Risk Mechanisms in Hypertensive Heart Disease

Abstract

Abstract-In this report, some of the underlying pathophysiological alterations associated with the independent risk from hypertensive heart disease and left ventricular hypertrophy are discussed. Emphasized are the classically described coronary hemodynamic alterations of decreased coronary blood flow and flow reserve with increased coronary vascular resistance and minimal coronary resistance; more recent concepts of endothelial dysfunction are emphasized. Additionally, increased collagen deposition within the ventricular walls and perivascularly participates importantly. These changes are exacerbated by the aging process and perhaps by increased dietary salt intake. Consequences of these functional and structural changes include further endothelial dysfunction, impairment of coronary hemodynamics, and ventricular contractile function (diastolic as well as systolic Key Words: left ventricular hypertrophy Ⅲ coronary heart disease Ⅲ coronary hemodynamics Ⅲ fibrosis Ⅲ sudden death Ⅲ risk S ome time has passed since I summarized my thoughts on the multifactorial nature of the development and reversal of left ventricular hypertrophy (LVH) and on the underlying mechanisms of risk associated with hypertensive heart disease. 1,2 During these years, and before, a tremendous body of information has appeared on this subject, including epidemiological data confirming the concept that LVH is, indeed, an independent factor of risk conferring increased mortality 3,4 ; newer biological information about the underlying fundamental mechanisms associated with developing LVH and with ventricular remodeling 4 -14 ; the role of powerful local autocrine and paracrine mechanisms within the left ventricle (LV) 5,6,8,9,11 ; and, of course, the persistent problem of silent ischemia, cardiac failure, and sudden death in hypertensive patients with LVH. [13][14][15][16][17][18] Still persistent is the unresolved issue of pharmacological reversal of LVH and whether the phenomenon simplistically termed pharmacological "regression" of LVH is, in fact, solely reduction and remodeling of LV muscle mass. 2,19,20 Furthermore, the more complete elucidation of pathophysiological mechanisms associated with the underlying risk of LVH demands our attention. This overall concern is the primary focus of this report. Earlier-Described Mechanisms Underlying LVH RiskIn our previous reports, several mechanisms were offered to explain the underlying risk associated with LVH. 2,19,21 Because relatively little was known about LVH as a cardiovascular risk factor until recently, the intrinsic alterations associated with the hypertrophied myocyte and its epiphenomena were not considered. Evidence was cited from experimental studies suggesting that pathological hypertrophy was associated with a different myosin isozyme that might predispose the heart to cardiac failure or sudden death, 22 but this concept has not remained a viable option. A second possibility, supported by a flurry of reports, suggested that LVH predisposed the ventricle to arrhythmias and sudden de...

Perspective on Selected Issues in Cardiovascular Disease Research With a Focus on Black Americans

“…4 The development of hypertension and its relationship to CVD is multifactorial and likely includes both environmental and physiological/genetic components, including endothelial dysfunction, subendocardial fibrosis, and left ventricular hypertrophy (LVH). 5,6 The relationship of LVH to cardiac death 6,7 is of particular importance in blacks because of the higher prevalence of hypertension associated LVH in this ethnic group. Echocardiographic data from the Coronary Artery Risk Development in Young Adults study showed that LV mass was higher in blacks than in whites and correlated with systolic blood pressure.…”

Effects of Angiotensin II Type 1 Receptor Antagonist on Smooth Muscle Cell Phenotype in Intramyocardial Arteries from Spontaneously Hypertensive Rats

“…Myocardial ischemia reflected by the decrease in unit coronary blood flow might be closely related to LV dysfunction in patients with essential hypertension (3). Angiotensin (Ang) II cardial ischemia (6), and decreasing coronary artery periarteriolar collagen deposition in hypertension (7,8).…”

Sympathetic Response to Ventricular Extrasystolic Beats in Hypertension and Heart Failure

“…Furthermore, it is unknown whether the sympathetic responses to PVCs seen in healthy subjects differ from those observed in essential hypertension (EH) and CHF, ie, 2 cardiovascular diseases in which sympathetic neural activity is markedly increased 4 -11 and its role in the arrhythmogenesis has been documented. [12][13][14][15][16] In the present study, we investigated the behavior of the changes in MSNA, as directly quantified by microneurography, that follow spontaneous unprovoked PVCs in healthy subjects and in patients with EH or CHF. Because evidence in animals and man 1,17,18 suggests that the sympathetic changes after provoked PVCs are related to (1) the blood pressure (BP) changes induced by PVCs, (2) their degree of prematurity (expressed by the coupling interval time), and (3) the level of the resting sympathetic tone, we further investigated in the 3 groups the relationships between the MSNA adjustments to spontaneous PVCs and the above-mentioned variables.…”