The functional significance of ventricular geometry for the transition from hypertrophy to cardiac failure. Does a critical degree of structural dilatation exist?

Although it is generally accepted that ventricular geometric configuration plays an important role for manifestation of cardiac pumping failure, the relative significance of structural dilatation vs impaired myocardial performance- and the interaction of these factors-have not been thoroughly addressed. Besides its unfavorable effects on coronary circulation, cardiac energetics, and arrhythmogenesis, structural ventricular dilatation has direct consequences for stroke volume for geometrical reasons. As demonstrated by model calculations, the slope of the curve describing the relation between stroke volume and anatomical ventricular size is flattened and the maximum of the curve is shifted toward smaller end-diastolic volumes in the presence of reduced "contractility" or distensibility or after loss of contractile tissue. Further determinants of this curve are wall thickness and end-diastolic and systemic pressure. Based on the examples of human dilative cardiomyopathy and spontaneously hypertensive rats it can be shown that symptoms of pumping failure occur when the ventricular operating point has reached the maximum of the stroke volume-ventricular size relation or has even passed over the maximum, so that compensation via increase in ventricular size has been exhausted. However, neither ventricular dilatation nor severe myocardial impairment are a precondition for the occurrence of congestive symptoms if diastolic dysfunction is predominant or if hemodynamics and neuroendocrine reactions are substantially influenced by peripheral factors.