Change in Diastolic Left Ventricular Filling After One Year of Antihypertensive Treatment

Abstract

Background-It is well established that hypertensive patients with left ventricular (LV) hypertrophy have impaired diastolic filling. However, the impact of antihypertensive treatment and LV mass reduction on LV diastolic filling remains unclear. Methods and Results-Echocardiograms were recorded in 728 hypertensive patients with ECG-verified LV hypertrophy (Cornell voltage-duration or Sokolow-Lyon) at baseline and after 1 year of blinded treatment with either losartan or atenolol-based regimen. Systolic and diastolic blood pressures (BP) were reduced on average 23/11 mm Hg; isovolumic relaxation time and E/A ratio became more normal, and LV inflow deceleration time prolonged (all PϽ0.001).Directionally opposite changes in isovolumic relaxation time (IVRT) and deceleration time indicate improvement in active LV relaxation and passive chamber stiffness during early diastole. Prevalences of normal LV filling increased, abnormal relaxation and pseudonormalization decreased, and restrictive filling pattern remained unchanged (PϽ0.05).Patients with reduction in LV mass had smaller left atrial diameter, shortened IVRT, increased E/A ratio, and prolonged LV inflow deceleration time (all PϽ0.001). Patients without LV mass reduction had no change in diastolic filling parameters (PϭNS). IVRT shortening was independently associated with reduction in LV mass. Increase in E/A ratio was independently associated with reduction in diastolic BP, and increase in the deceleration time was independently associated with reduced end-systolic relative wall thickness. Conclusions-Antihypertensive therapy resulting in LV mass or relative wall thickness regression is associated with significant improvement of diastolic filling parameters related to active relaxation and passive chamber stiffness compared with patients without regression, independent of BP reduction; however, abnormalities of diastolic LV filling remain common.

Patients with a Hypertensive Response to Exercise Have Impaired Left Ventricular Diastolic Function

“…LV diastolic dysfunction associated with exercise intolerance in patients with hypertensive response to exercise but no resting hypertension was similar in degree to that of patients with both hypertensive response to exercise and resting hypertension. Consistent with previous reports, we observed a correlation between arterial hypertension and impaired LV diastolic performance in patients with hypertension (4,5). In increased systolic arterial pressure, there is an upward shift in the LV diastolic pressure-volume ratio, resulting in an increase in left atrial pressure indicated by an increased E/E′ (24), and slow LV relaxation, as indicated by a decreased E′.…”

“…Increase in systolic blood pressure (SBP) causes slow myocardial relaxation, left ventricular (LV) hypertrophy and potentially adverse effects on passive chamber stiffness (4,5). Thus, many patients with long-standing hypertension have Doppler echocardiographic evidence of impaired diastolic function, which may limit exercise tolerance.…”

Cardiovascular remodeling during long-term nocturnal home hemodialysis

“…Regression of LVH has been shown to improve systolic function, and reduce the risk of ventricular arrhythmias and atrial fibrillation [20–22]. Moreover, in patients with and without kidney failure, regression of LVH is associated with decreased all-cause mortality, rendering this a valid surrogate health outcome in this population [23, 24].…”

“…This study is the first to show a significant improvement in diastolic dysfunction from a grade of 3.4 to 1.2 after 1 year of NHD with an improvement in overall LV filling pressures. While regression of diastolic dysfunction has been associated with LVH regression in prior studies, it is not known whether this leads to improved survival or a reduction in cardiovascular events [20, 30]. …”

Blockade of the Renin-Angiotensin-Aldosterone System: Effects on Hypertensive Target Organ Damage

“…The regression of cardiac hypertrophy and fibrosis is accompanied by an improvement of LV diastolic function, with increased rate of active relaxation and decreased passive chamber stiffness [51,52]. The two phenomena, hypertrophy regression and diastolic improvement, are partly independent from each other.…”