Factors Influencing Regional Myocardial Contractile Response to Inotropic Stimulation

Author:

Skopicki Hal A.1,Abraham Stephen A.1,Weissman Neil J.1,Mukerjee Anil K.1,Alpert Nathaniel M.1,Fischman Alan J.1,Picard Michael H.1,Gewirtz Henry1

Affiliation:

1. the Departments of Medicine (Cardiac Unit), Radiology, and Nuclear Medicine, Massachusetts General Hospital, Harvard Medical School, Boston.

Abstract

Background We hypothesized that the response of a myocardial segment to maximal dobutamine reflects not only maximal blood flow but also tethering, metabolic, and β-blocker status. Methods and Results Patients with stable ischemic heart disease (n=27) had positron emission tomographic measurement of blood flow at rest and with adenosine, and echocardiography at rest and with dobutamine. Positron emission tomographic measurement of [ 18 F]fluorodeoxyglucose myocardial distribution also was made. Adenosine blood flow in segments that contracted normally at peak dobutamine was similar to that of segments that became hypokinetic (1.06±0.72 versus 1.02±0.77 mL·g −1 ·min −1 ). Segments that became akinetic failed to augment blood flow (0.68±0.30 mL·g 1 ·min 1 ). Fluorodeoxyglucose–blood flow mismatch was more common in segments with abnormal wall motion at peak dobutamine (24 of 59, 41%) versus those that contracted normally (63 of 269, 23%; χ 2 , 7.40; P <.01). In patients off β-blockers, segments that contracted normally at peak dobutamine increased blood flow with adenosine (0.70±0.31 to 0.86±0.46 mL·g 1 ·min 1 ; P <.05), whereas those that became abnormal did not (0.63±0.24 to 0.65±0.19 mL·g 1 ·min 1 ; P =NS). Segments of patients on β-blockers that contracted normally at peak dobutamine increased blood flow with adenosine (0.78±0.31 to 1.10±0.70 mL·g 1 ·min 1 ; P <.05), as did segments that became abnormal (0.74±0.34 to 1.06±0.82 mL·g 1 ·min 1 ; P =NS). However, segments adjacent to ones with abnormal wall motion at rest had higher frequency of abnormal response at peak dobutamine in groups on (48% versus 16%; χ 2 , 14.1; P <.001) and off (51% versus 21%; χ 2 , 10.9; P <.01) β-blockers. Conclusions Augmented contraction at maximal dobutamine depends not only on increased myocardial blood flow but also on tethering, metabolic, and β-blocker status. Furthermore, impaired flow reserve does not preclude a normal response to maximal dobutamine, since blood flow need not increase greatly to meet demand.

Publisher

Ovid Technologies (Wolters Kluwer Health)

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine

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