The inotropic and electrophysiological effects of plasma obtained from patients and experimental dogs during cardiogenic shock following acute myocardial infarction were studied. Changes in the isometric contraction and the intracellular action potential were determined in isolated papillary muscles of rabbits. Control plasma collected from normal subjects produced no significant changes in the contraction or the electrical parameters. Plasma from shock patients decreased peak force by 42% and the maximum rate of force development by 38% in comparison to control values; the time to peak of contraction, the relaxation time and the action potential parameters were not significantly altered. Corresponding results were obtained with plasma from dogs before and during experimental cardiogenic shock. Biochemical determinations failed to identify a single specific "myocardial depressant factor" in the plasma of patients and dogs with cardiogenic shock. The results suggest that (1) various humoral factors released during cardiogenic shock may depress the contractile function of cardiac muscle and (2) that the observed negative intropic effect is not due to electrical changes in the cell membrane.

Action Potentials↗

PubMedDate not supplied

End-systolic pressure-volume and end-systolic stress-volume relationships in patients with aortic stenosis and with normal valvular function.

In order to study the effect of left ventricular hypertrophy on the endsystolic pressure-volume relationship, three left ventricular angiograms were performed in ten patients with normal valvular function but with varying left ventricular function (group 1) after 0.15 mg/kg propranolol and 1 mg atropine: at rest, after isosorbide-dinitrate at a decreased afterload and after methoxamine at an enhanced afterload. In eight patients with aortic stenosis (group 2) two left ventricular angiograms were performed: at rest and after isosorbide-dinitrate. Heart rate was kept constant by atrial pacing. Left ventricular mass in group 1 was 89 g/m2 and in group 2 180 g/m2. In group 1 the slope k of the end-systolic pressure-volume relation was related to the ejection fraction (EF) at rest: k = 0.024 . e0.072 EF; r = 0.93. In group 2 this relation was shifted to the left (P less than 0.001): k = 0.135 . e0.057 EF; r = 0.81. The relations, however, between the slope k of the end-systolic stress-volume relation and the ejection fraction were close together in group 1 and in group 2 and crossed at an ejection fraction of 67%. It is concluded: 1. In patients with aortic stenosis the end-systolic pressure-volume relation is steeper than in patients without valvular dysfunction at a given ejection fraction, so the relation between the slope k and the ejection fraction is shifted to the left. 2. The end-systolic stress-volume relationship is not altered in patients with aortic stenosis and seems to be advantageous for the evaluation of left ventricles with substantial hypertrophy due to pressure load.

Adult↗

PubMedDate not supplied

Comparison between the effect of postextrasystolic potentiation and the effect of nitrates on left ventricular function for the differentiation between reversible and irreversible left ventricular asynergy.

In patients with coronary heart disease (CHD) it is important to differentiate between reversible and irreversible left ventricular (LV) asynergy. Therefore global and regional LV function was investigated in the postextrasystolic beat (PES) and after isosorbide dinitrate (ISDN). In 24 patients LV angiograms were performed before and after ISDN. The ejection fraction (EF) was determined in a sinus beat and in PES. Regional LV performance was measured by the shortening of the length axis and six short hemiaxes. In 12 patients with normal LV function at rest EF increased from .72 +/- .04 (+/- 1 SD) to .77 +/- .04 (P less than 0.05) after ISDN and rose further to .81 +/- .02 in the PES (P less than 0.05). In 12 patients with CHD and LV asynergy EF increased from .43 +/- .12 to .47 +/- .13 after ISDN (P less than 0.05) and rose further to .57 +/- .13 in the PES (P less than 0.02). After ISDN 23/39 asynergic axes improved, 15/39 axes did not change, 1/39 axis decreased its shortening by 12%. In the PES 26/39 axes improved, 6/39 axes did not change; 7/39 axes showed less shortening, presumably due to a systolic shift of blood into dyskinetic regions with LV scar. It is concluded: The PES affects viable myocardium more than does ISDN; the PES is easier to perform and permits a more precise distinction between reversible and irreversible LV dyskinesis.

Coronary Disease↗

PubMedDate not supplied