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Updated: May 5, 2026

Reduction in Left Ventricular Wall Stress and Improvement in Function in Failing Hearts using Algisyl-LVR
Published on: April 8, 2013
Midwall mechanics are improved after regression of hypertensive left ventricular hypertrophy and normalization of
S Perlini1, M L Muiesan, C Cuspidi
1Clinica Medica I,IRCCS San Matteo, Università di Pavia, Pavia, Italy. sperlini@unipv.it
Insights
Regression of hypertensive left ventricular hypertrophy (LVH) improves heart function, with geometric normalization playing a key role. This improvement in myocardial function persists even after blood pressure increases again.
Area of Science:
- Cardiology
- Cardiovascular Physiology
- Echocardiography
Background:
- Hypertensive left ventricular hypertrophy (LVH) is common, but its impact on left ventricular (LV) myocardial function after regression is not fully understood.
- The relationship between LVH regression, normalization of cardiac geometry, and myocardial function requires further investigation.
Purpose of the Study:
- To investigate whether substantial regression of hypertensive LVH and normalization of LV geometry are linked to improved LV myocardial function.
- To determine the relative contributions of reduced LV systolic stress and normalized LV geometry to improved midwall function.
Main Methods:
- 152 patients with hypertensive LVH underwent 1 year of antihypertensive treatment (lisinopril +/- hydrochlorothiazide).
- Echocardiography assessed LV mass, relative wall thickness, and midwall fractional shortening before, during, and after treatment.
- 24-hour ambulatory blood pressure monitoring evaluated blood pressure and calculated end-systolic wall stress.
Main Results:
- Antihypertensive treatment significantly reduced blood pressure, end-systolic wall stress, and LV mass index.
- LVH regression was associated with increased midwall fractional shortening and decreased relative wall thickness.
- Improved midwall function persisted after treatment withdrawal, linked to preserved relative wall thickness despite increased wall stress.
Conclusions:
- Regression of concentric LVH is associated with improved midwall systolic function.
- Normalization of LV geometry, rather than solely the reduction in LV systolic stress, is the primary driver of improved systolic function.
Background:
It is still unclear whether substantial regression of hypertensive left ventricular hypertrophy (LVH) and normalization of chamber geometry are associated with improved left ventricular (LV) myocardial function.
Methods And Results:
Midwall mechanics were evaluated in 152 patients undergoing 1 year of effective antihypertensive treatment. Two-dimensionally directed M-mode echocardiography was performed as follows: (1) after a 4-week placebo "run-in" period, (2) after 1 year of treatment with 20 mg/d lisinopril (alone or associated with 12.5 to 25 mg/d hydrochlorothiazide), and (3) after a final 1-month placebo period to allow blood pressure (24-hour average ambulatory monitoring) to return to pretreatment levels. Treatment-induced reductions in blood pressure (from 149+/-16/95+/-11 to 131+/-12/83+/-10 mm Hg, P:<0.05) and circumferential end-systolic wall stress (from 84+/-22 to 72+/-19 g/cm(2), P:<0.05) were associated with a marked reduction in LV mass index (from 159+/-30 to 133+/-26 g/m(2), P:<0.05). LVH regression was accompanied by an increase in midwall fractional shortening (from 19.7+/-2.7% to 20.9+/-2.7%, P:<0.05) and by a decrease in relative wall thickness (from 48.2+/-7.7% to 44.1+/-6.7%, P:<0.05). The improvement in midwall function associated with afterload reduction and substantial LVH regression persisted after antihypertensive therapy withdrawal and restoration of the hypertensive state. Despite a significant increase in end-systolic wall stress, further LV chamber remodeling did not occur. The preservation of relative wall thickness was associated with a persistent improvement in midwall systolic function.
Conclusions:
Regression of concentric LVH is associated with an improvement of midwall systolic function, which is more dependent on the normalization of LV geometry than on the reduction in LV systolic stress.
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