Open AccessThe imbalance between coronary reserve and wall stress explains the severity of ventricular dysfunction in hypertension
Author(s) -
Frimm Clovis De Carvalho,
Pereira Valéria F. A.,
Rodrigues Ana Clara T.,
Tsutsui Jeane M.,
Cúri Mariana
Publication year - 2005
Publication title -
clinical cardiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.263
H-Index - 72
eISSN - 1932-8737
pISSN - 0160-9289
DOI - 10.1002/clc.4960280106
Subject(s) - medicine , cardiology , fractional flow reserve , coronary flow reserve , diastole , coronary vasodilator , vasodilation , blood pressure , coronary artery disease , myocardial infarction , coronary angiography
Abstract Background : The pathophysiologic role of coronary reserve impairment in hypertensive cardiac dysfunction is still debated. Previously, we demonstrated that satisfactory coronary vasodilatation may coexist with ventricular systolic dysfunction. It is conceivable that coronary reserve might otherwise be inappropriate for enhanced myocardial oxygen demand and may thus affect cardiac performance negatively. Hypothesis : Myocardial supply‐demand imbalance contributes to the severity of ventricular dysfunction in hypertension (HTN). Methods : Fractional shortening (%) and end‐systolic stress (10 3 ·dyn·cm −2 ) were determined using echocardiography, and coronary reserve was calculated using trans‐esophageal Doppler echocardiography. Coronary reserve/ stress (cm 2 ·dyn −1 ) was utilized as a measure of supply‐demand. Groups NL (20 healthy subjects), HTN1 (15 patients, fractional shortening ≥ 30), HTN2 (19 patients, 20 ≤ fractional shortening <30), and HTN3 (21 patients, fractional shortening < 20) were constituted. Results : Compared with NL and HTN1, groups HTN2 and HTN3 had significantly (p < 0.05) greater end‐systolic stress (NL = 72 ± 16, HTN1 = 72 ± 23, HTN2 = 143 ± 32, HTN3 = 186 ± 70). Coronary reserve was impaired in HTN3 alone (NL = 3.5 ± 0.6, HTN1 = 3.4 ± 1.0, HTN2 = 3.1 ± 1.0, HTN3 = 2.6 ±1.1), but coronary reserve/stress was reduced in both HTN2 andHTN3 (NL = 50 ± 12, HTN1 = 53 ± 21, HTN2 = 22 ± 7, HTN3 = 15 ± 7). Stepwise regression analysis identified diastolic internal dimension, end‐systolic stress, and coronary reserve/stress as independently associated with fractional shortening. Conclusion : The imbalance between supply‐demand explains the severity of hypertensive cardiac dysfunction and adds information to cardiac enlargement and elevated wall stress.