Angina can be defined in pathophysiological terms as a pain with cardiac origins, resulting from O2 deficit at the myocardial level. Atherosclerosis is by affecting and reducing the diameter of the coronary arteries, the most common cause of myocardial ischemia. A patient with atherosclerotic lesion (stenosis) which reduces at least 50% arterial diameter has significantly decreased the coronary flow reserve and develops myocardial ischemia in situations with increased metabolic need. Angina pectoris is clinically the most common manifestation of myocardial ischemia and results from changes at the cellular level, represented by metabolic shift from aerobe to the anaerobe cycle. Perpetuation of ischemic aggression leads to degradation and progressive loss of metabolic functions, electrical and mechanical ventricular myocardium, with the appearance of rhythm disorders and also, leading to heart failure events.
Angina pectoris develops when the blood flow at the coronary level is no longer adequate to the demand of O2 myocardial metabolism, the phenomenon is known as the period of myocardial ischemia. Reported to cellular myocardial ischemia may be the result of a request for O2 increased, or reduced intake. Heart rate, contractile status and blood parietal myocardial are major determinants of metabolic energy of the requirement and demand of O2. Metabolic balance of the myocardium is dependent on the ability of extraction of circulating O2 and O2 intake itself, which is directly dependent of the coronary flow. Human myocardium has a reduced ability to increase circulating O2 extraction (venous O2 saturation at rest is about 30%), so that the main mechanism in the event of increased metabolic demand is represented by the increase in coronary blood flow. The ability to dilate the coronary arteries and increase coronary blood flow, as a response to increased metabolic demand is known as the coronary flow reserve (CFR). It depends on the resistance of the coronary vascular tree and extravascular environment (infarction and interstitial), on the composition of circulating blood supply and in normal conditions, on a maximal dilatation of the coronary vessels which allow a 4-6 times increase in blood flow at rest.
Adequate knowledge of the pathophysiological mechanisms involved in the etiology of angina pectoris is important to explain and to properly approach therapeutically in different manifestations of ischemic heart disease.
The main clinical circumstances of occurrence of anginal manifestations are:
– Patient with stable hemoglobin which by atherosclerosis it losses its vasodilatory mechanisms of self-regulation of the coronary flow, by vasoconstriction, or by acute coronary thrombosis has a reduced intake of O2 myocardial;
– Patient presenting with uncontrolled hypertension, a fast heart rate, or increased inotropism and to which the metabolic demand of O2 is high.
– patient who is deficient in O2 intake, explained by alteration of the O2 transport function of blood circulating, situation being common in anemic states, hemoglobinopathies, or in different lung diseases characterized by low O2 saturation.
The appearance of chest pain is correlated with anaerobic metabolic pathway activation and development of lactic acidosis, accompanied by the release of lactate in coronary circulation, serotonin, bradykinin, histamine, reactive O2 species and especially adenosine. This result in degradation during myocardial ischemia, of ATP (adenosine acid triphosphoric) his circulating at extracellular level and A1 receptor stimulation of nerve endings associated to myocardial and coronary with the developmental vasodilatation pressure. The nerve ending correspond to spinal nerves I-IV and follows an upward path through the thalamus and spinal cords and from here to the cerebral cortex. Peculiarities of anatomical distribution of the nerve plexuses explain why the most common clinical forms of manifestation of chest pain have topographies at the chest, neck, shoulder, or left arm level.