Other recent studies did not observe a close relationship between left ventricular mass and diastolic function. Trimarco et al observed that treatment with a nonselective P-blocking agent improved diastolic function lowering blood pressure, but this effect was independent from left ventricular mass reduction. The study of Shahi et al showed that an angiotensin-converting enzyme inhibitor agent, alone or in addition of a diuretic, reduces left ventricular mass, but does not change left ventricular diastolic function.
In absence of echocardiographically defined hypertrophy, the impairment of left ventricular filling may be explained by an increase of muscle stiffness due to changes in cardiac muscle properties that could be related to alterations in myocardial collagen content and type, and perhaps to changes in distribution of cardiac myosin isozyme patterns. Other factors, besides structural ones, can influence the left ventricular relaxation and early filling. These include the following: dynamic factors such as inotropic state, loading conditions (preload and afterload) at the end of systole, heart rate, sympathetic tone, coronary blood flow and myocardial perfusion in early diastole, and alterations in intracellular calcium kinetics (decreased rate of reuptake of calcium by the sarcoplasmic reticulum).