The effect of repetitive periods of coronary occlusion on myocardial adenine nucleotides, lactate, and infarct size was studied. In one series of dogs, the circumflex artery was occluded for one, two, or four 10-min episodes, each separated by 20 min of reperfusion. Hearts were excised and sampled for metabolic assays after one or more periods of ischemia before or after reperfusion. One 10-min period of ischemia caused a 61% loss of ATP and 41% loss of adenine nucleotides from the most severely ischemic subendocardial zone. Reperfusion resulted in rapid restoration of the adenylate charge but in only slight repletion of the adenine nucleotide pool. However, two or even four 10-min periods of ischemia caused no further adenine nucleotide loss. In contrast, 40 min of continuous coronary occlusion caused an 87% depletion of ATP and 67% of the adenine nucleotide pool from the same subendocardial region. Collateral blood flow was similar during all occlusions, but lactate accumulation was less during later occlusions. In a second series of experiments, myocardial necrosis was quantitated 4 days after four 10-min periods of ischemia. Necrosis was observed in only one of six dogs and, in this dog, was only 1.5% of the anatomic area at risk. Thus intermittent reperfusion prevents cumulative metabolic deficits and myocardial ischemic cell death, perhaps by restoring the capacity for high-energy phosphate (HEP) production and/or washing out deleterious catabolites. A first episode of ischemia also slows HEP utilization in subsequent episodes.

A new diagnostic and therapeutic endoscopic system consisting of an excimer pulse dye laser is presented. This report demonstrates the accumulation of hematoporphyrin derivative (HpD) in atheroma as shown by the fluorescence of HpD using this equipment. Atheroma was induced in the aorta of WHHL (Watanabe heritable hyperlipidemic) rabbits, 5 mg kg−1 HpD was injected intravenously and the rabbits were sacrificed 24 h later. The aorta was dissected and the localization of HpD was examined. Characteristic peaks of the fluorescence of HpD at 630, 665 and 690 nm wavelength were detected in the atheromatous lesion. However, in the fatty plaque, the emission peak at 630 nm was lower and the 665 nm peak faded away. No fluorescence with peaks was detected in the normal area. The ratio of fluorescence intensity in atheroma, border zones and normal areas was 10.4 : 5.0 : 1.0. On normal rabbits made atherosclerotic by diet and balloon damage, an ultra thin endoscopic catheter was inserted from the descending aorta of atherosclerotic rabbits under anesthesia. Essentially the same data was obtained by these studies in vivo as was obtained in the in vitro studies. The above data suggests the possibility of future applications of this equipment for diagnosis of atheroma.

In addition to electrocardiogram (ECG), analysis of creatinine phosphokinase (CPK), lactate dehydrogenase (LDH) and their isoenzymes is commonlyemployed to diagnose acute myocardial infarction (AMI). The aim of this study was to observe the efficiency of isomers of CPKfor early diagnosis of AMI. ECG, though useful in many ways, is not 100% sensitive. The drawback involved with CPK and LDH isoenzymes is the time lag factor in diagnosing AMI early enough for interventional therapy. Recently the subunits of these isoenzymes, namely MMand now the MB isomers are being tested for their effectiveness in the early diagnosis ofAMI. In our experience MB isomers were found to be accurate markers in the early diagnosis of AMI. They were especially valuable in diagnosing myocardial infarction not detectable by ECGin cases such as non-Q AMI, cardiomyopathy, and bundle branch block among other such cases. (Internal Medicine 33: 210-215, 1994)

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