Current data do not allow an accurate determination of the proportion of cardiovascular mortality and morbidity directly attributable to cardiac remodeling. The parameters of left ventricular (LV) remodeling include heart size, shape and mass, ejection fraction, end-diastolic and end-systolic volumes, and peak force of contraction.
Measures of myocardial hypertrophy, such as wall thickness indices or myocardial mass, provide some indication of the changes in overall myocardial structure. There is no consensus echocardiographic definition of LV hypertrophy, and sequential measures can show considerable individual variability. Nevertheless, echocardiographic LV mass is a powerful predictor of cardiovascular mortality. The risk of cardiovascular events is directly related to ventricular mass, with the relationship becoming steeper above a mass of 140 g/m2.
Left ventricular volumes
Relatively small increases in ventricular volume are associated with a major independent increase in the risk of death in patients with coronary artery disease, recent myocardial infarction or heart failure. Post-myocardial infarction patients experiencing subsequent morbid events had greater increases in echocardiographic LV diastolic and systolic volumes than patients without such events.
End-diastolic volume reflects both structural remodeling and diastolic filling (end-diastolic myocyte fiber length). End-systolic volume is influenced by both the end-diastolic volume and fiber shortening. White et al identified end-systolic volume as the most potent predictor of survival: end-diastolic volume or the ejection fraction in a multivariate model added no further predictive value.
Left ventricular ejection fraction
A decreased LV ejection fraction carries a poor prognosis in heart failure. In the Vasodilator-Heart Failure Trials (V-HeFT I and II), mortality increased nonlin-early with the decline in ejection fraction, most sharply with ejection fractions <25%. Conversely, improvements in the ejection fraction carry an improved prognosis. The V-HeFT and Survival And Ventricular Enlargement (SAVE) studies also suggest that serial LV ejection fraction measures provide important additional prognostic information. There is thus a case for monitoring the ejection fraction or chamber size to assess response to therapy and making the appropriate adjustments. Early risk stratification of post-myocardial infarction remodeling Cardiovascular death and/or LV dilatation occur in >50% of survivors of acute myocardial infarction with LV dysfunction in the first 3.5 years of follow-up. Progressive LV dilatation is associated with distortion of the ventricular shape, deterioration in systolic function, and an increased risk of adverse cardiovascular events. Groups at high risk of progressive dilatation and adverse cardiovascular events include the elderly, those with a history of previous myocardial infarction, low ejection fraction, or early heart failure, and those with persistent changes in the echocardiographic indices of LV geometry and function.
The Global Utilization of Streptokinase and tPA for Occluded coronary arteries (GUSTO I) angiographic investigators showed that the end-systolic volume index at 90 to 180 minutes into reperfusion therapy is a strong predictor of 30-day and 1-year mortality rates. Male gender, prior angina or myocardial infarction, body weight <70 kg, heart rate >80 beats/min, systolic blood pressure <110 mm Hg, and anterior infarction were independent predictors of high end-systolic volume index. The clinical variables identified are consistent with those described by Gaudron et al as significant predictors of progressive ventricular enlargement and chronic dysfunction: ejection fraction and stroke index at 4 days, ventriculographic infarct size, anterior infarction, and Thrombolysis In Myocardial Infarction (TIMI) grade of infarct artery perfusion. Several observations emphasize that ejection fraction and infarct location are incomplete predictors of LV remodeling. In a 7-year follow-up of myocardial infarction survivors, 25% of patients with an LV ejection fraction <40% had no significant LV dilatation. Conversely, 53% of those with an LV ejection fraction >40% had a significant increase in chamber volume. Thus, early determination of the LV ejection fraction does not identify a group of patients who could benefit from early and aggressive treatment.
Many studies have also reported expansion and LV enlargement in patients with inferior infarction. The most recent reports have failed to identify infarct location as an independent predictor of LV dilatation. Even the extent of infarction may be an incomplete predictor of LV remodeling, as the incidence of LV dilatation in patients with large infarcts ranges from 35% to 50%. Early LV dilatation may also regress.
Although a large myocardial infarction generally triggers LV remodeling, estimation of infarct size may be insufficient for predicting LV dilatation because expansion requires transmural spread of the myocardial necrosis. Thus in subendocardial infarction, a protective outer layer of perfused myocardium prevents stretching of the infarcted segment and limits volume expansion.
The absence of residual infarct zone viability may discriminate patients with progressive LV dilatation after myocardial infarction from those who maintain normal LV geometry despite the persistence of infarct-related artery patency and an absence of residual stenoses.
Postinfarct electrocardiographic changes
The interrelation between infarct size, scar formation, and dysfunctional, but viable and normal adjacent myocardium, generates different local electrical fields that may be responsible for the surface electrocardiographic (ECG) changes over time. Recently, the Gruppo Italiano per lo Studio della Soprav-vivenza nell’Infarto miocardico (GISSI)-3 Echo Substudy showed that serial ECG analysis predicted postinfarct LV remodeling. Normalization of negative T waves during follow-up appeared more strictly related to recovery of regional dysfunction than QRS changes. Lack of resolution and late appearance of new negative T waves predicted unfavorable remodeling with progressive deterioration of ventricular function.
An elevated plasma angiotensin-converting enzyme (ACE) activity soon after the onset of myocardial infarction may be a significant predictor of LV dilatation and thus identify patients at risk. A risk stratification strategy that includes emerging factors with a strong potential influence on the remodeling process, such as myocardial viability in the infarct zone and LV hemodynamic variables, is mandatory.
The surrogate remodeling measures most frequently determined in large randomized studies are the ejection fraction and LV end-diastolic and end-sys-tolic volumes. The chronic effects of therapy on these measures currently serve as a guide to the remodeling process. However, they do not provide a clear picture of the changes in underlying cardiac pathophysiology. Measurement of the neurohor-
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