Acute Ischemic Heart Failure

syndromesDr Asadullah Soomro

Adult cardiologistPrince sultan cardiac centre Al-Hassa

Kingdom of Saudi Arabia. Email;hssbasadsoomro@gmail.com

Ischemic heart failure syndrome type 11, with more than 100 times

hospitalization. Guess what is this??

SOOMRO,S

HEART FAILURE WORLD

IATROGENIC HEART FAILURE

SYNDROMES

MIXED ISCHEMIC

HEART FAILURESYNDROMES WITH

STRUCTURAL HEART DEFECTS

ISCHEMIC HEART

FAILURE SYNDROMES

NON ISCHEMIC

HEART FAILURE

SYNDROMES

1 2

34

Type 1V“ Orphan Ischemic

heart failure Syndromes”

“ Myth or reality”

Ischemic Type 1V Heart failure

syndromesConventional 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.

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.

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.

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.

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.

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.

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 .

Background of Ischemic Type 1V Heart failure

syndromesAt 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.

Case No 1 ( 100020548)Date &time of admission 17. 3. 2015, at 6.11 PmMode 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)

DIAGNOSISAcute 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.

Executive Summary50 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%.

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%

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%)

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.

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.

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.

PAST HISTORY6 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.

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.

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.

CBC/Biochemistry (100020548)

8.4.2015

After CABG 7.4.2015

18.3.2015

50-100

Troponin

8.8 8.7 17.1 6.5 WBC

10.2 10 10 15.3 HEMOGLOBIN %

45,23,40 279 193 325 PLATELETS

1.8 PTT> 120

3.1 0.9 INR

21.8 5.2 4.6 GLUCOSE

8.1,6.9 9.1 7.7 BUN

170,171 113 87 CREATININE

840,947 493 99 CPK

Negative Sickling 315,313 125 17 CKMB

4.8 T3, 158,150 146 138 SODIUM

15.2 T4 4.8 , 5.2 3.9 3.9 POTASSIUM

2.4 TSH 1.5 2.1 CALCIUM

1.02 0.7 MAGNESIUM

420 564 URIC ACID

1.4 3.7 CHOLESTEROL

0.8 0.8 TRIGLYCERIDE

0.5 1.0 HDL

0.5 2.1 LDL

Troponin

Liver function test (10020548)

8.4.2015 7.4.2015Post CABG

31.3.14 18.3.2015 Name of Test

B+Ve Bloodgroup

22.7 33.0 Total Bilirubin

5.1 19.0 Direct Bilirubin

Negative

HCV 1915 697 27 30 ALT

Negativ

Hbs 2784 695 47 36 AST

Negativ

HIV 2976 3185 299 354 LDH

18.4 / 9 14 ,13 32 72.4/22 T protein/

Albumin

190 117 Alpo4

Transfusion ( total 101 units)

( Haemorrhagic shock)

Fresh FrozenPlasma

22Units

RBC

26Units

Cryo precipitate

23Units

Platelets

30Units

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.

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.

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.

Acute Extensive anterior wall STEMI complicated by ( De-novo) HF.

Type 1 , Ischemic Heart failure syndrome

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

& angina.

“Which is Benign,Which is

Malignant”

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.