{"title":"冠心病患者静息和运动时的右心室功能。","authors":"K R Karsch, S Scheufler, H Blanke, P Rentrop","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>Biplane cineventriculograms of the right ventricle at rest and during exercise were made of 16 patients with a right coronary artery stenosis of greater than 50% and less than 90% to explain the alteration of the volumes and function of the right ventricle during exercise-induced angina pectoris. The right ventricular enddiastolic volume increases from 113 +/- 6.6 ml/m2 to 133.9 +/- 9.8 ml/m2 (P less than 0.001). The endsystolic volume increases from 48.9 +/- 4.1 ml/m2 to 52.9 +/- 5.3 ml/m2. The stroke volume index increases from 64 +/- 5.5 ml/m2 to 81 +/-8.3 ml/m2 (P less than 0.001). At the same time the ejection fraction increases from 56.5 +/- 2.9% to 60.2 +/- 3.2% (P less than 0.05). The left ventricular enddiastolic pressure increases from 12.8 +/- 1.5 mm Hg to 26.6 +/- 1.6 mm Hg (P less than 0.001). The enddiastolic pressure of the right ventricle increases from 5.8 +/- 0.5 to 12.2 +/- 0.8 mm Hg (P less than 0.001). The mean velocity of diameter shortening, VD, increases from 0.9 +/- 0.06 D/s to 1.12 +/- 0.09 D/s (P less than 0.05). Exercise-induced angina pectoris leads to a considerable increase of the left ventricular enddiastolic pressure and therefore to an increase of the right ventricular afterload. The increase of afterload in patients with a right coronary artery stenosis is compensated by a considerable increase of the enddiastolic volume: the pump-function during exercise-induced angina pectoris is maintained by an increase of preload.</p>","PeriodicalId":72971,"journal":{"name":"European journal of cardiology","volume":null,"pages":null},"PeriodicalIF":0.0000,"publicationDate":"1980-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Right ventricular function at rest and during exercise in patients with coronary heart disease.\",\"authors\":\"K R Karsch, S Scheufler, H Blanke, P Rentrop\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>Biplane cineventriculograms of the right ventricle at rest and during exercise were made of 16 patients with a right coronary artery stenosis of greater than 50% and less than 90% to explain the alteration of the volumes and function of the right ventricle during exercise-induced angina pectoris. The right ventricular enddiastolic volume increases from 113 +/- 6.6 ml/m2 to 133.9 +/- 9.8 ml/m2 (P less than 0.001). The endsystolic volume increases from 48.9 +/- 4.1 ml/m2 to 52.9 +/- 5.3 ml/m2. The stroke volume index increases from 64 +/- 5.5 ml/m2 to 81 +/-8.3 ml/m2 (P less than 0.001). At the same time the ejection fraction increases from 56.5 +/- 2.9% to 60.2 +/- 3.2% (P less than 0.05). The left ventricular enddiastolic pressure increases from 12.8 +/- 1.5 mm Hg to 26.6 +/- 1.6 mm Hg (P less than 0.001). The enddiastolic pressure of the right ventricle increases from 5.8 +/- 0.5 to 12.2 +/- 0.8 mm Hg (P less than 0.001). The mean velocity of diameter shortening, VD, increases from 0.9 +/- 0.06 D/s to 1.12 +/- 0.09 D/s (P less than 0.05). Exercise-induced angina pectoris leads to a considerable increase of the left ventricular enddiastolic pressure and therefore to an increase of the right ventricular afterload. The increase of afterload in patients with a right coronary artery stenosis is compensated by a considerable increase of the enddiastolic volume: the pump-function during exercise-induced angina pectoris is maintained by an increase of preload.</p>\",\"PeriodicalId\":72971,\"journal\":{\"name\":\"European journal of cardiology\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":0.0000,\"publicationDate\":\"1980-02-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"European journal of cardiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"European journal of cardiology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Right ventricular function at rest and during exercise in patients with coronary heart disease.
Biplane cineventriculograms of the right ventricle at rest and during exercise were made of 16 patients with a right coronary artery stenosis of greater than 50% and less than 90% to explain the alteration of the volumes and function of the right ventricle during exercise-induced angina pectoris. The right ventricular enddiastolic volume increases from 113 +/- 6.6 ml/m2 to 133.9 +/- 9.8 ml/m2 (P less than 0.001). The endsystolic volume increases from 48.9 +/- 4.1 ml/m2 to 52.9 +/- 5.3 ml/m2. The stroke volume index increases from 64 +/- 5.5 ml/m2 to 81 +/-8.3 ml/m2 (P less than 0.001). At the same time the ejection fraction increases from 56.5 +/- 2.9% to 60.2 +/- 3.2% (P less than 0.05). The left ventricular enddiastolic pressure increases from 12.8 +/- 1.5 mm Hg to 26.6 +/- 1.6 mm Hg (P less than 0.001). The enddiastolic pressure of the right ventricle increases from 5.8 +/- 0.5 to 12.2 +/- 0.8 mm Hg (P less than 0.001). The mean velocity of diameter shortening, VD, increases from 0.9 +/- 0.06 D/s to 1.12 +/- 0.09 D/s (P less than 0.05). Exercise-induced angina pectoris leads to a considerable increase of the left ventricular enddiastolic pressure and therefore to an increase of the right ventricular afterload. The increase of afterload in patients with a right coronary artery stenosis is compensated by a considerable increase of the enddiastolic volume: the pump-function during exercise-induced angina pectoris is maintained by an increase of preload.