Pathophysiology of chest pain in patients with cardiomyopathies and normal coronary arteries.

Abstract

To clarify the pathogenesis of chest pain in patients with cardiomyopathies, we compared coronary blood flow and other indicators of ischemia at rest and during pacing-induced tachycardia in nine patients with cardiomyopathy (four hypertrophic and five congestive) and in five control subjects. Coronary blood flow was reduced at rest and during pacing in cardiomyopathy patients compared with controls. In patients with hypertrophic cardiomyopathy, pacing induced chest pain in all, increased ST-segment depression in three patients and increased coronary venous lactate concentration. With pacing, two of five patients with congestive cardiomyopathy had chest discomfort and three had increased ST-segment depression, but coronary venous lactate concentration did not change significantly. In both groups of cardiomyopathies, the ratio of the systolic and diastolic pressure-time indexes tended to decrease more than in controls during pacing. Thus, myocardial perfusion is decreased in patients with cardiomyopathy, both at rest and during pacing. The changes detected during pacing point to subendocardial ischemia as the likely mechanism for angina in hypertrophic and possibly also in congestive cardiomyopathy.

Verapamil prevents silent myocardial perfusion abnormalities during exercise in asymptomatic patients with hypertrophic cardiomyopathy.

“…The mechanism could relate to an increase in myocardial oxygen demand beyond the capacity of the vascular bed to supply oxygen (primarily in those patients with obstruction to left ventricular outflow) to a vascular bed that has not grown in proportion to the degree of hypertrophy, to a limitation of coronary reserve due either to elevated left ventricular-filling pressures, or to functional or fixed vascular abnormalities of the small intramural coronary arteries. 2,3 In this regard, in a histopathologic study of patients with HCM at necropsy,7 wall thickening and luminal compromise of intramural coronary arteries were observed in over 80% of patients; although these abnormalities were most commonly present in the ventricular septum, they were not confined to this region of the left ventricle. Of particular relevance to the results of the present study is the fact that abnormal intramural coronary arteries are also frequently seen in young, previously asymptomatic patients who died suddenly from HCM.…”

“…Thus, the verapamil dosage at the time of repeat study ranged from 240 to 480 mg/day (mean, 453), and this dosage was maintained for a mean of 6.7 days (range, 2-56) before the repeat study. The verapamil studies were performed [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16] weeks (mean, 6±5) after the initial control studies.…”

Difference in Coronary Blood Flow Dynamics between Patients with Hypertension and Those with Hypertrophic Cardiomyopathy.

“…In patients with left ventricular hypertrophy (LVH), it has been reported that myocardial ischemia may occur in the absence of epicardial coronary artery disease (1)(2)(3)(4)(5). It has been suggested that an imbalance between oxygen supply and demand due to the greatly increased myocardial mass might be a mechanism for myocardial ischemia (6).…”

Coronary flow reserve in hypertrophic cardiomyopathy: relation with microvascular dysfunction and pathophysiological characteristics

“…[2][3][4][5] In previous studies the reduction of CFR in HCM patients has been related to single haemodynamic, 13 echocardiographic 9,10 and histological characteristics. [14][15][16][17] This is the first study to relate a combination of haemo- dynamic (LV end-diastolic pressure, LV outflow tract gradient), echocardiographic (indexed LV mass) and histological (% luminal area of the arterioles) characteristics to the reduction in CFR.…”

“…7,8 A number of mechanisms are associated with the decrease in CFR, including diastolic dysfunction, 9,10 systolic compression of the septal coronary branches, 11,12 the existence and degree of LV outflow tract gradient, 13 small-vessel disease of the intramyocardial arterioles [14][15][16] and inadequate capillary density relative to the increase in myocardial mass. 17 Although all mechanisms have a role in creating an imbalance between oxygen supply and demand, their relative contribution to the decrease in CFR has not yet been evaluated in HCM patients. The aim of the present study is to investigate to which extent each of the aforementioned variables contribute to the reduction of CFR in HCM patients.…”