• Giuseppe Barletta.
• A.O. Careggi, Cardiovascular Medicine, Florence, Italy. g.barletta@dac.unife.it
• Int. J. Cardiol. 2003 Feb 1;87(2-3):245-52.

BackgroundDobutamine-inducible left ventricular obstruction lacks a sound clinical meaning. This phenomenon may be related to an abnormal response of the heart to the sympathetic stimulation, and head-up tilt would elicit intraventricular obstruction in patients known to develop it during dobutamine administration, through the synergistic effects of reduced preload, hypercontractility, and reflex increase in the cardiac sympathetic tone.MethodsTwenty-one patients with normal coronaries and available dobutamine stress-echocardiography underwent 60 degrees -head-up tilt on echocardiographic and electrocardiographic monitoring in drug-free and nitroglycerin infusion (0.3 mcg/kg/min) protocols. Twelve patients had (group 1: 7 males, aged 61+/-7 years), and nine had not (group 2: 3 males, aged 60+/-9 years) developed left ventricular obstruction during dobutamine stress-echocardiography. Doppler echocardiographic measurements of left ventricular diameters, function and outflow tract flow velocity were performed; power heart rate variability was analysed on short electrocardiographic recordings (low/high frequency ratio); plasma catecholamines were determined at baseline and during the tilt manoeuvres.ResultsIntraventricular obstruction did not develop in group 1. There were baseline differences in ventricular dimensions and mitral early-to-late velocity ratio between group 1 and 2, but hemodynamic behaviour during either tilt manoeuvre was similar. Low/high frequency ratio, that was similar at baseline and similarly increased on head-up tilt, increased significantly less on nitroglycerin-tilt in group 1. No difference in plasma catecholamines was found.ConclusionsReflex cardiovascular adaptive responses as those elicited by passive tilt are not involved in dynamic intraventricular obstruction in dobutamine-inducible obstruction patients, data indicating that left ventricular geometry and hypercontractility are not sufficient pathophysiological determinants.

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