Left ventricular filling is usually normal in uncomplicated coronary disease

Isao K. Inouye, Alan T. Hirsch, Debra Loge, Julio F. Tubau, Barry M. Massie

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10 Scopus citations

Abstract

Abnormalities in left ventricular filling have been described as an early finding in coronary artery disease (CAD) and more recently, in hypertension (HTN). The present study was undertaken to compare the prevalence and pattern of diastolic dysfunction in these two entities. Three groups of patients were studied: 10 normal volunteers (NLS), 39 HTN patients, and 30 CAD patients. The CAD patients were divided into two subgroups-one with normal ejection fraction (mean 0.60 ± 0.06) and the second with either a depressed ejection fraction (EF) or a history of HTN (mean EF 0.44 ± 0.15). The diastolic indices examined were peak filling rate (PFR, in end-diastolic volume [EDV]/sec), time to peak filling rate (TPFR, in msec), and first-third filling fraction ( FF1 3, in sec-1). The PFR in CAD and HTN was significantly reduced (1.86 ± 0.63 and 2.29 ± 0.49 vs 2.70 ± 0.35 EDV/sec in NLS, p < 0.025 and p < 0.001, respectively), with the CAD group also being significantly lower than the HTN group (p < 0.005). TPFR was prolonged in HTN, but not in CAD. FF1 3 was reduced in both HTN and CAD (0.38 ± 0.11 and 0.50 ± 0.14 vs 0.61 ± 0.06 sec-1 in NLS, p < 0.001 and p < 0.025, respectively), but it was significantly lower in HTN than in CAD (p < 0.001). However, when the subgroup of CAD patients with normal global systolic function was examined separately, diastolic indices were only slightly depressed. More importantly, only one, two, and five patients had PFR, TPFR, and FF1 3, respectively, which were below the normal values of our laboratory.

Original languageEnglish (US)
Pages (from-to)326-331
Number of pages6
JournalAmerican Heart Journal
Volume110
Issue number2
DOIs
StatePublished - Aug 1985

Bibliographical note

Funding Information:
From the Cardiology Service of the Veterans the Department of Medicine and Cardiovascular University of California-San Francisco. This work was supported in part by National Heart, Lung, and Blood Institute Grant No. HL 28146. Dr. Massie was supported as a Clinical Investigator of the Veterans Administration Research Service. for publication Dec. 21, 1984: revision received Feb. 15, 198.5; Apr. 2, 1985. requests: Barry Massie, M.D., Cardiology Center, 4150 Clement St., San Francisco,

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