Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling

Citation
F. Barilla et al., Recovery of contractility of viable myocardium during inotropic stimulation is not dependent on an increase of myocardial blood flow in the absence of collateral filling, J AM COL C, 33(3), 1999, pp. 697-704
Citations number
38
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
ISSN journal
07351097 → ACNP
Volume
33
Issue
3
Year of publication
1999
Pages
697 - 704
Database
ISI
SICI code
0735-1097(19990301)33:3<697:ROCOVM>2.0.ZU;2-M
Abstract
OBJECTIVES The purpose of this study was to determine whether contractile r ecovery induced by dobutamine in dysfunctioning viable myocardium supplied by nearly occluded vessels is related to an increase in blood flow in the a bsence of collaterals. BACKGROUND Dobutamine is used to improve contractility in ventricular dysfu nction during acute myocardial infarction. However, it is unclear whether a significant increase in regional blood flow may be involved in dobutamine effect. METHODS Twenty patients with 5- to 10-day old anterior infarction and great er than or equal to 90% left anterior descending coronary artery stenosis u nderwent Tc-99m-Sestamibi tomography (to assess myocardial perfusion) at re st and during low dose (5 to 10 mu g/kg/min) dobutamine echocardiography. R est echocardiography and scintigraphy were repeated >1 month after revascul arization. Nine patients had collaterals to the infarcted territory (group A), and II did not (group B). RESULTS Baseline wall motion score was similar in both groups (score 15.9 /- 1.3 vs. 17.4 +/- 2.0, p = NS), whereas significant changes at dobutamine and postrevascularization studies were detected (F[2,30] = 409.79, p < 0.0 001). Wall motion score improved significantly (p < 0.001) in group A both at dobutamine (-5.3 +/-:2.2) and at postrevascularization study (-5.5 +/- 1 .9), as well as in group B (-3.9 +/- 2.8 and -4.5 +/- 2.4, respectively). B aseline Tc-99m-Sestamibi uptake was similar in both groups (62.9 +/- 9.7% v s. 60.3 +/- 10.4%, p = NS), whereas at dobutamine and postrevascularization studies a significant change (F[2,30] = 65.17, p < 0.0001) and interaction between the two groups (F[2,30] = 33.14, p < 0.0001) were present. Tracer uptake increased significantly in group A both at dobutamine (+10.9 +/- 7.9 %, p < 0.001) and at postrevascularization study(12.1 +/- 8.7%, p < 0.001). Conversely, group B patients showed no change in tracer uptake after dobut amine test (-0.4 +/-: 5.8, p NS), but only after revascularization (+8.8 +/ - 7.2%, p < 0.001). CONCLUSIONS The increase in contractility induced by low dose dobutamine in fusion in dysfunctional viable myocardium supplied by nearly occluded vesse ls occurs even in the absence of a significant increase in blood flow. (C) 1999 by the American College of Cardiology.