Ischemic heart failure syndromes.

1. Acute Ischemic
Heart Failure
syndromes
Dr Asadullah Soomro
Adult cardiologist
Prince sultan cardiac centre Al-Hassa
Kingdom of Saudi Arabia.
Email;hssbasadsoomro@gmail.com

2. Ischemic heart failure syndrome type 11, with more than 100 times hospitalization. Guess what is
this??

3. SOOMRO,S
HEART FAILURE
WORLD
IATROGENIC
HEART
FAILURE
SYNDROMES
MIXED
ISCHEMIC
HEART FAILURE
SYNDROMES WITH
STRUCTURAL
HEART DEFECTS
ISCHEMIC
HEART
FAILURE
SYNDROMES
NON
ISCHEMIC
HEART
FAILURE
SYNDROMES
1 2
34

4. Type 1V
“ Orphan Ischemic heart
failure
Syndromes”
“ Myth or reality”

5. Ischemic Type 1V Heart failure
syndromes
Conventional criteria for diagnosing Coronary
artery disease in individual patient with symptoms of
heart failure include documented acute or old
Myocardial infarction or documented typical symptoms
of stable or unstable angina , supported by reversible
myocardial ischemia, and evidence of CAD on
coronary angiogram. ( type 1 to type
111)
How ever ,in type 1V ischemic heart failure without
coronary angiogram true prevalence of ischemic heart
failure is under estimated.

6. Ischemic Type 1V Heart failure
syndromes
Elderly patients with primarily symptoms of heart failure
( type 1V) with LV Systolic dysfunction or perserved
function , 52% have CAD on coronary angiogram,
and 37%have hibernating myocardium on
myocardial perfusion imaging .
Non invasive assesment thus seriously underestimates
the prevalence of CAD and fails to identify those
patients who may benefit from revascularization.
Most cases of type 1V HF are attributable to CAD.

7. Ischemic Type 1V Heart failure
syndromes
1) Very Elderly patients with low ejection fraction are
not studied to rule out CAD as cause of heart failure .
2) Similarly elderly hypertensive patients with perserved
systolic function are usually neglected indeed
,therefore CAD as a cause of heart failure is
overlooked.
3) Heart failure with global systolic dysfunction and
LBBB despite having atheroscelrotic risk factors are
also neglected as dilated cardiomyopathy and are
presumed not suitable for coronary angiography, or
delayed , hence do not benefit from late
revascularization.

8. Ischemic Type 1V Heart failure
syndromes
4) Elderly DM,HTN & CKD ,COPD with MR & TR
associated with paroxysmal or permanent atrial
fibrillation , and low ejection fraction are denied
coronary angiography to rule out CAD as cause
of heart failure until present with acute STEMI.
5) Adults with Corrected congenital heart defects ,
with residual sequele ,baseline abnormal EKG
and ventricular dysfunction especially those
associated metabolic syndrome , are also
overlooked to rule out CAD as a etiology or
precipitant of heart failure.

9. Ischemic Type 1V Heart failure
syndromes
6) Last not the least although rare but yet we see
some patients with long standing risk factors , who
are presented with malignant cardiac
dysrrhythmias and first time symptoms of
heart failure , with severe transient LV
systolic dysfunction ,resuscitated successfully with
out EKG evidence of myocardial infarction .
They are also neglected to rule out significant CAD
with otherwise good targets of revascularization.

10. Ischemic Type 1V Heart failure
syndromes
History , EKG and Echocardiogram ,found evidence
of CAD in 42% men and 25% women predicting
HF.
However careful history in patients with high
probability of CAD may help in diagnosis of type
1V ischemic heart failure in many patients.
More recent studies using different techniques have
found higher prevalence of type 1V ischemic heart
failure syndromes .
Average 61% ( 68% in men & 38% in women) in
east Finland.

11. Back ground of
Ischemic Type 1V Heart failure syndromes
In 1995 while working at Dow Medical college & civil
hospital Karachi Pakistan, I first time discovered this small
group of ischemic heart failure patients, who were labelled
as dilated / ischemic cardiomyopathy without objective
evidence of CAD.
They had severe LV systolic dysfunction with recurrent
hospitalizations.
To establish etiology and with a view to assess if they have
suitable revascularization targets, we did coronary
angiogram in few such high risk patients.
We found in them small caliber ,multi vessel severely diffuse
,multiple lesions ,( as an ischemic etiology and precipitant
of decompensation indeed).
Considered unsuitable for revascularization , therefore
stopped further testing .

12. Background of
Ischemic Type 1V Heart failure syndromes
At that time , based on above coronary morphological
features ,I classified ischemic heart failure in four
groups .
372 HF patients audit was first time presented , in Dow
medical golden jublee symposium and later in
cardiology congress organized by pakistan cardiac
society , but was overlooked by most of the physicians.
After coming to Kingdom of Saudi Arabia ,
I continued ineterst in ischemic heart failure
syndromes, and discovered few patients with
ischemic type 1V heart failure syndromes with
more or less same coronary morphological
features. Following is one of the good example to
share in this regard.

13. Case No 1 ( 100020548)
Date &time of admission 17. 3. 2015, at 6.11 Pm
Mode of Admission: Through ER.
Date & time of Expiry: 8 . 4 . 2015 , at 10.50 Pm
(Expired on 21th day of hospitalization & 48 hours of
CABG)
DIAGNOSIS
Acute decompensated Ischemic heart failure syndrome
with Syncope .
Severe LV systolic dysfunction moderate MR, Severe TR
& pulmonary hypertension ( type 1V)
stage C . severe diffuse 3 VD
CAD .
Post CABG , haemorrhagic / cardiogenic shock
Acute hypoxic liver injury, cardio-renal syndrome.

14. Executive Summary
50 year non saudi male hypertensive & smoker
,presented to KFHH ER with history of progressive
breathlessness & fatigue for the last 6 months
became severe at rest on the day of admission.
No H/o chest pain suggestive of angina or
myocardial infarction.
Evaluated by on call ,and admitted as hypertensive
acute decompensated heart failure syndrome,
echocardiogram showed severe global LV systolic
dysfunction EF < 20%.

15. Cont,
After HF stablization ,to rule out CAD underwent
Coronary angiogram which showed severe
diffuse 3VD CAD.
Discussed in combined meeting and was
recommended for viability study, which showed
dilated LV prominent RV with increase lung
uptake.
There were two totally reversible defect in LAD &
LCX territory.
However RCA had irreversible
( non viable scar) defect EF, 19%

16. Cont,
He was re discussed and was accepted
for high risk PCI.
Later reviewed by interventionalist team
and deferred for PCI.
Again third time discussed in combined
meeting and was accepted for high risk
CABG ( Euro-score 6.4 &
mortality around 5-10%)

17. Cont,
Prepared for CABG IABP was inserted on
6th April, evaluated by pulmonologist and CT
chest was done for pleural effeusion prior to
CABG.
On 7 th April underwent CABG, all arteries
were deeply intramyocardial.
Had 4 grafts, LIMA to mid LAD, SVG to
Diagonal & PDA of the RCA. OM
was totally occluded.

18. Cont,
In recovery suddenly became hypotensive VT/Vib ,
re-opened again, bleeding points were secured,
another SV Grafting was done to LAD.
In view of his haemodynamic instability along with
IABP ,ECMO was inserted and shifted to ICU
in critical condition, on multiple ionotropes .
Bleeding continued through drains ,platelets
dropped to 42 along with HB% ,transfused
various & multiple blood products ( total 101,
Rbc, Platelets, fresh frozen plasma & Cryo
precipitates) , all invain.

19. Cont,
On 8th April again shifted to OR because of
bleeding, re-thoracotomy done, clots removed,
areas of bleeding close to LAD were again sutured.
Chest packed with three large swabs, and shifted
back to ICU.
On maximum haemodynamic support (
IABP ,ECMO & multiple ionotrops) Dialysed
through CRRT , subsequently developed hypoxic
hepatitis ( AST,ALT & LDH) in thousands.
On the same day around 10 .20 pm developed
bradycardia which progressed to asystole ,
resuscitation done but failed and expired at 10.50
Pm.

20. PAST HISTORY
6 months back was admitted to PSBJ H with H/O
progressive breathlessness FC11 & syncope .
Fell down from the bed while he was sitting alone
,recovered spontaneously after some time , sustained
fascial injury with bleeding ,therefore went to
hospital EKG & X-rays were done ,but prior to full
evaluation left against medical advise (
LAMA).
Last time admitted to KFHH with worsening of symptoms of
heart failure, however considered as suspected corona virus
and remained in isolation ward untill cleared from dammam
reports that corona is negative.

21. Echocardiogram (26.3.15)
Moderately dilated LA /LV with severe global LV
systolic dysfunction EF < 20%.
Normal RA/ RV size, and function.
Moderate Mitral Regurgitation.
Severe TR, PASP= 50 – 55 mm.
Intact septa , IVC mildly dilated.
No pericardial effusion. No Clot.

24. Coronary Angiogram
( 26.3.2015)
LM: 30% plaque mid and at bifurcation.
LAD: Type 3 vessel , mid 90% diffuse disease, distally
graftable .
LCX: Non dominant . CTO proximally, filling from
RCA.
RCA: Dominant, diffuse disease, 50% proximal, 75%
mid and 90% distal. PLVB diffusely diseased, PDA
occluded filling from LCA .
Conclusion :
Severe 3 VD diffuse disease for discussion.

37. CBC/Biochemistry (100020548)
8.4.2015After CABG7.4.201518.3.2015
50-100Troponin8.88.717.16.5WBC
10.2101015.3HEMOGLOBIN %
45,23,40279193325PLATELETS
1.8PTT> 1203.10.9INR
21.85.24.6GLUCOSE
8.1,6.99.17.7BUN
170,17111387CREATININE
840,94749399CPK
NegativeSickling315,31312517CKMB
4.8T3,158,150146138SODIUM
15.2T44.8 , 5.23.93.9POTASSIUM
2.4TSH1.52.1CALCIUM
1.020.7MAGNESIUM
420564URIC ACID
1.43.7CHOLESTEROL

38. Liver function test (10020548)
8.4.20157.4.2015
Post CABG
31.3.1418.3.2015Name of
Test
B+VeBlood
group
22.733.0Total
Bilirubin
5.119.0Direct
Bilirubin
NegativeHCV19156972730ALT
NegativHbs27846954736AST
NegativHIV29763185299354LDH
18.4 / 914, 133272.4/22T protein/
Albumin
190117Alpo4

39. Transfusion ( total 101 units)
( Haemorrhagic shock)
Fresh
Frozen
Plasma
22
Units
R
B
C
26
Units
Cryo
precipitate
23
Units
Plate
lets
30
Units

40. 54 year Afghani male, admitted on saturday 25th july 2015 at around 7am with extensive anterior wall
STEMI, underwent primary PCI to Single vessel totally proximally occluded LAD successfully with DES
deployment TIMI 111 flow.
Immedietely post PCI in CCU develop acute heart failure ( De-novo), simple. haemodynamically stable
without major organ dysfunction.Echo showed severe LV systolic dysfunction and no mechanical
complication.

41. 54 year Afghani male, admitted on saturday 25th july 2015 at around 7am with extensive anterior wall STEMI.EKG on right taken at 5 am in
one of the private hospital where he presented with H/O chest pain after 8 hours. EKG shows sinus tachycardia , Q waves with ST elevation in
leads 1,aCL ,V2 to V6. cardiac markers were elevated in thousands at admission. Presumbly late presentation of MI .Did PCI to totally
occluded LAD .LCX & RCA were normal. Post PCI develop acute pulmonary edema.

42. 54 year Afghani male, admitted on saturday 25th july 2015 at around 7am with
extensive anterior wall STEMI.
Coronary angiogram shows single vessel proximal acute thrombotic occlusion of
LAD after septal branch. LAD before and after PCI.

43. Acute Extensive anterior wall STEMI complicated by ( De-
novo) HF.
Type 1 , Ischemic Heart failure syndrome

44. Acute Ischemic Heart Failure syndrome ( de –nove)
Type 1V, Without clinical evidence of myocardial infarction & angina.

45. “Which is Benign,
Which is Malignant”

46. Two other ischemic heart failure
type 1V and type 1 .
( Acute anterior wall STEMI,
simple HF, SVD ,post PCI to
LAD)
Coronary anatomy and
morphology.