title: Absence of arteriosclerosis in intramyocardial coronary arteries: a mystery to be solved?
abstract: Several studies show that portions of intramyocardial coronary arteries are spared of arteriosclerosis, involving morphological, embryological, biochemical and pathophysiological aspects. Endothelial function is significantly affected in the segment of transition, as estimated by the vasoactive response to Ach. These findings suggest that myocardial bridge can provide protection against arteriosclerosis by counteracting the negative effects of endothelial dysfunction. The intramyocardial portion's protection phenomenon deserves further scientific research on all research fronts. Improved morphological, biomechanical and especially physiological and embryological knowledge may be the key to a future window of opportunity for chronic arterial disease therapy and prevention. In addition, this review discusses possible therapeutic approaches for symptomatic coronary ischemia caused by myocardial bridges.
authors.affiliation: Surgery and Anatomy Department, Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, Ribeirão Preto, SP, Brazil.
authors.forename: Edvaldo Luiz
authors.initials: EL
authors.lastname: Ramalli
authors.forename: Leonardo Henrique
authors.initials: LH
authors.lastname: Braga
authors.forename: Patricia Martinez
authors.initials: PM
authors.lastname: Evora
authors.forename: Agnes Afrodite Sumarelli
authors.initials: AA
authors.lastname: Albuquerque
authors.forename: Andrea Carla
authors.initials: AC
authors.lastname: Celotto
authors.forename: André Lupp
authors.initials: AL
authors.lastname: Mota
authors.forename: Paulo Roberto Barbosa
authors.initials: PR
authors.lastname: Evora
mesh_terms: D000273:Adipose Tissue / Q000378:metabolism; D003324:Coronary Artery Disease / Q000517:prevention & control*; D003326:Coronary Circulation / Q000502:physiology; D003331:Coronary Vessels / Q000033:anatomy & histology / Q000196:embryology; D019332:Endothelin-1 / Q000378:metabolism; D004730:Endothelium, Vascular / Q000503:physiopathology*; D006801:Humans; D054084:Myocardial Bridging / Q000473:pathology*; D019899:Paracrine Communication / Q000502:physiology; D007703:Peptidyl-Dipeptidase A / Q000378:metabolism
chemical_list: D019332:Endothelin-1; C488034:ACE protein, human; D007703:Peptidyl-Dipeptidase A