The following changes were noted during pacing-induced angina: The coronary sinus blood flow was less than it was during the control period and less than that in the myocardial ischemic group without induced angina. While myocardial oxygen consumption did not increase, myocardial metabolism became anaerobic. The possibility of myocardial dysfunction also was noted.
The purpose of this study is to determine why precordial ST elevation (V1 lead) occurs during acute occlusion of the right coronary artery (RCA). Nineteen patients with vasospastic angina, in whom ergonovine administration into RCA provoked spasms, were divided into 2 groups by precordial ST change during spasms. Group I (n = 6) had precordial ST elevation; group II (n = 13) had no precordial ST elevation. A subgroup, IIA was comprised 6 patients in group II with spasms in the RCA proximal segment (segment number less than 2 of AHA coronary classification). None had left coronary dominancy. There was no difference in collateral flow during spasms. Location of spasms in group I was in the RCA proximal segment, and was significantly more proximal compared to group II. There was no difference in sigma ST in II, III, aVF between group I and II or IIA. Max ST elevation time by which duration of ischemia was estimated was significantly longer in group I than in group IIA. Three patients in group I displayed precordial ST depression before elevation, in all of whom in sigma ST in II, III, aVF was higher during precordial ST elevation than during depression. During acute occlusion in the RCA proximal segment, precordial ST elevation is caused by ischemia of the right ventricular anterior wall. Furthermore, precordial ST elevation can occur in a patient with RCA dominance, even if ischemic injury in the left ventricular infero-posterior wall increases progressively.
We report two cases in which the tips of guide catheters were damaged by rotational burrs during rotational coronary atherectomy of aorto-ostial lesions. There were no signs of embolization caused by the material of the guide catheters during and after the interventions.
A 17-year-old male with mitochondrial myopathy was transferred to our hospital because of respiratory distress and a rapidly deteriorating level of consciousness. He had a markedly increased cardiac output with low systemic vascular resistance and decreased arteriovenous oxygen difference. Severe lactic acidosis, rhabdomyolysis and acute renal failure were also present. He was treated in the intensive care unit with continuous hemofiltration and hemodialysis. This case demonstrates that cardiac failure in mitochondrial encephalomyopathy may be caused by myocardial abnormalities as well as by reduced systemic vascular resistance secondary to disturbed oxidative metabolism.(Internal Medicine 32: 798-801, 1993)
