This morning report from RSSA provides details on a 60-year-old male patient presenting with chest pain. Key details include:
- The patient presented with chest pain for over 30 minutes, accompanied by cold sweats. Initial vitals and exam findings are provided.
- The patient has a history of NSTEMI 1 year ago with 3 vessel CAD on angiography but refused further treatment. He also has a history of hypertension for 20 years.
- Initial labs, ECGs, chest x-ray, and past medical records are summarized. Echocardiogram from last year showed LV hypertrophy and diastolic dysfunction. Coronary angiogram showed 3 vessel CAD.
-
Difference Between Skeletal Smooth and Cardiac Muscles
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brief prabowo nsteacs.pptx
1. Morning Report
Physician in Charge
IV : dr. Anastasia / dr. Savitri
IIIA (Ward/IW) : dr. Erick, dr. Ira dan dr. Cik Kahadi
IIIB : dr. Kaputrin dan dr. Teguh
Chief : dr. Yordan dan dr. Astrid
Supervisor : dr. Budi Satrijo, Sp. JP(K)
Supervisor Incovit : dr. Indra Prasetya, Sp.JP(K)
MR Consultant : dr. Budi Satrijo, SpJP (K)
2. SUBJECTIVE
Mr. P/60 yo/ID 11536070
CHIEF COMPLAINT : Chest Pain
Patient complained about chest pain at 06.00 AM (2 hours before RSSA admission) with VAS
score 8/10, when he was lying on bed. It was heavy-like sensation, without radiated to the back, with
duration more than 30 minutes, and accompanied with cold sweating. Nausea (-), vomiting (-), SOB (-
). There was no stabbing like sensation and chest pain was not affected with inspiration, positional
changes, or food intake. Because the chest pain still persisted, patient directly went to RSSA.
In ER RSSA at 00.30 AM, patient said that chest pain still already felt with VAS 8/10 mmHg. GCS
was 456, BP 160/112 mmHg, HR 81 bpm, RR 26x/min and Sat 99% on NC 3 lpm NC. He was given drip
NTG 40 mcg/min, loading aspilet 4 tab, and CPG 4 tab, and his BP was improved 130 / 90 mmHg, and
chest pain improved with VAS 4/10.
Previously, he suffered from similar chest pain, with VAS score 6/10 while at rest. It was
occured At 05.00 AM (19 hours before RSSA admission). He was taking isosorbide dinitrate 5 mg, with
6 times of repetition, but the chest pain did not Improved.
3. SUBJECTIVE
Mr. P/60 yo/ID 11536070
PAST MEDICAL HISTORY :
ā¢ He had suffered from similar chest pain 1 year ago and checked at private hospital in Malang. He was
diagnosed with NSTEMI, and was referred to other hospital for further management. Coronary
angiography was perform and the result was CAD 3VD + LM disease. Then he planned to be referred to
cardiologist outpatient clinic for consideration for elective PCI or CABG. But patient never came to
control at RSSA because he refused for operation. After that Patient never controlled to any cardiologist
and also didnāt take any medication
ā¢ History of DOE (+) while doing moderate-heavy activities since 1 month. OE, PND, Leg swelling,
palpitation, and syncope was denied
4. SUBJECTIVE
Mr. P/60 yo/ID 11536070
RISK FACTOR :
ā¢ He had hypertension since 20 years ago, didnāt routinely consume medication
ā¢ He is an a passive smoker for the last 1 year
ā¢ History of diabetes mellitus, CKD, CAD and other disease was denied.
FAMILY HISTORY :
History of hypertension on her family was denied
There was no sudden cardiac death and cardiac disease in her family.
He was the 2nd son out of 5 siblings.
Screening for covid-19
There was no cough, fever, sore throat, anosmia, dysgeusia in the last 14 days ago.
History of traveling to red zone area was denied
History of contact with patient confirmed COVID-19 was denied
He lives in orange zone area
He hasnāt yet vaccinated covid-19
6. ECG at RSSA (April 18th 2022) at 00.30
Sinus rhythm, HR 100 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III.
ST segmen depression V2 (3 mm), V3(4 mm), V4(4.5 mm). T wave normal. QTc 337 msec. LVH(-), RVH (-), LAE (-), RAE(-).
Conclusion : Sinus tachycardia with ischemia
7. ECG at CVCU (March 4th 2022)
Sinus rhythm, HR 100 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III. ST
segmen depression V2 (1 mm), V3(1.5 mm), V4(0.5 mm). Biphasic T wave at V2,V3,V4. QTc 397 msec. LVH(-), RVH (-), LAE (-),
RAE(-).
Conclusion : Sinus tachycardia, with ST-T changes (+)
ECG at RSSA (April 18th 2022) at 2.30
8. ECG at CVCU (March 4th 2022)
Sinus rhythm, HR 98 bpm, FA LAD, HA N. normal P wave, PR Int 160 ms. narrow QRS 80 ms. Pathological Q waves in lead III. ST
segmen depression V2 (2 mm), V3(1 mm), V4(1 mm). T wave normal. QTc 486 msec. LVH(-), RVH (-), LAE (-), RAE(-).
Conclusion : Sinus tachycardia, ischemia, and prolonged QTc.
ECG at Persada Hospital (May 30th 2021)
9. CXR at Persada Hospital (May 30th 2021)
AP position, symmetrical, enough inspiration,
enough KV
Soft tissue: Normal
Bone: Costae D/S normal
ICS D/S normal
Trachea: In the middle
Cor: Site: N
Size: CTR 56%
Cardiac waist (+)
Aorta dilatation (+)
Hemidiaphragm:
D: dome shape
S: hard to evaluate
Vascular apex D increased
Costophrenic angles: D: sharp, S: hard to evaluate
Pulmo : Infiltrate (-)
Conclusion :
Cardiomegaly with HHD configuration
Aorta dilatation
10. CXR at RSSA (April 18th 2022)
AP position, symmetrical, less inspiration, enough
KV
Soft tissue: Normal
Bone: Costae D/S normal
ICS D/S normal
Trachea: In the middle
Cor: Site: N
Size: CTR 67%
Cardiac waist (-)
Hemidiaphragm:
D: dome shape
S: hard to evaluate
Bronchovesicular pattern dextra and sinistra
increased
Costophrenic angles: D: sharp, S: hard to evaluate
Pulmo : Infiltrate (-)
Conclusion :
Cardiomegaly with HHD configuration
Susp. Pleural effusion sinistra
17. Coronary angiography at Persada Hospital
LM : stenosis 10% mid-distal
LAD : stenosis 95-99% at osteal-proximal.
CTO at proximal, got collateral from
contralateral
Intermediate : stenosis 90% at osteal-
proximal
LCx : co-dominsasnt. Stenosis 90% at
osteal-proximal. Stenosis 60-70% at distal
RCA : stenosis 60% at osteal-mid. stenosis
40% at RPL. Stenosis 80% at PDA
Conclusion : CAD 3VD
Suggest to : CABG/high cost PCI
18. Assessment
1. NSTEMI killip II (Very high risk criteria) TIMI 5/7, GRACE 140 CRUSADE 27
2. HF st C fc II dt CAD, HHD
3. Hypertension st II
4. History of smoker
38. Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 42
39. Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 43
40. Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 44
41. Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 45
42. Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation 46
43. 47
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
44. 48
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
45. 49
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
46. 50
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
47. 51
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
49. 53
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
50. 54
Jean-Philippe Collet. 2020. ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation
52. Intraprocedural stent thrombosis (IPST)
INTRODUCTION
a rare complication leading to poor outcome including STEMI
and sudden cardiac death
47 (0.7%) of 6,591
patients with incident
IPST
ļ§ Death within 30 days was higher (12.9% vs 1.4%)
ļ§ Mortality within one year was also higher (19.9% vs. 2.7%)
ļ§ 0.5-2% in the case of elective PCI
ļ§ 6% in the case of PCI with acute coronary syndromes
Safety concerns regarding an increased risk of stent thrombosis with drug eluting stent (DES) persist while the
incidence, timing, and predictors of stent thrombosis with DES have not been determined
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
Iqbal J, et al. EuroIntervention. 2013,9:62-69
53. Definition of Intraprocedural Stent Thrombosis
(IPST)
Intra-procedural stent thrombosis (IPST) is deļ¬ned as an angiographically conļ¬rmed
intraluminal ļ¬lling defect within the stent that results in occlusive or non-occlusive
thrombolysis in myocardial infarction (TIMI) grade-0 or 1 anterograde ļ¬ow, secondary to the
development of new or increasing thrombus within or adjacent to a recently implanted stent,
occurring during the index procedure or before the percutaneous coronary intervention
(PCI) is completed.
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
Brener et al. JACC: Cardiovascular Interventions. Vol. 6. 2013: 36-43
IPST has an incidence of 0.7% after drug eluting stent (DES), and <0.01% after bare metal stent (BMS)
implantation in patients without acute myocardial infarction (AMI), thrombus-containing lesions and dissections. It
occurs in <1% of patients with ST-segment elevation myocardial infarction (STEMI).
54. The Academic Research Consortium (ARC) has
standardized the deļ¬nitions of ST by categorizing
the speciļ¬city of the adjudicated event (deļ¬nite,
probable, or possible) and its timing relative to
PCI (acute, subacute, late, and very late).
Intra-procedural stent thrombosis (IPST) (i.e., the development of occlusive or non-occlusive new thrombus in or
adjacent to a recently implanted stent before the PCI procedure is completed) is excluded from the ARC ST
deļ¬nitions.
Brener et al. JACC: Cardiovascular Interventions. Vol. 6. 2013: 36-43
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092
55. End Point Definition of Stent
Thrombosis by
The Academic Research Consortium
(ARC)-2
Garcia et al. Circulation. 2018:137:2635ā2650
56. The most important aspect for the diagnosis and treatment of IPST is
clinical suspicion of early stent thrombosis.
Diagnosis of Intraprocedural Stent thrombosis
(IPST)
The typical clinical presentation of stent thrombosis consists of chest pain and ischemic
electrocardiographic changes in the target vessel territory. However, ST can also present as
sudden death, or it can be asymptomatic in the setting of collateral vessels.
Hyo-Sun Shin, et al. J Lipid Atheroscler. 2014;3(1):43-
48
57. Coronary intervention-related MI is arbitrarily defined by an elevation of cTn values more than five times
the 99th percentile URL in patients with normal baseline values. In addition, one of the following
elements is required:
1. New ischaemic ECG changes
2. Development of new pathological Q waves
3. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a
pattern consistent with an ischaemic aetiology;
4. Angiographic findings consistent with a procedural flow-limiting complication such as coronary
dissection, occlusion of a major epicardial artery or a side branch occlusion/thrombus, disruption of
collateral flow, or distal embolization.
Criteria for PCI-related MI 48 h after the index procedure (type 4a MI)
Thygesen K, et al. 2018. European Heart Journal 2019, 40: 237ā269
58. When a filling defect is detected angiographically:
ļ§ Intravascular ultrasound (IVUS) may be used to detect the underlying
mechanism of ST (underexpansion, malapposition, edge dissection).
ļ§ Optical coherence tomography (OCT) is very suitable for visualization
of the stent surface for its higher resolution (10 mm), and its ability to
detect the presence of (sub) clinical thrombus has been experimentally
confirmed.
In this patient, as soon as the action predilatation with balloon and stent, we found ischaemic ECG changes and thrombus
intracatheter in the end of procedure. The ECG monitor back to the baseline soon after we gave loading Ticagrelor 180 mg,
Atorvastatin 40 mg and intracoronary heparin 1000 mg.
Diagnosis of Intraprocedural Stent thrombosis
(IPST)
Genereux P, et al. 2014. Journal of the American College of Cardiology Vol. 63, No. 7, 2014: 619-629
59. Pathophysiology of Stent
Thrombosis
Many factors are involved including procedural factors/stent, patient factors and lesion
characteristics. Patients with acute coronary syndrome, inflammation and tissue necrosis
were exposed to the circulation so as to strengthen the activity of platelets and easily
formed thrombus.
The material in the form of a polymer stent Cypher (sirolimus) and Taxus
(paclitaxel) DES can cause infiltration of eosinophils suspected
hypersensitivity reaction that can trigger platelet adhesion and activation
cascade coagulant.
Brener et al. JACC: Cardiovascular Interventions. Vol. 6. 2013: 36-43
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092
60. There are two kinds of thrombus:
ļ§ White thrombus : a platelet-rich thrombus, usually only lead to partial occlusion
ļ§ Red thrombus : a rich thrombus fibrin and erythrocytes.
White thrombi composed approximately one-third of specimens retrieved during PCI in a
contemporary sample of patients from a high-volume referral center. Patients with white thrombi
had less ischemic time and had smaller vessels when compared with those with red thrombi.
THROMBUS
Quadros AS, et al. 2012. American Heart Journal Volume 164, Number 4: 554-560
61. Torrado, J. et al. J Am Coll Cardiol. 2018;71(15):1676ā95
Pathogenic Mechanisms
of Stent Thrombosis
63. Device-related factors (or stent thrombogenicity), including stent material, surface coating, and the interaction with
adjunctive therapy such as intracoronary brachytherapy.
Platelet activation was greater during the 30 days after implantation of an open-cell versus a closed-cell stent,
which was potentially related to the different scaffolding properties of the stents.
The content of the drugs currently on the DES can be prothrombogenic. Rapamycin and Paclitaxel works by
blocking the migration and proliferation of smooth muscle cells that plays a role in neointimal formation
and restenosis. However, both drugs induce endothelial expression of tissue factor that will bind to the clotting
factor so that the formation of fibrin.
STENT FACTORS
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
64. Patient- or lesion-specific factors, including vessel size, acute coronary syndrome/unstable
angina, plaque characteristics, local platelet/coagulation activity, coronary blood flow, and left
ventricular ejection fraction.
A polymorphism of platelet glycoprotein IIIa gene (PlA2) may also be associated with an
increased risk of stent thrombosis.
Other patient characteristics that favor the development of stent thrombosis include diabetes
mellitus, chronic kidney disease, smoker, cancer, DAPT non-responsive, premature cessation of
DAPT, advanced age and hypersensitivity to polymer or drug.
PATIENT- OR LESION-SPECIFIC FACTORS
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092
65. PREDICTORS OF IPST
Over the past several years, many researchers have investigated potential predictors
of stent thrombosis especially acute and sub-acute categories and identified a number
of angiographic, clinical, procedural and post-procedural risk factors of stent thrombosis
A risk score has been proposed to personalize risk assessment for the occurrence of ST and may be used to identify patients
who might beneļ¬t the most from more aggressive antiplatelet therapy after stent implantation.
Iqbal J, et al.. Euro Intervention 2013; 9: 62-69
66. Predictors of Early and (Very) Late Stent Thrombosis
Claessen et al. JACC: Cardiovascular Interventions. Vol. 7. 2014:1081-1092
67. Predictors of IPST
Clinical risk score for prediction of
stent thrombosis and risk
stratification as developed by Baran
et al
8 significant predictors, with a stratification of
patients in low, medium, and high risk
groups, and has been validated using 1-year
data from 4,820 patients.
PATIENTāS SCORE: 12
Iqbal J, et al.. Euro Intervention 2013; 9: 62-69
68. Predictors of IPST
Stent Thrombosis Risk Score
(STRS) in predicting early stent
thrombosis (ST) after primary
Percutaneous Coronary Intervention
(PCI).
A total of 569 patients were included, the median
age was 56 years. Early ST was observed in 33
(5.8%) patients.
Early ST rate was 3.3% at STRS of 0-2, which
raised to 5.0% at STR of 3-4, and 17.2% at
STRS of ā„5
PATIENTāS SCORE: 3
Kumar R, et al. Journal Of The Saudi Heart Association 2020;32:256-262
69. Predictors of IPST
Association of the CHA2DS2VASc Score
with Acute Stent Thrombosis
3,460 consecutive patients with STEMI who
underwent a PPCI.
CHA2DS2VASc scores ā„ 4 were independently
associated with acute stent thrombosis.
Patients with a CHA2DS2VASc score of 4 had a
4.3 times higher risk of acute stent thrombosis
compared to those with a CHA2DS2VASc score of
1.
PATIENTāS SCORE: 3
Tanik OZ, et al. 2019. Med Princ Pract 2019;28:115ā123
70. Predictors of IPST
Integer-Based Risk Score for 1-Year
Deļ¬nite/Probable Stent Thrombosis in
Patients With Acute Coronary
Syndromes
6,139 patients undergoing PCI with stent
implantation for ACS.
Risk scores 1 to 6 were considered low risk
(1.36%), 7 to 9 intermediate risk (3.06%), and ā„10
high risk for ST (9.18%).
PATIENTāS SCORE: 6
Brener SJ, et al. 2013. JACC: Cardiovascular Interventions Vol.6, No.1,2013: 36-43
71. Stent Thrombosis Management
If ST is the case then action targets PTCA for revascularization of blood
vessels should be done immediately. Guidewire selected must be soft and
floppy to ensure free through the lumen of the stent and not crossing through the strut
stent
Aspiration trombhectomy intra coronary thrombus is effective for the treatment of ST especially on stents with a diameter of more than
2.5 mm, large blood vessels and large thrombus. Intracoronary thrombus aspiration can prevent distal embolization.
The existence of intra coronary thrombus is also an indication of the provision of Glycoprotein IIb-IIIa inhibitors.
The success of overcoming the acute thrombosis, characterized by normal blood flow (TIMI 3 flow) with
stenosis <50%.
Nikesh Jain et al. Cardiology and Cardiovascular Research 2019; 3(2): 31-36
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
72. Dual anti-platelet (DAPT) should be given as early as possible, especially in all patients
with acute coronary syndrome patients.
Acetylsalicylic acid (ASA) and the P2Y12 receptor antagonists such as clopidogrel, prasugrel and ticagrelor served to increase the
effectiveness of treatment and prevention of stent thrombosis.
PLATO Trial ļ The effectiveness of Ticagrelor vs Clopidogrel in preventing stent thrombosis
The incidence of stent thrombosis could still occur at 0.5-2% in the case of elective PCI and more than 6% in the case of PCI
with acute coronary syndromes despite using dual antiplatelet
Stent Thrombosis Management
ANTI-PLATELET
Nikesh Jain et al. Cardiology and Cardiovascular Research 2019; 3(2): 31-36
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
73. Selection of anticoagulation during PCI procedures is also important
ļ Unfractionated heparin (UFH) is the main option while undergoing
PCI.
From the research HORIZON-AMI, comparing UFH-Glycoprotein IIa/IIIb with direct thrombin
inhibitors bivalirubin as monotherapy, showed a 0.3 vs 1.4%, P <0.001 in the incidence of
Acute ST.
It is important choose the right size stents and perform high-pressure post-dilation effectively (> 14 atm)
To further optimize the prevention ST, lesions calsified, can be handled with the use of rotational atherectomy
so that expansion and better positioning stent.
The use of intracoronary imaging modalities such as Intra Vascular Ultra Sound (IVUS) and Optical
Coherence Tomography (OCT) is very helpful as guiding the expansion and apposition of the stent to be
more adequate
Stent Thrombosis Management
ANTICOAGULANT
PROCEDURE OPTIMIZATION
Nikesh Jain et al. Cardiology and Cardiovascular Research 2019; 3(2): 31-36
Oktaviono YH. Folia Medica Indonesiana Vol. 52. 2016 : 66-73
74. INTEGRATED STRATEGY OF IPST IN THIS PATIENT
Patient Characteristic Lession Characteristic Stent Characteristic
ļ§ Male, 49 y.o
ļ§ Insulin treated DM Type
II
ļ§ Smoker
ļ§ History of ACS 1 month
prior admission
ļ§ CAD 3VD with Left
Main Disease
ļ§ Lession length > 20
mm with calcification
ļ§ Multiple stenting
ļ§ Length 38mm
Moderate Risk of Early
Stent Thrombosis
Evidence IPST:
Ischemic ECG Changes
Thrombus Intracatheter
DAPT with Asetyl Salycilic +
Ticagrelor
High Intensity Statin
TIMI Flow 3, residual stenosis 0%
ECG returned to baseline
No chest discomfort during and post
procedure
2nd Generation DES
(Everolimus-eluting
platinum chromium stent)
75. Conclusions
ļ¼Intraprocedural Stent Thrombosis was a strong predictor of mortality in patients
undergoing PCI.
ļ¼This case showed that the present widespread use of DES instead of BMS for coronary
implantation although decreased the future risk of repeat revascularization, increased the
risk of thrombosis.
ļ¼Prior risk stratification, selection of 2nd generation DES, early potent antiplatelet treatment
and anticoagulant of choice with UFH might be used to reduce the risk of IPST in patients
undergoing stent implantation.