{"title":"Coronary microvascular disease in hypertensives.","authors":"A R Lucarini, E Picano, A Salvetti","doi":"10.3109/10641969209036171","DOIUrl":null,"url":null,"abstract":"<p><p>Arterial hypertension can badly affect coronary circulation through several mechanisms that are not mutually exclusive, namely, coronary artery disease, left ventricular hypertrophy, and microvascular disease. Theoretical and experimental data suggest that coronary microvascular disease may exist in hypertensives, in whom it can cause both a reduction of coronary flow reserve and a shift to the right of the coronary flow autoregulation curve. To address this issue, we used dipyridamole- echocardiography test, which causes ischemic-like ST segment depression with no detectable changes in left ventricular function in different subsets of patients with microvascular disease (Syndrome X; Hypertrophic cardiomyopathy; acute heart rejection). We found that dipyridamole infusion can cause a similar pattern of response (i.e., echocardiographically silent ST segment depression) in mild-moderate essential hypertensives with normal epicardial coronary arteries, without left ventricular hypertrophy, with increased forearm minimal vascular resistances and with a reduced coronary reserve. This pattern of response identifies hypertensives with higher risk of ventricular arrhythmias, is amplified by acute reduction of diastolic blood pressure and can be reversed, together with the reduction of forearm vascular resistances by chronic antihypertensive treatment. Taken together these findings suggest that microvascular coronary disease can exist in hypertensives with two adverse consequences, consistent with the experimental background: the reduction of coronary flow reserve as well as a shift to the right of the coronary flow autoregulation curve.</p>","PeriodicalId":10339,"journal":{"name":"Clinical and experimental hypertension. Part A, Theory and practice","volume":"14 1-2","pages":"55-66"},"PeriodicalIF":0.0000,"publicationDate":"1992-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.3109/10641969209036171","citationCount":"20","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Clinical and experimental hypertension. Part A, Theory and practice","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.3109/10641969209036171","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 20
Abstract
Arterial hypertension can badly affect coronary circulation through several mechanisms that are not mutually exclusive, namely, coronary artery disease, left ventricular hypertrophy, and microvascular disease. Theoretical and experimental data suggest that coronary microvascular disease may exist in hypertensives, in whom it can cause both a reduction of coronary flow reserve and a shift to the right of the coronary flow autoregulation curve. To address this issue, we used dipyridamole- echocardiography test, which causes ischemic-like ST segment depression with no detectable changes in left ventricular function in different subsets of patients with microvascular disease (Syndrome X; Hypertrophic cardiomyopathy; acute heart rejection). We found that dipyridamole infusion can cause a similar pattern of response (i.e., echocardiographically silent ST segment depression) in mild-moderate essential hypertensives with normal epicardial coronary arteries, without left ventricular hypertrophy, with increased forearm minimal vascular resistances and with a reduced coronary reserve. This pattern of response identifies hypertensives with higher risk of ventricular arrhythmias, is amplified by acute reduction of diastolic blood pressure and can be reversed, together with the reduction of forearm vascular resistances by chronic antihypertensive treatment. Taken together these findings suggest that microvascular coronary disease can exist in hypertensives with two adverse consequences, consistent with the experimental background: the reduction of coronary flow reserve as well as a shift to the right of the coronary flow autoregulation curve.