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CLINICAL STUDIES

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

Francesco Barillà, MD^*, Giuseppe De Vincentis, MD, Enrico Mangieri, MD^*, Massimo Ciavolella, MD, PhD^* , Gaetano Pannitteri, MD^*, Francesco Scopinaro, MD, Giuseppe Critelli, MD^* and Pietro Paolo Campa, MD^*

^* 2nd Section of Cardiology, Institute of Cardiac Surgery, University "La Sapienza," Rome, Italy
Section of Nuclear Medicine, University "La Sapienza," Rome, Italy

Manuscript received March 23, 1998; revised manuscript received October 14, 1998, accepted November 18, 1998.

Reprint requests and correspondence: Dr. Francesco Barillà, 2nd Section of Cardiology, University of Rome "La Sapienza," Policlinico Umberto I, Viale Del Policlinico 155, 00161 Rome, Italy

OBJECTIVES

The purpose of this study was to determine whether contractile recovery induced by dobutamine in dysfunctioning viable myocardium supplied by nearly occluded vessels is related to an increase in blood flow in the absence of collaterals.

BACKGROUND

Dobutamine is used to improve contractility in ventricular dysfunction 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 90% left anterior descending coronary artery stenosis underwent ^99mTc-Sestamibi tomography (to assess myocardial perfusion) at rest and during low dose (5 to 10 µg/kg/min) dobutamine echocardiography. Rest echocardiography and scintigraphy were repeated >1 month after revascularization. Nine patients had collaterals to the infarcted territory (group A), and 11 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 < 0.0001). 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). Baseline ^99mTc-Sestamibi uptake was similar in both groups (62.9 ± 9.7% vs. 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 dobutamine 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 infusion in dysfunctional viable myocardium supplied by nearly occluded vessels occurs even in the absence of a significant increase in blood flow.

Abbreviations and Acronyms   ECG = electrocardiogram   LAD = left anterior descending artery   LDD = low dose dobutamine   LV = left ventricular   MI = myocardial infarction   PET = positron emission tomography   SPECT = single-photon emission computed tomography   WMS = wall motion score

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