Factors responsible for manifestation of cardiac failure. Quantitative analysis using the finite element method

Factors responsible for manifestation of cardiac failure. Quantitative analysis using the finite element method

J Mol Cell Cardiol 24 (Supplement V) (1992) October 3,1992 Oral presentation II: 8.00 - 9.40 Heart Failure and Transplantation 49 FACTORS RES...

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J Mol

Cell

Cardiol

24 (Supplement

V) (1992)

October 3,1992

Oral presentation II: 8.00 - 9.40

Heart Failure and Transplantation

49

FACTORS RESPONSIBLE FOR MANIFESTATION OF CARDIAC FAILURE. QUANTITATIVE ANALYSIS USING THE FINITE ELEMENT METHOD Bernhard Dierberger, Rainer W Giilch, Ruthard Jacob. Physiologisches Institut II, Universitlt Tiibingen, FRG Based on the pressure-volume diagram and model calculations, the relative significance of myocardial (contractility, distensibility), geometric (inner dimensions, wall thickness) and mechanical (end-diastolic pressure, systolic pressure load) factors for reduction of stroke volume and ejection fraction can be quantified. The methodological approach has been improved by assumption of an ellipsoid of rotation with decreasing wall thickness towards the apex region as well as by development of a program for calculation using the finite element method. Confirming previous results, the application of this method on various models of cardiac hypertrophy and insufficiency (rats with renal and spontaneously hypertension, experimental aortic stenosis and aorta-caval fistula; patients with dilative cardiomyopathy) revealed that myocardial factors play a decisive role, as a rule, whereas structural dilatation exerts a direct negative effect on stroke volume only in the presence of further adverse factors. Reduced ventricular compliance has a surprisingly great influence particularly in hypertensive rats and patients with dilative cardiomyopathie, whereby the effects resulting from fibrosis are usually more pronounced than those of increased wall thickness.

134

METABOLIC

DYNAMICS

IN THE REPERFUSED

HUMAN

HEART

FOLLOWING

TRANSPLANTATION

Ryszard T. Smolenski, Anne-Marie L. Seymour, Kameljit K&i, Ronald 0. Pritchard and Magdi H. Yacoub. M. R. S. Unit, IV. H. L. I. at Hare field Hospital, Hare field, U.K. Reperfusion conditions affect the viability of heart cells through a variety of mechanisms. In particular, the efficiency of glycolytic and oxidative metabolism may be altered which in turn may modify the energy status of the heart. In this study, myocardial uptake and release of various metabolites involved in energy metabolism were investigated within 45 min of reperfusion (RI of the donor human heart during transplantation. Analysis of coronary sinus KS) and arterial (A) blood samples showed the following: 1) A peak of lactate release after 2.5 min of R (fi CS-A 2mM) which continued for the next 10 min. An initial uptake of pyruvate in the first min of R (a CS-A -0.02 mM) and subsequent release up to 45 min of R (a CS-A 0.03-0.05 mMI. Thus, CS lactate/pyruvate ratio (80) was transiently elevated but recovered to the value of A (35) within 5 min. 2) CS pH value was lower by 0.1 units than A in the first min but recovered immediately. Inorganic phosphate followed the same pattern with a maximum release in the first min (fi CS-A 1 mM). 3) Prolonged release of nucleotide catabolites was observed with maximum at 2.5 min of R (a CS-A 0.02 mM) and D CS-A 0.01 mM after 10 min. 4) Oxygen uptake was minimal in the first min. but increased gradually over the 45 min of reperfusion Our results highlight abnormalities in myocardial energy metabolism during reperfusion following transplantation. The most profound were reversed within the first min but abnormalities in pyruvate metabolism persisted for at least 45 min.

140

TEE EFFECT OF COUNTERPULSATION FREQUENCY MUSCLE USED FOR CARDIAC ASSISTANCE.

ON METABOLISM

OF SKELETAL

Anne-Marie L Seymoy, Debbie VE Cumming, Kameljit Kalsi, Ronald D Pritchard, Samir S Shah, John R Pepper, Charles W Pattison & Magdi H Yacoub. Dept of Cardiothoracic Surgery, National Heart & Lung Institute, Harefield Hospital, Middlx UB9 6JH. U.K. The electrical stimulation regime and the counterpulsation frequency employed in skeletal muscle counterpulsation (SMC) initiates muscle contraction and fibre type transformation but must be designed to prevent muscle fatigue and damage. We have investigated the metabolic changes at counterpulsation frequencies of l:l, 1:2, and 1:4 using a mock circulation model in untrained latissimus dorsi in sheep. The muscle was subjected to a fatigue test at a stimulation protocol of 3 volts, 35 Hz and samples were taken throughout the experiment for metabolic analyses. NMR spectroscopy was used to measure the phosphocreatine to phosphocreatine + inorganic phosphate ratio (PCr/PCr+Pi), an index of oxidative capacity. ‘IXe power developed during muscle contraction was also determined. Results showed that the PCr/PCr+Pi ratio declined to 37% and 16% of control in the 1:l and 1:2 modes respectively, within the first 5 min of the fatigue test. In each case, there was a loss of power from 1.5 to 2 W/kg. This contrasted with the I:4 mode where, despite an initial decrease in the PCr/PCr + Pi ratio, the muscle completed fhe full 30 min fatigue test maintaining an average power of 14 W/kg throughout. Histological findings from in vivo experiments, where post operative muscle damage was evident after stimulation in the 1: 1 and 1:2 modes, support these findings. We conclude that SMC in the 1:4 mode is less likely to cause muscle damage and fatigue and thus may be more appropriate for long term cardiac assistance. s.112