Acidity Theory of Atherosclerosis

Here is proposed a new hypothesis where acidity, evoked by stress, has an important role in the generator mechanism of atherosclerotic lesions, giving a new perspective for the understanding of its etiology and pathogenesis. The acidity theory of atherosclerosis is inside the response to injury concept. It has the following sequence of events: I. Sympathetic dominance by continuous stress plus II. Deficiency in production of endogenous digitalis-like compounds (DLCs) with alterations of Na(+), K(+)-ATPase activity results in: III. Lowered pH (acidity) that increases perfusion pressure and provokes effects on contractility of coronary arteries leading to changes in hemodynamic shear stress and atherosclerosis as consequence. The heart is an organ of high metabolic activity, susceptible to drops in pH during ischemia and hypoxia. Chronic elevated sympathetic bias may accelerate the myocardial anaerobic glycolysis with a significant increase in lactate production. In hypertension the concentration of lactic acid in both venous and arterial blood may be significantly elevated. Lactic acid in blood plasma is also significantly elevated during stress situations and indicative of stress levels. Psychosocial factors are independent significant predictors of carotid intima-media thickness (IMT) progression. Stress reduction through behavioral changes or use of sympatho-inhibitory drugs like Beta-blockers slow the progression of carotid IMT. Cardiac glycosides at lower daily doses also blocks excessive catecholamine release, resulting in very low mortality rate in prevention of acute coronary syndromes in patients with heart disease, as treated under the myogenic theory of myocardial infarction, a complementary hypothesis. Cardiac glycoside drugs show additional therapeutic possibilities, like re-elevation of lowered pH, appearing to attend the demand in insufficient production of endogenous DLCs, in some clinical conditions.