Dilatation of infarcted segments (infarct expansion) may occur during recovery from myocardial infarction, but the fate of noninfarcted segments is uncertain. Accordingly, left ventricular geometric changes were assessed by left ventricular angiography and M mode echocardiography on admission and 2 weeks later in 30 patients with their first acute transmural myocardial infarction. All patients demonstrated chest pain, ST segment elevation with subsequent development of Q waves (15 anterior, 15 inferior), and elevation of cardiac enzymes. Sequential left ventricular angiographic and hemodynamic findings were available in these patients by virtue of their participation in a study of thrombolysis in acute myocardial infarction. By that study design, all patients treated successfully with thrombolytic therapy and demonstrating improvement of flow in an occluded coronary artery underwent repeat cardiac catheterization. At 2 weeks there was a significant decrease in left ventricular and pulmonary capillary wedge pressures (p < .0 1), whereas both left ventricular end-diastolic (LVEDV) and end-systolic (LVESV) volume indexes increased (p < .01). The increase in LVEDV correlated directly with the percentage of the ventriculographic silhouette that was akinetic or dyskinetic at the initial catheterization (r = .71, p < .001). To assess regional changes in both infarcted and noninfarcted segments, serial endocardial perimeter lengths of both the akinetic-dyskinetic segments (infarction zone) and of the remainder of the cardiac silhouette (noninfarction zone) were measured in all patients who demonstrated at least a 20% increase in their LVEDV at 2 weeks after myocardial infarction. Notably, there was a mean increase of 13% in the endocardial perimeter length of infarcted segments and a 19% increase in the endocardial perimeter length of noninfarcted segments. Serial M mode echocardiographic studies showed no significant change in the wall thickness of noninfarcted myocardial segments. Hemodynamic changes that occurred in this subgroup of patients included significant decreases in left ventricular end-diastolic and pulmonary capillary wedge pressures (p < .05) and significant increases in angiographic cardiac index (p < .01) and LVESV index (p < .01). We conclude that in patients who manifest cardiac dilatation in the early convalescent period after myocardial infarction, there is remodeling of the entire left ventricle including infarct expansion of akineticdyskinetic segments and volume-overload hypertrophy of noninfarcted segments. The magnitude of the remodeling process is directly proportional to infarct size as assessed by the extent of wall motion abnormality present during the acute phase of infarction. Moreover, the remodeling changes that occur are associated with hemodynamic improvement, including lower left ventricular filling pressures and increased cardiac output, but these hemodynamic changes appear to occur at the expense of a significant increase in left ventricular chamber volumes.

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Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19+0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69±0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressurevolume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values.We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.

In 103 patients who underwent placement of 106 percutaneous wire-guided intraaortic balloon catheters between August 1983 and January 1986, all placements were successful and the average duration of counterpulsation was 3.4 +/- 1.6 days. During counterpulsation, 45 patients developed limb ischemia that required premature balloon removal in 29 patients. The development of limb ischemia was significantly related to the presence of diabetes (risk ratio 2.0), peripheral vascular disease (risk ratio 1.9), female gender (risk ratio 1.8) and the presence of a postinsertion ankle-brachial pressure index less than 0.8 (risk ratio 7.9). There was no association between the development of limb ischemia and age, body surface area, balloon size (10.5F/12F) or adequacy of anticoagulation. Fifteen patients underwent vascular surgery for treatment of balloon-related limb ischemia, which was associated with one operative death. Nine patients had persistent limb ischemia (seven asymptomatic, two symptomatic) at the time of hospital discharge. Improvements in wire-guided balloon technology have increased the probability of successful balloon placement over that of surgical placement and have reduced the incidence of major aortic injury, but there is no evidence that these improvements have reduced the incidence of limb ischemia or its sequelae. This should be borne in mind before proceeding with balloon insertion in patients with one or more risk factors for developing limb ischemia.

Sulfonylurea therapy appears to attenuate the magnitude of ST-segment elevation during an AMI, resulting in failure to meet criteria for thrombolytic therapy and as a consequence leading to inappropriate withholding therapy in this subset of diabetic patients.