Diastolic Heart Failure: A Concise Review

Abstract

The concept of “diastolic” heart failure grew out of the observation that many patients who have the symptoms and signs of heart failure had an apparently normal left ventricular (LV) ejection fraction. Thus it was assumed that since systolic function was “preserved” the problem must lie in diastole, although it is not clear by whom or when this assumption was made. Nevertheless, many guidelines followed on how to diagnose “diastolic” heart failure backed up by indicators of diastolic dysfunction derived from Doppler echoardiography. Diastolic heart failure is associated with a lower annual mortality rate of approximately 8% as compared to annual mortality of 19% in heart failure with systolic dysfunction, however, morbidity rate can be substantial. Thus, diastolic heart failure is an important clinical disorder mainly seen in the elderly patients with hypertensive heart disease. Early recognition and appropriate therapy of diastolic dysfunction is advisable to prevent further progression to diastolic heart failure and death. There is no specific therapy to improve LV diastolic function directly. Medical therapy of diastolic dysfunction is often empirical and lacks clear-cut pathophysiologic concepts. Nevertheless, there is growing evidence that calcium channel blockers, beta-blockers, ACE-inhibitors and ARB as well as nitric oxide donors can be beneficial. Treatment of the underlying disease is currently the most important therapeutic approach.

The effects of oat ingredients on blood pressure in spontaneously hypertensive rats

“…Impaired LV relaxation is associated with hypertension as a major consequence and leads to diastolic dysfunction by adversely affecting the adequate filling of LV. In half of the cases of heart failure, diastolic dysfunctional abnormalities are present with an increased risk of mortality (Aziz, Tk, Enweluzo, Dutta, & Zaeem, 2013). SHR treated with vehicle showed & Contaldo, 1997), (Mattioli, Zennaro, Bonatti, Bonetti, & Mattioli, 2004).…”

Cardioprotective effects of 5‐hydroxymethylfurfural mediated by inhibition of L‐type Ca2+ currents

“…A slight acute increase in LVEDP after addition of 5‐HMF is difficult to reconcile with an inhibitory action on Ca 2+ channels, but has been observed by others using established Ca 2+ channel blockers in vitro (Amende et al, ; Schmidlin et al, ; Hara et al, ) and in vivo (Kass et al, ; Nishimura et al, ; Cockrill et al, ). It should be noted that these acute effects have to be distinguished from the often observed protective effects after long‐term treatment with Ca 2+ channel blockers on diastolic dysfunction, attributed to indirect haemodynamic improvements (Aziz et al, ). Moreover, it has been suggested that Ca 2+ channel blockers applied at relatively high concentrations interfere with the Ca 2+ uptake and release activity of the sarcoplasmic reticulum in cardiac and skeletal myocytes (Wang et al, ).…”

Biomechanics of Cardiac Function

“…Diastolic heart failure, or heart failure with preserved ejection fraction (HFpEF) has become increasingly studied and is responsible for half of all heart failure hospitalizations (7, 152, 210, 216). Risk factors for HFpEF include aging, diabetes, obesity, and hypertension, and HFpEF has a higher prevalence in women than men.…”

“…Similarly, peripheral artery stiffening increases the resistance of the circulatory system leading to hypertension and increased LV pressure (215). HFpEF hearts commonly show concentric remodeling characterized by normal LV volume, increased LV mass (thus decreased volume to mass ratio), increased wall thickness, and increased chamber and myocardial stiffness (7). HFpEF hearts undergo hypertrophy with a marked increase in fibrosis, which leads to increased wall stiffness.…”