2009
DOI: 10.1590/s2179-83972009000300014
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Discinergia ventricular esquerda reversível identificada por potenciação pós-extrassistólica em miocardiopatia chagásica crônica não é causada por hibernação miocárdica

Abstract: A grafia discinergia (e suas variações) foi mantida conforme o original. Projeto parcialmente financiado pelo CNPq (Processo N o 520478/95-9) e pela FAPESP (Processo N o 1995/6195-8).

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Cited by 4 publications
(2 citation statements)
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References 24 publications
(16 reference statements)
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“…The study was performed using post-extrasystolic potentiation, which is commonly observed during radiologicalcontrast left ventriculography, and showed that most myocardial areas with impaired wall motion indeed had a contractile reserve; that is, these areas were viable 59 . However, the hypothesis that hypokinetic areas of viable myocardium, unmasked through post-extrasystolic potentiation, would be predominant in regions exhibiting scintigraphic, reversible (ischemic) perfusion defects, was not confi rmed by the results of the study 60 .…”
Section: Pathophysiological Consequences Of Coronary Microvascular Pementioning
confidence: 80%
“…The study was performed using post-extrasystolic potentiation, which is commonly observed during radiologicalcontrast left ventriculography, and showed that most myocardial areas with impaired wall motion indeed had a contractile reserve; that is, these areas were viable 59 . However, the hypothesis that hypokinetic areas of viable myocardium, unmasked through post-extrasystolic potentiation, would be predominant in regions exhibiting scintigraphic, reversible (ischemic) perfusion defects, was not confi rmed by the results of the study 60 .…”
Section: Pathophysiological Consequences Of Coronary Microvascular Pementioning
confidence: 80%
“…40,41 However, the hypothesis was not supported; the viability hidden by dyssynergia and shown through postextrasystolic potentiation could predominate or only appear in regions showing reversible perfusion defects during myocardial scintigraphy. 42 The second and perhaps most decisive mechanism would result in cellular death and consequent repairing fibrosis. In this context, there are relevant therapeutic implications potentially capable of attenuating, slowing, or even hindering the progression of myocardial dysfunction occasioned by ischaemic microcirculatory dysfunctions.…”
Section: Physiopathological Consequences and Opportunities For Therapmentioning
confidence: 99%