Unloading effects of prazosin in patients with chronic aortic regurgitation

Jebavý, P; Koudelková, E; Henzlova, Milena J.

doi:10.1016/0002-8703(83)90479-9

Cited by 9 publications

(2 citation statements)

References 31 publications

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“…In principle, the increase in afterload and the constriction of pulmonary vessels can result in an increase in pulmonary artery pressure. 10,12) In the present study, systolic maximal LV pressure, calculated as the sum of the maximal aortic pressure and the LVOT pressure gradient, did not increase significantly in response to phenylephrine. Therefore, the elevation in pulmonary artery pressure may result from a phenylephrine-induced increase in pulmonary vessel contraction rather than an increase in afterload to the LV.…”

Section: Discussioncontrasting

confidence: 46%

“…6) Further, reversal of LVOT obstruction may induce a paradoxical increase in cardiac output and systemic blood pressure and thereby decrease diastolic LV filling pressure and pulmonary artery pressure. 10) Based on these properties, propranolol may be useful in the management of pulmonary congestion with LVOT obstruction in ACS. Effects of phenylephrine: Phenylephrine-induced peripheral vasoconstriction results in an increase in aortic pressure and ventricular loading, 11) thereby reducing the hyperdynamic motion of nonischemic myocardium and relieving LVOT obstruction.…”

Section: Discussionmentioning

confidence: 99%

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Different Effects of Propranolol, Phenylephrine, and Saline Volume Loading on Catecholamine-Induced Left Ventricular Outflow Tract Obstruction in Acute Coronary Syndrome

et al. 2006

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SUMMARYHemodynamic deterioration due to left ventricular outflow tract (LVOT) obstruction can occur during catecholamine infusion in patients with acute coronary syndrome (ACS). The purpose of the present study was to compare the utility of propranolol, phenylephrine infusion, and rapid saline loading for reversal of dobutamine-induced LVOT obstruction in a canine model of ACS. ACS was induced via left anterior descending artery ligation in 21 open-chest anesthetized dogs, and LVOT obstruction, defined as an LVOT gradient > 30 mmHg, was induced by dobutamine infusion (20 to 40 µg/kg/min). Subsequently, the effects of propranolol infusion (0.7 to 1.0 µg/kg/min, n = 8), phenylephrine infusion (10 to 200 µg/kg/min, n = 7), and saline loading (200 to 400 mL/hr, n = 6) were assessed by serial hemodynamic measurements. All interventions produced significant and comparable improvements in the LVOT pressure gradient (propranolol: 60 ± 16 to 15 ± 12; phenylephrine: 68 ± 15 to 12 ± 10; saline loading: 58 ± 18 to 22 ± 10 mmHg; P < 0.001 for baseline versus postintervention; P = NS for comparison between interventions). Phenylephrine produced the greatest elevation in aortic pressure (propranolol: +15 ± 13; phenylephrine: +51 ± 36; saline loading: +15 ± 15 mmHg; P < 0.05), while saline loading produced the greatest increase in cardiac output (propranolol: +0.05 ± 0.12; phenylephrine: +0.28 ± 0.37; saline loading: +0.73 ± 0.48 L/min; P < 0.05). Propranolol was the only intervention that produced a significant decrease in diastolic pulmonary artery pressure (16 ± 5 to 11 ± 3 mmHg, P < 0.05). Propranolol, phenylephrine infusion, and saline volume loading were similarly effective in reversing dobutamine-induced LVOT obstruction in this canine model of ACS. However, each intervention produced different hemodynamic effects with potentially different clinical indications. (Int Heart J 2006; 47: 287-295)

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Section: Discussioncontrasting

confidence: 46%

Section: Discussionmentioning

confidence: 99%