Angiotenison Converting Enzyme Counters Myocardial Fibrosis

The angiotensin-converting enzyme inhibitor, lisinopril, can counter myocardial fibrosis and improve left ventricular diastolic function in patients with hypertensive heart disease.



German researchers noted that in arterial hypertension, left ventricular hypertrophy includes myocyte hypertrophy and fibrosis, leading to left ventricular (LV) diastolic dysfunction and heart failure.



In a prospective double-blind trial, researchers enrolled 35 patients with primary hypertension, LV hypertrophy and left ventricular diastolic dysfunction. Patients were randomised to receive either lisinopril (n=18) or hydrochlorothiazide (n=17).



At baseline and after six months, three procedures were performed — left ventricular catheterisation with endomyocardial biopsy, Doppler echocardiography and 24-hour blood pressure monitoring. Myocardial fibrosis was measured by LV collagen volume fraction and myocardial hydroxyproline concentration.



With lisinopril, collagen volume fraction fell from 6.9±0.6 percent to 6.3±0.6 percent and myocardial hydroxyproline concentration also fell, from 9.9±0.3 to 8.3±0.4 micrograms/mg of LV dry weight. Both reductions were significantly greater than with hydrochlorothiazide.



The reductions were associated with a rise in the early filling and atrial contraction LV peak flow velocity ratio, from 0.72±0.04 to 0.91±0.06, and a decrease in isovolumic relaxation time from 123±9 to 81±5 minutes. These too were significantly superior to hydrochlorothiazide.



Normalised blood pressure did not significantly change in either group. While there was no LV hypertrophy regression with lisinopril, myocyte diameter was reduced with hydrochlorothiazide, from 22.1±0.6 to 20.7±0.7 micrometer.