{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,2]],"date-time":"2026-02-02T19:36:01Z","timestamp":1770060961301,"version":"3.49.0"},"reference-count":44,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2003,2]]},"abstract":"<jats:p>\n            An increase in left ventricular mass represents a compensatory response of hypertensive heart to augmented loading conditions. The concept of inappropriate mass has been proposed to define an increase in left ventricular mass higher than needed to compensate for increased workload. To assess whether inappropriate left ventricular mass is associated with more severe impairment of coronary vasodilator capacity, 64 untreated middle-aged hypertensive patients without significant coronary artery stenosis and 14 normotensive volunteers comparable for age and gender were studied by transthoracic and transesophageal echocardiography to evaluate left ventricular mass, geometry, and coronary flow velocity response to adenosine. Thirty-three patients had appropriate and 31 had inappropriate increase in left ventricular mass, whereas all normotensive control subjects had appropriate left ventricular mass. Compared with control subjects, minimum coronary resistance (0.87\u00b10.18 mm Hg per second\/centimeter) was increased in both hypertensive subgroups, more in those with inappropriate left ventricular mass (1.34\u00b10.23 versus 1.19\u00b10.23 mm Hg per second\/centimeter,\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01), who also exhibited lower afterload-corrected midwall shortening and ratio of peak early and peak late velocities of transmitral flow profile. In hypertensive patients, minimum coronary resistance was related positively to absolute and relative left ventricular wall thickness (\n            <jats:italic>r<\/jats:italic>\n            =+0.33 and +0.35, both\n            <jats:italic>P<\/jats:italic>\n            &lt;0.01) and negatively to midwall shortening and ratio of peak early and peak late velocities of transmitral flow (\n            <jats:italic>r<\/jats:italic>\n            =\u22120.32 and \u22120.31, both\n            <jats:italic>P<\/jats:italic>\n            &lt;0.02). Thus, in the hypertensive heart, a deviation of left ventricular mass from values compensatory for increased cardiac workload is associated with lower coronary vasodilator capacity, depressed left ventricular wall mechanics, and abnormal left ventricular diastolic filling pattern.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.0000049623.25854.b7","type":"journal-article","created":{"date-parts":[[2003,2,6]],"date-time":"2003-02-06T23:43:13Z","timestamp":1044574993000},"page":"224-229","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":25,"title":["Coronary Vasodilator Capacity and Hypertension-Induced Increase in Left Ventricular Mass"],"prefix":"10.1161","volume":"41","author":[{"given":"Michaela","family":"Koza\u0300kova\u0300","sequence":"first","affiliation":[{"name":"From the Department of Internal Medicine, University of Pisa (M.K., C.P.); the Department of Clinical and Experimental Medicine, Federico II University Hospital (G.d.S.), Naples; and Institute of Clinical Physiology (C.M.), CNR, Pisa, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Giovanni","family":"de Simone","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Pisa (M.K., C.P.); the Department of Clinical and Experimental Medicine, Federico II University Hospital (G.d.S.), Naples; and Institute of Clinical Physiology (C.M.), CNR, Pisa, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carmela","family":"Morizzo","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Pisa (M.K., C.P.); the Department of Clinical and Experimental Medicine, Federico II University Hospital (G.d.S.), Naples; and Institute of Clinical Physiology (C.M.), CNR, Pisa, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Carlo","family":"Palombo","sequence":"additional","affiliation":[{"name":"From the Department of Internal Medicine, University of Pisa (M.K., C.P.); the Department of Clinical and Experimental Medicine, Federico II University Hospital (G.d.S.), Naples; and Institute of Clinical Physiology (C.M.), CNR, Pisa, Italy."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_1_1_2","doi-asserted-by":"publisher","DOI":"10.1161\/circ.88.4.8403291"},{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.34.4.782"},{"key":"e_1_3_1_3_2","doi-asserted-by":"publisher","DOI":"10.7326\/0003-4819-114-5-345"},{"key":"e_1_3_1_4_2","doi-asserted-by":"publisher","DOI":"10.1056\/NEJM199005313222203"},{"key":"e_1_3_1_5_2","unstructured":"Wahlander H Friberg P. 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