PCI. Target activated clotting time (ACT) is around 300
seconds. All patients receive 300mg non-enteric coated
aspirin as a loading dose and 75-150mg to be continued as
a maintenance dose. In addition to aspirin an oral P2Y12
inhibitor (Clopidogrel, Prasugrel or Ticagrelor) is given to all
patients.
Clopidogrel was loaded at 600mg and continued at 75mg
daily for at least one year. There is a growing concern of
Clopidogrel resistance in recent years. A large ongoing trial
[TAILOR-PCI (Tailored Anti Platelet therapy following PCI)] is
evaluating the use of pharmacogenetic testing at the time
of PCI to improve ischemic outcomes with Clopidogrel in
patients with acute coronary syndromes or stable coronary
artery disease.3
The preferred P2Y12 inhibitors are Prasugrel [60mg p.o.
loading dose, and 10mg maintenance dose once daily or
Ticagrelor ( 180mg p.o.loading dose and 90mg maintenance
dose twice daily )]. These drugs have a more rapid onset of
action, greater potency, and are superior to Clopidogrel in
clinical outcomes. 4, 5
In our practice, we shifted from clopidogrel to prasugrel
gradually. Loading with prasugrel creates a new problem.
It has a rapid onset of action and a prolonged half-life
(5-7 days). Sometimes patients with STEMI have coronary
anatomy not suitable for PPCI and are good candidates for
urgent CABG surgery, but loading with prasugrel before
the procedure makes difficult to do urgent CABG surgery
as it poses a greater chance of bleeding. Prasugrel is also
contraindicated in patients with previous stroke/transient
ischemic attack and its use is generally not recommended in
patients aged more than 75 years or in patients with lower
body weight (less than 60kg) as it was not associated with
net clinical benefits in these outsets. In that case prasugrel is
used in these patients a reduced dose (5 mg).6
Neither prasugrel nor ticagrelor should be used in patients
with a previous hemorrhagic stroke, in patients on oral
anticoagulants or in patients with moderate-to-severe liver
disease. Cangrelor is a potent IV reversible P2Y12 inhibitor
with a rapid onset and offset of action. Cangrelor may be
considered in patients not pre-treated with oral P2Y12
receptor inhibitors at the time of PCI or in those who are
considered unable to absorb oral agents. 7
Considering all these advantages and disadvantages we have
our own practice protocol. We routinely load with 180mg
Ticagrelor, followed by 90mg twice daily. Due to higher costs
and fear of poor compliance, we do a pharmacogenetic test
for clopidogrel after one month. If the test is indicating
normal response to clopidogrel, we shift the patients from
ticagrelor to clopidogrel. If clopidogrel is resistant, we shift
the patients from ticagrelor to prasugrel at maintenance
dose.
In addition to antiplatelet therapies, all patients also received
higher intensity statin therapy, mostly 40 mg atorvastatin as
a loading dose and continued as maintenance dose at least
one year as high intensity therapy to keep the LDL level
below 70 mg/dl.
Recent trials on aspiration thrombectomy downgrade its
routine use. It is now a Class III recommendation.8 Three
recent randomized clinical trials, namely, Intracoronary
Abciximab and Aspiration Thrombectomy in Patients
With Large Anterior Myocardial Infarction (INFUSE-AMI)
trial, Thrombosis Aspiration During ST-Segment Elevation
Myocardial Infarction (TASTE) trial, and Trial Routine
Aspiration Thrombectomy With PCI vs. PCI Alone in Patients
With STEMI (TOTAL ) have demonstrated lack of evidence of
benefit from routine use of thrombectomy. 9 , 10, 11, 12
Up to 2015, here in Labaid Cardiac Hospital, we used routine
manual thrombectomy device almost in every case without
knowing long-term benefits. Now we do not use aspiration
device routinely.
In most of the cases, after passing the PTCA wire, the distal
landing zone is usually evident. So direct stenting can be
done without muchdifficulties. When evenafter crossing the
lesion , distal vessel is not visible, a low profile small balloon
is enough to visualize the distal landing zone.
As the price of stents has come down significantly globally,
now in majority cases we use new generation drug eluting
stents. 2017 ESC guidelines for the management of acute
myocardialinfarction inpatientspresentingwithST-Segment
elevation have recommended stenting with new generation
DES over BMS for PPCI. 13, 14, 15 , 16
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Conclusion
Acute STEMI is a life threatening cardiac emergency that
requires urgent revascularization. PPCI is the treatment of
choice for opening the infarct-related occluded artery within
12 hours of onset of ischemic type chest discomfort. Non-
culprit significant lesions can be treated at the same setting
or stage PCI can be planned during the index hospitalization.
All significant lesions must be treated in patients with
cardiogenic shock in same setting.
Non-enteric coated aspirin 300mg loading dose should
be given to all patients and 75-150 mg maintenance dose
should be continued.
New generation potent P2Y12 inhibitor (Prasugrel or
Ticagrelor) loading dose followed by maintenance dose
should be given to all patients.
High dose Statin (eg Atorvastatin 40-80mg) loading dose
should be given to all patients.
Heparin (UFH) 3000 units bolus should be given to all patients
before the procedure.
Bivalirudin IV bolus and maintenance dose should be given
to all STEMI patients during the procedure.
Thrombus suction is not a routine recommendation.
Direct stenting with a DES is a preferred option. Otherwise
a low profile small balloon can be useful to visualize
the distal landing zone. Routine use of intracoronary
adenosine is beneficial to combat slow/no flow and improve
microcirculation.
References
1. JeffreyL Andersonand David AMorrow.AcuteMyocardial
Infarction: Review article by Edward W. Campion N Engl
J med 2017: 376 2053-2064 May 25, 2017.
2. Ashish Shah and Dmitriy N Feldman. Outcome of
the HORIZONS-AMI trial: Bivalirudin enhances long-
term survival in patients with ST-elevation myocardial
infarction undergoing angioplasty. Vasc Health Risk
Manag. 2012; 8: 115-123.
3. Mehta SR, Tanguay JF et al. CURREN-OASIS Trial
Investigators. Lancet 2010; 376 (9748): 1233-1243
4. Wiviott SD, Braunwald E et al. TRITON-TIMI 38
investigators. Prasugrel versus Clopidogrel in patients
with acute coronary syndromes. N Engl Med 2007; 357
(20): 2001-2015
5. Wallentin L. Becker R.C, Budaj A et al. PLATO
Investigators. Ticagrelor versus Clopidogrel in patients
with acute coronary syndromes. N Engl J Med 2009; 361
(11) :1045 -1057
6. Roe MT, Armstrong PW, Fox KA et al. TRILOGY ACS
investigators. Prasugrel versus Clopidogrel for acute
coronary syndromes without revascularization. N Engl J
Med 2012; 367 (14): 1297-1309.
7. Bhatt DL, Stoone GW, Mahaffey et al. CHAMPION
PHOENIX Investigators. Effect of platelet inhibition with
Cangrelor during PCI on ischemic events. N Engl J Med
2013; 368 (14): 1303-1313.
8. Levine GN, Bates ER, Blankenship JC, et al. 2015 ACC/
AHA/SCAI Focused Update on Primary Percutaneous
Coronary Intervention for patients with ST-Elevation
Myocardial infarction. J Am Coll Cardial 2016; 67: 1235-
50.
9. Stone GW, Maehara, Witzenbich B, et al. Intracoronary
abciximab and aspiration thrombectomy in patients
with Large anterior myocardial infarction: the INFUSE-
AMI randomized trial. JAMA 2012; 307: 1817-26.
10. Fröbert O, Lagerqvist B, Olivecrona GK, et al. Thrombus
aspiration during ST-segment myocardial infarction. N
Engl J Med 2013; 169:1587-97
11. Laserqvist B, Fröbert O, Loivecrona GK, et al. Outcomes 1
year after thrombus aspiration for myocardial infarction.
N Engl J Med 2014; 271:1111-20
12. Jolly SS Cairns JA, Yusuf S, et al. Randomized trial
of primary PCI with or without routine manual
thrombectomy. N Engl J Med 2015; 372:1389-98
13. Kastrati A, Dibra A, Spaulding C, Laarman GJ, et al. meta-
analysis of randomized trials on drug-eluting stents vs.
bare-metal stents in patients with acute myocardial
infarction. Eur Heart J 2007;28(22):2706-2713
14. Raber L, Kelbaek H, Ostojic M. et al. COMFORTABLE
AMI Trial Investigators. Effect of biolimus-eluting
stents with biodegrable polymer vs. bare-metal
stents on cardiovascular events among patients with
acute myocardial infarctions; the COMFORTABLE AMI
randomized trial. JAMA 2012;308(8):777-787
15. Sabate M, Cequier A, Iniguez A, et al. Everolimus-
eluting stent vs. bare-metal stent in ST-segment
elevation myocardial infarction (EXAMINATION); 1
year results of randomized controlled trial. Lancet
2012;380(9852):1482-1490
16. SabateM,BrugalettaS,CequierA,etal.Clinicaloutcomes
in patients with ST-segment elevation myocardial
infarction treated with everolimus-eluting stents vs.
bare-metal stents (EXAMINATION); 5 year results of a
randomized trial; Lancet 2016; 387(10016):357-366
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A F M S Haque, S M M Rahman, S A Iqbal, NN Fatema, Z Khan
Department of Cardiology, Combined Military Hospital, Dhaka
Colonel A F M Shamsul Haque, FCPS (Med), Cardiologist
Brig Gen S M Mamunur Rahman, FCPS (Med), Cardiologist
Brig Gen Syed Asif Iqbal, FCPS (Med), Cardiologist
Brig Gen Nurunnahar Fatema, FCPS (Med), Paediatric Cardiologist
Col Zehad Khan, FCPS (Med), Consultant Cardiologist
Correspondence: Dr. Colonel A F M Shamsul Haque, FCPS (Med), FCPS (Card)
Department of Cardiology, CMH Dhaka, Bangladesh.
Email: afmshams@yahoo.com
Objective
Background
Methods
Results
Conclusion
The aim of this study was to evaluate the usefulness of TDI for the evaluation of Left ventricular filling
pressure.
Evaluation of LV diastolic filling pressure (LVEDP) provides important haemodynamic data that has
both diagnostic and prognostic importance especially in patients with coronary artery disease (CAD).
The mitral inflow velocity – to – mitral annulus velocity ratio (E/E’) by TDI (Tissue Doppler Imaging)
is a reliable means in CAD patients to determine the LV filling pressure. In this study non-invasive
echocardiographic TDI was compared with angiographic left ventricular end diastolic pressure (LVEDP)
to assess its correlation for its clinical application.
Consecutive forty patients scheduled for cardiac catheterization were studied with Doppler
echocardiography. Invasive measurement of LV pressures was obtained with cardiac catheters and the
LVEDP was measured. Doppler signals from the mitral inflow and TDI of the mitral annulus (medial
corner) were obtained. The ratio of mitral inflow velocity to early diastolic velocity of the mitral
annulus (E/E’) showed a good correlation with LVEDP. E/E’ <8 predicted normal LVEDP, and E/E’ >15
identified increased LVEDP. Variability was present in those with E/E’ of 8 to 15. A subset of those
patients with E/E’ 8 to 15 could be further defined by use of other Doppler data.
Tissue Doppler parameters were correlated with invasive (angiographic) parameters. Patients with E/E’
>15 can be classified as having elevated filling pressure. An E/E’ < 8 suggests normal filling pressure.
In the range of E/E’ of 8 to 15, other information must be applied. 4,7 In our study out of 40 patients 14
patients had E/E’ was > 15, 16 patients had E/E’ < 8 and rest of the patients had E/E’ in between 8 to
15. In the normal E/E’ group 75% had normal LVEDP and in the high E/E’ ratio group 71% patients had
elevated LVEDP. Variability was observed in patients who had E/E’ in between 8 to 15.
Doppler signals from the mitral inflow and TDI of the mitral annulus and its ratio provides good
assessment of LV filling pressures. However, accurate prediction of filling pressures requires
incorporating other parameters.
Introduction
Left ventricularend diastolic pressure(LVEDP) is an important
parameter that should be evaluated during management
of patients with heart disease. This is particularly true in
critically ill patients. Doppler echocardiography has become
the non-invasive and reproduciblemethod for the assessment
of systolic and diastolic function of the left ventricle and
also of the left ventricular filling pressure.1,6 Noninvasive
assessment by Doppler echocardiography provides a safe
and reproducible investigation comparable with invasive
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Haque A F M S, Rahman S M M, Iqbal S A et al Bangladesh J Cardiol, 2017; 07(01-02): 716-18
pressure monitoring. This study was designed to evaluate
the correlation of TDI variables for the assessment of LVEDP1.
The estimation of LV filling pressure is necessary in the
follow-up of disease progression and response to treatment
in most patients with heart disease and usually requires
invasive hemodynamic monitoring2. Diastolic dysfunction
is common in cardiac disease and contributes to the signs
and symptoms of heart failure. Doppler echocardiography
is widely used for the noninvasive assessment of diastolic
filling of the left ventricle (LV). The purpose of this study was
to evaluate the usefulness of TDI for the evaluation of Left
ventricular filling pressure.
Methods
Population
The study population of this prospective observational study
consisted of forty consecutive patients who were scheduled
for elective CAG in 2011 and 2012. Subjects 18 years or
older with sinus rhythm were eligible. Inclusion criteria
were CAD, Sinus rhythm and age>18 yrs. Exclusion criteria
were valvular heart disease, complete left bundle branch
block or complete right bundle branch block, pacemaker
dependence, cardiomyopathy, pericardial effusion and
post cardiac surgery. Demographic data including age, sex,
underlying disease, risk factors for coronary artery disease
and indications for catheterization were recorded.
Echocardiographic Measurements
Doppler studies were performed with GE Vingmed imaging
system by a combination of Doppler ultrasonography and
B-mode imaging in the Department of Cardiology, CMH
Dhaka. For mitral inflow evaluation, the sample volume of
PW Doppler was placed at the mitral valve tips using the
apical 4-chamber view3. The peak Doppler velocity of early
diastolic flow (E wave) was measured. With the PW TDI
program, a sample volume (5mm) was placed at the septal
corner of mitral annulus in the apical 4-chamber view. These
measurements allowed for obtaining the mitral inflow to
annulus ratio (E/E’).
Invasive Measurements
Fourty consecutive patients in sinus rhythm referred for
clinically indicated CAG made up the study group. Patients
were studied with Doppler echocardiography on the same
day before the procedure. CAG was performed through the
femoral approach. All recordings were obtained by a pigtail
catheter connected with a fluid-filled transducer before left
ventriculography by a polygraph machine. Theleft ventricular
end diastolic pressure (LVEDP) was obtained by computer
recording.
Results
Baseline characteristics
The data show that 22 (55%) of the cases were above 50 years
of age followed by 13 (32.5%) in the range of 41– 50 years and
5 cases (12.5%) were 40 or below. 35 patients were referred
* Figures in the parentheses indicate corresponding %.
for evaluation of angina and the remainder was referred for
symptoms of congestive heart failure.
Tissue Doppler Correlation with Invasive Parameters
Patients with E/E’>15 can be classified as having elevated
filling pressure. An E/E’< 8 suggests normal filling pressure.
In the range of E/E’ of 8 to 15, other information must be
applied.4,7 In our study out of 40 patients 14 patients had
E/E’ was >15, 16 patients had E/E’ <8 and rest of the patients
had E/E’ in between 8 to 15. In the normal E/E’ group 75% had
normal LVEDP and in the high E/E’ ratio group 71% patients
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Haque A F M S, Rahman S M M, Iqbal S A et al Bangladesh J Cardiol, 2017; 07(01-02): 716-18
had elevated LVEDP. Variability was observed in patients who
had E/E’ in between 8 to 15.
Discussion
This study supports that E/E’ is a reliable Doppler
echocardiographic parameter to estimate LVEDP2. The
noninvasive assessment of LV filling pressures can be an
important clinical tool. TDI of the mitral annulus during
diastole has been proposed as a new method for assessment
of cardiac function. Ommen, et al. reported that the
correlation of left ventricular diastolic pressure with the
medial annulus TDI were consistently equivalent or better
than the lateral annulus or the combinations of the medial
and lateral annulus4,7. In the present study, this combined
variable was a good Doppler predictor of elevated filling
pressure. However, there remains significant scatter with
E/E’, particularly with intermediate values of E/E’. We would
propose that the E/E’ ratio be used as the initial measurement
for estimation of LV filling pressures, particularly in those
patients. Patients with E/E’>15 can be classified as having
elevated filling pressure. An E/E’<8 suggests normal filling
pressure. In the range of E/E’ of 8 to 15, other information
must be applied. Ommen, et al. had similar results in their
study4. Further characterization of the intermediate E/E’
group is necessary.
Study Limitations
The motion of the mitral annulus is not entirely due to
myocardial contraction but rather is the summation of
contraction, rotation, and translation. The effects of each
of these may vary from patient to patient. The use of the
apical transducer position to sample the mitral annulus is an
attempt to minimize the translational and rotational effects
and focus on long-axis excursions of the LV cavity. The effects
of regional dysfunction on the motion of the annular plane
are not yet known.
Conclusion
Evaluation of LV diastolic filling pressure (LVEDP) provides
important haemodynamic data that has both diagnostic and
prognostic importance especially in patients with coronary
artery diseases. E/E’ is significantly correlated with LVEDP in
the population with coronary artery disease. Overall, the E/E’
ratio was the predictor of LV filling pressure.
References
1. Necla O, Kayak H K, Ali D, Umut A and Serdar A.
Determnation of left ventricular filling pressure by new
echocardiographic methods in patients with coronary
artery disease. Int J Cardiovasc Imaging 2008; 24:141–
147.
2. N Mansencal, E Bovier, T Joseph, J C Farcot, A Redheil,
P Lacombe, et al. Value of Tissue Doppler Imaging to
Predict Left Ventricular Filling Pressure in Patients with
Coronary Artery Disease. Echocardiography 2004; 21 (2):
133-138.
3. S Tongyoo, D Jakrapanichakul and N Chaowalit,
Estimation of Left Ventricular End- diastolic Pressure
by Tissue Doppler Imaging in Patients with Coronary
Artery Disease. Thai Heart Journal 2006; 19 (30): 105-
112.
4. Ommen SR, Nishimura RA, Appleton CP, Miller FA,
Redfield MM and Tajik AJ. Clinical utility of Doppler
echocardiography and tissue Doppler imaging in the
estimation of left ventricular filling pressure. Circulation
2000; 102:1788-94.
5. Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left
ventricle in health and disease: Doppler echocardiography
is the clinician’s Rosetta Stone. J Am Coll Cardiol 1997; 30:
8 –18.
6. Yamamoto K, Nishimura RA, Chaliki HP, et al.
Determination of left ventricular filling pressure by
Doppler echocardiography in patients with coronary
artery disease: critical role of left ventricular systolic
function. J Am Coll Cardiol 1997; 30:1819–1826.
7. Sherif F, Nagueh, Appleton P, Gillebert C, Paolo N, Otto A et
al. Recommendations for the Evaluation of Left Ventricular
Diastolic Function by Echocardiography. Journal of the
American Society of Echcardiography 2009; 108-118.
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Figure-1
Figure-2




Figure-3
Figure-4
Figure-5,6 &7
 Dominant R wave in infe-
rior leads indicate RVOT po-
sition of the lead.
 Early precordial transition
and lack of notching in the
inferior leads confirm septal
location of the lead.
 Morphology in lead I sug-
gest location of the RV lead
in the anterior part of the in-
terventricular septum.
Figure-8
Figure 1a
Figure 1b
Figure 2a
Figure 2b
Figure 3a
Figure 3b
Figure 3c
Figure 3d
Figure 4a
Figure 4b
Figure 4c
Figure 5
Figure 6
Figure-1
Figure-4
Figure-5
Figure-2 & 3
Figure-6
Figure-7
Figure-8
Figure-9
Figure-10
Figure-14
Figure-11
Figure-12
Figure-13
Figure-15
Figure-16










Table-1



Figure-1
Figure-2
Figure-3
Figure-4
Figure-5
Figure-6 Figure-9
Figure-7
Figure-8
Figure-10
Figure-11
Stress Echo and Mitral Regurgitation
Known Severe MR
1. Look for Exercise Capacity
2. Pulmonary HTN new/Worse
3. LV response
Mild or No MR and
Unexplained Dyspnea,
Pulmonary HTN
1. Exercise capacity
2. New or worsening MR
3. Worsening Pul HTN
4. LV response
Figure-12
Figure-13
Figure-14
Table-2
Class of
Recommendation
Class I
Class II
Class IIa
Class IIb
Class III
Evidence and/or general
agreement that a given
treatment or procdure
is beneficial, useful,
effective
Conflicting evidance
and/or a divergence
of opinion about the
usefulness/efficacy of
the given treatment or
Procedure
Weight of evidence/
opinion is in favour of
usefulness/efficacy.
Usefulness/efficacy is
less well established by
evidence/opinion
Evidence or general
agreement that the given
treatment or procedure is
not useful/effective, and
in some cases may be
harmful.
Is recommendied/
is indicated
Should be
considered
May be
considered
Is not
recommended
Definition Suggested
wording to use
Table-3
Patient A after treatment CXR of Patient A, CXR showing cardiomegalyFigure-1 Figure-2
Causes of Dilated Cardiomyopathy : Factors Identified as Causes of Myocardial Damage
Category Of Factors
Bacterial infections
Rickettsia
Parasites
Fungi
Neuromuscular disorders
Nutritional factors
Collagen vascular diseases
Hematological diseases
Coronary artery diseases
Drugs
Endocrine diseases
Metabolic disorders
Malformation syndromes
Coxsackie virus B, human immunodeficiency virus, echovirus, rubella, varicella, mumps, Epstein-Barr
virus, cytomegalovirus, measles, polio
Diphtheria, Mycoplasma, tuberculosis, Lyme disease, septicemia
Psittacosis, Rocky Mountain spotted fever
Toxoplasma, Toxocara, Cysticercus
Histoplasma, coccidioidomycoses, Actinomyces
Duchenne or Becker muscular dystrophies, Friedreich ataxia, Kearns-Sayre syndrome, other
muscular dystrophies
Duchenne or Becker muscular dystrophies, Friedreich ataxia, Kearns-Sayre syndrome, other
Kwashiorkor, pellagra, thiamine deficiency, selenium deficiency
Rheumatic fever, rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, Kawasaki disease
Thalassemia, sickle cell disease, iron deficiency anemia
Anomalous left coronary artery from pulmonary artery, infarction
Anthracycline, cyclophosphamide, chloroquine, iron overload
Hypothyroidism, hyperthyroidism, hypoparathyroidism, pheochromocytoma, hypoglycemia
Glycogen-storage diseases, carnitine deficiency, fatty acid oxidation defects, mucopolysaccharidoses
Cri-du-chat (cat-cry) syndrome
Table-1
ECG of Patient A, ECG showing normal sinus rhythm and LVHFigure-3
Echocardiography of Patient A, Echocardiography showing dilated LV and poor LV function.Figure-4
ECG on the day of admission showing widespread ST segment depression in both inferior and anterior leads (arrows).Figure-1
Coronary angiogram, anterior posterior (AP) view
showing 80-90% stenosis of left main (LM) coronary
artery involving ostium and mid part (arrow).
Coronary angiogram, LAO caudal view showing
critical ostial stenosis of LM coronary artery
(arrow).
Coronary angiogram, left anterior oblique
(LAO) cranial view showing critical LM coronary
stenosis with 30-40% stenosis at mid part of left
anterior descending artery (LAD), (arrows).
Coronary angiogram, LAO view showing
normal non dominant right coronary artery
(RCA) (arrow)..
Figure-2 Figure-4
Figure-3 Figure-5
ECG 2 years after CABG, appears normal.Figure-6
x-ray chest-huge cardiomegally
Non coronary sinus is hugely dilated with a
perforation in apex
Right atrium was opened ,about 4cm long
vegetation was found, was attached to the
connecting site of Non coronary aneurysmal sinus
Huge right atrial and right ventricular enlargement
Double ended pledgeted horizontal mattress suture was
applied to aneurysmal area around the perforation
excised vegetation
Figure-1
Figure-3
Figure-5
Figure-2
Figure-4
Figure-6
Double ended pledgeted horizontal mattress
suture was applied around the perforation site
in Right atrium
PTFE patch closure of aneurismal part of
Non coronary sinus
PTFE patch closure of aneurismal part of Non
coronary sinus
Figure-7
Figure-8
Figure-9
Angiographic view showing normal LM, about 70 to
75% narrowing of mLAD, 95% stenosis of d LCxFigure-1
Stent in m LAD before inflation
LM stenting covering dissection
Deployment of stent in mLADFigure-2
Figure 4 & 5
Figure-3
Expanded deployed stent in LM
Longitudinal stent collapse
After stenting flap seen in LM
Collapse stent in LM and deployed stent in mLAD
Figure-6
Figure-8
Figure-7
Figure-9
Almost normal RCA with TPM
Run of suction catheter
Antegrate flow after suction
Total Occlusion of mid left main
Figure-1
Figure-3
Figure-4
Figure-2
POBA done IABP for cardiogenic shock
POBA and dottering Slow flow
Figure-5 Figure-7
Figure-6 Figure-8
Slow flow disappeared
Normalisation of coronary flow after PCI
Total occlusion of LM before PCIFigure-9
Figure-10
Figure-11
After left subclavian puncture wire failed to advanced into right atrium due to PLSVC
PPI lead into right ventricle making a circular loop
into right atrium (AP view)
PPI lead into right ventricle (LAO view)
Figure-1 & 2
Figure-3 Figure-4
PPI lead into right ventricle (RAO view)Figure-5
V07 no1 2dec2017

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V07 no1 2dec2017

  • 1.
  • 2. BANGLADESH JOURNAL OF CARDIOLOGY EDITORIALBOARD CHIEF PATRON Dr. A. M. Shamim CHAIRMAN, EDITORIAL COMMITTEE Dr. Abduz Zaher, FRCP EDITORIAL BOARD Dr. A. K. Miah, PhD Dr. A. P. M. Sohrabuzzaman, FCPS Dr. Reyan Anis, FRCP Dr. Arun Kumar Sharma, FACC Dr. Md. Elias Ali, MD Dr. Lutfor Rahman, MS Dr. Md. Lokman Hossain, MS Dr. Mahbubul Islam, DA Dr. A. H. M. Abul Monsur, D Card EDITOR Dr. Baren Chakraborty, FRCP ASSISTANT EDITOR Dr. Mahbubor Rahman, FRCP Dr. Fahmida Zaman, FACC CHIEF EXECUTIVE Dr. (Brig Gen) Manzoor A. Mollah (Retd.) SECRETARY, PUBLICATION COMMITTEE Al-Emran Chowdhury EDITORIAL STAFF Kuddus Hawladar Nipun Md. Mizanur Rahman ADDRESS OF CORRESPONDENCE Editor, Bangladesh Journal of Cardiology, Labaid Cardiac Hospital, House 1, Road 4, Dhanmondi, Dhaka 1205, Bangladesh Tel : 88-02-8610793-8, 9670210-3, Fax : 880-02-9615497, Mobile : 01819425302, E-mail : baren_chakraborty@yahoo.com
  • 5. Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11 APM Sohrabuzzaman, F Zaman, N Mohammad, M E Ali, H Rahman, M Z Kabir, A Sohel, S S Pathan, M A Khayer, ASMN Islam, R J Tamanna Labaid Cardiac Hospital, Dhaka, Bangladesh Objective Background Methods Results Conclusion The objective of this trial was to see level of periprocedural cardiac biomarker as evidence of myocardial necrosis using Bivaluridin versus Abciximab in patients who were undergoing PCI in a tertiary care cardiac hospital. Prevention of hemorrhagic complications has emerged as a priority in patients undergoing PCI in addition to suppressing periprocedural ischemia. In patients with stable angina and NSTEMI, Bivalirudin has been shown to result in similar rates of composite ischemia as Heparin plus Abciximab, while significantly reducing major bleeding. Does Bivalirudin cause less myocardial necrosis as evidenced by Troponin I and CKMB in patients undergoing PCI is unknown. A prospective all comers’ intention to treat patients was included in the study. The laboratory was blinded about the study drugs of the patients. The use of drugs was in the discretion of the operator and was decided upon the purchasing capacity of the patients. Study period was January 2013 to December 2015. The patients included with STEMI >20 mins and <24 hours in duration. Patients with NSTEMI, Unstable angina and chronic stable angina were included. Principal exclusion criteria were any contraindication to the use of Bivalirudin or Abciximab. The study medications were UFH (5000 unit IV; subsequent boluses titrated to ACT 200-250secs); Bivalirudin (Bolus 0.75 mg/kg IV, infusion 1.75 mg/kg/h) during and 4 hours post procedure; or Abciximab (Bolus: 0.25mg/kg and infusion: 0.125 mcg/kg/min) during and 12 hours post procedure; Antiplatelets: Aspirin 300mg and Clopidogrel 600mg or Prasugrel 60mg preprocedure. Troponin I & CKMB were measured as a biochemical marker of myocardial necrosis at Pre-procedure (base line), Just after procedure (0 hours), 8 hours, 16 hours and 24 hours post procedure. Ninety three patients (male 80, female 13) age ranges from 31 to 80 years (mean ±SD:53.83±11.52) were enrolled. PCI was done in all cases. All patients got aspirin 300mg and clopidogrel 600mg or prasugrel 60mg preprocedure and Unfractionated Heparin (5000 unit IV*; subsequent boluses titrated to ACT 200-250secs) during procedure. Bivalirudin was used in 69 (74.2%) and Abciximab in 24 (25.8%) of patients. Mean difference of Troponin I in Bivalirudin and Abciximab group at different times did not reveal statistical significance (Figure 1); but CK-MB level did better outcome (Figure 2). In this small scale trial of patients undergoing PCI in a single centre compared Abciximab and Bivalirudin to prevent myocardial necrosis as evidenced by Troponin I & CKMB resulted non-inferior outcome with Bivalirudin. Introduction An invasive strategy of coronary angiography, with revascularization when appropriate is recommended for high-risk patient who have an acute coronary syndrome (ACS).1,2,3 Anti-coagulation is a mainstay of treatment for patient with ACS and is recommended by international guidelines.4,5,6 Prevention of hemorrhagic complications has emerged as a priority in patients undergoing PCI in addition to suppressing peri-procedural ischemia. Identification of most appropriate adjunctive antithrombotic therapy before, APM Sohrabuzzaman, MD, FCPS, Senior Consulatant Fahmida Zaman, FACC, Consultant Nur Mohammad, MD, Consultant Md Elias Ali, MD, Senior Consultant Habibur Rahman, D Card, Consultant Mohammad Ziaul Kabir, D Card Consultant Atiquzzaman Sohel, D Card, Consultant Shiblee Sadik Pathan, D Card Consultant Mohammad Abul Khayer, D Card, Consultant ASM Nazmul Islam, D Card, Consultant Rownak Jahan Tamanna, MD, Consultant Correspondence: A P M Sohrabuzzaman, MD, FCPS Director, Cardiac Cath Lab & Heart Rhythm Services, Labaid Cardiac Hospital, Professor, School of Health Science, State University of Bangladesh, Dhaka, Bangladesh. e mail: aicd.pace@yahoo.com Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 6. Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11 during, and after percutaneous coronary intervention (PCI) has been the target of extensive research for the past three decades.1 Intravenous Heparin is traditionally regarded as the standard anticoagulant strategy to prevent peri-procedural ischemic events during PCI. Moreover it has hypersensitivity reaction, Bleeding complication, Heparin induced thrombocytopenia (HIT), transient elevation of serum aminotransferase and hyperkalemia. Because of large intra and interindividual variability and indirect mechanism of action of Heparin alternative option have been developed.4,7,8 Abciximab is a glycoprotein IIb/IIIa inhibitor (GPI) with potent platelet antiaggregative effects.1,9 Although the administration of Abciximab during PCI was not associated with a clinical benefit in patient in stable condition who were given loading dose of clopidogrel before intervention.1,10,11 Howeverpotent antiplatelet effectcausesthrombocytopenia and increase risk of bleeding, which in turn is strongly correlated with an unfavorable prognosis.1,12 Bivaluridin is a direct thrombin inhibitor that has increasingly been used in patient undergoing PCI since the time that the first study comparing Heparin plus a glycoprotein IIb/ IIIa inhibitor with Bivaluridin the randomized evaluation in PCI Linking Angiomax to Reduced Clinical Events-2 (REPLACE-2) trial suggest noninferiority of the Bivaluridin strategy.13 A recent randomized controlled trial (RCT) comparing Bivaluridin with Heparin alone, however found a significant increase in the rate of myocardial infarction (MI) with Bivaluridin and no difference in bleeding events, suggesting that the diverging result among RCTs might be influenced by the concomitant administration of a GPI with Heparin. In patients with stable angina and Non ST Elevation MI (NSTEMI), Bivalirudin has been shown to result in similar rates of composite ischemia as Heparin plus Abciximab, while significantly reducing major bleeding.4,14 Peri-procedural myocardial necrosis causes decrease cardiac function and has adverse long term clinical outcome. In this era none of the authors show interest to find out evidence of myocardial necrosis during and after procedure. All the authors have interest to see clinical outcome, bleeding manifestation and thrombotic events in recent past. Available laboratory evidence of myocardial necrosis in Bangladesh are raise of creatinine kinase MB (CK-MB) and troponin-I. Does Bivaluridin cause less myocardial necrosis as evidenced by Troponin I and CK-MB in patientswho undergone PCI is unknown? The objective of this trial was to see level of periprocedural cardiac biomarker as evidence of myocardial necrosis using Bivaluridin versus Abciximab in patients who were undergoing PCI in a tertiary care cardiac hospital. Methods A prospective all comers intention to treat patients was included in the study. The laboratory was blinded about the study drugs. The use of drugs was in the discretion of the operator and was decided upon the purchasing capacity of the patients. Study period was January 2013 to December 2015. The patients who got the study drugs were included. Principal exclusion criteria were any contraindication to PCI and use of Bivalirudin or Abciximab. Prior thrombolytic, current use of warfarin, history of bleeding diathesis or known coagulopathy (including HIT), or will refuse blood transfusions, history of intracerebral mass, aneurysm, AVM, or hemorrhagic stroke; stroke or TIA within 6 months or any permanent neurologic deficit; GI or GU bleed within 2 months, or major surgery within 6 weeks; recent or known plateletcount<100,000cells/mm3orheamoglobin<10g/dL, Planned elective surgical procedure that would necessitate interruption of thienopyridines during the first 6 months post enrollment. The study was approved by institutional review board or ethics committee and all patients gave written informed consent. Patient was randomly assigned, in an open-lebel fashion according to the purchasing capacity of the study drugs. The patients were divided into two groups Bivalirudin versus Abciximab group. The study medicatons were Antiplatelets: Aspirin 300mg and Clopidogrel 600mg or Prasugrel 60mg preprocedure and UFH (5000 unit IV; subsequent boluses titrated to ACT 200-250secs) during procedure in both groups. In Bivalirudin group, Bivalirudin (Bolus 0.75 mg/kg IV, infusion 1.75 mg/kg/h) during and 4 hours post procedure and in Abciximab group, Abciximab (Bolus: 0.25mg/ kg and infusion: 0.125 mcg/kg/min) during and 12 hours post procedure. Troponin I & CKMB were measured as a biochemical marker of myocardial necrosis at Pre-procedure (base line), just after procedure (0 hours), 8hours, 16 hours and 24 hours post-procedure. After collection of laboratory data primary analysis were performed for all patient who underwent randomization according to intention to treat principle. We used SPSS version 15 for statistical analysis. Result was expressed as mean difference. Results Total Ninety three patients (male 80, female 13) age ranges from 31 to 80 years, Median age 54 years. Patients were enrolled during the period January 2013 to December 2015. All patients had PCI as intention treat purpose. All patients got aspirin 300mg and clopidogrel 600mg or prasugrel 60mg preprocedure and Unfractionated Heparin (5000 unit IV bolus; subsequent boluses titrated to ACT 200-250 secs) during procedure. Bivalirudin was used in 69 (74.2%) and Abciximab in 24 (25.8%) of patients. Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 7. Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11 Among 93 patients 42 (45.2%) had primary PCI, 32(34.4%) had STEMI, 9(9.7%) had NSTEMI, 6(6.5%) had unstable anigina, Table-1 Table-3 Table-2 Diagnosis of the study patients (n=93) Comparison of mean Troponin I (ng/ml) level in Bivalirudin and Abciximab group at different times (n=93) Type of vessels of the study patients (n=93) 4(4.3%) had Chronic stable angina. (Table-1) Vessels involvement during PCI, single vessel 77 patients, double vessel 14 patients, and triple vessel 2 patients. Among the single vessel PCI, LAD were 36(38.7%), RCA were Diagnosis Number Percentage Primary 42 45.2 STEMI 32 34.4 NSTEMI 9 9.7 UA 6 6.5 CSA 4 4.3 19.3 28.6 34.6 35.1 31.4 18.7 69.9 40.7 36.8 35.7 Vessel Name of Vessels Number Percentage Single LAD 36 38.7 RCA 32 34.4 LCX 9 9.7 Double LAD+LCX 4 4.3 LAD+RCA 8 8.6 LCX+RCA 2 2.2 Triple LAD+LCX+RCA 2 2.2 32 (34.4%), LCX were 9 (9.7%) were done (Table-2) In Bivaluridin vs Abciximab group base line troponin I (mean) was 19.3 vs 18.7, at 0 hours- 28.6 vs 69.9, at 8hours-34.6 vs 40.7, at 16 hours-35.1 vs 36.8 and after 24 hours-31.4 vs 35.7. (Table-3) Whereas CK-MB (mean) in Bivaluridin vs Abciximab group at base line 98 vs 77, at 0 hours 135 vs 239, at 8hours 159 vs 250, at 16 hours-110 vs 148 and after 24 hours-84 vs 112. (Table-4) In this study we found slightly higher troponin I level in Abciximab group at different times after PCI within 24 hours of observation but it was not statistically significant (Figure 1) and much higher in CK-MB level in Abciximab group at different times but did not reveal statistical significance (Figure 2). In this small scale study Bivaluridin resulted non inferior outcome to prevent myocardial necrosis asevidenced by Troponin I and CKMB with Abciximab. Discussion In this small study we had used Bivlirudin in 74% cases and Abciximab in 26% cases. We found less myocardial necrosis in CKMB level only in Bivalirudin group than that of Abciximab Figure-1 Mean difference of Troponin I Status by Bivalirudin and Abciximab used Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 8. Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11 Figure-2 Mean difference of CKMB status by Bivalirudin and Abciximab used Table-4 Comparison of mean CK-MB (IU/ml) level in Bivalirudin and Abciximab group at different times (n=93) Group Baseline 0 hours 8 hours 16 hours 24 hours Bivaluridin(n=69) 98 135 159 110 84 Abciximab(n=24) 77 239 250 148 112 group during PCI for 24hours observation. Bivalirudin is cheaper than Abciximab in Bangladesh. So patient were more capable to purchase Bivalirudin than Abciximab.Hence number of patient were high in Bivaluridin group. Myocardial infarction resulting elevation of biomarkers at study entry make it difficult to detect myocardial injury after the procedure. To diagnose procedure related myocardial necrosis at least 50% increase above the level of biomarker recorded before procedure.1 In HORIZONS-AMI study they found that Bivaluridin was superior to Abciximab and Heparin in patient undergoing primary PCI for STEMI.1,11 Bivaluridin is also superior in patients with acute NSTEMI shown in ACUITY clinical trial.1,12 There were no significant differences in the peak creatine kinase level or creatine kinase MB fraction between the Bivalirudin group and the group that received Heparin plus Abciximab.15 In our study Abciximab group had higher cardiac biomarker level. This was might be due to higher myocardial necrosis during procedure or acute coronary events like acute STEMI patients were more in this study. Before any comment on Abciximab that causes more periprocedural myocardial necrosis randomization should be done in 1:1 fashion and preprocedure diagnosis should be same in both groups. Treatment with Abciximab may decrease the short and long term risk of death 15,16,17 and these agents are used in more than 90% of patient who undergo primary PCI in the United States and in the majority of such patients in Europe.15,18,19 But in this subcontinent specially South Asian countries Bivalirudin is more costeffective than Abciximab.In our study we found that Bivalirudin is non-inferior than Abciximab in periprocedural myocardial necrosis. There were several strength of this study including there was no sponsor of this study and laboratory was completely blind about patient’s diagnosis and medications used. On the other hand few limitation also we advocate these were; randomization was not 1:1 fashion, baseline diagnosis were not unique, base line cardiac biomarker were not same in all cases. Moreover we did not focus on bleeding menifestation, stent thrombosis, periprocedural cardiac events. In conclusion this small scale, prospective all comers intention to treat trial of patients undergoing PCI in a single centre showed that Bivalirudin was non-inferior to that of Abciximab to prevent periprocedural myocardial necrosis as evidenced by Troponin I and CKMB. Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 9. Sohrabuzzaman APM, Zaman F, Mohammad N et al Bangladesh J Cardiol, 2017; 07 (01-02): 707-11 Reference 1. Kastrati A, Neumann F J, Schuiz S, Massberg S, Byrne R A, Ferenc M et al. Abciximab and Heparin versus Bivalirudin for non-ST-Elevation Myocardial Infarction. N Engl J Med 2011; 365:1980-89 2. Wright RS, Anderson JL, Adams CD, et al. 2011 ACCF/AHA focused update of the guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline): a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation 2011;123:2022-2060 3. Bassand JP, Hamm CW, Ardissino D, et al. Guidelines for the diagnosis and treatment of non-ST-segment elevation acute coronary syndromes. Eur Heart J 2007; 28:1598-1660 4. Navarese EP, Schulze V, Andreotti F, Kowalewski M, Kołodziejczak M, Kandzari DE, et al Comprehensive meta-analysis of safety and efficacy of bivalirudin versus heparin with or without routine glycoprotein IIb/IIIa inhibitors in patients with acute coronary syndrome. JACC Cardiovasc Interv. 2015;8(1 ):201-213. 5. O’Gara P T, Kushner FG, Ascheim DD, et al. 2013 ACCF/ AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 61:e78–e140 6. Hamm C W, Bassand JP, Agewall S et al.(2011) ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST- segment elevation: The Task Force for the management of acute coronary syndromes (ACS) in patients presenting without persistent ST-segment elevation of the European Society of Cardiology (ESC). Eur Heart J 32:2999–3054 7. Steinberg DH, Shah P, Kinnaird T et al.(2008) Bleeding risk and outcomes of Bivalirudin versus Glycoprotein IIb/IIIa inhibitors with targeted low-dose unfractionated Heparin in patients having percutaneous coronary intervention for either stable or unstable angina pectoris. Am J Cardiol 2008;( 102):160–164 8. Navarese EP, De Luca G, Castriota F, et al. Low- molecular-weight heparins vs. unfractionated heparin in the setting of percutaneous coronary intervention for ST-elevation myocardial infarction: a meta-analysis. J Thromb Haemost 2011; 9:1902–1915. 9. Neumann FJ, Hochholzer W, Pogatsa-Murray G, Schomig A, Gawaz M. Antiplatelet effects of abciximab, tirofiban and eptifibatide in patients undergoing coronary stenting. J Am Coll Cardiol 2001;37:1323-1328 10. Kastrati A, Mehilli J, Schuhlen H, et al. A clinical trial of abciximab in elective percutaneous coronary intervention after pretreatment with clopidogrel. N Engl J Med 2004;350:232-238 11. Mehilli J, Kastrati A, Schuhlen H, et al. Randomized clinical trial of abciximab in diabetic patients undergoing elective percutaneous coronary interventions after treatment with a high loading dose of clopidogrel. Circulation 2004;110:3627-3635 12. Ndrepepa G, Berger PB, Mehilli J, et al. Periprocedural bleeding and 1-year outcome after percutaneous coronary interventions: appropriateness of including bleeding as a component of a quadruple end point. J Am Coll Cardiol 2008;51:690-697 13. Lincoff AM, Bittl JA, Harrington RA, et al. Bivalirudin and provisional glycoprotein IIb/IIIa blockade compared with heparin and planned glycoprotein IIb/IIIa blockade during percutaneous coronary intervention: REPLACE-2 randomized trial. JAMA 2003;289:853-863. 14. Shahzad A, Kemp I, Mars C, et al. Unfractionated heparin versus bivalirudin in primary percutaneous coronary intervention (HEAT-PPCI): an open-label, single centre, randomised controlled trial. Lancet 2014;384:1849– 1858. 15. Gregg WS, Bernhard W, Giulio G, Jan ZP, Bruce RB, Dariusz D et al Bivelirudin during Primary PCI IN Acute Myocardial Infarction. N Engl J Med 2008; 358:2218- 2230. 16. De Luca G, Suryapranata H, Stone GW, et al. Abciximab as adjunctive therapy to reperfusion in acute ST-segment elevation myocardial infarction: a meta-analysis of randomized trials. JAMA 2005;293:1759-1765 17. Kandzari DE, Hasselblad V, Tcheng JE, et al. Improved clinical outcomes with abciximab therapy in acute myocardial infarction: a systematic overview of randomized clinical trials. Am Heart J 2004;147:457- 462 18. Dauerman HL, Frederick PD, Miller D, French WJ. Current incidence and clinical outcomes of bivalirudin administration among patients undergoing primary coronary intervention for stent thrombosis elevation acute myocardial infarction. Coron Artery Dis 2007;18:141-148 19. Fox KA, Steg PG, Eagle KA, et al. Decline in rates of death and heart failure in acute coronary syndromes, 1999-2006. JAMA 2007;297:1892-1900 Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 10. Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15 1M Rahman, 1M E Ali, 1S Nazneen, 1S S Pathan, 1M A Khayer, 2M A Hossain, 3S M D Hossain, 4R Islam 1. Labaid Cardiac Hospital, Dhaka 2. Bangladesh Medical College, Dhaka 3. Khulna Medical College, Khulna 4. Uttara Adhunik Medical College, Dhaka Objective Background Methods Results Conclusion The aim of this study is to evaluate the feasibility, efficacy and outcomes of primary percutaneous coronary intervention (PPCI) done in Labaid Cardiac Hospital (LCH) from 2004 to 2017. Primary PCI is the preferred method of treatment of Acute ST segment Elevation Myocardial Infarction (STEMI) in a PCI-capable hospital within 12 hours of onset of ischemic type chest discomfort. A full- time dedicated heart team is required to accomplish this goal. Since the inception of LCH in 2004 only one patient underwent PPCI in first year. Since then, the number of patients has been increasing significantly. Total 697 patients underwent PPCI upto August, 2017. Most of them were followed up clinically and a few angiographically. 25 patients (3.58%) died during the index hospitalization, 19 patients (2.72%) developed stent thrombosis of whom acute stent thrombosis occurred in 7 patients, subacute thrombosis occurred in 8 patients and remaining 4 patients developed late stent thrombosis. Major bleeding occurred in 30 patients (4.30%) required blood transfusions. All of them had femoral artery puncture approach. Only 2 patients (0.28%) developed intracranial hemorrhage which was managed conservatively. Primary PCI is a very effective, life-saving method of treatment of acute STEMI, reduces overall major adverse cardiovascular events (MACE). Labaid Cardiac Hospital is a major center in the country as a round the clock PCI-capable superspeciality hospital. Introduction Acute myocardial infarction is the leading cause of sudden cardiac death, cardiogenic shock, ischemic cardiomyopathy, congestive heart failure and arrhythmias. It poses a great threat to modern medicine after invention of antibiotics and reasonable control of communicable diseases. Increasing incidence of diabetes mellitus, hypertension, dyslipidemias and consumption of tobacco are the major risk factors for ischemic heart disease. Sedentary modern urban life style, air and sound pollutions, food adulteration, excess social and family stress contribute to the development of cardiovascular diseases. On top of these global factors, South Asian population are facing a different genetic/ Mahbubor Rahman, FRCP, Senior Consultant and CCU Incharge Md Elias Ali, MD, Senior Consultant Shaheena Nazneen, D Card, Consultant Shiblee Sadik Pathan, D Card, Consultant Mohammad Abul Khayer, D Card, Consultant Md Amir Hossain, FCPS, Associate Professor of Cardiology S M Delwar Hossain, D Card, Assisstant Professor of Cardiology Rakibul Islam, FACC, Professor of Cardiology Correspondence: Mahbubor Rahman, FRCP Labaid Cardiac Hospital Room 313, House 1, Road 4 Dhanmondi R/A, Dhaka 1205, Bangladesh. Phone: +8801716914634, email: mahbubordr@gmail.com Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 11. Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15 geographical pattern of narrow, diffuse coronary artery diseases. After introduction of PPCI, the outcomes of STEMI have been improved a lot. The mortality and morbidity have been decreased significantly. There are many obstacles in widespread use of PPCI in Bangladesh including poor public hospital facilities, higher cost in private hospitals, lack of insurance coverage, less number of PCI capable hospitals, lack of infrastructures at peripheral cities, lack of trained manpower, lack of public awareness, unbearable traffic congestions in the capital city and many more. Despite these hurdles, LCH introduced PPCI in 2004 when it started it’s journey. Since then, number of PPCI has been increasing steadily. Methods We started PPCI in 2004 and did only one case in that year. In the year of 2016 we did PPCI on 162 patients. Upto August 2017, total number of PPCI has reached to 697. Of them 520 (74.60%) were male, age difference between 21 years and 91 years (Mean age 58.5 years, SD 6.7), 230 (32.99%) patients had diabetic, 354 (50.78%) patients were hypertensive, 380 (54.51%) patients were current male smokers, 321 (46.05%) were dyslipidemic. Average duration of ischemic type chest pain before reaching the emergency department was 6.5 hours, mean door to balloon time was 62 minutes, SD 9. Upto 2011 (total 95 patients, 13.62%) GP IIb/IIIa inhibitors (abciximab and Eptifibatide) were used as adjunctive anti- platelet agents. After the publication of results of HORIZON AMI trial, the scenario was dramatically changed. Since then, most of our patients (602 patients, among them 500 patients (83.05%) received bivalirudin. Results We have followed up 615 patients (88.23%) mostly clinically and a few angiographically. Clinical follow up includes telephonic communication and out patient basis ECG, Echocardiographic assessment, biochemical evaluation, nuclear imaging of ischemia and viability of myocardium. Among 697 patients, 352 (50.50%) had infarct related single vessel disease (SVD), 190 (27.85%) patients had double vessel disease (DVD) and 132 patients (18.93%) had triple vessel disease (TVD). Only 23 patients (3.29%) had severe left main disease, 58 patients (8.32%) presented with cardiogenic shock of whom 12 patients (20.68%) died during the index hospitalization. Left anterior descending (LAD) artery was involved in 56% cases, Right Coronary Artery (RCA) was involved in 30% cases and in 10.61% cases left circumflex artery (LCX) was involved. Initial success rate of opening the infarct related artery was 96%. Total 25 patients (3.58%) died (of which 12 patients were in cardiogenic shock) during the index hospitalization. Ten patients died on the Cathlab table from cardiac arrest, mostly due to ventricular asystole. Only ten patients received intra- aortic balloon pump (IABP). All of them were in cardiogenic shock. Two patients survived who received IABP support. Nineteen patients (2.72%) developed stent thrombosis within 5 years, of whom 7 patients had acute stent thrombosis (within 24 hours), 8 patients had subacute stent thrombosis (within 30 days) and 4 patients had late and very late stent thrombosis. Upto 2012, 53% patients received bare metal stent (BMS) and 47% patients received drug eluting stent (DES) mostly of which were first generation DES. After that trend had changed, new generation DES with better outcomes facilitated their use. After 2015, 90% patients undergoing PPCI received DES. Slow flow/no flow phenomenon is a great challenge for interventional cardiologists. Apparent successful opening of the occluded artery doesn’t ensure the microcirculation and functionalrescueofischemicmyocardium.Latepresentations, huge thrombus burden, excessive manipulation of the lesion, use of thrombus aspiration catheter, predilatation with a big/used balloon, mismatch between artery and stent sizes, underapposed or edge dissections are the principal causes of slow/no flow phenomenon. Intracoronary administration of adenosine, diltiazem, nitroprusside, trinitrate, and adjunctive bivalirudin are the pharmacotherapies that help to overcome this problem in most cases. Auto reperfusion is an old method to deal with the problem but there is no substantial evidence to support its regular use. Major bleeding occurred in 30 patients (4.30%) required blood transfusions. Most of them received GP IIb/IIIa inhibitors. After the growing use of Bivalirudin incidence of major bleeding has significantly reduced. Only 2 patients (0.28%) developed intracranial hemorrhage, both of them received abciximab. Discussion Acute STEMI is the leading cause of death in coronary care units throughout the world. It has a tremendous impact on short and long term mortality and morbidity. With the new development of techniques and adjunctive anti-thrombotic agents, it’s outcomes have been improving rapidly and new trials have been directing the clinicians to a deeper insight of the disease and its management. Acute myocardial infarction is classified on the basis of the presence or absence of ST-Segment Elevation on the ECG and is further classified into six typesof infarctionsdue to coronary atherothrombosis (type 1), infarction due to a supply demand mismatchthatisnottheresultofacuteatherothrombosis(type 2), infarction causing sudden death without the opportunity for biomarker or ECG confirmation (type 3), infarction related to a PCI (type 4a), infarction related to thrombosis of a coronary stent (type 4b), and infarction related to coronary artery bypass grafting (CABG) surgery (type 5)1. Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 12. Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15 For patients with STEMI, urgent reperfusion of the culprit occluded artery often achieved via PPCI, reduces mortality and other MACE. Adjunctive antithrombotic antiplatelet therapies are used during PPCI to reduce MACE rates. The most commonly used agents include unfractionated heparin (UFH) or low molecular weight heparin (LMWH) plus/minus glycoprotein IIb/IIIa inhibitors (GPI). These agents reduce the rates of pre-procedural ischemic and thrombotic events, thoughthese benefitscomeat thecost ofincrease in bleeding complications. Bivalirudin is a direct thrombin inhibitor with a short half-life and linear pharmacokinetics, which results in a predictable serum concentrations and anticoagulant effect. Bivalirudin has emerged as an efficacious and safe alternative to heparin plus GPI both in stable coronary artery disease and acute coronary syndrome patients.2 In our practice, we usually load the patient with 3000 units IV UFH before the procedure. After getting the angiographic views of the culprit lesion, we give the initial 0.75mg/ kg bolus dose of Bivalirudin followed by an infusion at a rate of 1.75mg/kg/hr for two hours after the completion of PCI. Target activated clotting time (ACT) is around 300 seconds. All patients receive 300mg non-enteric coated aspirin as a loading dose and 75-150mg to be continued as a maintenance dose. In addition to aspirin an oral P2Y12 inhibitor (Clopidogrel, Prasugrel or Ticagrelor) is given to all patients. Clopidogrel was loaded at 600mg and continued at 75mg daily for at least one year. There is a growing concern of Clopidogrel resistance in recent years. A large ongoing trial [TAILOR-PCI (Tailored Anti Platelet therapy following PCI)] is evaluating the use of pharmacogenetic testing at the time of PCI to improve ischemic outcomes with Clopidogrel in patients with acute coronary syndromes or stable coronary artery disease.3 The preferred P2Y12 inhibitors are Prasugrel [60mg p.o. loading dose, and 10mg maintenance dose once daily or Ticagrelor ( 180mg p.o.loading dose and 90mg maintenance dose twice daily )]. These drugs have a more rapid onset of action, greater potency, and are superior to Clopidogrel in clinical outcomes. 4, 5 In our practice, we shifted from clopidogrel to prasugrel gradually. Loading with prasugrel creates a new problem. It has a rapid onset of action and a prolonged half-life (5-7 days). Sometimes patients with STEMI have coronary anatomy not suitable for PPCI and are good candidates for urgent CABG surgery, but loading with prasugrel before the procedure makes difficult to do urgent CABG surgery as it poses a greater chance of bleeding. Prasugrel is also contraindicated in patients with previous stroke/transient ischemic attack and its use is generally not recommended in patients aged more than 75 years or in patients with lower body weight (less than 60kg) as it was not associated with net clinical benefits in these outsets. In that case prasugrel is used in these patients a reduced dose (5 mg).6 Neither prasugrel nor ticagrelor should be used in patients with a previous hemorrhagic stroke, in patients on oral anticoagulants or in patients with moderate-to-severe liver disease. Cangrelor is a potent IV reversible P2Y12 inhibitor with a rapid onset and offset of action. Cangrelor may be considered in patients not pre-treated with oral P2Y12 receptor inhibitors at the time of PCI or in those who are considered unable to absorb oral agents. 7 Considering all these advantages and disadvantages we have our own practice protocol. We routinely load with 180mg Ticagrelor, followed by 90mg twice daily. Due to higher costs and fear of poor compliance, we do a pharmacogenetic test for clopidogrel after one month. If the test is indicating normal response to clopidogrel, we shift the patients from ticagrelor to clopidogrel. If clopidogrel is resistant, we shift the patients from ticagrelor to prasugrel at maintenance dose. In addition to antiplatelet therapies, all patients also received higher intensity statin therapy, mostly 40 mg atorvastatin as a loading dose and continued as maintenance dose at least one year as high intensity therapy to keep the LDL level below 70 mg/dl. Recent trials on aspiration thrombectomy downgrade its routine use. It is now a Class III recommendation.8 Three recent randomized clinical trials, namely, Intracoronary Abciximab and Aspiration Thrombectomy in Patients With Large Anterior Myocardial Infarction (INFUSE-AMI) trial, Thrombosis Aspiration During ST-Segment Elevation Myocardial Infarction (TASTE) trial, and Trial Routine Aspiration Thrombectomy With PCI vs. PCI Alone in Patients With STEMI (TOTAL ) have demonstrated lack of evidence of benefit from routine use of thrombectomy. 9 , 10, 11, 12 Up to 2015, here in Labaid Cardiac Hospital, we used routine manual thrombectomy device almost in every case without knowing long-term benefits. Now we do not use aspiration device routinely. In most of the cases, after passing the PTCA wire, the distal landing zone is usually evident. So direct stenting can be done without muchdifficulties. When evenafter crossing the lesion , distal vessel is not visible, a low profile small balloon is enough to visualize the distal landing zone. As the price of stents has come down significantly globally, now in majority cases we use new generation drug eluting stents. 2017 ESC guidelines for the management of acute myocardialinfarction inpatientspresentingwithST-Segment elevation have recommended stenting with new generation DES over BMS for PPCI. 13, 14, 15 , 16 Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 13. Rahman M, Ali M E, Nazneen S et al Bangladesh J Cardiol, 2017; 07(01-02): 712-15 Conclusion Acute STEMI is a life threatening cardiac emergency that requires urgent revascularization. PPCI is the treatment of choice for opening the infarct-related occluded artery within 12 hours of onset of ischemic type chest discomfort. Non- culprit significant lesions can be treated at the same setting or stage PCI can be planned during the index hospitalization. All significant lesions must be treated in patients with cardiogenic shock in same setting. Non-enteric coated aspirin 300mg loading dose should be given to all patients and 75-150 mg maintenance dose should be continued. New generation potent P2Y12 inhibitor (Prasugrel or Ticagrelor) loading dose followed by maintenance dose should be given to all patients. High dose Statin (eg Atorvastatin 40-80mg) loading dose should be given to all patients. Heparin (UFH) 3000 units bolus should be given to all patients before the procedure. Bivalirudin IV bolus and maintenance dose should be given to all STEMI patients during the procedure. Thrombus suction is not a routine recommendation. Direct stenting with a DES is a preferred option. Otherwise a low profile small balloon can be useful to visualize the distal landing zone. Routine use of intracoronary adenosine is beneficial to combat slow/no flow and improve microcirculation. References 1. JeffreyL Andersonand David AMorrow.AcuteMyocardial Infarction: Review article by Edward W. Campion N Engl J med 2017: 376 2053-2064 May 25, 2017. 2. Ashish Shah and Dmitriy N Feldman. Outcome of the HORIZONS-AMI trial: Bivalirudin enhances long- term survival in patients with ST-elevation myocardial infarction undergoing angioplasty. Vasc Health Risk Manag. 2012; 8: 115-123. 3. Mehta SR, Tanguay JF et al. CURREN-OASIS Trial Investigators. Lancet 2010; 376 (9748): 1233-1243 4. Wiviott SD, Braunwald E et al. TRITON-TIMI 38 investigators. Prasugrel versus Clopidogrel in patients with acute coronary syndromes. N Engl Med 2007; 357 (20): 2001-2015 5. Wallentin L. Becker R.C, Budaj A et al. PLATO Investigators. Ticagrelor versus Clopidogrel in patients with acute coronary syndromes. N Engl J Med 2009; 361 (11) :1045 -1057 6. Roe MT, Armstrong PW, Fox KA et al. TRILOGY ACS investigators. Prasugrel versus Clopidogrel for acute coronary syndromes without revascularization. N Engl J Med 2012; 367 (14): 1297-1309. 7. Bhatt DL, Stoone GW, Mahaffey et al. CHAMPION PHOENIX Investigators. Effect of platelet inhibition with Cangrelor during PCI on ischemic events. N Engl J Med 2013; 368 (14): 1303-1313. 8. Levine GN, Bates ER, Blankenship JC, et al. 2015 ACC/ AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for patients with ST-Elevation Myocardial infarction. J Am Coll Cardial 2016; 67: 1235- 50. 9. Stone GW, Maehara, Witzenbich B, et al. Intracoronary abciximab and aspiration thrombectomy in patients with Large anterior myocardial infarction: the INFUSE- AMI randomized trial. JAMA 2012; 307: 1817-26. 10. Fröbert O, Lagerqvist B, Olivecrona GK, et al. Thrombus aspiration during ST-segment myocardial infarction. N Engl J Med 2013; 169:1587-97 11. Laserqvist B, Fröbert O, Loivecrona GK, et al. Outcomes 1 year after thrombus aspiration for myocardial infarction. N Engl J Med 2014; 271:1111-20 12. Jolly SS Cairns JA, Yusuf S, et al. Randomized trial of primary PCI with or without routine manual thrombectomy. N Engl J Med 2015; 372:1389-98 13. Kastrati A, Dibra A, Spaulding C, Laarman GJ, et al. meta- analysis of randomized trials on drug-eluting stents vs. bare-metal stents in patients with acute myocardial infarction. Eur Heart J 2007;28(22):2706-2713 14. Raber L, Kelbaek H, Ostojic M. et al. COMFORTABLE AMI Trial Investigators. Effect of biolimus-eluting stents with biodegrable polymer vs. bare-metal stents on cardiovascular events among patients with acute myocardial infarctions; the COMFORTABLE AMI randomized trial. JAMA 2012;308(8):777-787 15. Sabate M, Cequier A, Iniguez A, et al. Everolimus- eluting stent vs. bare-metal stent in ST-segment elevation myocardial infarction (EXAMINATION); 1 year results of randomized controlled trial. Lancet 2012;380(9852):1482-1490 16. SabateM,BrugalettaS,CequierA,etal.Clinicaloutcomes in patients with ST-segment elevation myocardial infarction treated with everolimus-eluting stents vs. bare-metal stents (EXAMINATION); 5 year results of a randomized trial; Lancet 2016; 387(10016):357-366 Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 14. Haque A F M S, Rahman S M M, Iqbal S A et al Bangladesh J Cardiol, 2017; 07(01-02): 716-18 A F M S Haque, S M M Rahman, S A Iqbal, NN Fatema, Z Khan Department of Cardiology, Combined Military Hospital, Dhaka Colonel A F M Shamsul Haque, FCPS (Med), Cardiologist Brig Gen S M Mamunur Rahman, FCPS (Med), Cardiologist Brig Gen Syed Asif Iqbal, FCPS (Med), Cardiologist Brig Gen Nurunnahar Fatema, FCPS (Med), Paediatric Cardiologist Col Zehad Khan, FCPS (Med), Consultant Cardiologist Correspondence: Dr. Colonel A F M Shamsul Haque, FCPS (Med), FCPS (Card) Department of Cardiology, CMH Dhaka, Bangladesh. Email: afmshams@yahoo.com Objective Background Methods Results Conclusion The aim of this study was to evaluate the usefulness of TDI for the evaluation of Left ventricular filling pressure. Evaluation of LV diastolic filling pressure (LVEDP) provides important haemodynamic data that has both diagnostic and prognostic importance especially in patients with coronary artery disease (CAD). The mitral inflow velocity – to – mitral annulus velocity ratio (E/E’) by TDI (Tissue Doppler Imaging) is a reliable means in CAD patients to determine the LV filling pressure. In this study non-invasive echocardiographic TDI was compared with angiographic left ventricular end diastolic pressure (LVEDP) to assess its correlation for its clinical application. Consecutive forty patients scheduled for cardiac catheterization were studied with Doppler echocardiography. Invasive measurement of LV pressures was obtained with cardiac catheters and the LVEDP was measured. Doppler signals from the mitral inflow and TDI of the mitral annulus (medial corner) were obtained. The ratio of mitral inflow velocity to early diastolic velocity of the mitral annulus (E/E’) showed a good correlation with LVEDP. E/E’ <8 predicted normal LVEDP, and E/E’ >15 identified increased LVEDP. Variability was present in those with E/E’ of 8 to 15. A subset of those patients with E/E’ 8 to 15 could be further defined by use of other Doppler data. Tissue Doppler parameters were correlated with invasive (angiographic) parameters. Patients with E/E’ >15 can be classified as having elevated filling pressure. An E/E’ < 8 suggests normal filling pressure. In the range of E/E’ of 8 to 15, other information must be applied. 4,7 In our study out of 40 patients 14 patients had E/E’ was > 15, 16 patients had E/E’ < 8 and rest of the patients had E/E’ in between 8 to 15. In the normal E/E’ group 75% had normal LVEDP and in the high E/E’ ratio group 71% patients had elevated LVEDP. Variability was observed in patients who had E/E’ in between 8 to 15. Doppler signals from the mitral inflow and TDI of the mitral annulus and its ratio provides good assessment of LV filling pressures. However, accurate prediction of filling pressures requires incorporating other parameters. Introduction Left ventricularend diastolic pressure(LVEDP) is an important parameter that should be evaluated during management of patients with heart disease. This is particularly true in critically ill patients. Doppler echocardiography has become the non-invasive and reproduciblemethod for the assessment of systolic and diastolic function of the left ventricle and also of the left ventricular filling pressure.1,6 Noninvasive assessment by Doppler echocardiography provides a safe and reproducible investigation comparable with invasive Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 15. Haque A F M S, Rahman S M M, Iqbal S A et al Bangladesh J Cardiol, 2017; 07(01-02): 716-18 pressure monitoring. This study was designed to evaluate the correlation of TDI variables for the assessment of LVEDP1. The estimation of LV filling pressure is necessary in the follow-up of disease progression and response to treatment in most patients with heart disease and usually requires invasive hemodynamic monitoring2. Diastolic dysfunction is common in cardiac disease and contributes to the signs and symptoms of heart failure. Doppler echocardiography is widely used for the noninvasive assessment of diastolic filling of the left ventricle (LV). The purpose of this study was to evaluate the usefulness of TDI for the evaluation of Left ventricular filling pressure. Methods Population The study population of this prospective observational study consisted of forty consecutive patients who were scheduled for elective CAG in 2011 and 2012. Subjects 18 years or older with sinus rhythm were eligible. Inclusion criteria were CAD, Sinus rhythm and age>18 yrs. Exclusion criteria were valvular heart disease, complete left bundle branch block or complete right bundle branch block, pacemaker dependence, cardiomyopathy, pericardial effusion and post cardiac surgery. Demographic data including age, sex, underlying disease, risk factors for coronary artery disease and indications for catheterization were recorded. Echocardiographic Measurements Doppler studies were performed with GE Vingmed imaging system by a combination of Doppler ultrasonography and B-mode imaging in the Department of Cardiology, CMH Dhaka. For mitral inflow evaluation, the sample volume of PW Doppler was placed at the mitral valve tips using the apical 4-chamber view3. The peak Doppler velocity of early diastolic flow (E wave) was measured. With the PW TDI program, a sample volume (5mm) was placed at the septal corner of mitral annulus in the apical 4-chamber view. These measurements allowed for obtaining the mitral inflow to annulus ratio (E/E’). Invasive Measurements Fourty consecutive patients in sinus rhythm referred for clinically indicated CAG made up the study group. Patients were studied with Doppler echocardiography on the same day before the procedure. CAG was performed through the femoral approach. All recordings were obtained by a pigtail catheter connected with a fluid-filled transducer before left ventriculography by a polygraph machine. Theleft ventricular end diastolic pressure (LVEDP) was obtained by computer recording. Results Baseline characteristics The data show that 22 (55%) of the cases were above 50 years of age followed by 13 (32.5%) in the range of 41– 50 years and 5 cases (12.5%) were 40 or below. 35 patients were referred * Figures in the parentheses indicate corresponding %. for evaluation of angina and the remainder was referred for symptoms of congestive heart failure. Tissue Doppler Correlation with Invasive Parameters Patients with E/E’>15 can be classified as having elevated filling pressure. An E/E’< 8 suggests normal filling pressure. In the range of E/E’ of 8 to 15, other information must be applied.4,7 In our study out of 40 patients 14 patients had E/E’ was >15, 16 patients had E/E’ <8 and rest of the patients had E/E’ in between 8 to 15. In the normal E/E’ group 75% had normal LVEDP and in the high E/E’ ratio group 71% patients Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 16. Haque A F M S, Rahman S M M, Iqbal S A et al Bangladesh J Cardiol, 2017; 07(01-02): 716-18 had elevated LVEDP. Variability was observed in patients who had E/E’ in between 8 to 15. Discussion This study supports that E/E’ is a reliable Doppler echocardiographic parameter to estimate LVEDP2. The noninvasive assessment of LV filling pressures can be an important clinical tool. TDI of the mitral annulus during diastole has been proposed as a new method for assessment of cardiac function. Ommen, et al. reported that the correlation of left ventricular diastolic pressure with the medial annulus TDI were consistently equivalent or better than the lateral annulus or the combinations of the medial and lateral annulus4,7. In the present study, this combined variable was a good Doppler predictor of elevated filling pressure. However, there remains significant scatter with E/E’, particularly with intermediate values of E/E’. We would propose that the E/E’ ratio be used as the initial measurement for estimation of LV filling pressures, particularly in those patients. Patients with E/E’>15 can be classified as having elevated filling pressure. An E/E’<8 suggests normal filling pressure. In the range of E/E’ of 8 to 15, other information must be applied. Ommen, et al. had similar results in their study4. Further characterization of the intermediate E/E’ group is necessary. Study Limitations The motion of the mitral annulus is not entirely due to myocardial contraction but rather is the summation of contraction, rotation, and translation. The effects of each of these may vary from patient to patient. The use of the apical transducer position to sample the mitral annulus is an attempt to minimize the translational and rotational effects and focus on long-axis excursions of the LV cavity. The effects of regional dysfunction on the motion of the annular plane are not yet known. Conclusion Evaluation of LV diastolic filling pressure (LVEDP) provides important haemodynamic data that has both diagnostic and prognostic importance especially in patients with coronary artery diseases. E/E’ is significantly correlated with LVEDP in the population with coronary artery disease. Overall, the E/E’ ratio was the predictor of LV filling pressure. References 1. Necla O, Kayak H K, Ali D, Umut A and Serdar A. Determnation of left ventricular filling pressure by new echocardiographic methods in patients with coronary artery disease. Int J Cardiovasc Imaging 2008; 24:141– 147. 2. N Mansencal, E Bovier, T Joseph, J C Farcot, A Redheil, P Lacombe, et al. Value of Tissue Doppler Imaging to Predict Left Ventricular Filling Pressure in Patients with Coronary Artery Disease. Echocardiography 2004; 21 (2): 133-138. 3. S Tongyoo, D Jakrapanichakul and N Chaowalit, Estimation of Left Ventricular End- diastolic Pressure by Tissue Doppler Imaging in Patients with Coronary Artery Disease. Thai Heart Journal 2006; 19 (30): 105- 112. 4. Ommen SR, Nishimura RA, Appleton CP, Miller FA, Redfield MM and Tajik AJ. Clinical utility of Doppler echocardiography and tissue Doppler imaging in the estimation of left ventricular filling pressure. Circulation 2000; 102:1788-94. 5. Nishimura RA, Tajik AJ. Evaluation of diastolic filling of left ventricle in health and disease: Doppler echocardiography is the clinician’s Rosetta Stone. J Am Coll Cardiol 1997; 30: 8 –18. 6. Yamamoto K, Nishimura RA, Chaliki HP, et al. Determination of left ventricular filling pressure by Doppler echocardiography in patients with coronary artery disease: critical role of left ventricular systolic function. J Am Coll Cardiol 1997; 30:1819–1826. 7. Sherif F, Nagueh, Appleton P, Gillebert C, Paolo N, Otto A et al. Recommendations for the Evaluation of Left Ventricular Diastolic Function by Echocardiography. Journal of the American Society of Echcardiography 2009; 108-118. Generated by Foxit PDF Creator © Foxit Software http://www.foxitsoftware.com For evaluation only.
  • 17.
  • 21.  Dominant R wave in infe- rior leads indicate RVOT po- sition of the lead.  Early precordial transition and lack of notching in the inferior leads confirm septal location of the lead.  Morphology in lead I sug- gest location of the RV lead in the anterior part of the in- terventricular septum. Figure-8
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  • 46. Figure-6 Figure-9 Figure-7 Figure-8 Figure-10 Figure-11 Stress Echo and Mitral Regurgitation Known Severe MR 1. Look for Exercise Capacity 2. Pulmonary HTN new/Worse 3. LV response Mild or No MR and Unexplained Dyspnea, Pulmonary HTN 1. Exercise capacity 2. New or worsening MR 3. Worsening Pul HTN 4. LV response
  • 47. Figure-12 Figure-13 Figure-14 Table-2 Class of Recommendation Class I Class II Class IIa Class IIb Class III Evidence and/or general agreement that a given treatment or procdure is beneficial, useful, effective Conflicting evidance and/or a divergence of opinion about the usefulness/efficacy of the given treatment or Procedure Weight of evidence/ opinion is in favour of usefulness/efficacy. Usefulness/efficacy is less well established by evidence/opinion Evidence or general agreement that the given treatment or procedure is not useful/effective, and in some cases may be harmful. Is recommendied/ is indicated Should be considered May be considered Is not recommended Definition Suggested wording to use Table-3
  • 48.
  • 49. Patient A after treatment CXR of Patient A, CXR showing cardiomegalyFigure-1 Figure-2
  • 50. Causes of Dilated Cardiomyopathy : Factors Identified as Causes of Myocardial Damage Category Of Factors Bacterial infections Rickettsia Parasites Fungi Neuromuscular disorders Nutritional factors Collagen vascular diseases Hematological diseases Coronary artery diseases Drugs Endocrine diseases Metabolic disorders Malformation syndromes Coxsackie virus B, human immunodeficiency virus, echovirus, rubella, varicella, mumps, Epstein-Barr virus, cytomegalovirus, measles, polio Diphtheria, Mycoplasma, tuberculosis, Lyme disease, septicemia Psittacosis, Rocky Mountain spotted fever Toxoplasma, Toxocara, Cysticercus Histoplasma, coccidioidomycoses, Actinomyces Duchenne or Becker muscular dystrophies, Friedreich ataxia, Kearns-Sayre syndrome, other muscular dystrophies Duchenne or Becker muscular dystrophies, Friedreich ataxia, Kearns-Sayre syndrome, other Kwashiorkor, pellagra, thiamine deficiency, selenium deficiency Rheumatic fever, rheumatoid arthritis, systemic lupus erythematosus, dermatomyositis, Kawasaki disease Thalassemia, sickle cell disease, iron deficiency anemia Anomalous left coronary artery from pulmonary artery, infarction Anthracycline, cyclophosphamide, chloroquine, iron overload Hypothyroidism, hyperthyroidism, hypoparathyroidism, pheochromocytoma, hypoglycemia Glycogen-storage diseases, carnitine deficiency, fatty acid oxidation defects, mucopolysaccharidoses Cri-du-chat (cat-cry) syndrome Table-1
  • 51. ECG of Patient A, ECG showing normal sinus rhythm and LVHFigure-3
  • 52. Echocardiography of Patient A, Echocardiography showing dilated LV and poor LV function.Figure-4
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  • 55. ECG on the day of admission showing widespread ST segment depression in both inferior and anterior leads (arrows).Figure-1
  • 56. Coronary angiogram, anterior posterior (AP) view showing 80-90% stenosis of left main (LM) coronary artery involving ostium and mid part (arrow). Coronary angiogram, LAO caudal view showing critical ostial stenosis of LM coronary artery (arrow). Coronary angiogram, left anterior oblique (LAO) cranial view showing critical LM coronary stenosis with 30-40% stenosis at mid part of left anterior descending artery (LAD), (arrows). Coronary angiogram, LAO view showing normal non dominant right coronary artery (RCA) (arrow).. Figure-2 Figure-4 Figure-3 Figure-5
  • 57. ECG 2 years after CABG, appears normal.Figure-6
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  • 61. x-ray chest-huge cardiomegally Non coronary sinus is hugely dilated with a perforation in apex Right atrium was opened ,about 4cm long vegetation was found, was attached to the connecting site of Non coronary aneurysmal sinus Huge right atrial and right ventricular enlargement Double ended pledgeted horizontal mattress suture was applied to aneurysmal area around the perforation excised vegetation Figure-1 Figure-3 Figure-5 Figure-2 Figure-4 Figure-6
  • 62. Double ended pledgeted horizontal mattress suture was applied around the perforation site in Right atrium PTFE patch closure of aneurismal part of Non coronary sinus PTFE patch closure of aneurismal part of Non coronary sinus Figure-7 Figure-8 Figure-9
  • 63.
  • 64. Angiographic view showing normal LM, about 70 to 75% narrowing of mLAD, 95% stenosis of d LCxFigure-1
  • 65. Stent in m LAD before inflation LM stenting covering dissection Deployment of stent in mLADFigure-2 Figure 4 & 5 Figure-3
  • 66. Expanded deployed stent in LM Longitudinal stent collapse After stenting flap seen in LM Collapse stent in LM and deployed stent in mLAD Figure-6 Figure-8 Figure-7 Figure-9
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  • 68.
  • 69. Almost normal RCA with TPM Run of suction catheter Antegrate flow after suction Total Occlusion of mid left main Figure-1 Figure-3 Figure-4 Figure-2
  • 70. POBA done IABP for cardiogenic shock POBA and dottering Slow flow Figure-5 Figure-7 Figure-6 Figure-8
  • 71. Slow flow disappeared Normalisation of coronary flow after PCI Total occlusion of LM before PCIFigure-9 Figure-10 Figure-11
  • 72.
  • 73.
  • 74. After left subclavian puncture wire failed to advanced into right atrium due to PLSVC PPI lead into right ventricle making a circular loop into right atrium (AP view) PPI lead into right ventricle (LAO view) Figure-1 & 2 Figure-3 Figure-4
  • 75. PPI lead into right ventricle (RAO view)Figure-5