Antianginals

Antianginals

INTRODUCTION

Angina is caused by an accumulation of metabolites in the striated muscles and is associated with severe chest pain that occurs when the coronary flow is inadequate to supply oxygen required for the heart. Angina pectoris is the most common condition affecting significant number of population, involving tissue ischaemia in which vasodilators are used. Ischaemic heart disease is the most common serious health problem today. By far, the most frequent cause of angina is atheromatus obstruction of large coronary vessels (atherosclerotic angina and classic angina). However, in the transient spasm, localized portions of these vessels can also cause myocardial ischaemia and pain (spastic angina or variant angina). In theory, the imbalance between oxygen delivery and myocardial oxygen demand can be corrected by decreasing oxygen demand or by increasing delivery (by increasing coronary flow). Oxygen demand can be reduced by decreasing the cardiac work or according to recent studies, by shifting myocardial metabolism to substrates that require less oxygen per unit of adenosine triphosphate (ATP) production. In variant angina, spasm of coronary vessels can be reversed by nitrates or calcium channel blockers. It should be emphasized that all the vasodilators are effective in angina and, conversely, that some agents useful in angina (e.g. propranolol) are not vasodilators. Unstable angina, an acute coronary syndrome, is said to be present when there are episodes of angina at rest and when there is a change in character, frequency, and duration of chest pain as well as precipitating factors in patients with previously stable angina. In most cases, formation of nonocclusive thrombi at the site of a fissured or ulcerated plague is the mechanism.