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The Science Journal of the Lander College of Arts and Sciences

Abstract

Takotsubo Cardiomyopathy (TTC) is a temporary heart-wall motion abnormality with the clinical presentation of a myocardial infarction. Found predominantly in postmenopausal women, TTC most often appears with apical ballooning and mid-ventricle hypokinesis. Often induced by an emotional or physical stress, TTC is reversible and excluded as a diagnosis in patients with acute plaque rupture and obstructive coronary disease. The transient nature and positive prognosis of this cardiomyopathy leaves a dilemma as to what precipitates it. This paper explores the theories of the pathogenesis of TTC including coronary artery spasm, microvascular dysfunction, and catecholamine excess. A thorough analysis of the pathogenesis was conducted using online databases. The coronary artery spasm theory involves an occlusion of a blood vessel caused by a sudden vasoconstriction of a coronary artery. This condition was confirmed in some patients with TTC using provocative testing, but failure to induce a coronary artery spasm in many patients led to its dismissal as a primary pathogenic mechanism. It is however a significant occurrence in patients with TTC and cannot be dismissed entirely. The microvascular dysfunction theory is challenged in the limited and underdeveloped methods of testing for its presence. However, using the corrected Thrombolysis in Myocardial Infarction frame count method to evaluate the flow of contrast in coronary arteries, researchers were able to indicate diffuse impaired coronary microcirculation in the myocardium. The theory involving catecholamines is based on the catecholamine surge that many patients experience with emotional or physical stressors. The stressor leads to excitation of the postsynaptic sympathetic neuron and the adrenal medulla, stimulating an influx of norepinephrine and epinephrine and the resulting hypokinesis of the apical portion of the left ventricle. Further research focused on this theory discovered the protective nature of estrogen against the catecholamine surge, explaining the prevalence of TTC in post-menopausal women. Genetic research perpetuates this theory by presenting predisposed genetic factors that prevent TTC. Analysis of the three theories found the catecholamine theory to be the most probable mechanism behind TTC, but further research is necessary to confirm TTC pathogenesis.

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