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Myocardial ischaemia is responsible for angina, unstable angina, and, less commonly, shortness of breath secondary to ischaemic left ventricular dysfunction (angina equivalent) as well as cardiac arrhythmias. This article will deal with the mechanisms of myocardial ischaemia likely to be encountered in patients presenting with the chronic coronary insufficiency and stable symptoms of angina. It will not deal with the vessel wall based mechanisms of unstable or acute coronary syndromes which are covered elsewhere in this series.
The undergraduate, see-saw diagram showing the perfect match between myocardial oxygen consumption (MV̇o2) and oxygen delivery to the myocardium remains at the core of our understanding of myocardial ischaemia. Changes in MV̇o2, because of their relation to symptomatology and the rather more tractable nature of this parameter experimentally, have been concentrated on as a mechanism explaining myocardial ischaemia. However, not only is it plausible that changes in oxygen delivery influence the process of myocardial ischaemia, but to explain the day to day symptoms of patients with angina, changes in both MV̇o2 and oxygen delivery together or separately must occur. Accordingly, an understanding of the mechanisms involved in regulating both of these parameters is important.
MYOCARDIAL OXYGEN CONSUMPTION
MV̇o2 is determined in large part by the parameters shown in table 1.1 Some of these, on a daily basis, remain relatively fixed (for example, myocardial mass), but it is the change in myocardial workload that is the most obvious when talking to patients who give a clear story of a relation (though not precise generally) between their symptoms and exercise. Experimentally myocardial work has required instrumentation for its quantification, however, the systolic blood pressure · heart rate double-product has been demonstrated to be a useful surrogate2 and is of clinical utility. These two component parameters are useful, …