Hypertension and heart failure: a dysfunction of systole, diastole or both?

Abstract

The pathological myocardial hypertrophy associated with hypertension contains the seed for further maladaptive development. Increased myocardial oxygen consumption, impaired epicardial coronary perfusion, ventricular fibrosis and remodelling, abnormalities in long-axis function and torsion, cause, to a varying degree, a mixture of systolic and diastolic abnormalities. In addition, chronotropic incompetence and peripheral factors such as lack of vasodilator reserve and reduced arterial compliance further affect cardiac output particularly on exercise. Many of these factors are common to hypertensive heart failure with a normal ejection fraction as well as systolic heart failure. There is increasing evidence that these apparently separate phenotypes are part of a spectrum of heart failure differing only in the degree of ventricular remodelling and volume changes. Furthermore, dichotomizing heart failure into systolic and diastolic clinical entities has led to a paucity of clinical trials of therapies for heart failure with a normal ejection fraction. Therapies aimed at reversing myocardial fibrosis, and targets outside the heart such as enhancing vasodilator reserve and improving chronotropic incompetence deserve further study and may improve the exercise capacity of hypertensive heart failure patients. Hypertension heart disease with heart failure is simply not a dysfunction of systole and diastole. Other peripheral factors including heart rate and vasodilator response with exercise may deserve equal attention in an attempt to develop more effective treatments for this disorder.

Cardiac Autonomic Functions Derived From Short-Term Heart Rate Variability Recordings Associated With Nondiagnostic Results of Treadmill Exercise Testing

“…28) Some studies showed that heart rate response was blunted in hypertensive patients with or without heart failure. 29) Our present study also demonstrated that the nondiagnostic group had higher BMI and more hypertension than the negative group. Study limitations: First, our study was limited by a crosssectional rather than a longitudinal design.…”

Bone marrow mononuclear cells induce beneficial remodeling and reduce diastolic dysfunction in the left ventricle of hypertensive SS/MCWi rats

“…While blood pressure reduction is a major treatment goal in hypertensive heart disease, reducing ischemia and reversing pathological remodeling are key to preventing mortality and morbidity due to diastolic dysfunction (29). Recent evidence from work using bone marrow mononuclear cells (BMMNC) to treat myocardial infarction has shown a robust proangiogenic and antifibrotic effect of exogenous BMMNC therapy in ischemic hearts (8).…”

Diastolic Dysfunction: Association with Hypertension and Potential Target for Antihypertensive Therapy

“…Markers of collagen turnover and extracellular matrix proliferation cause detectable changes in left ventricular compliance and longitudinal axis mechanics and function even before LVH is detectable [8,9]. This remodeling of the extracellular matrix is thought to be pivotal in causing abnormalities of ventricular relaxation and ventricular compliance that characterize diastolic dysfunction, and it occurs in association with myocyte hypertrophy or independent of the development of LVH [19,23]. In patients with LVH, myocardial fibrosis is particularly increased in the subendocardial region [24].…”

“…Furthermore, there is a decrease in capillary density in the hypertrophied ventricle and a reduction in myocardial flow reserve. These factors are thought to predispose to myocardial ischemia even in the absence of epicardial coronary stenosis [4,19]. In addition, there is clustering of hypertension and other atherogenic and dysmetabolic risk factors such as obesity, sleep apnea, and dysmetabolic syndrome that directly and indirectly impair left ventricular function.…”