Hypertension and Coronary Microvascular Disease

Strauer, B. E.; Schwartzkopff, B.

doi:10.1007/978-1-4615-5385-4_23

Cited by 1 publication

(2 citation statements)

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“…This has been demonstrated in experimental hypertension 70,71 as well as clinically. 32,54,72,73 For example, in the spontaneously hypertensive rat (SHR) treated with either an ACE inhibitor, an angiotensin II (type 1) receptor antagonist, or both (in studies designed to produce equivalent reductions in arterial pressure with each of these 3 treatment options), it was possible to demonstrate significant physiological improvement using these therapies. [71][72][73] Most intriguing was the greater-than-additive flow reserves with combination therapy.…”

Section: Coronary Insufficiency Coronary Flowmentioning

confidence: 99%

“…32,54,72,73 For example, in the spontaneously hypertensive rat (SHR) treated with either an ACE inhibitor, an angiotensin II (type 1) receptor antagonist, or both (in studies designed to produce equivalent reductions in arterial pressure with each of these 3 treatment options), it was possible to demonstrate significant physiological improvement using these therapies. [71][72][73] Most intriguing was the greater-than-additive flow reserves with combination therapy. 71 This can be explained by the coronary vasodilation induced by inhibition of angiotensin II-mediated constriction with the ACE inhibitor, further inhibition of additionally generated angiotensin II by intracardiac chymase, 74 augmented bradykinin-induced vasodilation induced by the ACE inhibitor, 7,75 as well as the beneficial effect on the endothelially produced natural vasodilator nitric oxide.…”

Section: Coronary Insufficiency Coronary Flowmentioning

confidence: 99%

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Risk Mechanisms in Hypertensive Heart Disease

Fröhlich

1999

Hypertension

162

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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...

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