Regional Left Ventricular Performance in the Year following Myocardial Infarction

Abstract

The relationship of abnormal regional myocardial performance to left ventricular (LV) function 2-12 months following transmural myocardial infarction was investigated in 25 patients by quantitative biplane angiocardiography. Abnormally contracting segments (ACS) (akinetic or dyskinetic) of the LV were identified in 24 patients. Their sites correlated with the electrocardiographic locations of infarction. ACS were expressed as a percentage (ACS%) of the end-diastolic ventricular circumference, and the percentages obtained correlated with ejection fraction (EF) (r = —0.838, P = 0.0001) using a quadratic regression equation. The group of patients (N = 8) with heart failure (paroxysmal nocturnal dyspnea and/or ventricular gallop sound) demonstrated a significantly lower mean value for EF ( P = 0.0003) and a significantly larger mean value for ACS% ( P = 0.0041) than the group of patients (N = 16) without heart failure. EF sharply separated the two groups. ACS% was a poor separator because in the majority of patients in both groups it was between 14 and 38%. Since EF sharply separated the heart failure and non-heart failure groups but ACS% did not, a theoretic model was developed to assess the contribution of the remaining myocardium to LV function. The curve described by the model did not differ significantly from the curve derived from the quadratic regression equation. Data from heart failure and non-heart failure patients were generally separated by a point (EF = 0.30, ACS = 23%) on the theoretic curve. Abnormal function of the nonakinetic myocardium was considered to be present when observed EF was lower than predicted EF for the observed ACS%. Thus, within the year following transmural myocardial infarction, the relative size of an abnormally contracting region of the ventricle was quantitatively related to impairment of LV function. The spherical model not only provided a framework for relating the clinical status of a patient to both ventricular function and size of the ACS, but also offered a means of estimating the function of the myocardium that appeared angiographically to be nonakinetic.

The ischemic segment and left ventricular function during exercise angina

“…According to our results, ejection fraction during maximum angina on effort is determined by the size of the ischemically impaired area. This finding could be seen as analogous to the correlation between size of i1}farct scar and EF found by Field et al (13) in old infarction. Differences between Field's equation and ours are due to: 1. different structure of the impaired area, which is scar tissue in Field's patients and ischemic myocardium in ours; 2. the fact that the compensatory hypertrophy of the normal myocardium found in old infarction is absent in our patients with normal ventricles at rest (31).…”

“…In some patients, however, the resting ventriculogram shows local wall motion abnormalities of viable myocardium, perfused by severely narrowed vessels (6,26). In these patients, there is a localized imbalance of oxygen supply and demand, already at rest (13). Inadequate oxygen supply is known to cause loss of contractility.…”

Serial M‐mode echocardiographic mapping in myocardial infarction: A quantitative evaluation of left ventricular wall motion abnormalities

“…Several reports point to good correlations between the ECG determined site of infarction and LV cineangio- (Field et al, 1973;Gelberg et al, 1979) and echocardiographically (Heikkila et al, 1975;Parisi et al, 1981) determined wall motion disturbances. In contrast, others have pointed to certain shortcomings when comparing electrocardiographically localized infarct extension with autopsy findings (Erhardt 1974;Horan et al, 1971).…”

Importance of temporal heterogeneity in assessing the contraction abnormalities associated with acute myocardial ischemia.

“…The basic observation that functionally and tempor ally disordered ventricular contraction occurs in response to myocardial ischemia/infarction is well established and the detection of such abnormal patterns of myocardial contraction in man has become an accepted criterion for inferring the presence of myocardial ischemia, infarction, or scarring.23 32 Of the different patterns of abnormal contraction that have been described, dyskinesis or paradoxical systolic bulging of a myocardial segment is the most clearly defined and its mechanisms have been extensively studied.25' 27. 33 The timing in systole of such paradoxical bulging has received less attention, although significant variation has been noted during frame-by-frame analysis of angiographic stud-25~30, 34,35 uhs ies.…”