• Clinical cardiology · Jul 2005

    Adjunctive handgrip during dobutamine stress echocardiography: invasive assessment of myocardial oxygen consumption in humans.

    • Ijaz A Khan, F Javier Otero, Jose Font-Cordoba, Marti McCulloch, Richard G Sheahan, Rohit Parmar, and Christopher R DeFilippi.
    • Division of Cardiology, University of Maryland School of Medicine, Baltimore, Maryland 21201-1595, USA.
    • Clin Cardiol. 2005 Jul 1;28(7):349-52.

    BackgroundAdjunctive isometric exercise in the form of sustained submaximal handgrip (HG) is considered to increase the sensitivity of dobutamine stress echo (DSE) for detection of functionally significant coronary artery disease.HypothesisThe study was undertaken to quantify invasively the impact of HG in humans on hemodynamics and myocardial oxygen consumption (MVO2) during DSE.MethodsAn invasive hemodynamic evaluation was performed during DSE and with addition of adjunctive HG in 11 subjects. Coronary sinus (CS) blood flow, right-sided and systemic pressures, oxygen saturations, and transthoracic two-dimensional echocardiography were obtained at each 3-min stage and after adding HG at peak DSE. Myocardial oxygen consumption was calculated by the Fick method and circumferential end-systolic wall stress (ESWS) by Mirsky's formula.ResultsAt peak DSE, heart rate, left ventricular ejection fraction, CS flow, and MVO2 increased, whereas pulmonary capillary wedge pressure (PCWP) and circumferential end-systolic wall stress (ESWS) decreased from baseline. Compared with peak DSE, the addition of isometric HG at peak DSE caused an increase in PCWP (7 +/- 3 vs. 8.4 +/- 3 mmHg, p < 0.05), ESWS (112 +/- 25 x 103 vs. 125 +/- 32 x 103 dyne x s x cm2, p = 0.02), and CS flow (260 +/- 92 vs. 301 +/- 105 ml/min, p < 0.05). There was a minimal increase in left ventricular volumes, heart rate, and systolic blood pressure. The MVO2 increased from 29 +/- 8 ml/min at peak DSE to 31 +/- 9 ml/min with adjunctive HG (p = 0.03).ConclusionHandgrip adjunctive to peak DSE results in a modest increase in MVO2, primarily by an increase in end-systolic wall stress.

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