PubMed · 394972
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D Cardus. 1978. Exercise testing: methods and uses.. https://pubmed.ncbi.nlm.nih.gov/394972/
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Vagal stimulation at precise times in successive cardiac cycles can elicit sinus arrhythmias. Two mechanisms have been identified that can, but do not necessarily, cause these vagally induced sinus arrhythmias. First, changes in cycle length elicited by a given concentration of acetylcholine (ACh) depend on the phase of the pacemaker cell action potential when the ACh binds to muscarinic receptors. Second, acetylcholinesterase degrades ACh rapidly enough for the mean concentration of ACh per cardiac cycle to vary from cycle to cycle. We used a mathematical model of the underlying cellular physiology, to examine whether these mechanisms are responsible for arrhythmogenesis. Computer simulation showed that both mechanisms contribute to the vagally induced sinus arrhythmias.
This review paper deals with recent data concerning the physiopathology of chronic heart failure. Broadly speaking, the cause of chronic heart failure is arterial hypertension and/or coronary disease. Myocardial hypertrophy is only one example of biological adjustment to the environment, and chronic heart failure, an adaptation disease, indicates its limits. Diastolic dysfunction includes 3 elements. Relaxation is slowed down by a decrease in density of Ca(2+)-ATPase in the sarcoplasmic reticulum and by a fall in Na+/Ca2+ exchange activity. The decline of tissue compliance is mainly explained by probably hormonal changes in collagen. Changes in isomyosins account for abnormalities of atrial contraction. At the beginning of mechanical overload, the fall in systolic function enables the heart to produce a normal tension. The determinant element is slowing down of intracellular calcium movements. Enlarged hearts generate arrhythmias. The origin is probably the presence of unstable calcium homeostasis.
A computer simulation of ventricular conduction is presented with a discrete element ventricular conduction model. The model is shown to be capable of demonstrating normal ventricular rhythm, including QRS and T-waves, plus a variety of rhythm disturbances including missed beats, electrical alternans and self-sustaining instability with arrhythmias. The morphology of the range of alternans produced bears a strong resemblance to certain clinically recognised arrhythmias.