Treatment of Angina - New Attitudes and Emerging Changes in Management

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Abstract

Angina pectoris is a symptom that is usually, in the developed world, caused by obstruction to the coronary arteries by the enlargement of atheromatous lesions; there are other causes. The symptom can limit lifestyle, but more importantly is a repetitive reminder to the patient of the presence of heart disease, causing continual anxiety because of the belief that angina is the portent of early death. That is not true; the annual mortality in the absence of severe disease and with reasonable left ventricular function ranges between 1 and 3% (see Figure 1).1 Angina pectoris has been a rather dull topic in cardiovascular medicine because of a lack of new ideas and a conventional approach to management. That is set to change. Angina pectoris was known many centuries ago,2 but the first clear and elegant description was by Heberden in the 18th century.3 The exact cause and pathophysiology was established by the work of many physicians such as Hunter, Black, Fothergil, Jenner, Parry, and Burns, showing the link of angina to the heart and to abnormalities of the coronary arteries.4 Osler wrote eloquently about angina,5 but it was Obratzow and Straschenko6 in 1910 and then Herrick7 who first described myocardial infarction in a patient.

Citation
US Cardiology, 2007;4(1):31-4

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Angina pectoris is a symptom that is usually, in the developed world, caused by obstruction to the coronary arteries by the enlargement of atheromatous lesions; there are other causes. The symptom can limit lifestyle, but more importantly is a repetitive reminder to the patient of the presence of heart disease, causing continual anxiety because of the belief that angina is the portent of early death. That is not true; the annual mortality in the absence of severe disease and with reasonable left ventricular function ranges between 1 and 3% (see Figure 1).1 Angina pectoris has been a rather dull topic in cardiovascular medicine because of a lack of new ideas and a conventional approach to management. That is set to change. Angina pectoris was known many centuries ago,2 but the first clear and elegant description was by Heberden in the 18th century.3 The exact cause and pathophysiology was established by the work of many physicians such as Hunter, Black, Fothergil, Jenner, Parry, and Burns, showing the link of angina to the heart and to abnormalities of the coronary arteries.4 Osler wrote eloquently about angina,5 but it was Obratzow and Straschenko6 in 1910 and then Herrick7 who first described myocardial infarction in a patient.
Recent work has established the role of the unstable, fissured, or eroded atheromatous plaques in the coronary arteries,8–11 thrombosis in the coronary artery leading to myocardial infarction,12,13 and the effects of platelet activation and accumulation of atheromatous material in the vessel wall.14–16 Most of these acute abnormalities in the vessel wall lead to acute coronary syndromes or myocardial infarction and carry a poor early prognosis. Chronic (stable) angina pectoris, in contrast, is usually a consequence of a fixed obstruction within the coronary artery. The atheromatous plaque may expand outwards from the lumen of the artery and only late in the progression of atheroma does the lesion reduce the size of the lumen. The extent to which the lumen is occluded by a lesion in the absence of an acute coronary syndrome is a poor guide to the stability of the plaque or the future natural history.17 The differences in pathology between these different coronary syndromes almost certainly account for the differences in prognosis and the better prognosis of stable angina pectoris.

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