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Acute myocardial infarction complicated by acute heart failure

DIMITRIS KARATZASAttikon University Hospital, Athens, Greece

CLINICAL CASES SESSION

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Patient: 65 years, white, female

Admission: December 10th 2010

Complain: Acute dyspnea

Cardiovascular Risk FactorsCardiovascular Risk Factors: Known CADHypertensionDiabetes type 2

CLINICAL CASE

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Cardiovascular Past History: Cardiovascular Past History:

20072007 coronary angiography ???

Follow-up? Other exams (ECG, Echo)?

CLINICAL CASE

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5 days before admission

Respiratory infection (fever 38 C)

3 h before admission

Worsening dyspnea decides to go the hospital

CLINICAL CASE

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Blood Pressure: 90 / 60 mm Hg HR: 100 bpm

Cardiovascular Exam: Jugular venous distensionS1; S2; S3;No murmurs

Chest Exam: rales over the lung bases

Abdominal Exam: normal

Extremities: no edema

PHYSICAL EXAMINATION (at ER admission)

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ECG (admission)

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65 yo, white, female

Known CAD,

Dyspnea

EKG compatible with ongoing lateral AMI

Low BP

CASE SUMMARY

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LABORATORY – at admission

Markers of necrosis:

cTnI (0,32 ng/ml)

CK (220 UI/L)

CK-Mb (29 UI/L)

Creatinine: 1.4 mg/dl

Hb: 8.5 g/dl

Potassium: 5.4 mEq/L

Sodium: 141 mEq/L

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1. Send to the CCU I.V. thrombolytics2. Send to the cath Lab primary PTCA3. First stabilize with I.V. diuretics and I.V

nitroglycerin, than send to the cath lab4. Install intra-aortic balloon counterpulsation

AT THIS TIME, WHAT SHOULD WE DO?

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ER decision:

Oxygen by nasal canula 3 L/min Morphine 2 mg I.V. Aspirin Clopidogrel 300 mg I.V. furosemide 40 mg Send to the cath lab

CORONARY ANGIOGRAPHY

LAD 100%LCx: 99%, 100%RCA: 70% proximal and multiple 75-90% distal

Decided Procedure: PCI to LCx

CORONARY ANGIOGRAPHY

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INTRAAORTIC BALOON COUNTERPULSATION

IABP positioned before high risk PTCA (standard procedure)

Pumping started at 1:1

I.V. Heparin bolus + infusion

Procedures: PCI to LCx (2 stents)

CORONARY INTERVENTION

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Reevaluation in CCU

BLOOD PRESSURE: MAP>80 mm Hg

Creatinine: 1.6 mg/dl

Hb: 10.8 g/dl

Potassium: 4.4 mEq/L

Sodium: 140 mEq/L

72 hours later the IABP was removed

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Three days later the patient was transfered to the wardThe echo study showed an EF=40%.......

On the 10th day the patient suffered cardiac arrest due to ventricullar fibrillation

Follow-up

Blood Pressure: 96 / 72 mm Hg Heart Rate: 104 bpm

Neurological status: confused

Cardiovascular Exam: Increased jugular vein distensionS1; S2; S3;No murmurs

Chest Exam: rales over 2/3 of the lungs

Abdominal Exam: normal

Extremities: peripheral hypoperfusioncyanosis

ICU ADMISSION

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Patient intubated– Mechanical ventilation started– FiO2 60%– PEEP 10 mm Hg

IABP inserted (1:1)

Swan – Ganz assessments

NEXT STEPS

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Hemodynamic measurements

MAP: 70 mm HgCO: 2.1 L/minCI: 1.6 L/min/m2

SVRI: 3400 dyne sec/cm-5

PVRI: 345 dyne sec/cm-5

PCWP: 24 mm HgRAP: 14 mm HgSVO2 : 60 %

> 704 – 8

2.8 – 4.21970 – 2390

225-3155 – 15

0 – 8> 70

Procedures: PCI to LAD ....

CORONARY INTERVENTION (2)

Procedures: PCI to LAD & RCA

CORONARY INTERVENTION (2)

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The patient remained to the CCU for 7 days due to respiratory infection and then she was transfered to ICU for further treatment....

Follow-up

Acute Heart Failure Complicating Acute Coronary Syndromes

A Deadly Intersection

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Acute Heart failure and ACS

Patients with ACS and heart failure on admission

Patients with ACS and heart failure during hospitalization (after thrombolysis, PCI or no reperfusion therapy)

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…the problem

Approximately 10% to 20% of patients with ACS have concomitant HF, and up to 10% of ACS patients develop HF during hospitalization

80% of all in-hospital morbidity and mortality is concentrated in the group of patients with ACS and acute heart failure

The short-term risk of adverse clinical outcomes in patients with ACS complicated by HF is directly proportional to the level of troponin elevation.

The prognosis of ACS complicated by HF is directly related to the degree of HF as measured by the Killip classification.

Compared with those with Killip class I HF, patients with an ACS in Killip class II or III HF are 4 times more likely to die during the index hospitalization, whereas those with cardiogenic shock (class IV) have a 10-fold higher mortality.

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GRACE investigators

HF at admission was associated with a 4-fold increase in hospital mortality rates (12.0% versus 2.9%).

This was true across all ACS(16.5% versus 4.1% in STEMI)(10.3% versus 3% in NSTEMI)(6.7% versus 1.6% in unstable angina)

The mortality rates were 2.9%, 9.9%, and 20.4%, for patients in Killip classes I II and III

Circulation 2004Circulation 2004

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HF Leads to Early and Sustained Increases in Mortality

n

No heart failure at admissionHeart failure at admission

MO

RTA

LITY

Time to death within 6 months

11 729 11 671 11 117 11 002 10 915 10 863 10 7716543210

0

0,1

0,2

0,3

Cumulative in-hospital and postdischarge mortality rate was 20.7% in pts with HF on admission vs 5.9% in pts without HF

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GRACE investigators

Regardless of LVSD, AHF in the presence of ACS is associated with a striking increase in short-term mortality (42% of the VALLIANT cohort presented with AHF and did not have quantitative evidence of LVSD).

Determinants of in-hospital and short-term mortality risk, including increasing age, female gender, prior infarction, diabetes, hypertension, and higher heart rate.

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GRACE investigators

Focusing early aggressive pharmacological, procedural, and interventional strategies at this group may lead to early benefits in overall survival.

Even if only a relatively small modification in risk for the heart failure subgroup were achieved, significant absolute reduction would occur in morbidity and mortality for the entire ACS population

Clinicians should intensify their application of proven therapies. Yet, contrary to this principle, ACS patients who develop AHF are significantly less likely to undergo cardiac catheterization and subsequent revascularization and also are less likely to receive pharmacotherapies with established mortality reduction such as ACE inhibitors, - blockers, and statins.

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AHF in pts with STEMI treated with primary PCI

European Journal of Heart Failure 2008

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AHF in pts with STEMI treated with primary PCI

The systematic application of primary PCI may prevent the subsequent development of HF, but, when HF develops, the prognosis remains severe.

Therefore, an aggressive strategy should be recommended particularly in patients who have clinical signs of HF on admission or who have an AMI with a large risk area

European Journal of Heart Failure 2008

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Guidelines recommendation

In patients with ST-segment elevation myocardial infarction, emergency primary PCI is universally recommended for patients with CHF (class IB indication).

Guidelines also recommend an early invasive strategy (ie, diagnostic angiography with intent to perform revascularization) in initially stabilized patients with NSTE-ACS (without serious comorbidities or contraindications to such procedures) who have an elevated risk for clinical events, including patients with symptoms or signs of CHF (class IA).

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However…

observations in large, contemporary, multinational cohorts reflective of current practice suggest marked underuse of revascularization among patients with NSTE-ACS complicated by CHF.

A critical window exists to improve the survival of those with AHF complicating ACS. Although AHF is present on admission or develops early during ACS, the mortality risk in patients continues to accelerate beyond the early period out to at least 30 days.

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Take home messages …

Patients with ACS complicated by HF have a 4-fold increased risk of in-hospital mortality

However these patients are less likely to undergo coronary angiography and revascularization and to receive pharmacological therapy for CAD than ACS patients without HF.

Targeting the most severely affected pts derives the most benefit.

Smarter use of existing therapies can improve clinical outcome

Thank you