Alcohol ingestion often provokes attacks in patients with vasospastic angina. Type 2 aldehyde dehydrogenase (ALDH2) deficiency, which is based on a single point mutation (Glu487Lys) of the ALDH2 gene, is common in the Japanese population, but rare among the Caucasian population. We investigated how the genotype of ALDH2 affects the characteristics of alcohol-induced vasospastic angina. Ninety-one patients with vasospastic angina who had ingested alcohol daily or occasionally were studied. Patients had been diagnosed as vasospastic angina by a provocation test with an intracoronary injection of ergonovine or acetylcholine during coronary angiography. The Glu487Lys mutation was detected by allele specific PCR. We interviewed the patients to obtain information concerning the relationship between alcohol ingestion and anginal attacks. Alcohol ingestion induced attacks in 16 of 66 patients without the Glu487Lys mutation, 8 of 22 in heterozygotes, and 1 of 3 in mutant homozygotes. The intervals between alcohol ingestion and the onset of anginal attacks were shorter in homozygotes (0.17 hours) and heterozygotes (1.5+/-0.6 hours) for ALDH2*2 than in normal homozygotes for ALDH2*1 (5.4+/-0.6 hours). The amount of ethanol which induced attacks was significantly greater in normal homozygotes than in homozygotes (11 ml) and heterozygotes (42.5+/-7.1 ml) for ALDH2*2 (96.1+/-13.4 ml in normal patients). The frequency of anginal attacks induced by alcohol ingestion did not differ between ALDH deficient and normal homozygotes. In ALDH deficient patients, however, anginal attacks were induced by a smaller amount of alcohol immediately after its ingestion. Thus, the ALDH2 genotype modifies the characteristics of the anginal attacks as a co-factor for the induction of vasospastic angina after alcohol ingestion.

The effect of changes in preload on regional myocardial motion in acute ischaemia was examined by miniature ultrasonic gauges after left anterior descending coronary artery occlusion in eight open chest dogs with the pericardium preserved. Left ventricular end-diastolic pressure was varied by blood withdrawal and infusion. When preload changed, isovolumetric shortening in the non-ischaemic region was inversely related to that in the ischaemic region. When preload decreased, stroke volume decreased and was accompanied by a decrease in end-diastolic length and ejection shortening in the non-ischaemic region together with an increase in isovolumetric bulging in the ischaemic region. When preload increased, these variables changed in opposite directions. These results indicate that in acute ischaemia: (1) changes in isovolumetric shortening in the non-ischaemic and ischaemic regions were related with each other when the level of volume expansion varied, and suggest that; (2) stroke volume is affected by end-diastolic length, ejection shortening in the non-ischaemic region and isovolumetric bulging in the ischemic region.

M., KANAZAWA, M., HANEDA, T. and TAKISHIMA, T. Significance of the Right Ventricular Free Wall in Dogs with and without Pulmonary Constriction. Tohoku J. Exp. Med., 1995, 177 (2), [93][94][95][96][97][98][99][100][101][102][103][104][105][106] To evaluate the role of the right ventricular (RV) free wall in cardiac function, RV and left ventricular (LV) wall segment lengths were measured by ultrasonic crystals in 10 open chest dogs with the pericardium preserved. Right coronary artery (RCA) was perfused separately by own blood and the flow was reduced stepwise until active shortening (aL) of the RV segment disappeared or RCA flow became zero (Ischemia). The experiment was repeated with and without pulmonary stenosis (PS). At Ischemia, RV and LV systolic pressures decreased. RV end-diastolic length increased and RVaL decreased. LV enddiastolic length and LVaL were reduced. LV stroke volume concurrently fell. These changes became more prominant with PS. The critical level of RCA flow, at which RVaL began to change, was higher with PS (5.27±2.85 ml/min, mean± S.D.) than without PS (1.44± 1.16, p <0.01). Based on the relationships between RVaL and percent changes in RV developed pressure and stroke volume, the degree of the decreases in RV developed pressure and stroke volume at RVAL of zero were estimated to be about 20%. These results indicate that the RV free wall partly contributes to maintaining the RV function, especially during RV pressure overload, critical coronary flow; pressure load; right ventricular function; stroke volumeThe significance of the right ventricular free wall in cardiac function has long been questioned. Following a report by Starr et al. (1943), the right ventricular free wall has been thought not to participate in maintaining cardiac function. In contrast, right ventricular infarction sometimes shows a severely depressed state of cardiac function in the clinical settings (Cohn et al. 1974;Coma-Canella et al. 1979;Lorell et al. 1979;Coma-Canella and Lopez-Sendon 1980;Lloyd et al. 1981;Lopez-Sendon et al. 1981). In addition, the right ventricular stroke volume is known to be mainly maintained by bellows action, which consists of the cooperative movements of both the right ventricular free wall and the interventricular septum (Rushmer et al. 1953). Thus, it appears that the right ventricular free wall partly contributes to maintaining right ventricular function. Therefore, the present study was designed to clarify the significance of the right ventricular free wall in cardiac function. We induced a depression of right ventricular free wall function through the stepwise reduction in right coronary artery flow, and examined the changes in cardiac function, especially changes in the right ventricular developed pressure and left ventricular stroke volume in relation to the right ventricular free wall movement, under conditions with and without pulmonary stenosis. MATERIALS AND METHODS Surgical preparationsTen mongrel dogs weighing from 13.6 to 23.5 kg (mean 17.9 kg) were anesthetized with intra...

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