Unstable Angina : Atherosclerotic Etiology, Myogenic Pathophysiology and Cardiotonic Therapeutic
According the Myogenic Theory the pathophysiological mechanism of unstable angina is represented primarily by an episodic and spontaneous regional myocardial insufficiency, provoking reciprocal regional myocardial ischemia with spontaneous recovery and successive recurrence of the manifestations assuming chronic form, or evolving to the acute myocardial infarction and even to sudden death. Such myocardial and symptomatic instability is identified by the electrocardiography, echocardiography, scintigraphy, hemodynamic avaliation or magnetic resonance imaging mainly during painful episodes, taking shape as the precedent stage of myocardial infarction.
In a retrospective study from the past fifty years, therapeutical trials realized with the use of coronary dilators, beta blockers, antiaggregate platelets, anticoagulants and thrombolytics, looking for the unstable angina pectoris (UA) interruption, were ever marked by failure in the clinical events, what certainly jeopardizes the Thrombogenic Theory basis. On the other side, the use of cardiotonic drugs preconized by the Myogenic Theory (MT) was ever successful in all cases of UA, serving as a confirmation for the MT.
Cardiotonics use in UA shows immediate stop regarding the painful crisis in crescendo, with the return to the symptomatic and myocardial stability with functional preservation of the myocardium and prevention of myocardial infarction to long term. In 199 patients with UA treated with the use of cardiotonics we have had an absolute success in all cases with the sole exception of 1 patient (0.4%) which evolved to MI and 0% of mortality.
Concerning the actual tendency to interpret the unstable angina as an infectious etiology resulted from inflammatory blood cells it represents in our point of view just a pure and weak speculation. Experiments in animals with normal coronary arteries shows that the trigger of accentuated myocardial ischemia followed by myocardial reperfusion, provoke identical blood reactions with the invasion of white blood cells and derived products. We believe that such recordings must be interpreted as non-specific mechanisms of auto-defense, usually observed in different clinical conditions or in front of the aggression of any organs by any physical, chemical or infectious agents.
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