Assessment of timing right ventricular assist device withdrawal using left ventricular assist device filling characteristics

Right ventricular assist devices (RVAD) are often needed on a short term basis in patients who develop RV failure after left ventricular assist device (LVAD) implantation. The purpose of this study was to use LVAD filling characteristics to help determine the timing for weaning a patient from RVAD support. Eleven patients (age 50 years +/- 15) supported with an LVAD (Novacor) and an RVAD (Biomedicus or ABIOMED) were studied. Eight patients (RV recovery group) were studied before RVAD removal and all were successfully weaned from RVAD support. Five patients (RV failure group) were studied at the time of RVAD placement to determine baseline characteristics of RV failure. Simultaneous measures of LVAD volume and routine hemodynamics were recorded during periods of high and low RVAD flow. The LVAD filling was assessed as the first derivative of LVAD volume and the mean filling rate for each cardiac cycle was calculated and averaged over 10 sec periods at both RVAD flows. The mean pump rate corrected filling rates did not change in the RV recovery group (89 +/- 13 vs. 87 +/- 8 ml/beat) and significantly decreased in the RV failure group (84 +/- 19 vs. 62 +/- 22 ml/ beat) (p < 0.001) with decreasing RVAD flow. These data suggest that LVAD filling rates may be used to assess RV systolic function and the proper timing of RVAD removal in selected patients.     

Low incidence of myocardial recovery after left ventricular assist device implantation in patients with chronic heart failure

BACKGROUND: Mechanical, histological, and biochemical improvement has been described in patients after left ventricular assist device (LVAD) support. Explantation of the LVADs without heart transplantation has been described in selected patients who received this therapy as a bridge to transplantation. METHODS AND RESULTS: A retrospective review of patients receiving a mechanical bridge to transplantation at Columbia Presbyterian Hospital after July 21, 1991, was performed to determine the incidence of patients in whom the device was successfully explanted. From August 1, 1996, to February 1, 1998, we prospectively attempted to identify potential explant candidates by the use of exercise testing. During this time, we recruited 39 consecutive patients after insertion of the Thermo Cardiosystems vented electric device to participate in the following study. Approximately 3 months after device implantation, a maximal exercise test with hemodynamic monitoring and respiratory gas analysis was performed with the LVAD in the automated mode. The electric device was interfaced with a pneumatic console such that the rate could be decreased to 20 cycles/min. Hemodynamic measurements were recorded as the device rate was decreased. A repeat exercise test was then performed if the patient remained hemodynamically stable. A retrospective chart review of 111 LVAD recipients at our institution identified only 5 successful explant patients. Eighteen of the 39 patients were studied. Fifteen patients exercised with maximal device support. At peak exercise, VO2 averaged 14.5+/-3.6 mL. kg-1. min-1; LVAD flow, 8.0+/-1.3 L/min; Fick cardiac output, 11.4+/-3.3 L/min; and pulmonary capillary wedge pressure, 13+/-4 mm Hg. Seven patients remained normotensive and could exercise at a fixed rate of 20 cycles/min. In these patients, peak VO2 declined from 17.3+/-3.9 to 13.0+/-6.1 mL. kg-1. min-1. In one of these patients, the device was explanted. CONCLUSIONS: Significant myocardial recovery after LVAD therapy in patients with end-stage congestive heart failure occurs in a small percentage of patients. Most of these patients have dilated cardiomyopathy. Exercise testing may be a useful modality to identify those patients in whom the device can be explanted.     

Altered myocardial phenotype after mechanical support in human beings with advanced cardiomyopathy

BACKGROUND: Left ventricular assist devices (LVAD) provide lifesaving circulatory support to patients awaiting heart transplantation. To date, the extent to which sustained mechanical unloading alters the phenotype of pathologic myocardial hypertrophy in dilated cardiomyopathy is unknown. METHODS: We examined left ventricular size, myocyte and myocardial immunoreactivity for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in eight patients with advanced dilated cardiomyopathy before and after LVAD support. The mean duration of congestive heart failure was 18 +/- 5 months, and LVAD support averaged 42 +/- 4 days before heart transplantation. RESULTS: Echocardiographically determined left ventricular mass decreased from 505 +/- 83 to 297 +/- 52 gm (p < 0.05) during LVAD support, whereas minimum myocyte diameter decreased from 28.1 +/- 0.9 to 21.7 +/- 0.6 microns (p < 0.01) in transmural myocardial tissue specimens. Overall left ventricular ANP immunopositivity decreased from 48% at LVAD placement to 12% at transplantation (p < 0.05), whereas BNP immunopositivity decreased from 28% to 4% after LVAD support. Moreover, a gradient of ANP and BNP immunostaining from subendocardium to epicardium observed before mechanical unloading diminished after LVAD support. Analysis of the relationship between left ventricular mass and ANP immunopositivity revealed a close and highly significant correlation between these variables. CONCLUSIONS: These studies demonstrate remarkable left ventricular plasticity even in the presence of advanced cardiomyopathy. Parallel reductions in myocardial mass and myocyte size with reductions in ventricular ANP and BNP immunostaining indicate a novel regression of the phenotype of pathologic hypertrophy within the human myocardium after LVAD support.     

Emergency versus elective/urgent left ventricular assist device implantation

BACKGROUND: The risk and outcome in patients undergoing left ventricular assist device (LVAD) implantation on an emergency basis is still unclear. METHODS: Since April 1993, 40 patients received a Novacor and 8 patients a Heartmate LVAD in our institution. Patients with emergency LVAD placement were compared with the remainder in a retrospective manner. Parameters studied included underlying heart disease, preimplantation dysfunction of kidney, liver, lung, and cerebrum, interval of mechanical support, outcome, and complications. RESULTS: Patients with emergency LVAD placement predominantly were seen with postcardiotomy heart failure (47%) or acute myocarditis (20%) (group A) whereas elective and urgent candidates for LVAD implantation mainly had dilative cardiomyopathy (67%) or ischemic heart disease (30%) (group B). The incidence of secondary organ failure was significantly higher for all organs in group A patients (p < .01). Mean support interval in patients who underwent emergency LVAD implantation was lower (74+/-79 days vs 115+/-80 days), and fewer patients could be forwarded to heart transplantation in this group (22% vs 78%, p < .01). Moreover, bleeding complications were increased in group A (66% vs 30%, p < .01), but not thromboembolism and infection. CONCLUSION: In conclusion, the overall success rate after emergency LVAD implantation was lower, with bleeding being the most frequent complication. To achieve acceptable outcomes in disastrous situations, LVADs should be placed as early as possible.     

The use of APACHE II scores to select candidates for left ventricular assist device placement. Acute Physiology and Chronic Health Evaluation

BACKGROUND: The growth in left ventricular assist device (LVAD) use has been hampered by high morbidity and mortality rates and cost. The purpose of this study was to help improve patient selection for LVAD placement by determining whether the Acute Physiology and Chronic Health Evaluation II (APACHE II) scoring system, a multiparameter, physiology-based predictor of outcome, could be used to predict outcome after LVAD placement and thus help determine optimum timing of LVAD placement. METHODS: This was a retrospective analysis of a prospective cohort observational study consisting of 2 groups: (1) 50 patients with severe heart failure who did not receive LVAD placement after initial evaluation and (2) 31 patients who did receive LVAD placement. Patients included in the study were in severe heart failure on the basis of 3 of the following: lung crackles, S3, peripheral edema, ejection fraction < 0.30, systolic blood pressure < 80 mm Hg, progressive prerenal azotemia, altered level of consciousness, gastrointestinal ischemia or congestion, or persistent although reversible pulmonary hypertension in spite of maximal medical therapy, including intravenous inotropes. The decision for LVAD placement was at the discretion of the attending physician. RESULTS: Both LVAD- and non-LVAD-treated patients were similar in cause of heart failure, APACHE II scores, and other baseline laboratory parameters. Survival time with a log-logistic model was better for LVAD-treated patients, p=.0266. Although Kaplan Meier analysis showed a trend toward better survival rates in the LVAD-treated patient, the Cox proportional hazards revealed that LVAD-treated patients had better survival (relative risk ratio, 95% confidence interval=0.305, 0.110 to 0.892; p=.0219) after adjustment for APACHE II score. Each unit increase in APACHE II independently predicted death (relative risk ratios, 95% confidence interval=1.139, 1.055 to 1.231; p=.0009). Patients with medium APACHE II (11 to 20) scores in particular benefitted from LVAD treatment. CONCLUSION: LVAD placement for severe heart failure (not restricted to cardiogenic shock) improves survival. APACHE II can aid in deciding the timing of LVAD placement in patients with heart failure who may not have attained conventional hemodynamic criteria for LVAD placement. Patients who had APACHE II scores between 11 and 20 derived the greatest benefit from LVAD placement.     

Thrombogenic and atherogenic lipid modifications in plasma and patients with coronary artery disease and after coronary artery bypass surgery

BACKGROUND: Although multiple studies have shown that the left ventricular assist device (LVAD) improves distorted cardiac geometry, the pathological mechanisms of the "reverse remodeling" of the heart are unknown. Our goal was to determine the effects of LVAD support on cardiac myocyte size and shape. METHODS AND RESULTS: Isolated myocytes were obtained at cardiac transplantation from 30 failing hearts (12 ischemic, 18 nonischemic) without LVAD support, 10 failing hearts that received LVAD support for 75+/-15 days, and 6 nonfailing hearts. Cardiac myocyte volume, length, width, and thickness were determined by use of previously validated techniques. Isolated myocytes from myopathic hearts exhibited increased volume, length, width, and length-to-thickness ratio compared with normal myocytes (P<0.05). However, there were no differences in any parameter between myocytes from ischemic and nonischemic cardiomyopathic hearts. Long-term LVAD support resulted in a 28% reduction in myocyte volume, 20% reduction in cell length, 20% reduction in cell width, and 32% reduction in cell length-to-thickness ratio (P<0.05). In contrast, LVAD support was associated with no change in cell thickness. These cellular changes were associated with reductions in left ventricular dilation and left ventricular mass measured echocardiographically in 6 of 10 LVAD-supported patients. CONCLUSIONS: These studies suggest that the regression of cellular hypertrophy is a major contributor to the "reverse remodeling" of the heart after LVAD implantation. The favorable alterations in geometry that occur in parallel fashion at both the organ and cellular levels may contribute to reduced wall stress and improved mechanical performance after LVAD support.     

Intrathoracic multicentric Castleman disease: CT findings in 12 patients

BACKGROUND: Intraaortic balloon pumping (IABP) and left ventricular assist device (LVAD) are used for left ventricular support when low cardiac output occurs after a coronary bypass operation for serious coronary artery disease. There are hemodynamic differences in blood flow in various kinds of coronary artery bypass grafts, caused by their inherent physiologic characteristics. The hemodynamic effects of left ventricular assistance with IABP and LVAD on blood flow through various coronary artery bypass grafts were investigated. METHODS: An ascending aorta-coronary bypass graft (ACB), an internal thoracic artery, and a descending aorta-coronary bypass graft were anastomosed to the left anterior descending coronary artery in a canine model. In this experimental model, the blood flow to the same coronary bed in the three types of grafts could be evaluated. Blood flow in the left anterior descending coronary artery through the three types of coronary bypass grafts was studied in this model during or in the absence of ventricular assistance. RESULTS: In the control study, the systolic blood flow did not differ among the three types of grafts, but the diastolic flow decreased in the following order: with the ACB, the internal thoracic artery, and the descending aorta-coronary bypass graft. The systolic flow during IABP and LVAD was similar to the control flows. Use of IABP increased the diastolic flow by 75.3%+/-12.4% of the control value in the ACB, 37.9%+/-25.0% in the internal thoracic artery, and 21.2%+/-11.4% in the descending aorta-coronary bypass graft. The LVAD increased the diastolic flow by 97.7%+/-18.7% of the control value in the ACB, 64.5%+/-25.7% in the internal thoracic artery, and 63.0%+/-27.9% in the descending aorta-coronary bypass graft. The diastolic blood flows in the left anterior descending coronary artery and the three types of grafts were significantly greater with IABP than the control values, and significantly greater with LVAD than with IABP and the control values. The degrees of increase of diastolic flows in the left anterior descending coronary artery and the ACB with IABP and LVAD were significantly greater than in the arterial grafts (p < 0.01). CONCLUSIONS: The diastolic flows in the internal thoracic artery and descending aorta-coronary bypass graft increased less than in the native left anterior descending coronary artery and ACB during left ventricular assistance, particularly with IABP. It is important for the selection of tactics for the management of catastrophic status after coronary bypass grafting to consider the hemodynamic characteristics of the graft.     

Extracorporeal life support as a post left ventricular assist device implant supplement

Extracorporeal life support (ECLS) is indicated following left ventricular assist device (LVAD) implant for right heart failure or pulmonary dysfunction. From December 1991 to December 1996, 100 patients were supported with the implantable HeartMate LVAD. Of these, 12 patients were supported with ECLS post LVAD implant. Pre-operatively, 10 patients (83%) were on an intra-aortic balloon pump, 9 patients (75%) were intubated, and 8 patients (67%) required ECLS bridge to LVAD implant. Six patients (50%) were men, and patient age ranged from 28 to 63 years (mean 46 +/- 10 years). Duration of ECLS averaged 3 +/- 2 days (range, 1-9 days). Eight patients (67%) required a right ventricular assist device (RVAD) with an ECLS circuit, three patients (25%) required peripheral veno-venous ECLS, and one patient peripheral veno-arterial ECLS. Forty-five percent supported with ECLS post LVAD survived to transplant compared with the 81% supported with LVAD only. Early in this experience, three patients had RVAD support only and all three patients died. RVAD support (with or without ECLS) was 11% overall and declined from 14% in the first 50 patients to 8% in the second 50. ECLS post LVAD is relatively uncommon and its use is associated with reduced survival, but helps salvage these critically ill patients.     

Loading sequence plays an important role in enhanced load sensitivity of left ventricular relaxation in conscious dogs with tachycardia-induced cardiomyopathy

BACKGROUND: Left ventricular relaxation rate in the failing heart depends more on the systolic load than in the normal heart. To elucidate the mechanisms for the enhanced load sensitivity of left ventricular relaxation in heart failure, we examined the relative contributions of changes in end-systolic volume and loading sequence to the left ventricular relaxation rate. METHODS AND RESULTS: In seven conscious dogs, the time constant (Td) of left ventricular pressure decay, end-systolic volume, systolic circumferential force, and time to peak force during caval occlusion were compared before and after development of tachycardia-induced heart failure. Rapid ventricular pacing decreased the slope of the end-systolic pressure-volume relation from 4.5 to 2.8 mm Hg/mL (P < .01) and prolonged Td from 33 to 49 ms (P < .01). In normal conditions, caval occlusion reduced end-systolic force (-580 g, P < .01) and end-systolic volume (-7 mL, P < .01) but did not change Td or time to peak force. In heart failure, however, caval occlusion shortened Td (-11 ms, P < .01), with a concomitant decrease in the time to peak force (-30 ms, P < .01), while end-systolic volume and force declined slightly. Consequently, for a comparable reduction in end-systolic force, Td decreased more in heart failure than in normal hearts, suggesting enhanced load sensitivity. Moreover, changes in Td correlated well with those in the time to peak force (r = .79, P < .01) but not with those in end-systolic volume. CONCLUSIONS: Loading sequence rather than elastic recoil seems to play the predominant role in the enhanced load sensitivity of left ventricular relaxation in heart failure.     

Human cadaver skin viability for in vitro percutaneous absorption: storage and detrimental effects of heat-separation and freezing

To evaluate the clinical results of circulatory support for severe heart failure after operation, we examined 62 patients (39 males and 23 females) who underwent circulatory support for postoperative heart failure from 1984 to 1996. Their ages ranged from 22 to 78 (mean 52) years. In 62 patients, 35 had valvular, 25 had ischemic, and 2 had congenital heart disease. Postoperation, 29 patients underwent venoarterial bypass (VAB), 20 had biventricular bypass (BVB), and 8 had left ventricular bypass (LVB). The remaining 5 patients received a pulsatile left ventricular assist device (LVAD). The weaning and discharge rates of the patients by type of support were 51.7% and 31.0% with VAB, 75.0% and 55.0% with BVB, 87.5% and 37.5% with LVB, and 60.0% and 40.0% with LVAD, respectively. The complete results of this series (64.5% weaning rate and 40.3% discharge rate) were acceptable.     

Hemodynamic effect of inhaled nitric oxide in dilated cardiomyopathy patients on LVAD support

Recently it has been shown that inhaled nitric oxide (NO), which has been proven to contribute to improvement in critical pulmonary hypertension, may provide a favorable effect early after left ventricular assist device (LVAD) support. To improve right ventricular function, inhalation of NO was added to treatment with conventional catecholamines for four consecutive dilated cardiomyopathy (DCM) patients following institution of LVAD. In two patients 1 hr after inhalation of NO, central venous pressure (CVP), mean pulmonary arterial pressure (PAm), and pulmonary vascular resistance (PVR) were improved. These results led to better LVAD output and resulted in an adequate cardiac index. On the other hand, a right VAD (RVAD) was implemented in one patient whose high CVP, PAm, and PVR continued; he was weaned after 8 days of RVAD support. Another patient who had a high CVP but normal PAm and PVR before and after inhalation of NO had no improvement in his hemodynamic state. These data suggest that inhaled NO may improve systemic circulation by reducing right ventricular afterload and may become a promising and convenient therapy before placing RVAD in DCM patients under LVAD support. RVAD should be conducted in patients with right ventricular failure or when pulmonary hypertension is associated with impaired right ventricular reserve, even after inhalation of NO.     

Stress-induced left ventricular outflow tract obstruction: a potential cause of dyspnea in the elderly

OBJECTIVES: We sought to identify the pattern of disturbed left ventricular physiology associated with symptom development in elderly patients with effort-induced breathlessness. BACKGROUND: Limitation of exercise tolerance by dyspnea is common in the elderly and has been ascribed to diastolic dysfunction when left ventricular cavity size and systolic function appear normal. METHODS: Dobutamine stress echocardiography was used in 30 patients (mean [+/-SD] age 70 +/- 12 years; 21 women, 9 men) with exertional dyspnea and negative exercise test results, and the values were compared with those in 15 control subjects. RESULTS: Before stress, left ventricular end-diastolic and end-systolic dimensions were reduced, fractional shortening was increased, and the basal septum was thickened (2.3 +/- 0.5 vs. 1.4 +/- 0.2 cm, p < 0.001, vs. control subjects) in the patients, but posterior wall thickness did not differ from that in control subjects. Left ventricular outflow tract diameter, measured as systolic mitral leaflet septal distance, was significantly reduced (13 +/- 4.5 vs. 18 +/- 2 mm, p < 0.001). Isovolumetric relaxation time was prolonged, and peak left ventricular minor axis lengthening rate was reduced (8.1 +/- 3.5 vs. 10.4 +/- 2.6 cm/s, p < 0.05), suggesting diastolic dysfunction. Transmitral velocities and the E/A ratio did not differ significantly. At peak stress, heart rate increased from 66 +/- 8 to 115 +/- 20 beats/min in the control subjects, but blood pressure did not change. Transmitral A wave velocity increased, but the E/A ratio did not change. Left ventricular outflow tract velocity increased from 0.8 +/- 0.1 to 2.0 +/- 0.2 m/s, and mitral leaflet septal distance decreased from 18 +/- 2 to 14 +/- 3 mm, p < 0.001. In the patients, heart rate rose from 80 +/- 12 to 132 +/- 26 beats/min and systolic blood pressure from 143 +/- 22 to 170 +/- 14 mm Hg (p < 0.001 for each), but left ventricular dimensions did not change. Peak left ventricular outflow tract velocity increased from 1.5 +/- 0.5 m/s (at rest) to 4.2 +/- 1.2 m/s; mitral leaflet septal distance fell from 13 +/- 4.5 to 2.2 +/- 1.9 mm (p < 0.001); and systolic anterior motion of mitral valve appeared in 24 patients (80%) but in none of the control subjects (p < 0.001). Measurements of diastolic function did not change. All patients developed dyspnea at peak stress, but none developed a new wall motion abnormality or mitral regurgitation. CONCLUSIONS: Although our patients fulfilled the criteria for "diastolic heart failure," diastolic dysfunction was not aggravated by pharmacologic stress. Instead, high velocities appeared in the left ventricular outflow tract and were associated with basal septal hypertrophy and systolic anterior motion of the mitral valve. Their appearance correlated closely with the development of symptoms, suggesting a potential causative link.     

Paradoxical hypertension after reversal of heart failure in patients treated with intensive vasodilator therapy

Hypertension is a major cause of heart failure, evolving from left ventricular hypertrophy to systolic and diastolic dysfunction. Although effective heart failure therapy has been associated with a lowering or no change in systemic arterial blood pressure in long-term follow-up, this study describes the symptomatic, clinical, and left ventricular functional response of a subgroup of heart failure patients with a prior history of hypertension who demonstrated a paradoxical hypertensive response despite high-dose vasodilator therapy. We prospectively identified 45 patients with a past history of hypertension who had become normotensive with symptomatic heart failure. Of these 45 heart failure patients, 12 became hypertensive while receiving therapy in follow-up, with systolic blood pressure > or = 140 mm Hg (Group A). The remaining 33 patients did not have a hypertensive response to therapy (Group B). In the 12 Group A patients, 60+/-10 years old, with symptomatic heart failure for 6.3+/-4.3 years, vasodilator therapy was intensified in the 2.0+/-0.5 years of follow-up, achieving final doses of enalapril 78+/-19 mg and isosorbide dinitrate 293 +/-106 mg per day. New York Heart Association classification improved from 2.9+/-0.8 to 1.3+/-0.5 (P < or = .0001), with a reduction in heart-failure-related hospitalizations. Left ventricular ejection fraction increased from 17+/-6% to 40+/-10% (P < .0001). Follow-up blood pressure at 1 to 3 months was unchanged. However, both systolic and diastolic blood pressure increased at final follow-up, rising from 116+/-14 to 154+/-13 mm Hg (P = .0001) and from 71+/-9 to 85+/-14 mm Hg (P = .004), respectively. Renal function remained unchanged. Although both groups had similar clinical responses, there were more blacks and women in the hypertensive Group A. Effectively, 12 of 45 (27%) heart failure patients with an antecedent history of hypertension demonstrated a paradoxical hypertensive response to vasodilator therapy. The recurrence of hypertension in a significant portion of patients successfully treated for heart failure has important clinical implications.     

Acute alterations in systolic ventricular interdependence-mechanical dependence of right ventricle on left ventricle following acute alteration of right ventricular free wall

The purpose of the study was to examine whether systolic ventricular interdependence can be acutely altered by changes in the mechanical properties of the ventricular wall. In eight acute canine studies, we released an aortic constriction during diastole. We measured right ventricular (RV) pressure changes (dPr) caused by sudden changes in left ventricular (LV) pressure (dPl). Measurements were obtained during control, 10 min after right coronary artery occlusion, and then 15 min after injecting glutaraldehyde into the RV free wall. By superimposing the pressure tracings of the beats immediately before and after the aortic release, the instantaneous pressure difference ratio (dPr/dPl) was calculated during systole. Maximal value of the pressure difference ratio decreased from control 0.11 +/- 0.04 to ischemia 0.08 +/- 0.03; (p < 0.05) and increased with glutaraldehyde 0.15 +/- 0.06; (p < 0.05). Thus, acute ischemia in RV free wall decreased the magnitude of systolic ventricular interdependence from LV to RV, while glutaraldehyde, which stiffens the RV free wall, increased the magnitude.     

Influence of longer term left ventricular assist device support on valvular regurgitation

The authors previously published data that describe acute alterations in ventricular dimensions and in the severity of mitral and tricuspid regurgitation (MR/TR) after initiation of left ventricular assist device (LVAD) pumping. In the current study, measurements of ventricular size and regurgitant jet area acquired after LVAD implantation are presented. Eight patients had LVAD implanted pending cardiac transplantation (duration of assist 70-279 days; mean, 162 +/- 29 days). Echocardiograms were obtained at the time of LVAD implant and later during LVAD support (mean time for late echo, 95 +/- 32 days post-implant). Comparisons of pre-implant with late post-implant data showed: increased TR jet area (4.8 +/- 1.0 cm2 vs. 8.0 +/- 1.7 cm2 P < 0.05); increased right ventricular (RV) end-systolic dimension (31 +/- 4 vs 40 +/- 5 mm, P < 0.05); and increased RV end-diastolic dimension (35 +/- 4 vs. 45 +/- 5 mm, P < 0.065). Decreased MR jet area and decreased LV dimensions (P < 0.05) also were noted on comparison of pre-implant and late post-implant data. There were no significant differences between any immediate post-implant and late post-implant echocardiographic measurements. No patient had clinical evidence of RV failure. LV mechanical assist causes an acute increase in TR, presumably by volume loading the RV. TR and RV enlargement persisted but did not discernibly worsen on subsequent post-implant echocardiograms. LV dimensions and MR remained less than the pre-implant values on later post-implant determinations.     

Clinical results and radiographic appearance of the Rashkind double umbrella device in patients with occlusion of the ductus arteriosus

BACKGROUND: The Rashkind double umbrella device for patent arterial duct occlusion has been used in many patients. Its radiographic appearance has not been sufficiently described. OBJECTIVE: To present the varying radiographic appearances of the Rashkind double umbrella device on the chest X-ray. MATERIALS AND METHODS: The chest radiographs of 69 patients (median age 60 months; median weight 17 kg), who underwent closure of their patent arterial duct between March 1990 and August 1994, were reviewed. The following parameters were evaluated: 1) the size of the heart (cardio-thoracic ratio) and pulmonary vessels, 2) the position of the device in AP/PA and lateral projections. The results of occlusion of the patent arterial duct were also reviewed. RESULTS: Sixty-two of 69 (90 %) patients had complete occlusion after a follow-up between 2 months and 3(1)/2 years. The cardio-thoracic ratio showed significant reduction at follow-up (P < 0.001). The two different size devices could be well differentiated in the AP and the lateral projection. In 14 patients (20 %) the device was in an asymmetrical position. There was no significant correlation between position of the device and success of occlusion in our material. CONCLUSION: Complete occlusion of the arterial duct using Rashkind double umbrella devices can be achieved in 90 % of our population. In 20 % the device will have an asymmetrical position. There is no correlation between asymmetrical position of the device in the chest radiograph and residual shunting.     

Adverse effects and recovery after total intravenous anesthesia in children

INTRODUCTION: The asynchrony of the left ventricle--i.e., its nonuniform contraction and relaxation--is an important factor for left ventricular function. Heart failure is often related to abnormal systolic function, sometimes associated with a diastolic dysfunction. We studied the relationship of left ventricular asynchrony to left ventricular function in patients with nonischemic heart failure. MATERIAL AND METHODS: Radionuclide angiography at rest was performed in 25 patients with nonischemic heart failure and in 26 age and sex matched normal subjects. In addition to ejection fraction and peak filling rate, two indices of left ventricular asynchrony were calculated: the coefficient of variation of regional time to end systole and the coefficient of variation of regional time to peak filling rate. These factors indicate how disperse are the regional values of time to end systole and of time to peak filling rate. In fact, the higher the value, the greater the asynchrony. RESULTS: A significant (r = .46, p < .05) inverse correlation was found between the ejection fraction and the coefficient of variation of regional time to end systole in both the normal subjects and the heart failure patients, while the ejection fraction correlated significantly (r = .46, p < .05) with the coefficient of variation of regional time to peak filling rate only in the patients. Moreover, the peak filling rate was inversely correlated (r = .57, p < .05) with the coefficient of variation of regional time to peak filling rate in the heart failure patients but not in the normal subjects. CONCLUSIONS: These results suggest that left ventricular systolic and diastolic asynchrony may contribute to impair left ventricular systolic and diastolic function in patients with nonischemic heart failure.     

Influence of inhaled nitric oxide on systemic flow and ventricular filling pressure in patients receiving mechanical circulatory assistance

BACKGROUND: In patients with left ventricular (LV) dysfunction, inhaled nitric oxide (NO) decreases pulmonary vascular resistance (PVR) but causes a potentially clinically significant increase in left atrial pressure (LAP). This has led to the suggestion that inhaled NO may reach the coronary circulation and have a negative inotropic effect. This study tested an alternative hypothesis that LAP increases because of volume shifts to the pulmonary venous compartment caused by NO-induced selective pulmonary vasodilation. METHODS AND RESULTS: The Thermo Cardiosystems Heartmate is an LV assist device (LVAD) that can be set (by controlling pump rate) to deliver fixed or variable systemic blood flow. Eight patients (between 1 and 11 days after LVAD implantation) were administered inhaled NO (20 and 40 ppm for 10 minutes), and LAP, systemic flow, and pulmonary arterial pressure were measured in both fixed and variable pump flow modes. In both modes, inhaled NO lowered PVR (by 25 +/- 6% in the fixed mode, P < .001, and by 21 +/- 5% in the variable mode, P < .003). With fixed pump flow, LAP rose from 12.5 +/- 1.2 to 15.1 +/- 1.4 mm Hg (P < .008). In the variable flow mode, LAP did not increase and the assist device output rose from 5.3 +/- 0.3 to 5.7 +/- 0.3 L/min (P < .008). CONCLUSIONS: A selective reduction in PVR by inhaled NO can increase LAP if systemic flow cannot increase. These data support the hypothesis that with LV failure, inhaled NO increases LAP by increasing pulmonary venous volume and demonstrate that inhaled NO has beneficial hemodynamic effects in LVAD patients.     

Subject''s perceptions of the crew interaction dynamics under prolonged isolation

BACKGROUND: Short-term variability of RR interval and blood pressure occurs predominantly at low frequency (LF; approximately 0.1 Hz) and high frequency (approximately 0.25 Hz). The arterial baroreflex is thought to be the predominant determinant of the LF component of RR variability. Patients with severe congestive heart failure (CHF) have an attenuated or absent LF oscillation in RR variability. The left ventricular assist device (LVAD) offers a unique possibility for analysis of spectral oscillations in RR interval independent of any effects of blood pressure that influence these oscillations via the baroreflex. METHODS AND RESULTS: We performed spectral analysis of RR, blood pressure, and respiration in 2 patients with CHF before and after LVAD implantation. LF components of the RR-interval and blood pressure variability were absent in both CHF patients before LVAD implantation. After LVAD implantation, spectral analysis of the RR interval showed restoration of a clear and predominant LF oscillation in the native hearts of both patients, with no such oscillation evident in the blood pressure profile. CONCLUSIONS: During total circulatory support with the LVAD, the LF oscillation in RR interval of the native heart, absent in CHF, is restored. This LF oscillation in RR interval occurs in the absence of LF oscillations in blood pressure and thus is unlikely to be explained by baroreflex mechanisms. Hence, the absence of LF oscillation in the RR interval in CHF is functional and is reversible by LVAD circulation. The presence of a predominant LF oscillation in RR interval independent of any oscillation in blood pressure suggests that the LF oscillation is a fundamental property of central autonomic outflow.     

Exercise performance and chronotropic response in heart failure patients with implantable left ventricular assist devices

During metabolic stress testing, 9 of 20 patients with left ventricular assist devices exhibited a lag in peak device rate by < or = 85% of peak native heart rate (group I), with peak device rates of 118 +/- 9 beats/min compared with group II, in which peak device rate nearly equaled peak native rates. Peak systolic blood pressure was significantly greater in group II than group I, but there was no significant difference in peak oxygen consumption, anaerobic threshold, or peak flows.