Increase of myocardial oxygen consumption due to active diastolic wall tension

A marked increase in left ventricular diastolic pressure\((\bar P_{LVD} )\) relative to volume is regularly observed during angina pectoris and may contribute to further deteriorations of myocardial perfusion in the ischemic myocardium and to pulmonary congestion as well. A possible simultaneous increase in myocardial oxygen consumption (MVO₂) due to a reversible diastolic tone during transient ischemia has not been taken into consideration in previous studies on alterations in ventricular diastolic properties. 13 closed-chest experiments were carried out in clinical catheterization technique with situations of high\((M\dot VO_2 )\) (18–50 mm Hg) relative to volume induced by right ventricular pacing (n=19; 172±5 beats/min) and catecholamine-induced reversible diastolic tone (n=17) in moderate hypothermia (31°C).\(\bar P_{LVD} \) was directly measured and indirectly calculated from its hemodynamic determinants using Bretschneider's equation (E_t) that does not consider ventricular diastolic pressure. In addition, an energy demand for maintenance of active diastolic wall tension (E₅) was calculated from\(M\dot VO_2 \) mean ventricular diastolic volume estimated from endsystolic and stroke volume, diastolic time and heart rate in ml O₂/min·100g. During pacing tachycardia with high\(\bar P_{LVD} \) (27.4±1.8 mm Hg) the\(\bar P_{LVD} \) (12.49±0.50 ml O₂/min·100 g) exceeds E_t (10.11±0.25 ml O₂/min·100 g) (p<0.001), partly due to neglect of E₅ (1.39±0.11 ml O₂/min·100 g). During catecholamine-induced high\(M\dot VO_2 \) (31.1±2.5 mm Hg) the\(\bar P_{LVD} \) (12.29±0.83 ml O₂/min·100 g) increases significantly (p<0.001) over E_t (10.43±0.81 ml O₂/min ·100 g). Addition of E₅ (1.76±0.14 ml O₂/min·100g) to E_t abolishes the differences between\(M\dot VO_2 \) and E_t yielding non-significantly different values. Results indicate by means of indirect energetic evidence the occurrence of a diastolic tone of the heart under unphysiologic conditions. Acute increases in\(\bar P_{LVD} \) during angina pectoris are supposed to increase\(M\dot VO_2 \) markedly due to an additional energy demand for maintenance of reversible active diastolic wall tension.