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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.

Increased morbidity due to hemorrhagic complications is associated with an invasive management strategy in patients with acute myocardial infarction. Our findings show the complex interaction of several factors in the occurrence of hemorrhagic events during thrombolytic therapy.

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Dilation of the left ventricle after myocardial infarction is common, occurs rapidly (within 2 weeks of infarction) and may be self-limited. To evaluate the time course of postinfarction left ventricular dilation and to assess the impact of successful coronary thrombolysis, serial radionuclide left ventricular volume analyses were performed in 36 patients undergoing attempted thrombolysis for acute transmural myocardial infarction. All patients underwent cardiac catheterization, coronary angiography and attempted thrombolysis within 7 h of the onset of symptoms. The site of coronary occlusion was the left anterior descending coronary artery in 17 patients, the right coronary artery in 18 and, in 1 patient, occluded bypass grafts to the right and left circumflex coronary arteries. Attempted reperfusion using a thrombolytic agent was successful in 22 individuals, occurring 5 +/- 1 h after the onset of symptoms. Gated radionuclide ventriculography was performed early (mean time 1 day after admission, n = 36), subacutely (mean time 11 days postinfarction, n = 36) and late after infarction (mean time 10.5 months, n = 25), and a geometric technique was used to measure serial left ventricular end-diastolic volume. Left ventricular end-diastolic volume for the entire group increased significantly (p less than 0.01) from 153 +/- 30 ml at baseline to 172 +/- 45 ml (at 11 days) to 220 +/- 63 ml (at 10.5 months). Twenty of 36 patients showed greater than 20% increase in left ventricular end-diastolic volume (dilation) with time. This appeared early in seven patients, occurred remote from infarction in seven others and showed a progressive pattern in six.(ABSTRACT TRUNCATED AT 250 WORDS)

Subjective estimates of the angiographic severity of coronary artery stenoses show variability and inaccuracy. We therefore tested the accuracy of a newly developed computerized image analysis system for quantitating vessel diameter from cineangiograms. Fourteen cylindrical phantoms of known diameter were filled with contrast medium and filmed over a wide range of clinically relevant radiographic conditions in order to develop regression equations that related computer-derived to anatomic diameters. Computer measurements of vessel diameter were unaffected by vessel size, magnification, focal spot size, thickness of scattering medium, kilovolt peak, or location within the radiographic field, but a correction factor was necessary for a small but significant (p < .01) linear dependence on contrast medium concentration. The accuracy of computerized vessel diameter measurements ranged between + 59 and 137 ,u for all conditions except for rapid vessel motion and contrast medium concentrations of 50% or less meglumine diatrizoate (Renografin 76), both of which resulted in reduced accuracy as well as in the inability to locate lumen edges of vessels less than 1 mm in diameter.Circulation 68, No. 2, 453-461, 1983. SUBJECTIVE VISUAL ESTIMATES of percent stenosis of a coronary artery from cineangiograms have been shown to be characterized by a large interobserver variabilityl-3 and a descrepancy between angiographic and postmortem estimates of lesion severity has been noted in a number of studies. further objectify measurements of luminal dimensions. Although the reproducibility of various objective methods of diameter measurement has been studied, the accuracy of these measurements has received little attention.The fact that radiographic vessel images have edge gradients rather than sharply demarcated edges is not widely appreciated by angiographers. 14 Accurate diameter measurement is dependent on precise localization of the anatomic vessel edge within the edge gradient, and the magnitude of error in diameter measurements associated with arbitrary assignment of the vessel edge within the edge gradient may be considerable. A new method for computerized edge detection of coronary arteries from digitized 35 mm cineangiographic images with the use of specific algorithms to locate spatially disparate points within the edge gradient has been developed. The hypothesis that each of these points can be mathematically related to the anatomic edge was tested by filming contrast mediumfilled cylindrical phantoms over a wide range of cineradiographic conditions and comparing computer-derived measurements of diameter from digitized frames with the known diameters.

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Nine patients with acute myocardial infarction had cardiac catheterization and intracoronary infusions of streptokinase 2.3 to 4.3 hours (mean, 3.5) after the onset of symptoms. Occluded coronary arteries were opened within approximately 20 minutes in all patients, but reocclusion occurred in one patient. The immediate effect of thrombolysis on myocardial salvage was assessed with the intracoronary injection of thallium-201. Improved regional perfusion, indicating myocardial salvage after recanalization, was observed in seven of the nine patients. One patient, who had also sustained a nontransmural infarction one week before, had no change after thrombolysis. In the ninth patient, recanalization of a coronary artery was followed by reocclusion and worsening of the myocardial-perfusion defect. Intracoronary thallium-201 studies two weeks and three months after streptokinase infusion in two patients were unchanged in comparison with scintiscans performed 1.5 hours after thrombolysis. These short-term observations suggest that recanalization of obstructed coronary arteries after intracoronary thrombolysis can salvage jeopardized myocardium, However, evaluation of the long-term effects of this procedure on survival and myocardial function will require controlled clinical trials.