Power output of skeletal muscle ventricles in circulation: short-term studies

Skeletal muscle ventricles (SMVs) were constructed from preconditioned latissimus dorsi muscles in eight dogs and then connected to each animal's systemic arterial circulation in short-term experiments. The lengths of time that SMVs could produce hemodynamic work as left ventricular assist devices were recorded. After 4 hr of continuous pumping at approximately 55 beats/min, six of eight SMVs were able to generate systolic pressures of 128 +/- 23 mm Hg and flows of 340 +/- 31 ml/min, representing 20 +/- 4% of the animals' cardiac output. After 8 hr of continuous pumping, five of the eight SMVs generated pressures of 110 +/- 15 mm Hg and flows of 308 +/- 88 ml/min, or 15 +/- 7% of the animals' cardiac output. The stroke work produced by the SMVs was intermediate between that of the animals' left and right ventricles. Although the SMVs were stimulated to contract at only about one-third the heart rate, the power output of the SMVs approximated that of the right ventricles because of the greater stroke work of the SMVs. Two SMVs functioned as LVADs for 14 hr. Deterioration in SMV function eventually occurred. In each case, however, complications such as anemia, hypoxia, and hypotension, which are inherent to prolonged short-term experiments of this type, contributed to the deterioration of SMV function. The results presented here suggest that skeletal muscle has the potential to directly support the circulation; however, the length of time such muscle pumps are capable of functioning has yet to be determined.     

Acute hemodynamic effect of oral nifedipine in severe chronic congestive heart failure

The temporal hemodynamic effects of oral nifedipine after a single dose of 20 to 40 mg were evaluated in 11 patients with severe chronic congestive heart failure (left ventricular ejection fraction 0.22 +/- 0.7 [mean +/- standard deviation]). Nifedipine significantly reduced systemic vascular resistance, from 1,850 +/- 493 to 1,315 +/- 398 dynes s cm-5 at 1 hour (29%), to 1,410 +/- 246 at 3 hours and to 1,523 +/- 286 at 6 hours (p less than 0.05). Cardiac index increased 21%, from 2.07 +/- 0.46 to 2.51 +/- 0.83 liters/min/m2 at 1 hour, to 2.38 +/- 0.53 liters/min/m2 at 3 hours (p less than 0.05) and to 2.24 +/- 0.41 liters/min/m2 at 6 hours. The group response of stroke volume to nifedipine was smaller. A peak increase of 17% was seen 3 hours after initiation of therapy (22.6 +/- 7.2 versus 25.5 +/- 6.1 ml/m2). This difference did not reach statistical significance. Mean blood pressure declined significantly, from 94 +/- 20 to 80 +/- 13 mm Hg at 1 hour, to 83 +/- 15 mm Hg at 3 hours and to 86 +/- 17 mm Hg at 6 hours (p less than 0.05) and was associated with no significant change in heart rate. The marked decrease in blood pressure resulted in a decrease in rate-pressure product from 12,272 +/- 4,230 to 10,500 +/- 2,074 mm Hg/min at 1 hour, to 10,374 +/- 2,735 mm Hg/min at 3 hours and to 11,047 +/- 3,813 mm Hg/min at 6 hours (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute hemodynamic effect of oral MDL 17,043 in severe congestive heart failure

MDL 17,043, when administered intravenously in humans, produces a significant and salutary hemodynamic response. To determine its acute effect when administered orally (3 mg/kg), 10 patients with severe congestive heart failure were studied by right-sided cardiac catheterization for 8 hours. At 4 hours after drug ingestion, there was significant improvement in several hemodynamic measurements. Cardiac index increased 38% over baseline (from 1.9 +/- 0.4 to 2.6 +/- 0.4 liters/min/m2, p less than 0.01), arteriovenous oxygen difference decreased by 30% (from 8.0 +/- 1.4 to 5.6 +/- 1.2 vol%, p less than 0.01), heart rate increased by 8% (from 85 +/- 16 to 92 +/- 16 beats/min, p less than 0.05), stroke volume index increased by 22% (from 23 +/- 5 to 28 +/- 4 ml/beat/m2, p less than 0.05), left ventricular stroke work increased by 24% (from 18 +/- 5 to 22 +/- 5 g-m/m2, p less than 0.01), mean arterial pressure decreased by 10% (from 79 +/- 6 to 71 +/- 9 mm Hg, p less than 0.01), mean right atrial pressure decreased by 40% (from 10 +/- 5 to 6 +/- 4 mm Hg, p less than 0.01), and mean pulmonary artery wedge pressure decreased by 36% (from 22 +/- 5 to 14 +/- 6 mm Hg, p less than 0.01). Cardiac index, arteriovenous oxygen difference, mean arterial pressure, right atrial pressure, and pulmonary artery wedge pressure remained significantly improved at 8 hours. These findings indicate that MDL 17,043 is active when administered orally and produces beneficial hemodynamic effects for as long as 8 hours.     

The effects of oral hydralazine on right ventricular end-diastolic pressure in patients with right ventricular failure

Hydralazine reduces pulmonary vascular resistance in patients with primary and secondary pulmonary hypertension, but the effects on right ventricular function of a change in resistance without a reduction in pulmonary arterial pressure are not known. We evaluated the hemodynamic effects of hydralazine, 50 mg, administered orally every 6 hours for 48 hours in 14 patients with right ventricular failure and pulmonary hypertension resulting from various causes. Hydralazine reduced mean right ventricular end-diastolic pressure from 17.4 +/- 5.6 to 11.6 +/- 5.3 mm Hg (p less than 0.001) and increased cardiac output and stroke volume by more than 40%. In nine patients who had no change in mean pulmonary arterial pressure after hydralazine, total pulmonary resistance decreased from 15.9 +/- 6.0 to 10.6 +/- 4.3 (p less than 0.001) and cardiac index increased from 2.07 +/- 0.51 to 2.97 +/- 0.91 (p less than 0.005). There was a close correlation between the reductions in total pulmonary resistance and right ventricular end-diastolic pressure (r = 0.73)). These data suggest that hydralazine can increase cardiac output and reduce right ventricular end-diastolic pressure even when pulmonary arterial pressure remains unchanged.     

Pericardial influences on right and left ventricular filling dynamics

The influence of the pericardium on right and left ventricular filling was studied using two-dimensional and Doppler echocardiography in 14 open-chest dogs. Doppler echo parameters of filling included early (E) and late (A) velocities and their ratio (E/A) for the mitral and tricuspid valves. Right and left ventricular volumes were calculated from orthogonal two-dimensional echocardiographic images. Data were compared at three levels of left ventricular end-diastolic pressure (6 +/- 2, 13 +/- 3, and 21 +/- 4 mm Hg) at matched heart rates before and after pericardiectomy. The instantaneous diastolic pressure gradient was measured in 12 of the dogs. Pericardiectomy resulted in an increase in early mitral velocity, peak early diastolic pressure gradient, and E/A but not early mitral velocity normalized for end-diastolic volume. In contrast, for the tricuspid valve flow, pericardiectomy did not change E but caused a marked increase in A and a decrease in E/A. Right ventricular end-diastolic volumes at matched left ventricular end-diastolic volumes were similar before and after the pericardium was removed. However, removal of the pericardium caused a significant decrease of the slope for the right (86.0 +/- 27.0 x 10(-4) versus 50.0 +/- 19.5 x 10(-4) mm Hg/ml, p less than 0.01), but not left, ventricular ln end-diastolic pressure-volume relation (21.2 +/- 9.2 x 10(-3) versus 21.4 +/- 5.3 x 10(-3) mm Hg/ml, p = NS), and a decrease of the pressure intercept for the left (3.0 +/- 2.0 versus 1.6 +/- 0.9 mm Hg, p less than 0.05), but not right, ventricular ln end-diastolic pressure-volume relation (2.8 +/- 1.4 versus 1.4 +/- 0.8 mm Hg, p = NS). In conclusion, filling of the two ventricles is affected by the pericardium over a wide range of physiological ventricular volumes and pressures. At matched left ventricular end-diastolic volume, pericardiectomy causes a fundamental alteration in right, but not left, ventricular filling.     

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.     

Beneficial effects of atrioventricular synchrony in dogs with right coronary artery embolization, and complete heart block

Complete heart block complicating right ventricular infarction frequently is accompanied by shock. Hemodynamic responses to different pacing modes were studied in six anesthetized, closed chest dogs following right coronary artery embolization with mercury and heart block induced by repetitive trans-septal DC shock. Hemodynamics were recorded at control, following right coronary artery embolization, during atrioventricular sequential pacing (DVI) and ventricular pacing (VVI). With respect to the hemodynamics recorded during VVI and DVI pacing; (1) The mean arterial pressure increased by 29.4% during DVI pacing (92.1 +/- 31.3 mm Hg vs 73.4 +/- 28.9 mm Hg p less than 0.005). This increase was primarily due to an augmentation in systolic arterial pressure. (2) The left ventricular end diastolic pressure increased by 35.8% during DVI pacing (16.3 +/- 5.3 mm Hg vs 12.0 +/- 4.3 mm Hg p less than 0.01). (3) Cardiac output improved by 33.8% during DVI pacing (2.34 +/- 0.75 L/min vs 1.76 +/- 0.59 L/min, p less than 0.0005). This was a consistent improvement in cardiac output with a narrow range of 27.1% to 39.0%. (4) There were no significant changes in right atrial, pulmonary, pulmonary capillary wedge pressures or in systemic vascular resistance. In dogs with right coronary artery occlusion and complete heart block DVI pacing is clearly superior to VVI pacing. This is probably because the atrial contribution to ventricular filling, in this model, is critically important to maintain an adequate cardiac output.     

Mild pressure loading alters right ventricular function in fetal sheep

Right ventricular function before and during 10 days of mild pressure loading (10 mm Hg increase in mean pulmonary arterial pressure) was compared with right ventricular function in unloaded near-term fetal sheep. Pressure loading did not alter fetal arterial blood gases or vascular pressures. The right ventricular function curve (stroke volume versus mean right atrial pressure) was not significantly altered by loading. However, the relation between right ventricular stroke volume and increased arterial pressure was dramatically shifted upward, indicating improved ventricular function after the 10-day loading period. Normalized free wall of the loaded right ventricles became thicker (1.2 +/- 0.2 versus 0.9 +/- 0.2 mm/kg, p less than 0.01) and heavier (2.7 +/- 0.4 g/kg versus 2.2 +/- 0.4 g/kg, p less than 0.05) than control, and the ratio of the equatorial radius of curvature to wall thickness decreased (3.2 +/- 0.5 versus 4.5 +/- 0.9, p less than 0.005). Left ventricular free wall and septal weights and thicknesses were not significantly changed. The in vitro diastolic pressure-volume curves of both ventricular chambers of loaded hearts shifted to the left, indicating smaller ventricles than controls at physiological filling pressures. These data suggest the transduction of right ventricular loading effects to the left ventricle. Improved right ventricular function after loading is predicted by the law of Laplace based on the decreased radius of curvature-to-wall thickness ratio.     

Myocardial relaxation: effects of preload on the time course of isovolumetric relaxation

We studied the effect of an isolated increase in preload on isovolumetric relaxation in the intact dog heart and isometric relaxation in isolated cardiac muscle (dog and rat) preparations. In eight anesthetized dogs, 8 to 12 ml of blood was infused into the left ventricle during a single diastole. The exponential time constant (T) of isovolumetric relaxation was measured in single-beat experiments in which the left ventricular systolic pressure increased (112 +/- 2 to 128 +/- 3 mm Hg; p less than .05, n = 62). In a second series of experiments, left ventricular systolic pressure was held constant (109 +/- 2 to 107 +/- 2 mm Hg; p = NS, n = 23) by simultaneous ventricular infusion and aortic unloading. In the first protocol, T increased from 28.0 +/- 0.4 to 30.7 +/- 0.4 msec (p less than .05), whereas in the second protocol (constant systolic pressure) there was no change in T. The time course of isometric relaxation was also studied in six rat left ventricular papillary muscles and four dog right ventricular trabecular muscles. Preload was varied from 30% to 100% of the peak of the isometric length-tension curve in each muscle. Over this wide range of preload, the isometric force decline recordings were superimposable as long as the comparisons were made at equal levels of total load. Thus an isolated increase in preload does not influence the time course of isovolumetric relaxation.     

Influence of acute right ventricular dysfunction on cardiac tamponade

Echocardiographic and hemodynamic data were measured in nine closed chest dogs during graded cardiac tamponade (pericardial pressure 5, 10, 15 mm Hg) before and after production of diffuse acute ischemic right ventricular dysfunction. Right ventricular dysfunction was produced by intracoronary injection of nonradioactive microspheres (mean diameter +/- SD 54 +/- 4 microns) and caused a significant increase in right atrial pressure (7.6 +/- 1.4 vs. 1.6 +/- 1 mm Hg, p less than 0.001) and cross-sectional areas of both the right atrium (8.3 +/- 0.3 vs. 5.6 +/- 0.2 cm2, p less than 0.001) and right ventricle (8.8 +/- 0.4 vs. 5.7 +/- 0.4 cm2, p less than 0.001). Right atrial and ventricular collapse required a significantly larger pericardial effusion and pericardial pressure after right ventricular infarction than before. Mean aortic pressure had fallen 1.9 +/- 2% and 6.5 +/- 6.9% at the time of right atrial collapse (p = NS before vs. after right ventricular dysfunction) and 3 +/- 4.1% and 20.1 +/- 20.8% at the time of right ventricular collapse (p less than 0.03) before and after right ventricular dysfunction, respectively. In the presence of ischemic right ventricular dysfunction, echocardiographic signs of cardiac tamponade are less sensitive and occur later in the hemodynamic progression of cardiac tamponade. Pulsus paradoxus with cardiac tamponade was not prevented by coexisting ischemic right ventricular dysfunction.     

Early tolerance to hemodynamic effects of high dose transdermal nitroglycerin in responders with severe chronic heart failure

Transdermal systems for delivery of nitroglycerin have been shown to provide sustained blood levels of the drug for at least 24 hours. Investigations of hemodynamic effects of transdermal nitroglycerin in patients with heart failure have demonstrated a transient reduction in pressure lasting less than the expected 24 hours. These findings could be due to the development of circulatory tolerance to the vasodilatory effects of nitroglycerin or to insufficient drug dosing. In the present study, we compared the hemodynamic effects of the first and the second doses of high dose (120 mg) transdermal nitroglycerin given 24 hours apart in 11 responders (greater than or equal to 20% reduction in mean pulmonary artery wedge pressure lasting greater than or equal to 2 hours). Initiation of nitroglycerin therapy resulted in a significant reduction in mean right atrial pressure lasting for 14 hours and in a reduction in mean pulmonary artery and mean pulmonary artery wedge pressures lasting 24 hours. After administration of the second dose, mean right atrial pressure at 2 hours (9 +/- 5 versus 7 +/- 4 mm Hg), 4 hours (8 +/- 5 versus 6 +/- 4 mm Hg) and 8 hours (8 +/- 5 versus 6 +/- 3 mm Hg) was higher than after the first dose (p less than 0.05). Both mean pulmonary artery and mean pulmonary artery wedge pressures were significantly higher after the second nitroglycerin dose.(ABSTRACT TRUNCATED AT 250 WORDS)     

Early reversal of right ventricular dysfunction in patients with acute pulmonary embolism after treatment with intravenous tissue plasminogen activator

To assess abnormalities of right heart function and their reversal with thrombolysis in pulmonary embolism, serial imaging and Doppler echocardiographic studies were performed before and after a 6 hour intravenous infusion of 80 to 90 mg of recombinant tissue-type plasminogen activator (rt-PA) in seven patients with segmental or lobar acute pulmonary embolism. None of the five men and two women had known prior pulmonary hypertension. Substantial clot lysis and improvement in pulmonary blood flow, as determined by serial pulmonary angiography and perfusion lung scanning, were achieved in all. Coincident with clot lysis, pulmonary artery systolic pressure decreased (from 42 +/- 11 to 26 +/- 7 mm Hg, p less than 0.005), right ventricular diameter decreased (from 3.9 +/- 1.0 to 2.0 +/- 0.5 cm, p less than 0.005) and left ventricular diameter increased (from 3.7 +/- 0.9 to 4.4 +/- 0.6 cm, p less than 0.01). Right ventricular wall movement, initially mildly, moderately or severely hypokinetic in one, two and four patients, respectively, normalized in five and improved to mild hypokinesia in two. Tricuspid regurgitation was present before lytic therapy in six patients. In five, flow velocity in the tricuspid regurgitant jets indicated a peak systolic right ventricular minus right atrial pressure gradient of 25 to 52 mm Hg. Tricuspid regurgitation was detected early after lytic therapy in only two patients. Systolic septal flattening was noted before but not after lysis. These findings confirm that pulmonary emboli may result in appreciable right ventricular dysfunction and dilation, resultant tricuspid regurgitation, abnormal septal position and decreased left ventricular size.(ABSTRACT TRUNCATED AT 250 WORDS)     

The transmitral pressure-flow velocity relation. Effect of abrupt preload reduction

Although recent animal and clinical studies suggest that Doppler-derived indexes may be useful for the characterization of ventricular diastolic behavior, the hemodynamic basis for the preload dependency of these indexes has not previously been fully elucidated. Accordingly, effects of reduction of left atrial load on the pressure-flow velocity relation were characterized in 10 anesthetized, closed-chest dogs during transient inferior vena caval occlusion by means of simultaneously recorded left atrial and left ventricular micromanometric pressure measurement and transesophageal Doppler echocardiograms. Within four or five beats after inferior vena caval balloon occlusion, left atrial loading was reduced as evidenced by a decrease in the slope of the left atrial v wave from 21 +/- 4 to 13 +/- 4 mm Hg/sec (p less than 0.001) and by a decrease in the first crossover point of left atrial and left ventricular pressures from 5.6 +/- 1.1 to 2.9 +/- 1.5 mm Hg (p less than 0.001). This decrease in left atrial loading resulted in reductions during early diastole of minimum left ventricular pressure (from 1.0 +/- 0.8 to -0.4 +/- 1.2 mm Hg, p less than 0.001), the maximum early forward (i.e., left atrial pressure greater than left ventricular pressure) transmitral pressure gradient (from 2.8 +/- 0.8 to 2.4 +/- 0.5 mm Hg, p less than 0.01); the slope of the rapid filling pressure wave (from 44 +/- 11 to 38 +/- 10 mm Hg/sec, p less than 0.025); and the area of the reversed (i.e., left ventricular pressure greater than left atrial pressure) transmitral pressure gradient (from 79 +/- 42 to 53 +/- 33 mm Hg.msec, p less than 0.05). During late diastole, both the heights and slopes of the left atrial and left ventricular a waves fell, resulting in a decrease in the maximum late transmitral pressure gradient (from 1.2 +/- 0.7 to 0.9 +/- 0.5 mm Hg, p less than 0.05). Vena caval occlusion also altered Doppler transmitral velocity profiles during both the early and late phases of diastole. Peak velocity of the E wave decreased (from 50 +/- 11 to 41 +/- 7 cm/sec, p less than 0.01) as did acceleration (from 880 +/- 222 to 757 +/- 258 cm/sec2, p less than 0.025) and deceleration (from 597 +/- 260 to 429 +/- 197 cm/sec2, p less than 0.025). Peak velocity of the A wave also fell (from 29 +/- 9 to 22 +/- 5 cm/sec, p less than 0.005). Abrupt inferior vena caval occlusion did not significantly change heart rate or mean aortic pressure.(ABSTRACT TRUNCATED AT 400 WORDS)     

Alterations in transesophageal pulsed Doppler indexes of filling of the left ventricle after pericardiotomy

The impact of pericardial constraint on patterns of left ventricular filling was measured by transesophageal pulsed Doppler echocardiography in 30 patients undergoing elective nonvalvular cardiac surgery. Peak early left ventricular filling velocity increased from 0.52 +/- 0.11 to 0.56 +/- 0.15 m/s (p less than 0.05) and early left ventricular filling fraction increased from 60 +/- 9% to 65 +/- 9% (p less than 0.005) after pericardiotomy. The study group was retrospectively subdivided into two groups based on the prepericardiotomy mean right atrial pressure, an index of intrapericardial pressure and hence pericardial constraint. In 13 patients with a mean right atrial pressure less than 6 mm Hg, no significant changes in early left ventricular filling were evident after pericardiotomy. In 17 patients with a mean right atrial pressure greater than or equal to 6 mm Hg indicative of a greater degree of pericardial constraint before pericardiotomy, significant increases in peak early filling velocity (0.52 +/- 0.13 to 0.57 +/- 0.19 m/s, p less than 0.05), peak early filling rate (4.29 +/- 0.67 to 4.66 +/- 0.86 stroke volumes/s, p less than 0.05) and early left ventricular filling fraction (57 +/- 7% to 63 +/- 8%, p less than 0.001) were measured after pericardiotomy. Thus, the pericardium does constrain early left ventricular filling and its effects are more pronounced in patients with an elevated right atrial pressure.     

Biventricular function in the adult respiratory distress syndrome

We examined biventricular function in patients with the adult respiratory distress syndrome (ARDS) by a combination of invasively determined pressures and flows and concomitant radionuclide angiography. Right (RVEF) and left (LVEF) ventricular ejection fractions were measured; right and left ventricular end-diastolic (EDVI) and end-systolic (ESVI) volume indices were calculated from the respective ejection fraction and measured thermodilution stroke volume. With an increase in the outflow pressure load on the right ventricle, measured as the mean pulmonary artery pressure (PAP), the RVEF fell (Y = 66.25 -1.01X; r2 = .42; p less than .001) and both the RVEDVI (y = 13.39 + 3.66X; r2 = .33; p less than .001) and RVESVI (Y = 23.9 + 3.57X; r2 = .41; p less than .001) increased. Progressive increases in the PAP also seemed associated with a change in left ventricular end-diastolic pressure-volume relationships: without pulmonary artery hypertension (PAP less than 20 mm Hg) the mean LVEDVI was 87.2 +/- 31.3 ml/m2 (mean +/- SD) and the mean PCWP was 5.0 +/- 2.8 mm Hg; with a mean PAP exceeding 30 mm Hg, the LVEDVI remained constant (90.4 +/- 26.9 ml/m2) although the PCWP was greater than previous (18.5 +/- 5.7 mm Hg; p less than .01). Analysis of right ventricular peak-systolic pressure end-systolic volume ratios implied a concurrent depression in right ventricular contractility at high levels of PAP. However, right ventricular "pump" function to maintain an adequate left ventricular preload remained unaltered regardless of the presence of pulmonary artery hypertension.     

Hemodynamic response to exercise after propranolol in patients with mitral stenosis.

Hemodynamic response to exercise before and 10 minutes after propranolol (5 mg intravenously) was studied in 10 young patients with pure mitral stenosis who had normal sinus rhythm and no cardiac failure. After propranolol the mean heart rate and cardiac index at rest were lower than during the control state (respectively, 95 +/- 4 versus 82 +/- 3 beats/min, P less than 0.005; 3.4 +/- 0.2 versus 2.8 +/- 0.1 liters/min per m2, P less than 0.025). As a result, the mean pulmonary wedge pressure and mean mitral valve gradient at rest were lower (respectively, 22 +/- 2 versus 18 +/- 2 mm Hg, P less than 0.005; 24 +/- 2 versus 17 +/- 2 mm Hg, P less than 0.001). During exercise after propranolol the values of pulmonary wedge pressure and mitral valve gradient were lower than control values during exercise (respectively, 39 +/- 3 versus 30 +/- 2 mm Hg, P less than 0.005; 44 +/- 3 versus 32 +/- 3 mm Hg, P less than 0.005), again because of the lower heart rate and cardiac index (130 +/- 6 versus 104 +/- 6 beats/min, P less than 0.001; 4.6 +/- 3 versus 3.7 +/- 2 liters/min per m2, P less than 0.01). Left ventricular end-diastolic pressure and stroke index showed no significant changes. Thus, propranolol may benefit patients with pure mitral stenosis with sinus rhythm and no cardiac failure whose symptoms occur during those reversible conditions characterized by an increase in heart rate or cardiac output, or both.     

Hemodynamic importance of systolic ventricular interaction, augmented right atrial contractility and atrioventricular synchrony in acute right ventricular dysfunction

To delineate the determinants of right ventricular performance with acute right ventricular dysfunction, surgical electrical isolation of the right ventricular free wall was produced in 13 dogs. During atrioventricular (AV) pacing, hemodynamic and wall motion measurements were normal. When not paced, the right ventricular free wall became asystolic, resulting in a depressed and bifid right ventricular systolic pressure (33 +/- 5 to 18 +/- 4 mm Hg) and decreased left ventricular systolic pressure (100 +/- 18 to 80 +/- 18 mm Hg) and stroke volume (14 +/- 4 to 10.3 +/- 3.5 ml) (all p less than 0.05). Ultrasound demonstrated right ventricular free wall dyskinesia, increased right ventricular end-diastolic size (155 +/- 13% of control), but decreased left ventricular size (69 +/- 11% of control) (both p less than 0.05). Right atrial pressure increased (5.8 +/- 2.5 to 7.6 +/- 2.8 mm Hg, p less than 0.05) with an augmented A wave and blunted Y descent, indicating pandiastolic right ventricular dysfunction. The septum demonstrated reversed curvature in diastole and bulged paradoxically into the right ventricle during early systole, generating the initial peak of right ventricular pressure and reducing its volume. Later, posterior septal motion coincided with maximal left ventricular pressure and the second peak of the right ventricular waveform. Left ventricular pacing alone led to further decreases in right ventricular systolic pressure and size, left ventricular systolic pressure and stroke volume. The previously augmented A wave was replaced by a prominent V wave. Therefore, when contractility of its free wall is acutely depressed, right ventricular performance is dependent on left ventricular-septal contractile contributions transmitted by the septum.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of the pericardium on the diastolic left coronary pressure-flow relationship in the isolated dog heart

We studied the effects of the pericardium on diastolic left coronary pressure-flow relationships in heart-blocked and isolated canine preparations. In these preparations, the left and right coronary arteries were dilated with adenosine and perfused by means of a pressurized arterial reservoir. The diastolic left heart pressure (LHP) was controlled by the height of a reservoir connected to the left atrium and left ventricle. The right atrial and ventricular pressure i.e., coronary outflow pressure, was kept constant at 0 mm Hg. Before and after pericardiectomy, diastolic coronary pressure-flow relationships were obtained at three values of LHP (0, 15, and 30 mm Hg) with driving pressure decreasing (2 mm Hg/sec or less) from approximately 60 mm Hg to the actual zero-flow pressure (Pf = 0) during a single long diastole induced by cessation of ventricular pacing. The slopes of the coronary pressure-flow relationships were approximated by a linear regression analysis in which the correlation coefficients were greater than .98 in all cases. Before pericardiectomy, with LHP increasing from 0 to 15 and 30 mm Hg, the value of Pf = 0 significantly increased from 7 +/- 1 to 16 +/- 1 (p less than .01) and 28 +/- 2 mm Hg (p less than .01), respectively. After pericardiectomy, it increased from 7 +/- 1 to 14 +/- 1 (p less than .01) and 17 +/- 2 mm Hg (p less than .01), respectively. When LHP was at 0 and 15 mm Hg, the pericardiectomy had no effect on the value of Pf = 0.(ABSTRACT TRUNCATED AT 250 WORDS)     

Differential effects on right ventricular function of transient right, left anterior descending and left circumflex coronary occlusions during percutaneous transluminal coronary angioplasty

Right ventricular function was studied by means of a thermodilution catheter before, during and after percutaneous transluminal angioplasty of the proximal right (group 1, n = 8), left anterior descending (group 2, n = 8) or left circumflex (group 3, n = 8) coronary artery. All patients had evidence of myocardial ischemia, with single-vessel disease affecting the proximal segment of one of the three major coronary arteries; no patient had had a previous myocardial infarction and all had normal cardiac function at baseline study. Cardiac index decreased during balloon inflation. Mean pulmonary artery pressure was unaffected in group 1 but increased in group 2 (from 19 +/- 5 to 31 +/- 11 mm Hg, p less than 0.01) and in group 3 (from 19 +/- 2 to 22 +/- 5 mm Hg, p less than 0.05). Right ventricular ejection fraction decreased from 62 +/- 9% to 52 +/- 10% (p less than 0.01) in group 1 and from 64 +/- 7% to 44 +/- 10% (p less than 0.005) in group 2, and returned to normal within 2 min after balloon deflation in both groups. In group 3, right ventricular ejection fraction was unchanged during balloon inflation (58 +/- 5% at baseline, 58 +/- 9% at 60 s, p = NS). Therefore, brief occlusion of the proximal segments of the left anterior descending or right coronary artery results in marked alteration of right ventricular performance that is probably caused by right ventricular free wall ischemia in the right coronary group and by the concomitant effects of septal ischemia and increased right ventricular afterload in the left anterior descending artery group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Is atrial activation beneficial in heart transplant recipients?

Because of the distortion of atrial morphology that occurs during cardiac allograft transplantation in humans, the beneficial effects of properly sequenced atrial and ventricular activation are unclear in these patients. To evaluate the atrial contribution to ventricular pump performance in heart transplant recipients, arterial pressure and cardiac output during pacing from either chamber were measured in nine patients 10 +/- 1 days after transplantation. Systolic, diastolic and mean systemic arterial pressures were significantly higher during atrial pacing compared with ventricular pacing: 143 +/- 23 versus 125 +/- 20 mm Hg, 73 +/- 15 versus 66 +/- 14 mm Hg and 94 +/- 17 versus 84 +/- 16 mm Hg, respectively (p less than 0.05 for all). In addition, cardiac output decreased from 5.5 +/- 1.4 to 4.6 +/- 1.5 liters/min (p less than 0.005) for atrial versus ventricular pacing. Thus, there is a significant atrial contribution to cardiac performance in patients after heart transplantation. This may have clinical implications in those patients who later require a permanent pacemaker.