Has a blood pressure disease, but rather as a vascular abnormality involving functional and structural changes in conduit arteries, branch points, and resistance arteries that generate reflected waves or oscillations in the arterial system. Endothelial dysfunction appears critical to all these changes. Thus, hypertensive patients at risk of cardiovascular events show decreased nitric oxide (NO) bioactivity. This is usually due to decreased endothelial NO secretion, but also may result from inactivation of secreted NO before its activity is expressed at the vascular site of action. Decreased NO activity can be expected to narrow the arterioles that control vascular resistance and thus to raise blood pressure.
Vascular remodeling, originally identified by Mulvaney, involves the rearrangement of vascular smooth muscle cells around a smaller lumen, leaving the vascular mass unchanged, but reducing the lumen diameter. Although the mechanism remains largely unelucidated, endothelial dysfunction may play a contributory role. This structural alteration in the microvasculature may therefore occur before the development of overt conduit artery disease and certainly before the development of atherosclerotic plaques.
Heart failure can no longer be defined as a disease in which ventricular emptying is impaired but as a progressive structural process altering the shape and volume of the chamber. The structural transformation is termed left ventricular remodeling, and it involves the myocytes and interstitial myocardial components, including collagen. In response to various pathologic stimuli (myocardial infarction, pressure and volume overload, idiopathic dilated cardiomyopathy, and myocarditis), the cardiomyocytes stretch, and local hormone and cytokine release increases. These changes, in turn, stimulate the expression of embryonic genes. Thus myocytes, which are typical terminally differentiated cells, become capable of a life-death cycle. In other words, the failing myocyte may survive (hypertrophy) or kill itself (apoptosis) in response to the same initial pathologic stimulus.
The neurohumoral abnormalities responsible for heart failure progression include: the sympathetic nervous system, shown by an elevated plasma norepinephrine level; the renin-angiotensin system, shown by an increase in plasma renin activity; increased plasma levels of aldosterone; increased endothelin system activity; and increased cytokine activity, shown by the increases in tumor necrosis factor-a and arginine vasopressin.
The degree of remodeling is influenced by the left ventricular hemodynamic load, which is itself determined, in terms of altered compliance and resistance, by the structural remodeling of the vasculature. Thus, the relationship between hypertension and heart failure is one of interaction between left ventricular and vascular remodeling.
There are a number of often conflicting studies of the relationship between blood pressure and left ventricular systolic function. In uncomplicated essential hypertension, left ventricular systolic chamber function was initially found to be normal or even above normal. This appeared to contradict the data from experimental animals showing progressive impairment of contractility in pressure-overload left ventricular hypertrophy, and the epidemiologic evidence that hypertension is the most important predictor of congestive heart failure in the general population. The paradox was resolved by the introduction of midwall fractional shortening (FS), which identified reduced myocardial systolic function in a large subgroup of hypertensive subjects whose chamber function remained intact thanks to the more concentric left ventricular geometry. Even so, the relationship between blood pressure and left ventricular systolic function remained elusive in some studies, notably those that could not exclude the possibility of a confounding effect by previous antihypertensive drug therapy on the complex interplay between blood pressure, left ventricular mass, and left ventricular function.
More recently, Schillaci et al showed an association between 24-hour blood pressure and left ventricular systolic function in a large treatment-naive hypertensive population. Their findings agree with the large body of experimental evidence that consistently indicates depressed myocardial contractility in pressure-overload hypertrophy.
In summary, the hemodynamic load imposed on the heart by vascular remodeling and the humoral abnormalities imposed on the vasculature by cardiac remodeling subtend the relationship between hypertension and heart failure borne out by the molecular, experimental, and clinical evidence.
pathophysiology; hypertension; vascular remodeling; etiology
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