Kiyomitsu Ikeoka

Clinical Course of Patients with Coronary Ectasia

Objective: To compare the clinical prognosis between patients with diffuse coronary ectasia and those with localized coronary ectasia. Design: Patients with coronary ectasia were divided into two groups based on the Markis classification (group D: types I–III and group L: type IV), and the clinical manifestations and prognosis were compared between the two groups. Results: Group D patients (52.1 ± 4 years) were significantly younger than group L patients (62.5 ± 7 years). During the study, 4 patients in group D died suddenly. Three of the patients had type I coronary ectasia, and 1 had left main coronary ectasia. Conclusion: The results of the present study indicate that patients with diffuse coronary ectasia and left main coronary ectasia should be followed carefully.

Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.

Variations of endothelium-dependent vasoresponses in congestive heart failure

Endothelium-dependent vasodilation decreases in patients with congestive heart failure (CHF). Whether this decreased vasodilation occurs simultaneously in different vascular beds has not been elucidated. We studied the vasomotor reactivity in both coronary and peripheral resistance vessels in a rat CHF model produced by ligating the left coronary artery. Variations in vessel diameter in response to vasoactive drug administration were measured using an in vitro system of coronary resistance vessels from cardiac muscle and peripheral resistance vessels from cremaster muscle. Vascular responses to acetylcholine were impaired in the early stage of CHF (at 2 weeks), whereas the reaction to bradykinin was preserved. NG-monomethyl-L-arginine (L-NMMA) inhibited the responses of acetylcholine; however, L-NMMA only partially inhibited the responses to bradykinin. Vascular reactivity to A23187 was preserved in the early stage and was impaired in the late stage of CHF (at 8 weeks). These reactions were inhibited by L-NMMA. The response to sodium nitroprusside remained constant in both stages of CHF. The responses were similar in the coronary resistance and peripheral resistance vessels. This suggests that acetylcholine transmission is impaired in the early stages of CHF but that with CHF of longer duration there is progressive impairment of nitric oxide production and release in both coronary and peripheral resistance vessels.

Positive indium-111 leukocyte imaging in post myocardial infarction syndrome

The diagnosis of post myocardial infarction syndrome (PMIS) is sometimes difficult because of the absence of a specific test. We report a 68-year-old man with PMIS who had a persistent accumulation of indium-111 oxine labeled leukocytes in the infarcted myocardium for 1 month. The uptake of leukocytes preceded the appearance of the main symptoms and disappeared with the clinical improvement after the therapy with steroids. Leukocyte imaging has a potential as a useful tool for early diagnosis, evaluation of therapy and assessing the mechanism of PMIS.