Previous reports have shown that increases in heart rate may result in enhanced left ventricular (LV) systolic and diastolic performance. To assess whether this phenomenon occurs in the presence of depressed LV function, the effects of pacing on LV pressure and volume were compared in seven patients with dilated cardiomyopathy (LV ejection fraction 0.19+0.11) and six patients with no or minimal coronary artery disease (LV ejection fraction 0.69±0.11). Patients with normal LV function demonstrated significant increases in LV peak-positive dP/dt, LV end-systolic pressure-volume ratio, LV peak filling rate, and a progressive leftward and downward shift of their pressure-volume diagrams, compatible with increased contractility and distensibility in response to pacing tachycardia. There was no change in LV peak-negative dP/dt or tau. Patients with dilated cardiomyopathy, in contrast, demonstrated no increase in either LV peak-positive dP/dt or the end-systolic pressurevolume ratio, and absence of a progressive leftward shift of their pressure-volume diagrams. Moreover, cardiomyopathy patients demonstrated no increase in LV peak-negative dP/dt or LV peak filling rate and a blunted downward shift of the diastolic limb of their pressure-volume diagrams. Tau, as determined from a derivative method, became abbreviated although never reaching control values.We conclude that patients with dilated cardiomyopathy may demonstrate little or no significant enhancement in systolic and diastolic function during atrial pacing tachycardia, suggesting a depression of both inotropic and lusitropic reserve.
Clinical depression has been identified as an independent risk factor for increased mortality in patients with coronary artery disease. Enhanced platelet activity has been suggested as the mechanism responsible for this adverse association. Selective serotonin reuptake inhibitors (SSRIs) are known to inhibit platelets in patients undergoing coronary stenting. We sought to determine whether concomitant therapy with SSRIs would yield additional anti-platelet benefit in patients with congestive heart failure (CHF) already treated with antecedent aspirin. A total of 88 patients with left ventricular ejection fraction (LVEF) -40% or CHF symptoms in the setting of preserved systolic function and NYHA Class II-IV were analyzed. Of these, 23 patients (26%) were chronic SSRI users (SSRIq), and 65 patients were free from SSRI therapy (SSRIy). All patients received aspirin (325 mg) for at least 1 month prior to platelet studies. Platelets were assessed by aggregometry, flow cytometry and a rapid analyzer. The SSRIq group exhibited a substantial decrease in platelet activity when compared with SSRIy patients, as manifested by a significant reduction in ADP-(Ps0.001), and collagen-induced (Ps0.02) aggregation, and the expression of PECAM-1 (Ps0.03), GPIb (Ps0.03), GP IIbyIIIa antigen (Ps0.02) and GP IIbyIIIa activity with PAC-1 antibody (Ps0.04) and P-selectin (Ps0.02). Therapy with SSRIs also resulted in the reduced formation of platelet-leukocyte microparticles (Ps 0.01). Epinephrine-induced aggregation in plasma, collagen-induced whole blood aggregation, closure time and expression of vitronectin receptor, CD63, CD107a, CD107b and CD151 did not differ between groups. In patients with CHF already on aspirin, SSRI therapy was associated with further inhibition of platelet function. This observation may help to explain some of the clinical benefits associated with SSRI therapy. Further clinical trials may help to elucidate the potential outcome benefits of SSRIs in other potential thrombotic circumstances.
We report the cases of four patients with end-stage renal disease and New York Heart Association class III or IV heart failure of nonischemic origin as documented by coronary angiography. Because of left ventricular dysfunction (left ventricular end-diastolic pressure, 23 to 30 mm Hg; ejection fraction, 20% to 35%), all four patients were initially considered poor surgical candidates for renal transplantation. These same four patients became asymptomatic, however, with markedly improved cardiac function (ejection fraction, 43% to 69%) detected as early as 6 and 14 days after renal engraftment. Therefore, there exists a subset of patients with end-stage renal disease in whom congestive heart failure should not be considered a contraindication to renal transplantation. We conclude that some dialysis-dependent patients who manifest symptomatic heart failure of nonischemic origin have a reversible cardiomyopathy and should not be denied renal transplantation.
Healthy elderly subjects (greater than or equal to 65 years) did not show the prominent low frequency (0.07-0.09 Hz) heart rate oscillations (Mayer waves) recorded in young adults immediately following passive upright tilt. This difference may be related to altered autonomic function with physiologic aging.
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Volume measurements obtained with an impedance catheter (impedance volume measurements) have been used previously in determining pressure-volume relationships in the right and left ventricles and in the right atrium. The purpose of the present study was to determine the utility of impedance volume techniques in the assessment of aortic pressure-volume relationships in animals and humans. Experiments to develop this methodology were first performed in ten anesthetized dogs, with simultaneous measurements of aortic pressure (micromanometer), diameter (ultrasonic crystals), and impedance volume. Transient (20 sec) inferior vena cava (IVC) occlusion and nitroprusside infusion resulted in a reproducible series of aortic pressure-volume and pressure-diameter points. In each case changes in impedance volume closely paralleled changes in diameter. From the wide range of pressure-volume points, it was possible to construct pressure-volume plots for a single cardiac cycle, as well as longer loops over a 20-40 mm Hg pressure range. End-systolic and end-diastolic pressure-volume points could subsequently be identified, which outlined a more precise pressure-volume relationship that was linear in six cases and curvilinear in four cases, depending on the level of aortic pressure. We extended these techniques to human subjects undergoing diagnostic cardiac catheterization. Studies using the impedance catheter in the aorta were performed in 11 patients. Aortic pressure-volume curves were elicited during Valsalva maneuver to obtain data over a range wider than that of a single cardiac cycle. Measurements of relative volume were calibrated with simultaneous M-mode echocardiography in three patients. We conclude that pressure-volume relationships in the aorta can be assessed with impedance volume techniques, making possible in vivo measurements of arterial compliance. Potential nonlinearities in aortic P-V relationships require that the assessment of aortic compliance encompass as much as possible of the physiologic range of pressure and volume.
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