Titlebook: Early Arrhythmias Resulting from Myocardial Ischaemia; Mechanisms and Preve James R. Parratt Book 1982 The contributors 1982 arrhythmia.car

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ocardial infarction. Fatal complications of coronary disease have been reported to decrease by about 25 per cent in the latest report of the Persantine-Aspirin Reinfarction Study Research Group (1980). The significance of this and other similar trials has recently been discussed by Sherry (1980).

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s for this are many but surely include the difficulties involved in producing a consistent quantitative model in which to assess the protective actions of putative antiarrhythmic drugs. For instance, our own experiences have shown that one-stage coronary artery ligation does not produce ventricular

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ors precipitating transient electrical instability of the heart, in often symptomless patients with coronary artery disease, is unknown. It is generally believed that catecholamines play an important part in precipitating ventricular fibrillation, and, since the cardiac effects of catecholamines are

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978-1-349-06262-1The contributors 1982

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Peking University Linguistics Researchnt medical advance (Zoll ., 1956), because the brevity of the event pre-empted studies of its causes (and still does) and because it commonly occurs without praecordial tightness or any precise clinical syndrome.

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ischaemia. The objective of this chapter is to identify the ischaemia-induced changes which may be critical to the genesis of arrhythmias. In order to achieve this it will be necessary to consider the nature and progression of ischaemic injury.

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https://doi.org/10.1007/978-3-031-24723-1nd ventricular fibrillation may result. The period of maximum vulnerability to fibrillation is between 5 and 10 min after the onset of occlusion, although a further burst of arrhythmias has been observed in some instances between 15 and 30 min of ischaemia (for references see chapter 6). Thereafter,