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SUMMARY Two-dimensional echocardiography underestimates left ventricular volume compared with cineventriculography. To exclude the influence of difference in heart rate, blood pressure, respiration phases and any effect of the contrast material on left ventricular function, simultaneous studies of twodimensional echocardiography and cineventriculography-echoventriculography were performed in 46 patients. Apical two-dimensional echocardiograms in the right anterior oblique (RAO) equivalent view were recorded before and during cineventriculography in the 300 RAO projection. End-diastolic and end-systolic volumes (EDV and ESV) were calculated using a disc method with a semiautomatic computer system. The echo transducer position relative to the left ventricular apex and long axis was analyzed. For EDV determined by two-dimensional echocardiography and cineventriculography, the linear regression equation was radiologic methods.'4 Thus, patient-related problems could explain the systematic underestimation of left ventricular volume as determined by two-dimensional echocardiography. Differences in heart rate, blood pressure and respiration, and possible influences of contrast agents have been reported.4In this study we analyzed left ventricular volumes and ejection fractions from simultaneous recordings of two-dimensional echocardiograms in the apical right anterior oblique (RAO) equivalent view and cineventriculograms in the RAO plane, eliminating any perturbing influences on left ventricular volume. Methods PatientsThe study was performed in 46 patients, 39 males and seven females, who were undergoing catheterization for evaluation of clinically suspected coronary artery disease (table 1). The mean age (± SEM) was 51.2 + 6.9 years. Thirty-seven patients had significant coronary artery disease, nine showed features of primary congestive cardiomyopathy, two had arterial hypertension, four mitral regurgitation, one patient had mitral valve prolapse, one obstructive cardiomyopathy, and one aortic insufficiency. Three patients appeared to be normal. Fifteen of the 37 patients with coronary artery disease showed asynergy of the anterior wall and 13 asynergy of the posterior wall. CatheterizationThe left ventricle was catheterized retrogradely through a percutaneous puncture of the right femoral artery. The patients were fasting and not premedicat-

Thrombolytic therapy for acute myocardial infarction reduces early mortality, but full recovery of left ventricular function after reperfusion is delayed. Therefore, the relations among reperfusion, survival and the time course of left ventricular functional recovery were examined in 226 patients treated with intracoronary streptokinase; 77% (134 patients) had sustained reperfusion and 31 patients had no reperfusion or had reocclusion by day 3. Wall motion was measured from contrast ventriculograms performed in the acute period and 3 days later in the central and peripheral infarct regions and the noninfarct region by the centerline method in 165 patients. Patients with reperfusion had better survival (p less than 0.05, mean follow-up 4.5 years) and a higher ejection fraction at 3 days (52 +/- 12 versus 46 +/- 10%, p less than 0.02) attributable to a significantly different change in peripheral infarct region function between the acute and 3 day studies (0.1 +/- 1.0 versus -0.3 +/- 0.9 SD, p less than 0.05). These early functional changes were significant in patients with anterior myocardial infarction and showed similar trends in those with inferior myocardial infarction. On Cox regression analysis, function measured at 3 days was more predictive of survival than was function measured acutely (chi square for acute ejection fraction = 11.48 versus 24.59 at 3 days). Although, as previously reported, greater than 45% of total recovery of left ventricular function occurs later, the ejection fraction achieved by day 3 is already predictive of survival. Thus, the mechanism by which successful thrombolytic therapy enhances survival is improvement of regional and global left ventricular function early after acute myocardial infarction.

SUMMARY Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 1.2 hours (±+ SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 + 63,200 IU of streptokinase over 26.1 21.5 minutes, patency of the occluded vessels was reached.PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 + 7.3% to 58.6 19.5% (area method) and from 71.4 + 12.4% to 39.2 + 19.7% (diameter method). The improvement was 31.5 18.4% and 32.2 ± 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred.The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period.PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.

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SUMMARY In 50 patients with proven acute myocardial infarction (AMI), left ventricular hemodynamics (pulmonary end-diastolic pressure [PAEDP]; cardiac index [CI]; stroke volume index [SVI]; and SVI/PAEDP were related to the size of the acute infarct. Acute infarct mass was calculated from serial determinations of serum creatine phosphokinase (CPK) every two hours, using a computer program. In 15 cases postmortem measurement of acute infarct size after staining with Nitro-BT was made and correlated with calculated infarct size. Correlation in this limited number of cases was good with a mean difference of 7 g. Acute infarct mass in 38 survivors was 46 ± 5 g and was significantly smaller (P < 0.05) than in the 12 nonsurvivors (76 ± 12 g.) PAEDP in surviving patients was significantly lower (17 ± I mm Hg) and SVI (36 ml/m2) and SVI/PAEDP (2.4 ml/m2/mm Hg) significantly higher than in the nonsurvivors (PAEDP: 24 mm Hg; SVI: 23 ml/m2; SVI/PAEDP: 0.86 ml/m2/mm Hg) (P < 0.001 for all differences). Similar significant differences were observed between patients not in shock and those in cardiogenic shock. Although in 39 patients, in whom the infarction was their first, infarct mass was larger (58 ± 6 g) than in 11 patients with repeat infarctions (37 ± 8 g), left ventricular hemodynamics were slightly more impaired in reinfarctions (PAEDP: 21 ± 3 mm Hg; Cl: 2.60 L/min/m') than in first infarctions (PAEDP: 18 ± I mm Hg; CI: 2.82 L/min/m'). for the parameters cardiac index, PAEDP, and acute infarct mass precluded their usefulness, when taken individually, in predicting survival.When a relationship between hemodynamics and infarct size was looked for, four constellations of individual patients were identified. These groups were defined by PAEDPs of above or below 18 mm Hg and infarct sizes above or below 65 g. Class A patients (N = 22) had a small infarct (29 ± 4 g) and good pump function (PAEDP: 13 mm Hg; SVI: 40 ml/m'; SVI/PAEDP: 3.27 ml/m'/mm Hg); prognosis was good for these patients. In class B (N = 13) the infarct was large (96 ± 8 g) and pump function markedly impaired (PAEDP: 26 mm Hg; SVI: 24 ml/mi; SVI/PAEDP: 0.98 ml/m'/mm Hg); 54% of these patients died. Five patients in class C had, in the presence of a large infarct (84 g), only a slightly elevated PAEDP of 17 mm Hg and an almost normal SVI of 37 ml/mi. In contrast, the ten class D patients had an infarct size (34 g) similar to that in class A, but high PAEDP (23 mm Hg) and moderately reduced SVI (31 ml/ml). In this group a high incidence of reinfarctions (six out of ten) occurred.It is concluded that infarct mass calculated from serial CPK analysis, as a single parameter, cannot be used to predict mortality or development of cardiogenic shock in an individual patient. In conjunction with hemodynamic monitoring of left ventricular pump function, however, infarct mass is of considerable importance for assessment of the hemodynamic function of the residual myocardium.loss, appearance of Q waves, and alterations of the ST segment); 3) elevation of creatine phospho...

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