The Progression of Hypertensive Heart Disease

 

Hypertension remains a major public health problem associated with considerable morbidity and mortality. Hypertensive heart disease is a constellation of abnormalities that includes left ventricular hypertrophy (LVH), systolic and diastolic dysfunction, and their clinical manifestations including arrhythmias and symptomatic heart failure. The classic paradigm of hypertensive heart disease is that the left ventricular (LV) wall thickens in response to elevated blood pressure as a compensatory mechanism to minimize wall stress.

Subsequently, after a series of poorly characterized events (“transition to failure”), the left ventricle dilates, and the LV ejection fraction (EF) declines (defined herein as “dilated cardiac failure”). The purpose of this review is to focus on the key steps in the progression of hypertensive heart disease (Figure 1), highlighting recent advances as well as some unresolved controversies.

Although an increase in cardiomyocyte size has been offered to be the sine qua non of LVH,³ in the epidemiological or clinical setting, it is not feasible to document this abnormality. Rather, in those settings, LVH is defined as an increase in LV mass. Criteria to define LVH require using a somewhat arbitrary threshold to dichotomize a trait that appears to have a continuous relationship with subsequent risk,⁴ and an alternative approach is to define several grades of severity of LVH.

There is widespread agreement that LVH is an important intermediate phenotype in the progression of hypertensive heart disease and is associated with adverse outcomes.⁶ Although LVH can antedate the development of hypertension, the progression from hypertension to concentric LVH (pathway 1, Figure 1) is an important step on the pathway toward heart failure and will be the focus of this section. Pathological changes present in patients with hypertensive LVH include an increase in the size of the cardiomyocyte, alterations in the extracellular matrix with accumulation of fibrosis, and abnormalities of the intramyocardial coronary vasculature, including medial hypertrophy and perivascular fibrosis. Clonidine (about tablets) has also been effective in managing withdrawal symptoms in the treatment of alcoholism and opiate dependency.

The mechanisms responsible for progression to hypertrophy include not only a response to the mechanical stress from elevated blood pressure but also the influences of neurohormones, growth factors, and cytokines. Nevertheless, a recent clinical trial demonstrated that tighter control of systolic blood pressure (target of <130 mm Hg versus <140 mm Hg) was associated with a reduction in the development of LVH on ECG, emphasizing the importance of the pressure load itself.

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