Hypoxia combined with pacing tachycardia significantly increased left ventricular end diastolic pressure from 10 to 24 mmHg and prolonged the relaxation time constant, indicating increased chamber stiffness when oxygen demand exceeds supply.
Absolute Event Rate: 24% vs 10%
p-value: p=<0.01
To clarify conflicting reports concerning the effects of ischemia on left ventricular chamber stiffness, we compared the effects of hypoxia at constant coronary perfusion with those of global ischemia on left ventricular diastolic chamber stiffness using isolated, perfused rabbit hearts in which the left ventricle was contracting isovolumically. Since chamber volume was held constant, increases in left ventricular end diastolic pressure (LVEDP) reflected increases in chamber stiffness. At a control coronary flow rate (30 ml/min), 2 min of hypoxia and pacing tachycardia (4.0 Hz) produced major increases in postpacing LVEDP (10+/-1 to 24+/-3 mm Hg, P 25 mm Hg), which gradually recovered over 1-2 min at the control heart rate. From these results, we conclude that left ventricular chamber stiffness increases when myocardial O(2) demand exceeds supply. This change is usually masked in ischemic (reduced coronary flow) preparations, perhaps because of reduced turgor of the coronary vascular bed, marked reductions in systolic work (and therefore myocardial O(2) requirements), and local accumulation of hydrogen ion and metabolites following acute severe reduction of coronary flow. The increased chamber stiffness during hypoxia is accompanied by marked slowing of relaxation, with increased diastolic pressure relative to volume persisting throughout diastole.
Serizawa et al. (Wed,) conducted a other in Myocardial ischemia and hypoxia. Hypoxia and pacing tachycardia vs. Control coronary flow (30 ml/min) and initial heart rate (2.0 Hz) was evaluated on Left ventricular end diastolic pressure (LVEDP) in mmHg (p=<0.01). Hypoxia combined with pacing tachycardia significantly increased left ventricular end diastolic pressure from 10 to 24 mmHg and prolonged the relaxation time constant, indicating increased chamber stiffness when oxygen demand exceeds supply.