The failure of the blood pressure to fall during the late strain phase of the Valsalva maneuver in patients with heart failure may result from the left ventricle operating on a flat portion of its function curve or from maintenance of left ventricular volume despite decreased systemic venous return. To test these possibilities, we studied the effect of the Valsalva maneuver (40 cm H20 for 15 sec) on left ventricular volume in 12 normal subjects with a mean left ventricular ejection fraction of 0.65 ± 0.07 (± SD) and in eight patients with nonischemic cardiomyopathy, evidence of pulmonary congestion, and a mean left ventricular ejection fraction of 0.23 0.09. Left ventricular volume and right ventricular area were determined by apical two-dimensional echocardiography. In both groups the right ventricular end-diastolic area decreased during the late strain phase of the Valsalva maneuver. In normal subjects it decreased from 9.3 ± 1.5 to 5.6 ± 1.6 cm2 (p < .001) and in patients it decreased from 13 ± 2.2 to 10 ± 2.9 cm2 (p < .001). In normal subjects, left ventricular end-diastolic volume decreased from the control level during the Valsalva maneuver, and this was apparent in both the fourchamber (96 ± 21 to 68 ± 18 ml, p < .01) and two-chamber views (97 + 15 to 56 20 ml, p < .01). In the patients, left ventricular end-diastolic volume was not significantly different from control in either view (199 ± 70 to 195 + 78 and 214 ± 77 to 218 + 86 ml, respectively). In normal subjects, a decrease in stroke volume from control during the Valsalva maneuver was evident in both views (61 + 13to40 ± 11 ml,p< .01 and63 ± 9to33 ± 16ml,p< .01),butinthepatientstherewasnochange in stroke volume in either view during the Valsalva maneuver (45 ± 21 to 45 ± 23 and 49 + 12 to 49 + 17 ml). We conclude that in patients with pulmonary congestion and reduced left ventricular ejection fraction, left ventricular stroke volume does not fall during the strain phase of the Valsalva maneuver because left ventricular end-diastolic volume is maintained. 10, 1984; accepted Nov. 8, 1984. Presented in part at the 56th Annual Scientific Sessions of the American Heart Association. To test these possibilities we studied the effect of a standardized Valsalva maneuver on right ventricular end-diastolic cross-sectional area, left ventricular enddiastolic volume, and left ventricular stroke volume determined by two-dimensional echocardiography in normal volunteers and patients with nonischemic cardiomyopathy in whom clinical findings were consistent with congestive heart failure.

The beta-adrenergic and calcium channel blocking drugs, which individually and combined have proven efficacious in the treatment of angina pectoris, appear to have opposing effects on coronary artery vasomotion. Previous studies have shown that beta-adrenergic blockade may potentiate and calcium channel blockade reverse coronary vasoconstriction during adrenergic cold stimulation in patients with coronary artery disease. To assess the coronary hemodynamic effects of combined drug therapy, thermodilution coronary sinus and great cardiac vein flow and mean arterial pressure were measured during serial cold pressor testing, both before and after 0.1 mg/kg of intravenous propranolol and again after the addition of 10 mg of sublingual nifedipine in 21 patients (9 without [group A1] and 12 with [group A2] greater than 50% narrowing of the left anterior descending coronary artery). In an additional 15 patients (6 patients without [group B1] and 9 with [group B2] left anterior descending artery stenosis), serial cold pressor testing was performed reversing the drug order. Despite significant increases in mean arterial pressure (p less than 0.01) during cold pressor testing, coronary sinus resistance responses after propranolol plus nifedipine were not statistically significant for any group. However, regional coronary resistance responses differed between patients with and without left anterior descending artery stenosis. In group A1, great cardiac vein resistance was unchanged after propranolol plus nifedipine. In group A2, great cardiac vein flow decreased significantly after propranolol plus nifedipine from 8 +/- 17 to -4 +/- 12% (p less than 0.01 versus control), and great cardiac vein resistance increased from 4 +/- 21 to 15 +/- 19% (p less than 0.01 versus control). A similar significant response was observed for groups B1 and B2. Regional coronary vasoconstriction during adrenergic stimulation after combined drug therapy was only observed in patients with significant left anterior descending artery stenosis. These data suggest that in some patients with severe coronary artery disease, combined beta-adrenergic and calcium channel blockade modified regional coronary responses to adrenergic stimulation with an inhomogeneous distribution of blood flow to potentially ischemic regions without affecting total coronary blood flow. These data also imply that an improvement in anginal symptoms after combined drug therapy may be due primarily to mechanisms that reduce myocardial oxygen demand rather than to improved myocardial oxygen supply.

No abstract