K Kiryu, T Nakamura, M Kaneko, M Oikawa, T Yoshihara
{"title":"赛马心源性猝死的心脏病理学研究。","authors":"K Kiryu, T Nakamura, M Kaneko, M Oikawa, T Yoshihara","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Twenty thoroughbred race horses were selected for postmortem cardiopathological study of sudden cardiac death; ten of the twenty horses died suddenly. In order to define accurately the morphological changes observed in these ten hearts, ten other thoroughbred race horses considered to have normal hearts were selected as a control group and studied by postmortem coronary angiography. Of the ten horses that died suddenly, eight were witnessed to have died either during or shortly after training or racing. The death was instantaneous except in one horse, which showed ventricular tachycardia and died 4.5 h after a race. The other two died unexpectedly in the stable at night. Pathologically, the horses that died suddenly generally showed multifocal myocardial lesions that were ischemic and fibrotic. These lesions were found in the atrial tissue close to the sinoatrial (SA) node and in the atrioventricular (AV) junction, including the upper portion of the interventricular septum. Such myocardial lesions were often associated with vascular changes including arterio- and/or arteriolosclerosis. Angiographically, the SA node appeared to be perfused by atrial branches of the left and right coronary arteries. One branch originating from the left coronary artery gave off a few branches into the AV junction. These pathological findings, mainly consisting of both atrial lesions and lesions in the AV junction, were similar to those observed in horses with either atrial fibrillation, SA block, or paroxysmal ventricular tachycardia. A finding of particular interest was the angiographic demonstration that the blood supply to the AV junction partly came from the SA node artery.(ABSTRACT TRUNCATED AT 250 WORDS)</p>","PeriodicalId":77157,"journal":{"name":"Heart and vessels. Supplement","volume":"2 ","pages":"40-6"},"PeriodicalIF":0.0000,"publicationDate":"1987-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cardiopathology of sudden cardiac death in the race horse.\",\"authors\":\"K Kiryu, T Nakamura, M Kaneko, M Oikawa, T Yoshihara\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Twenty thoroughbred race horses were selected for postmortem cardiopathological study of sudden cardiac death; ten of the twenty horses died suddenly. In order to define accurately the morphological changes observed in these ten hearts, ten other thoroughbred race horses considered to have normal hearts were selected as a control group and studied by postmortem coronary angiography. Of the ten horses that died suddenly, eight were witnessed to have died either during or shortly after training or racing. The death was instantaneous except in one horse, which showed ventricular tachycardia and died 4.5 h after a race. The other two died unexpectedly in the stable at night. Pathologically, the horses that died suddenly generally showed multifocal myocardial lesions that were ischemic and fibrotic. These lesions were found in the atrial tissue close to the sinoatrial (SA) node and in the atrioventricular (AV) junction, including the upper portion of the interventricular septum. Such myocardial lesions were often associated with vascular changes including arterio- and/or arteriolosclerosis. Angiographically, the SA node appeared to be perfused by atrial branches of the left and right coronary arteries. One branch originating from the left coronary artery gave off a few branches into the AV junction. These pathological findings, mainly consisting of both atrial lesions and lesions in the AV junction, were similar to those observed in horses with either atrial fibrillation, SA block, or paroxysmal ventricular tachycardia. A finding of particular interest was the angiographic demonstration that the blood supply to the AV junction partly came from the SA node artery.(ABSTRACT TRUNCATED AT 250 WORDS)</p>\",\"PeriodicalId\":77157,\"journal\":{\"name\":\"Heart and vessels. Supplement\",\"volume\":\"2 \",\"pages\":\"40-6\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1987-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Heart and vessels. 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Cardiopathology of sudden cardiac death in the race horse.
Twenty thoroughbred race horses were selected for postmortem cardiopathological study of sudden cardiac death; ten of the twenty horses died suddenly. In order to define accurately the morphological changes observed in these ten hearts, ten other thoroughbred race horses considered to have normal hearts were selected as a control group and studied by postmortem coronary angiography. Of the ten horses that died suddenly, eight were witnessed to have died either during or shortly after training or racing. The death was instantaneous except in one horse, which showed ventricular tachycardia and died 4.5 h after a race. The other two died unexpectedly in the stable at night. Pathologically, the horses that died suddenly generally showed multifocal myocardial lesions that were ischemic and fibrotic. These lesions were found in the atrial tissue close to the sinoatrial (SA) node and in the atrioventricular (AV) junction, including the upper portion of the interventricular septum. Such myocardial lesions were often associated with vascular changes including arterio- and/or arteriolosclerosis. Angiographically, the SA node appeared to be perfused by atrial branches of the left and right coronary arteries. One branch originating from the left coronary artery gave off a few branches into the AV junction. These pathological findings, mainly consisting of both atrial lesions and lesions in the AV junction, were similar to those observed in horses with either atrial fibrillation, SA block, or paroxysmal ventricular tachycardia. A finding of particular interest was the angiographic demonstration that the blood supply to the AV junction partly came from the SA node artery.(ABSTRACT TRUNCATED AT 250 WORDS)