Heart failure during hospitalization for acute myocardial infarction a coronary care unit registry study, Gheorghi-ade et al observed a decrease in the incidence of heart failure from 30.7% between 1982 and 1985 to 23.9% between 1992 and 1995. Another coronary care unit experience from Minneapolis and Gothenburg showed heart failure rates of 27% of men and 37% of women after acute myocardial infarction (AMI) with mortality rates of 12% and 15%, respectively. Heart failure during hospitalization for AMI was age-related. Its incidence increased progressively from 14% in patients below 50 years of age to 39% in those over 80, and was associated with increased mortality rates of 26.2% and 64%, respectively.
Ali et al observed heart failure in 41.6% of their patients after a first AMI admitted within 24 hours of symptom onset. The distribution was bimodal, with a small early peak on admission (4%), followed by a second peak beginning 4 days later in 39% of the remaining patients. Predictors of early-peak failure were older age, diabetes mellitus, or previous cardiac symptoms. Those of late-peak failure were the same demographic factors, plus a history of hypertension, male gender, increased peak creatine phosphokinase and heart rate, and low left ventricular ejection fraction. In patients with vs without heart failure, in-hospital mortality was 5.3% vs 1.4%; outcome at 18 months follow-up was also poorer, with mortality rates of 14.9% vs 6.4%.
The late heart failure peak, 4 to 8 days after AMI, suggests that if predictors could be identified, appropriate preventive measures could be taken. Recurrent ischemia could be one culprit, as could activation of the renin-angiotensin system (RAS) or sympathetic nervous system. Both angiotensin II and norepinephrine are
increased early in AMI with evidence of heart failure. The observation that angiotensin-converting enzyme (ACE) inhibitors are effective in lowering heart failure and mortality rates in high-risk patients soon after AMI suggests that RAS activation has an important role in heart failure progression. In addition, the Metoprolol In Acute Myocardial Infarction (MIAMI) trial demonstrated that early intravenous metoprolol decreased heart failure and mortality rates in older high-risk patients with a history of hypertension and diabetes mellitus. Ali et al also found an association between P-blockade and a decreased incidence of in-hospital heart failure.
In summary, older patients with diabetes and preexisting coronary disease are more prone to in-hospital heart failure and death following a first AMI despite similarly aggressive thrombolytic therapy.
Heart failure beyond the acute phase of myocardial infarction
Gaudron et al showed that a quarter of patients develop limited left ventricular dilatation within 4 weeks of a first AMI. This helps to restore the cardiac index and stroke index at rest, and to preserve exercise performance. It thus remains compensatory. A slightly smaller fraction (20%) develops progressive structural left ventricular dilatation, which is compensatory at first, then progresses to noncompensatory dilatation, and ends in severe global left ventricular dysfunction. In these patients, depression of the global ejection fraction probably results from dysfunction of initially normally contracting myocardium. Significant predictors of progressive ventricular enlargement and chronic dysfunction include the ejection fraction and stroke index at 4 days, ventriculographic infarct size, anterior infarction, and the Thrombolysis In Myocardial Infarction (TIMI) grade of infarct artery perfusion. The in-hospital incidence of heart failure, which ranges from 10% to 30%, can be significantly decreased by early ACE-inhibitor therapy. St John Sutton et al evaluated left ventricular remodeling in a large cohort of the Survival And Ventricular Enlargement (SAVE) trial. Cardiovascular death and/or left ventricular dilatation occurred in >50% of survivors of AMI with left ventricular dysfunction in the initial 3.5 years of follow-up. Progressive left ventricular dilatation was associated with distortion of ventricular shape, deterioration in systolic function, and increased risk of adverse cardiovascular events. Patients with a history of MI, low ejection fraction, early heart failure, older age, and persistent changes in the echocardiographic indices of left ventricular geometry and function, form a particularly high-risk group for progressive dilatation and adverse cardiovascular events.
In older men and women with heart failure associated with prior MI in a long-term health care facility, Aronow et al found significantly higher mortality in those with an abnormal vs normal ejection fraction. Significant independent risk factors for total mortality were age, hypertension, diabetes mellitus, and an abnormal left ventricular ejection fraction.
After AMI with or without left ventricular dysfunction or heart failure, Kober et al showed that mortality declined steeply with time to a low plateau at 1 year. Similarly, the absolute importance of left ventricular systolic dysfunction and heart failure, estimated as differences in monthly mortality, also declined rapidly in the first year. However, the relative importance of these risk factors as predictors of mortality persisted for >5 years, although it too decreased with time. Both heart failure and LV dysfunction were also associated with other risk factors, such as three-vessel coronary disease and ventricular arrhythmias. Because these patients with greater problems tended to die earlier, the risk associated with heart failure and left ventricular dysfunction declined with time. In this study, the prognostic importance of new or transient heart failure was less than for established heart failure, but it maintained its prognostic importance, demonstrating that aggressive management is mandatory. These patients should receive ACE inhibitors, but transient heart failure may reflect severe three-vessel disease requiring revascularization. This study also showed that not all prognostic factors retain their relative importance. The prognostic importance of ventricular fibrillation is quickly exhausted. Other factors normally considered important (infarct location, previous AMI) showed only borderline significance in multivariate models.
Numerous studies have shown that left ventricular dysfunction is often potentially reversible, related to myocardial stunning, myocardial hibernation, or a combination of these two pathophysiological processes. In such patients left ventricular function may improve substantially, and even normalize, after revascularization. Moreover, enhanced left ventricular function with revascularization translates into symptomatic benefit in patients with perioperative heart failure symptoms.
In patients with viable myocardium included in the meta-analysis by Allman et al, annual mortality was significantly lower in those treated with revascularization (3.2%) than in those treated medically (16%). This trend was uniform across all the studies, and independent of the method used to identify viable myocardium. Even the degree of improvement in outcome with revascularization in these patients did not depend on whether the evidence of viable myocardium was provided by positron emission tomography, single photon emission tomography with thallium-201, or low-dose dobutamine stress echocardiography. Annual mortality in revascularized patients with little if any evidence of viable myocardium is significantly worse than in those with viable myocardium: 7.7% vs 3.2%. In several studies, perioperative mortality rates were impressively high (10%) in patients without, and negligible in those with, viable myocardium.
The data of Allman et al indicate that is not necessarily wrong to recommend revascularization in patients with minimal evidence of viable myocardium since the outcome is not significantly worse than with medical therapy. Management decisions in this latter subgroup clearly need to be made on a case-by-case basis, factoring in other considerations such as age, coronary anatomy, and comorbidity. Randomized studies are needed to elucidate the role of revascularization in the management of patients with ischemic left ventricular dysfunction who do not have angina, as well as the role of viability testing in the decision-making process.
pathophysiology; left ventricular dysfunction; myocardial infarction; prognosis; myocardial viability; neurohumoral activation
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