Increased LVEDP=Dyspnea

When studied hemodynamically, most patients with diastolic dysfunction have normal sized left ventricles and elevated left ventricular diastolic pressures (LVEDP) at rest when congestion is not present. This is a marker of increased stiffness. More refined hemodynamics indicate that left ventricular relaxation is slowed. Because of these changes, these patients have an inability to increase left ventricular end diastolic volume (LVEDV) without a great increase in end diastolic pressures. This inability to use the Frank-Starling mechanism of increasing LVEDV limits exercise since any increased volume markedly increases LVEDP and clinical dyspnea.

Hence a vicious cycle develops since the increased left ventricular pressure results in shortness of breath. This generates anxiety, increased sympathetic tone, an increased heart rate and possibly an arrhythmia such as atrial fibrillation. Ischemia secondary to coronary stenosis impairs relaxation further and increases LVEDP. Hypertension intensifies the impaired diastole further by enhancing concentric hypertrophy, a myocardium which is strong, but stiff. The inability to increase LVEDV compromises the ability to increase cardiac output, which, in turn, also stimulates the sympathetic and rennin angiotensin-aldosterone systems leading to volume retention and a further increase in LVEDP.