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We experienced a patient in whom coronary spasms were induced by an ergonovine provocation test during coronary angiography at the sites of coronary artery ectasia. The patient was a 45-year-old male with chest pain at rest, which promptly disappeared when given sublingual nitroglycerin. Similar attacks occurred frequently even with the administration of drugs after admission, but no significant changes were observed in electrocardiography (ECG) during the attacks or by repeated Holter ECG. The results of exercise ECG and provocation tests such as Valsalva maneuver, hyperventilation, and cold pressor test were negative. Coronary angiography showed ectatic changes in the left coronary artery, and the coronary spasms were induced by ergonovine administration at the ectatic portion of the left anterior descending artery and left circumflex artery, and right coronary artery with chest symptoms similar to those observed during spontaneous attacks. However, there were no significant changes in ECG. This rare case suggests an involvement of spasms in the pathogenic mechanism of myocardial ischemia in coronary artery ectasia.

Although the incidence of ventricular arrhythmias following myocardial ischaemia lessens as ischaemia improves, it is not clear whether this is correlated with a reduction in the degree of ST segment elevation. To explore this further we examined the effects of change in heart rate and the administration of the calcium antagonist diltiazem, 0.02 mg·kg−1·min−1, on ST segment elevation and the alternans of ST segment elevation (STA) and on serious ventricular arrhythmia induced by 10 min occlusion of the left anterior descending coronary artery in 86 mongrel dogs. The dogs were divided into three groups: 26 dogs paced at a rate of 180 beats·min−1 (group A); 44 dogs paced at a rate of 120 beats·min−1 (group B); and 16 dogs paced at a rate of 180 beats·min−1 and given diltiazem intravenously from 25 min before the coronary occlusion (group C). The degree of ST segment elevation and STA within 3 min of ischaemia was significantly lower in group B than in group A. There was no marked difference in the degree of ST segment elevation between groups A and C, but the STA was lower in group C than in group A. Incidence of ventricular tachycardia and ventricular fibrillation was significantly lower in groups B and C than in group A, and the timing of their first appearance was 4.5(SEM 0.6), 4.2(0.9) and 3.0(0.4) min, respectively. We suggest that the reduction in serious ventricular arrhythmias associated with the decrease in heart rate was caused by the improvement of STA secondary to the improvement of ST segment elevation. However the reduction in these arrhythmias after diltiazem may be related to STA improvement due to other factors, such as the reduction of cellular damage, rather than to improved ST segment elevation.

The combination of the systolic anterior motion of the anterior leaflet of the mitral valve and/or the mitral annular calcification in the case of asymmetrical septal hypertrophy has been fully recognized. However, in concentric left ventricular hypertrophy the systolic anterior motion of the anterior mitral valve and the massive posterior submitral calcification have not been commonly reported. We present a case with mild concentric left ventricular hypertrophy and massive posterior submitral calcification which displace the entire mitral ring anteriorly, namely, toward the left ventricular outflow tract. In this case, typical left ventricular outflow obstruction with systolic anterior motion of the anterior mitral valve was seen. Thus, we considered that this rare condition may have contributed to the formation of the systolic anterior motion of the anterior mitral leaflet in this case. We have provided additional information regarding the possible causes of systolic outflow obstruction in hypertrophic obstructive cardiomyopathy.

Vectorcardiographic, electrocardiographic, and hemodynamic changes in isolated infarction (infarct confined to the right ventricular free wall) were studied in 19 mongrel dogs. An isolated right ventricular infarction was produced by embolizing the right coronary artery with Spongel under closed chest conditions. The size of the infarct, identified by TTC staining, accounted for 6-65% (35.9 +/- 22.0%, mean +/- SD) of the right ventricular free wall. The STx, STy, STz, and the spatial magnitude of the ST segment (STM) were continuously recorded with an automated, real-time vectorcardiographic ST-segment analyzer (ST-monitor) using the Frank lead system. The cardiac index (CI) ratio (CI after embolization/CI before embolization) of all dogs with larger infarcts (infarct greater than 35% of the right ventricle) was below 1.0. In dogs with smaller infarcts (% RVI less than or equal to 35%), there were no differences in the hemodynamic data before and 4 h after embolization. In dogs with larger infarcts, however, pulmonary arterial pressure and heart rate 4 h after embolization were significantly decreased compared with those before embolization. In addition, right atrial pressure 4 h after embolization in the larger infarct group was significantly elevated compared with that in the smaller infarct group. In dogs with larger infarcts, STx, STy, and STM were significantly larger than in those with smaller infarcts both 15 min and 4 h after embolization. There were no significant correlations between infarct size and change in vectorcardiographic ST segments in the smaller infarct group.(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of early perfusion after intracoronary infusion of urokinase (PTCR) in patients with acute myocardial infarction was assessed. Coronary perfusion was reestablished in 7 of 10 patients receiving intracoronary urokinase. We compared the recanalized group after intracoronary urokinase (n = 7) with the standard therapy group (n = 32). Left ventricular end-diastolic pressure, cardiac index, angiographic ejection fraction, radionuclide ejection fraction, defect score by Thallium-201 scintiscan and regional ejection fraction by the left ventriculogram, measured at about one month after the onset of acute myocardial infarction, were compared according to the site of the main coronary lesion (right coronary artery or left anterior descending coronary artery). No statistically significant differences between the recanalized group after the administration of intracoronary urokinase and the control group were found at each coronary lesion. On the other hand, the comparison between two patients with and without PTCR, who matched the clinical and coronary angiographic findings, showed that PTCR on acute myocardial infarction might be of value. However, evaluation of the long-term effects of coronary thrombolysis on survival and myocardial function will require controlled randomized trials of a large number of patients.