Left ventricular function in acute myocardial infarction

Abstract

A B S T R A C T Left ventricular catheterization was carried out in 40 patients with acute myocardial infarction. Left ventricular end-diastolic pressure (LVEDP) was elevated in 85% of the patients studied. In 14 patients with apparently uncomplicated infarcts, LVEDP averaged 15 mm Hg, and cardiac index (2.98 liter/min/m'), stroke volume (38.3 ml/m'), and stroke work (49.2 g-m/m') were within normal limits. In 12 patients with clinical signs of left ventricular failure, LVEDP averaged 29.9 mm Hg, cardiac index was at the lower limit of normal (2.79 liter/min/m'), but stroke volume (31.6 ml/m') and stroke work (37.3 g-m/m') were reduced.In 14 patients with clinical signs of shock, LVEDP averaged significantly lower than in the heart failure group (21.1 mm Hg), but cardiac index (1.59 liter/min/ m'), stroke volume (16.5 ml/m'), and stroke work (11.1 g-m/m') were markedly reduced. A large presystolic atrial "kick" (average amplitude 9.5 mm Hg) was an important factor in the high LVEDP in the patients with heart failure but not in those with shock. The first derivative of left ventricular pressure was significantly lower in shock than in the nonshock group. Although right atrial pressure (RAP) and LVEDP were significantly correlated (r = 0.49), wide discrepancies in individual patients rendered the RAP an unreliable indicator of the magnitude of left ventricular filling pressure.These data show the following: (a) LVEDP is usually elevated in acute myocardial infarction, even in absence of clinical heart failure; (b) cardiac output apparently is supported by increased LVEDP and compensatory tachycardia; (c) in patients with shock, left ventricular function usually is markedly impaired, but inadequate compensatory cardiac dilatation or tachycardia could contribute to the reduced cardiac output in some indiThis work was presented in part at the meeting of The

Influence of scar on left ventricular performance at the onset of myocardial ischemia: shock versus heart failure

“…This animal model of shock during myocardial ischemia appears to simulate myocardial infarction in man, in that it is associated with prior abnormality of ventricular muscle (8,9) and occurs after occlusion of a main branch of the left coronary artery (1). However, shock could occur in a different setting in the unusual instance of left main coronary artery occlusion without previous myocardial injury (4).…”

“…Thus, experimental models employing a previously normal myocardium have required embolization of multiple coronary arteries to produce hypotension (6), which does not closely parallel the usual vascular abnormalities associated with clinical myocardial infarction (7). Further, there is evidence in man suggesting that cardiac decompensation or shock during myocardial ischemia is usually associated with previous abnormality of the myocardium (8,9). 534 The Journal of Clinical Investigation Volume 50 1971…”

Relationship between pulmonary artery end-diastolic pressure and left ventricular filling pressure in patients in shock

“…The cause of shock was acute myocardial infarction in 12 patients, sepsis in five, postcardiac arrest in three, hypovolemia in three, drug overdose in one, and cerebrovascular accident in one.…”

“…The agents were infused in increasing amounts depending on clinical response (i.e., increases in systemic pressure, urine flow, improved sensorium, cardiac output), the limiting factors being an undue increase in heart rate or increased ventricular irritability. Four patients were treated with norepinephrine (4-12 ug/min), three with isoproterenol (3)(4)(5)(6)(7)(8)(9)(10)(11)(12)(13)(14) gg/min) and one patient in the latter group received 5 mg of glucagon (table 3). Two patients were studied before and after intravenous administration of 80 mg of ethacrynic acid while another subject was studied before and 10 min after administration of a 250-ml volume challenge.…”

Evolution of Abnormalities in Left Ventricular Function after Acute Myocardial Infarction

“…In three patients (9, 11, and 12), however, the ventricle responded to reduction in LVEDP with a rise in stroke volume. In six patients (4,5,7,8,10, and 11), similar volume manipulations were carried out in the follow-up studies. When cardiac function curves from different studies in the same patient were compared, no consistent pattern emerged.…”