dc.creatorHISS, Flavio C.
dc.creatorLASCALA, Thiago F.
dc.creatorMACIEL, Benedito C.
dc.creatorMARIN-NETO, Jose A.
dc.creatorSIMOES, Marcus V.
dc.date.accessioned2012-10-19T22:49:14Z
dc.date.accessioned2018-07-04T15:15:36Z
dc.date.available2012-10-19T22:49:14Z
dc.date.available2018-07-04T15:15:36Z
dc.date.created2012-10-19T22:49:14Z
dc.date.issued2009
dc.identifierJACC-CARDIOVASCULAR IMAGING, v.2, n.2, p.164-172, 2009
dc.identifier1936-878X
dc.identifierhttp://producao.usp.br/handle/BDPI/23991
dc.identifier10.1016/j.jcmg.2008.09.012
dc.identifierhttp://dx.doi.org/10.1016/j.jcmg.2008.09.012
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1620719
dc.description.abstractOBJECTIVES This study aimed at analyzing the association between myocardial perfusion changes and the progression of left ventricular systolic dysfunction in patients with chronic Chagas` cardiomyopathy (CCC). BACKGROUND Pathological and experimental studies have suggested that coronary microvascular derangement, and consequent myocardial perfusion disturbance, may cause myocardial damage in CCC. METHODS Patients with CCC (n = 36, ages 57 +/- 10 years, 17 males), previously having undergone myocardial perfusion single-positron emission computed tomography and 2-dimensional echocardiography, prospectively underwent a new evaluation after an interval of 5.6 +/- 1.5 years. Stress and rest myocardial perfusion defects were quantified using polar maps and normal database comparison. RESULTS Between the first and final evaluations, a significant reduction of left ventricular ejection fraction was observed (55 +/- 11% and 50 +/- 13%, respectively; p = 0.0001), as well as an increase in the area of the perfusion defect at rest (18.8 +/- 14.1% and 26.5 +/- 19.1%, respectively; p = 0.0075). The individual increase in the perfusion defect area at rest was significantly correlated with the reduction in left ventricular ejection fraction (R = 0.4211, p = 0.0105). Twenty patients with normal coronary arteries (56%) showed reversible perfusion defects involving 10.2 +/- 9.7% of the left ventricle. A significant topographic correlation was found between reversible defects and the appearance of new rest perfusion defects at the final evaluation. Of the 47 segments presenting reversible perfusion defects in the initial study, 32 (68%) progressed to perfusion defects at rest, and of the 469 segments not showing reversibility in the initial study, only 41 (8.7%) had the same progression (p < 0.0001, Fisher exact test). CONCLUSIONS In CCC patients, the progression of left ventricular systolic dysfunction was associated with both the presence of reversible perfusion defects and the increase in perfusion defects at rest. These results support the notion that myocardial perfusion disturbances participate in the pathogenesis of myocardial injury in CCC. (J Am Coll Cardiol Img 2009;2:164-72) (c) 2009 by the American College of Cardiology Foundation
dc.languageeng
dc.publisherELSEVIER SCIENCE INC
dc.relationJacc-cardiovascular Imaging
dc.rightsCopyright ELSEVIER SCIENCE INC
dc.rightsrestrictedAccess
dc.subjectmyocardial perfusion scintigraphy
dc.subjectchronic Chagas` cardiomyopathy
dc.subjectleft ventricular function
dc.subjectmicrocirculation
dc.titleChanges in Myocardial Perfusion Correlate With Deterioration of Left Ventricular Systolic Function in Chronic Chagas` Cardiomyopathy
dc.typeArtículos de revistas


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