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High-dose aprotinin was used in 20 patients undergoing primary or repeat operations on the thoracic or thoracoabdominal aorta using cardiopulmonary bypass and hypothermic circulatory arrest. The activated clotting times immediately before the establishment of hypothermic circulatory arrest exceeded 700 seconds in all but 1 patient. Three patients (15%) required reoperation for bleeding. Seven patients died during hospitalization, and 5 had postmortem examination. Platelet-fibrin thrombi were present in multiple organs including the coronary arteries of 4 patients with myocardial infarction or failure, the pulmonary arteries of 2 patients, 1 of whom died of acute right ventricular failure, the brains of 2 patients who sustained a stroke, and the kidneys of 4 patients, 3 of whom had development of renal dysfunction. Renal dysfunction occurred in 13 patients (65%), and all were 65 years of age or older. Five of these patients required hemodialysis. Among 20 age-matched patients who had similar operations without aprotinin, there was one hospital death (5%) from myocardial infarction, and renal dysfunction developed in 1 patient (5%), who did not require dialysis. None of these 20 patients required reoperation for bleeding. Although aprotinin has been shown to reduce blood loss in patients having cardiac operations employing cardiopulmonary bypass, this benefit was not attained in this group of patients with thoracic aortic disease in whom hypothermic circulatory arrest was used. Use of aprotinin in elderly patients undergoing these procedures was associated with an increased risk of renal dysfunction and failure, and of myocardial infarction and death.
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PMID:Renal dysfunction and intravascular coagulation with aprotinin and hypothermic circulatory arrest. 752 Jun 87

Right ventricular function was measured in ten patients with severe COPD (mean FEV1 = 0.48 +/- 0.2 L/s) as part of an evaluation for single lung transplant (SLT). Right ventricular ejection fraction (RVEF) was determined by two methods: first-pass radionuclide scan by multigated acquisition (MUGA) and by using a fast thermistor tipped RVEF/volumetric pulmonary artery catheter. None of the patients had clinical evidence of active right heart failure, although mild resting pulmonary hypertension (mean pulmonary artery pressure [PAP] = 24 +/- 4 mm Hg) that worsened with minimal exercise (mean PAP = 39 +/- 11 mm Hg) was present. There was a significant difference in RVEF measured by the two methods (mean MUGA RVEF = 57 +/- 10%, mean catheter RVEF = 27 +/- 8%; p < 0.00005). RVEF determined by both methods was correlated with hemodynamic and gas exchange variables obtained during rest and at maximal exercise. There were significant, yet inverse, correlations between RVEF measured by catheter and cardiac index measured during exercise (CIex), as well as with exercise pulmonary vascular resistance index (PVRI). There were no significant correlations found between MUGA RVEF and any gas exchange or hemodynamic variables. Significant correlations were found with the catheter-measured right ventricular end-diastolic volume (RVEDV) and CIex (r = 0.9 p < 0.005), with maximal oxygen consumption during exercise (VO2max) (r = 0.86 p < 0.0025), with exercise stroke volume index (SVI) (r = 0.76 p < 0.01), and exercise central venous pressure (CVP) (r = 0.62 p < 0.05). Echocardiographic studies revealed right ventricular dilatation and mild tricuspid regurgitation (TR) in all patients. The strong correlation between RVEDV, CIex, and VO2max supports the concept that in these patients, as long as there is no clinical evidence of right heart failure (resting CVP still within normal limits), those with the largest RVEDVs use the Frank Starling principle to their best advantage to remain more functional.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Right ventricular function in patients with severe COPD evaluated for lung transplantation. Lung Transplant Group. 778 38

The efficacy of two right ventricular assist systems for severe right ventricular failure caused by multiple ligation of the right coronary artery and right ventricular free wall with ventricular septal infarction was studied in 20 adult dogs in order to determine a better assist system in terms of hemodynamics and ventricular function. Two types of assist systems, a right ventricular bypass (RVAS) and an RVAS with intraaortic balloon pumping (IABP) were applied. The assist flow changed the preoperative aortic blood flow by 20%, 40%, 60% and 80%, respectively. The RVAS decreased the preload of RV and resulted in an effective RV assist. But RVAS did not effectively improve the aortic pressure (AP), left atrial pressure (LAP), aortic flow (AF), coronary sinus flow (CSF), left ventricular end diastolic pressure (LVEDP), LV stroke work (LVSW), or the endocardial viability ratio (EVR). On the other hand, RVAS with IABP significantly improves AP, LAP, AF, CSF, LVEDP, LVSW, and EVR as compared with the data of RVAS only. The optimal assist flow during RVAS with IABP might be 40-60% of the preoperative aortic blood flow.
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PMID:[Experimental study of right ventricular assists for severe right ventricular failure]. 780 20

The cardiac valvular surgical experience of patients in the Duke Carcinoid Database was reviewed to assess operative outcome. Of the 604 patients in the database, 19 patients with carcinoid heart disease were identified by cardiac catheterization or echocardiography, or both. Eight of these underwent tricuspid valve replacement surgery with bioprostheses (2 also had open pulmonic valvuloplasty). Compared with patients medically managed, surgically treated patients were similar with the exception that they had higher right atrial mean (17 +/- 6 vs 9 +/- 4 mm Hg, p = 0.03) and v-wave (27 +/- 6 vs 17 +/- 7 mm Hg, p = 0.04) pressures. Of the 8 surgical patients, 5 (63%) died within 30 days. Causes of death included tricuspid valve thrombosis, cerebral vascular accident, coagulopathy, renal failure, and intractable right heart failure. High comorbidity was present in all 8 patients. There was a weak trend (p = 0.17) toward lower Charlson comorbidity indexes in survivors (6.7 +/- 0.6) compared with nonsurvivors (7.6 +/- 0.9). Age was significantly lower (p = 0.036) in survivors (46 +/- 13 years) compared with nonsurvivors (69 +/- 4 years). Extended follow-up revealed 2 patients who survived beyond a decade. Review of 47 carcinoid valve replacement cases (Duke Carcinoid Database and 39 published cases) revealed a 30-day mortality of 56% for patients > 60 years of age, and 0% for those < or = 60 years of age (p < 0.0001). Although valve replacement surgery can afford prolonged palliation from carcinoid heart disease, it is associated with a significant mortality risk. Careful preoperative risk stratification by age and comorbidity may provide a means for optimal selection of surgical candidates.
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PMID:Predictors of outcome of tricuspid valve replacement in carcinoid heart disease. 786 94

Changes in the right ventricular function measured with a thermodilution ejection fraction catheter have been recorded in open-chest normal pigs and pigs with acute right heart failure (RVF) undergoing left ventricular assistance with a pneumatic-sac-type device (LVAD). To produce acute right heart failure, 5 pigs underwent ligation of the right ventricular free wall coronary arteries. Compared with normal pigs, cardiac output in ligated pigs fell by 21% (7.5 +/- 0.5 vs 9.5 +/- 1.2 L/min; p < 0.05) and the right ventricular end diastolic pressure rose (11.4 +/- 2.6 vs 5.7 +/- 3.6 vs mmHg: p < 0.05). With the left ventricular assist device connected, the right atrial pressure was increased to 3, 5, 7, 10 and 12 mmHg by volume loading while maintaining the haematocrit at 35 +/- 6%. The right ventricular stroke work index (RVSWI) increased with volume loading in normal pigs. In RVF pigs, RVSWI increased significantly with the LVAD (59.2 +/- 5.8 vs 23.5 +/- 7.8 mmHg ml/min/kg, p < 0.01), approaching that of normal pigs (62.3 +/- 4.8 mmHg ml/min/kg). Similar changes were observed in the cardiac output and right ventricular stroke volume. These results show that, in this model of open-chest, mild, acute right heart failure, left ventricular assistance allows right ventricular function to return to normal, despite volume overloading, by decreasing right ventricular after load and increasing right ventricular compliance.
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PMID:Right heart function during left ventricular assistance in an open-chest porcine model of acute right heart failure. 807 Sep 45

Although bridging to cardiac transplantation has become a therapeutic option for transplant candidates whose condition deteriorates while they are awaiting a donor heart, short-term efficacy has not been proved and long-term survival has not been reported. We retrospectively reviewed data on 44 patients who had circulatory assist devices placed as a bridge to transplantation between May 1985 and April 1993. The 35 male and nine female patients ranged in age from 12 to 65 years (mean 43.8 years). Thirty-one patients were supported with 32 Thoratec (18 left ventricular, 14 biventricular), 11 Novacor, and two Jarvik J-7-70 devices. The duration of device support was from 4 hours to 440 days (mean 45.5 days). Fifteen patients did not receive a donor organ because of infection (ten patients), renal failure (five patients), bleeding (nine patients), cerebrovascular accident (three patients), ventricular fibrillation (one patient), and right heart failure (one patient), and all died. Two patients were weaned from support and survived without transplantation. Twenty-seven patients underwent transplantation, and 26 survived (96%). Overall survival was 64% (28/44). Duration of survival ranged from 2 to 96 months (mean 35 months). Among the 28 hospital survivors, there were four late deaths (all transplant recipients) at 3, 6, 14, and 68 months. Posttransplantation actuarial survivals at 1, 5, and 8 years are 88%, 83%, and 66%. Twenty-three of the 24 patients presently alive are in New York Heart Association functional class I. These data demonstrate the short- and long-term efficacy of bridging to transplantation with circulatory support devices. The excellent survival and full functional recovery of patients undergoing transplantation ensure that donor organs are not being "wasted" on the sickest patients.
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PMID:Eight years' experience with bridging to cardiac transplantation. 830 66

Thirty-four patients with chronic lung disease in stable condition were studied at supine rest (RS), at rest with the legs raised (LR), and during two levels of exercise: E1, 0 or 20 W, E2, 20 or 40 W. Five patients had normal spirometry (group 1), six patients had normal vital capacity but FEV1/VC below 70% (group 2), and 23 patients had VC below 95% of normal and FEV1/VC below 70% (group 3); group 3 was subdivided into group 3a (n = 14) without, and group 3b (n = 9) with a history of right heart failure (RHF). Right ventricular end-diastolic (RVEDV) and end-systolic (RVESV) volumes were computed from stroke volume and right ventricular ejection fraction (RVEF). RVEF at rest was correlated with lung function variables. Changes in RVEF from LR to E2 were normal, i.e. above 0.05, except for in group 3b, where RVEF did not increase with exercise. Relation between RVESV and pressure, and changes in stroke volume with RVEDV from LR to E2 were also abnormal in group 3b. These results show that in patients with chronic lung disease RVEF at rest reflects lung function, whereas its adaptation to exercise is impaired only in patients who have experienced RHF episodes.
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PMID:Right ventricular pressure-volume relations in chronic lung disease. 845 70

This study investigated the mechanism of right ventricular failure during bypass of the left side of the heart by precisely assessing right ventricular function with use of a conductance catheter. Bypass of the left side of the heart was established with a centrifugal pump in 10 mongrel dogs weighing 11 to 19 kg. Right ventricular function during left heart bypass was evaluated by two parameters that were both derived from measurement of relative change in right ventricular volume by the conductance catheter technique. One parameter was the right ventricular end-systolic pressure-volume relationship as a load-independent index, and the other was the peak right ventricular pressure-right ventricular stroke volume relationship as a "force-velocity relationship." These parameters were measured in both normal and failing hearts while afterload was increased by bilateral intrapulmonary balloon inflation. Moreover, changes in these relationships were observed by varying assist ratios of left heart bypass from 0% to 100%. Failing heart models were induced by normothermic aortic clamping for 20 minutes. The right ventricular end-systolic pressure-volume relationship in normal hearts did not change, irrespective of the assist ratio of left heart bypass, whereas that in failing hearts decreased from 4.25 +/- 1.41 mm Hg/ml without bypass of the left side of the heart to 3.53 +/- 1.30 mm Hg/ml after 100% assist of left heart bypass (p < 0.05). In the peak right ventricular pressure-right ventricular stroke volume relationship, right ventricular stroke volume was almost constant in normal hearts when afterload was increased regardless of the assist ratio of left heart bypass. Moreover, right ventricular stroke volume was maintained at a higher level during bypass of the left side of the heart compared with that without left heart bypass. However, that slope of the relationship in failing hearts was inversely linear and became significantly steeper after 100% assist of bypass of the left side of the heart compared with that without left heart bypass (-0.131 +/- 0.042 versus -0.051 +/- 0.038, p < 0.005). Therefore ++these two slopes of the relationship intersected at a point that was considered the critical point of afterload during bypass of the left side of the heart. In other words, right ventricular stroke volume was decreased by 100% left heart bypass above the critical point of afterload. In conclusion, this study demonstrates not only that bypass of the left side of the heart results in an increase in right ventricular stroke volume in both normal and failing hearts at the physiologic range of afterload, but also that right ventricular function against higher afterload is impaired by 100% assist of bypass of the left side of the heart in failing hearts.
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PMID:Analysis of right ventricular function during bypass of the left side of the heart by afterload alterations in both normal and failing hearts. 862 7

This experimental study was designed to assess the influence of failure of the right side of the heart or pulmonary hypertension, or both, on the performance of a novel miniaturized left ventricular assist device. In small-sized dogs (n = 50) ischemic global left ventricular failure was induced and support was provided by the HIA-VAD displacement pump (stroke volume 10 or 25 ml) installed as a left ventricular assist device. In three groups of animals (n = 10 each) pulmonary hypertension was created before induction of global left ventricular failure. During left ventricular assist device support temporary ischemic failure of the right side of the heart was induced in four groups of animals (n = 10 each). In the group subjected to left ventricular failure, support with the left ventricular assist device, and right ventricular failure during left ventricular assist, left atrial pressure and cardiac index were significantly lower than in the group subjected to left ventricular failure and left ventricular assist alone (2 +/- 6 versus 11 +/- 6 mm Hg and 1.6 +/- 0.4 versus 1.0 +/- 0.4 L/(min/m2), respectively, p < 0.05). In the group subjected to pulmonary hypertension, left ventricular failure, and left ventricular support, left atrial pressure dropped to values near zero but cardiac index remained unaltered as compared with results with the same regimen without pulmonary hypertension. However, when right ventricular failure was added (that is, pulmonary hypertension, left ventricular failure, left ventricular support, and right ventricular failure during support with the left ventricular assist device) left atrial pressure dropped to negative values (p < 0.05) and cardiac index progressively deteriorated. When, in an additional group of dogs, biventricular support was installed in the latter regimen, circulation was initially well supported but oxygenation deteriorated in 60% of cases. We conclude that (1) adequate right ventricular function was indispensable during support with the left ventricular assist device, (2) the combination of pulmonary hypertension and right ventricular failure led to the "low left ventricular assist device output syndrome," and (3) biventricular mechanical support in the presence of pulmonary hypertension may be complicated by the alveolar leakage syndrome.
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PMID:Effects of failure of the right side of the heart and increased pulmonary resistance on mechanical circulatory support with use of the miniaturized HIA-VAD displacement pump system. 875 17

Patients with obstructive sleep apnea demonstrate both acute and chronic hemodynamic changes attributable to their disease. Acutely, these patients experience repetitive nocturnal hemodynamic oscillations. Sudden increases in heart rate and arterial pressure occur in association with decreases in left ventricular stroke volume immediately following apnea termination. These hemodynamic changes are likely attributable primarily to the effects of oxygen desaturation and arousal, an abrupt change in state. These acute changes occur against a background of altered cardiovascular control. Patients with sleep apnea, even when sleeping without obstructions, fail to display the normal nocturnal decline in arterial pressure of 10-15% from the waking value. The absence of a nocturnal decline may have chronic consequences, such as development of left ventricular hypertrophy. Another chronic hemodynamic consequence of sleep apnea may be sustained diurnal hypertension. Epidemiologic studies suggest individuals with sleep disordered breathing are at greater risk of daytime hypertension, even after controlling for other risk factors. Although sleep apnea may contribute to pulmonary, as well as systemic hypertension, sleep apnea alone does not appear to be a cause of decompensated right heart failure. Although knowledge of the hemodynamic consequences of sleep apnea has grown in recent years, much remains to be learned.
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PMID:Hemodynamic consequences of obstructive sleep apnea. 884 30


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