Monitoring fibrillar collagen turnover in hypertensive heart disease

A substantial increase in fibrillar collagen has been observed in the cardiac ventricles of animals w1x and humans w2x with arterial hypertension. Either reactive or reparative hypertensive myocardial fibrosis is the result of both increased collagen types I and III synthesis by fibroblasts and unchanged or decreased extracellular collagen degradation w3x. Hemodynamic and non-hemodynamic factors may be involved in the disequilibrium between collagen synthesis and degradation that occurs in hypertension w4x.

As shown experimentally w1x and clinically w5,6x, a rise in collagen content increases myocardial stiffness and promotes abnormalities of cardiac function. In addition, the perivascular accumulation of collagen fibers may impair the vasodilator capacity of intramyocardial coronary arteries and contribute to the decrease in coronary reserve, which is commonly seen in the hypertensive heart w7x.

On the other hand, alterations in the electrical activity of the left ventricle in hypertensive patients have been shown to be related to the degree of myocardial fibrosis w6x.

CITA DEL ARTÍCULO  Cardiovasc Res. 1997 Aug;35(2):202-5