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Factors influencing regional myocardial contractile response to inotropic stimulation: Analysis in humans with stable ischemic heart disease

  • Hal A. Skopicki
  • , Stephen A. Abraham
  • , Neil J. Weissman
  • , Anil K. Mukerjee
  • , Nathaniel M. Alpert
  • , Alan J. Fischman
  • , Michael H. Picard
  • , Henry Gewirtz
  • Massachusetts General Hospital

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

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 [18F]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%; χ2, 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%; χ2, 14.1; P<.001) and off (51% versus 21%; χ2, 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.

Original languageEnglish
Pages (from-to)643-650
Number of pages8
JournalCirculation
Volume94
Issue number4
DOIs
StatePublished - 1996

Keywords

  • adenosine
  • coronary disease
  • echocardiography
  • myocardial contraction
  • regional blood flow

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