Vascular determinants of univentricular support

The dynamic coupling between cardiac pump performance and vascular arterial-venous capacitive and resistive properties was examined analytically and experimentally to determine the feasibility of maintaining systemic and pulmonary circulation, devoid of the right heart. Analysis of the cardiovascular system (excluding neurohumoral factors), used a mathematical representation of the major determinants involved in cardiac output and demonstrated that change in pump flow output has reciprocal effects on the venous and arterial pressures. Independent of the pump's performance characteristics, cardiac output reserve was restricted, reaching a critical plateau (50% of normal) because of the rapidly depleting pulmonary venous pressure, concurrent with the translocation of the venous stressed volume to the arterial side of the circulation. Animal experiments aided by computer modeling confirmed that near normal flow can be sustained by actively mobilizing or augmenting blood volume, or by reducing selectively the unstressed volume and venous pooling. A single blood pump, in a form of a mechanical substitute, or the biologic left heart acting alone, can support the entire circulation. The right heart is not essential for normal pulmonary circulation, but serves to maintain low systemic venous pressure and a relatively high left heart flow reserve state. Peripheral vascular parameters, i.e., stressed volume and venous capacitance, serve a vital role in preserving the mechanical self regulation of cardiac output.     

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.     

An intracorporeal (abdominal) left ventricular assist device. Initial clinical trials

We have initiated clinical trials with an intracorporeal (abdominal) partial artificial heart and ten preterminal postcardiotomy patients have been studied. During profound left ventricular failure, the device captures the entire cardiac output from the apex of the left ventricle at low pressures (20 to 40 mm Hg) and ejects (at 80 to 150 mm Hg) into the infrarenal abdominal aorta; the biological aortic valve opens only intermittently and the entire systemic circulation is pump generated. The device is six to ten times more effective than intra-aortic balloon pumping in man and has maintained systemic perfusion during clinical asystole and ventricular fibrillation. We have documented that the profoundly depressed postcardiotomy left ventricle, initially incapable of ejection, can recover during total left ventricular unloading with the abdominal left ventricular assist device support over a seven-day period.     

Homozygous deletion of the p16INK4A gene occurs more frequently in CD2+ than in CD2+ T-cell acute lymphoblastic leukemia

Right ventricular assist devices are an important part of the armamentarium of cardiac surgeons for the treatment of right-sided circulatory failure after cardiac transplantation or insertion of a left ventricular assist device. However, right ventricular assist device insertion can be technically challenging in the setting of pulmonary hypertension because of a number of concomitant anatomic and physiologic phenomena. We present a technique for the insertion of the right ventricular assist device outflow cannula that is easier and faster to insert, and safer to explant, especially if cardiopulmonary bypass is to be avoided.     

Hemodynamic and physiologic changes during support with an implantable left ventricular assist device

To evaluate hemodynamic effectiveness and physiologic changes on the HeartMate 1000 IP left ventricular assist device (Thermo Cardiosystems, Inc., Woburn, Mass.), we studied 25 patients undergoing bridge to heart transplantation (35 to 63 years old, mean 50 years). All were receiving inotropic agents before left ventricular assist device implantation, 21 (84%) were supported with a balloon pump, and 7 (28%) were supported by extracorporeal membrane oxygenation. Six patients died, primarily of right ventricular dysfunction and multiple organ failure. Nineteen (76%) were rehabilitated, received a donor heart, and were discharged (100% survival after transplantation). Pretransplantation duration of support averaged 76 days (22 to 153 days). No thromboembolic events occurred in more than 1500 patient-days of support with only antiplatelet medications. Significant hemodynamic improvement was measured (before implantation to before explantation) in cardiac index (1.7 +/- 0.3 to 3.1 +/- 0.8 L/min per square meter; p < 0.001), left atrial pressure (23.7 +/- 7 to 9 +/- 7.5 mm Hg; p < 0.001), pulmonary artery pressure, pulmonary vascular resistance, and right ventricular volumes and ejection fraction. Both creatinine and blood urea nitrogen levels were significantly higher before implantation in patients who died while receiving support. Renal and liver function returned to normal before transplantation. We conclude that support with the HeartMate device improved hemodynamic and subsystem function before transplantation. Long-term support with the HeartMate device has a low risk of thromboemboli and makes a clinical trial of a portable HeartMate device a realistic alternative to medical therapy.     

Intravenous nitroglycerin in acute respiratory failure of patients with chronic obstructive lung disease, secondary pulmonary hypertension and cor pulmonale

We have studied the hemodynamic effects of an intravenous single dose of nitroglycerin in 13 patients with secondary pulmonary hypertension and Cor Pulmonale, during the acute course of respiratory failure and under assisted ventilation. We observed a significant decrease in systolic, diastolic and mean pulmonary arterial pressures, and in pulmonary resistance and systolic right ventricular work index, without any change in right or left pre-loads. The systolic arterial pressure decreased slightly, without any change in cardiac index or diastolic pressure. The arterial and mixed venous oxygen contents, and the pulmonary shunting ( Qs/Qt) were unchanged. These results suggest that nitroglycerin may be a useful therapy in patients in the acute stages of pulmonary hypertension resulting from chronic lung disease and under assisted ventilation. In addition, the lack of change in cardiac index, intrapulmonary shunting and oxygen content suggests that this decrease in pulmonary resistance is not linked with any deleterious effect in oxygen transfer.     

Effects of halothane on global and regional biventricular performances and on coronary hemodynamics before and during right coronary artery stenosis in the dog

BACKGROUND: Previously, it was suggested that right ventricular (RV) free wall dysfunction does not necessarily elicit global hemodynamic alterations. This was investigated in a canine model of halothane-induced right coronary artery (RCA) insufficiency. METHODS: Two concentrations (0.8% and 1.6% end tidal) of halothane on global and regional RV and left ventricular (LV) performance and on coronary, pulmonary, and systemic hemodynamics were studied in 10 open-chest dogs first before and, subsequently, during critical RCA stenosis. RESULTS: In the absence of stenosis, halothane caused progressive and comparable depression of regional and global RV and LV function and reduction of RCA flow. Halothane administered during RCA stenosis caused disproportionate decreases in RCA flow and segment shortening and increases in systolic segment lengths in the area supplied by the stenosed RCA that were approximately twice as great as before stenosis. Such severe regional RV dysfunction was not accompanied by greater depression of global RV and LV pump function (systolic pressures and stroke volume). CONCLUSIONS: In the canine heart with its dominant left coronary system, RCA insufficiency (on the basis of halothane-induced hypotension) caused regional RV dysfunction suggesting ischemia that was not accompanied by global hemodynamic alteration.     

Paradoxic pulmonary vasoconstriction in response to acetylcholine in patients with primary pulmonary hypertension

Pulmonary vascular reactivity was assessed during diagnostic heart catheterization in two patients with pulmonary hypertension unexplained by pulmonary or cardiac disease and in five patients with atypical chest pain and normal coronary arteriograms. Acetylcholine, an endothelium-dependent vasodilator that also has a direct contracting effect on vascular smooth muscle cells, was infused in the right atrium in a step-wise increasing dose in order to obtain final blood concentrations in the pulmonary circulation ranging from 10(-6) mol/L to 10(-4) mol/L. In the five control patients, acetylcholine induced a dose-related decrease of pulmonary vascular resistance (-52 percent +/- 9 percent). In the patients with primary pulmonary arterial hypertension, however, acetylcholine caused a paradoxic increase of pulmonary arterial pressure and of pulmonary vascular resistance. Thus, it appears that endothelium-dependent vasodilation is impaired in the pulmonary circulation of patients with primary pulmonary arterial hypertension. Endothelial dysfunction in the pulmonary circulation may play a role in the pathophysiology of this disease.     

Pathophysiologic studies of the pulmonary and coronary circulations in man

Studies of the pulmonary circulation in normal man, performed with external radiation detectors, have shown that pulmonary blood volume is about 10% of total blood volume. Pulmonary blood volume was unchanged in patients with acute or chronic left atrial hypertension and in normal persons during expansion of total blood volume in spite of marked increases in pulmonary vascular pressures. However, pulmonary blood volume was greatly increased in patients with polycythemia rubra vera and a large total blood volume and in patients with a left to right shunt but normal pulmonary intravascular pressure. Studies of regional myocardial perfusion with injection of xenon-133 solution into the left coronary artery revealed localized areas of ischemia distal to stenotic lesions even when the patient was at rest. During angina produced by pacing, more severe ischemia occurred, thus suggesting that functional factors reduce local perfusion below resting levels. In patients with "variant" angina, intravenous injection of thallium-201 chloride during spontaneous attacks has revealed large cold areas in myocardial scintigrams not present under control conditions, thus suggesting severe transmural reduction of perfusion in heart muscle corresponding to S-T segment elevation in the electrocardiogram.     

Comparative study of artificial circulation for the liver after cardiogenic shock: pulsatile or nonpulsatile?

Because of multiple organ failure (MOF), the survival rate of patients with mechanical circulatory support has not been satisfactory, The purpose of this study is to estimate the effects of pulsatile and nonpulsatile artificial circulation on hepatic microcirculation and function. Cardiogenic shock was induced experimentally by ligating of left anterior descending branch in pigs. For the right ventricular assist device, a nonpulsatile pump (Nikkiso HPM-15) was employed. The left ventricular function was supported by either a nonpulsatile pump (Nikkiso HPM-15: NP group) or a pulsatile pump (Zeon Medical: P group). NP group was further divided into 80% support (NP-1 group) and 100% support (NP-2 group) of the control cardiac output. All groups were maintained at an equivalent mean aortic pressure of 3 hours. We measured the hepatic artery blood flow, portal vein flow and hepatic regional blood flow. For the metabolic and hepatic oxygen metabolic data, GOT, GPT, arterial blood ketone body ratio (AKBR), lactate/pirubic acid (L/P), and hyaluronic acid were evaluated. The mean aortic pressure was higher in the NP-2 group than in the other groups. The hepatic arterial blood flow was significantly higher in the P group than in the others. The AKBR and hepatic oxygen metabolism showed significant improvement in the P group in comparison with others. The regional blood flow in the liver showed improvements in the P and NP-2 groups. These findings suggested that pulsatile circulation may be beneficial for microcirculation of the liver; and the augmented nonpulsatile flow had effects similar to those of pulsatile flow in hepatic circulation.     

Analytic processing elicits right ear superiority in monaurally presented speech

Experiments were designed to assess the performance of an intracorporeal (abdominal) left ventricular assist device (ALVAD) in the presence of induced tachycardias, multiple premature ventricular contractions (PVC's), and ventricular fibrillation in calves. Performance criteria were the degree of left ventricular unloading and the per cent cardiac output assumed by the ALVAD. During synchronous pumping, left ventricular unloading was complete and the entire cardiac output was captured by the device. During induced tachycardias up to rates of 120 beats per minute, these degrees of performance were maintained. At rates in excess of 120 beats per minute, performance declined due to decreased biologic stroke volumes and prosthetic filling times. In the presence of induced PVC's, performance during synchronous pumping decreased because of erratic R-wave sensing. Left ventricular unloading was complete but irregular, and the total cardiac output was captured. When asynchronous pumping was utilized, mean left ventricular systolic pressures increased, but total cardiac output was still captured. During induced ventricular fibrillation, ALVAD actuation maintained cardiac outputs equal to control values for periods up to 5 1/2 hours. These experiments indicate that, during normal sinus rhythm, synchronous pumping is optimal; asynchronous pumping is optimal during complex dysrhythmias; and either can be utilized to support the circulation with varying degrees of left ventricular unloading.     

Pulmonary hypertension is not a risk factor for RVAD use and death after left ventricular assist system support

Unlike transplantation candidates, patients with pulmonary hypertension (PHTN) and a high transpulmonary gradient do not appear to be at increased risk for right ventricular dysfunction after left ventricular assist system implant. To verify this observation, we reviewed 63 patients supported with the HeartMate (Thermo Cardiosystems, Inc, Woburn, MA) left ventricular assist system. Patients were divided into two groups: patients with PHTN (47 patients) had mean pulmonary artery pressure > 30 mm Hg and/or pulmonary vascular resistance > 4 Wood units, and the remainder of patients did not have PHTN (16 patients). Both groups were similar in age (mean, 51 years), gender distribution (% men, 83% vs 94%, not significant), and number of patients with ischemic cardiomyopathy (72% vs 69%, not significant). More patients in the group without PHTN required extracorporeal membrane oxygenation support (38% vs 12%, p = .06). Right ventricular assist device support was instituted in five (11%) patients with PHTN and four (25%) patients without PHTN. A significantly larger number of patients without PHTN died while on support (14% vs 44%, p = .01). Survival after transplantation in both groups was > 90%. Patients with PHTN have higher transpulmonary gradient, show a significant decrease in pulmonary pressure after left ventricular assist system implantation, and have a higher transplantation rate compared to patients without PHTN. A larger patient cohort is needed to determine if the absence of PHTN is a risk factor for RVAD need and poor outcome after LVAS support.     

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.     

Evaluation of a pulsatile pediatric ventricular assist device in an acute right heart failure model

BACKGROUND: The development of pulsatile ventricular assist devices for children has been limited mainly by size constraints. The purpose of this study was to evaluate the MEDOS trileaflet-valved, pulsatile, pediatric right ventricular assist device (stroke volume = 9 mL) in a neonatal lamb model of acute right ventricular failure. METHODS: Right ventricular failure was induced in ten 3-week-old lambs (8.6 kg) by right ventriculotomy and disruption of the tricuspid valve. Control group 1 (n = 5) had no mechanical support whereas experimental group 2 (n = 5) had right ventricular assist device support for 6 hours. The following hemodynamic parameters were measured in all animals: heart rate and right atrial, pulmonary arterial, left atrial, and systemic arterial pressures. Cardiac output was measured by an electromagnetic flow probe placed on the pulmonary artery. RESULTS: All results are expressed as mean +/- standard deviation and analyzed by Student's t test. A p value less than 0.05 was considered statistically significant. Base-line measurements were not significantly different between groups and included systemic arterial pressure, 80.6 +/- 12.7 mm Hg; right atrial pressure, 4.6 +/- 1.6 mm Hg; mean pulmonary arterial pressure, 15.6 +/- 4.2 mm Hg; left atrial pressure, 4.8 +/- 0.8 mm Hg; and cardiac output, 1.4 +/- 0.2 L/min. Right ventricular injury produced hemodynamics compatible with right ventricular failure in both groups: mean systemic arterial pressure, 38.8 +/- 10.4 mm Hg; right atrial pressure, 16.8 +/- 2.3 mm Hg; left atrial pressure, 1.4 +/- 0.5 mm Hg; and cardiac output, 0.6 +/- 0.1 L/min. All group 1 animals died at a mean of 71.4 +/- 9.4 minutes after the operation. All group 2 animals survived the duration of study. Hemodynamic parameters were recorded at 2, 4, and 6 hours on and off pump, and were significantly improved at all time points: mean systemic arterial pressure, 68.0 +/- 13.0 mm Hg; right atrial pressure, 8.2 +/- 2.3 mm Hg; left atrial pressure, 6.4 +/- 2.1 mm Hg; and cardiac output, 1.0 +/- 0.2 L/min. CONCLUSIONS: The results demonstrate the successful creation of a right ventricular failure model and its salvage by a miniaturized, pulsatile right ventricular assist device. The small size of this device makes its use possible even in small neonates.     

Differential responsiveness of murine T lymphomas to local growth and invasion factors may determine metastasis formation in the ovaries

Iodine-123-metaiodobenzylguanidine [123I-MIBG] has been used to evaluate the cardiac sympathetic nervous system. We evaluated the effect of pulmonary hypertension on the sympathetic neuronal function of the left ventricle in patients with pulmonary hypertension. We studied 20 patients with either chronic lung disease or pulmonary vascular disease. The patients were divided into a pulmonary hypertensive group and a control group. Single photon emission tomography was performed in the resting state 15 min and 4 h after administration of 123I-MIBG. Regions of interest (ROI) were set in the left ventricular (LV) free wall, the interventricular septum (IVS) and outside the LV free wall on short-axis images. The washout rate and the ROI/LV uptake ratio were calculated in each ROI. The IVS:LV uptake ratio was significantly lower in the pulmonary hypertensive group than in the control group. Our results suggest that left heart sympathetic neuronal dysfunction initially occurs in the IVS before it involves the LV free wall subsequently.     

Mechanical circulatory support for post cardiotomy cardiogenic shock in infants

Eleven infants weighing 2.3 to 7.8 kg underwent mechanical circulatory support for post cardiotomy cardiogenic shock. Initiated pre-operatively in two patients, extracorporeal membrane oxygenation was used in a total of eight patients aged 6 days to 3 months in association with repair of cyanotic congenital heart disease with increased pulmonary blood flow or with a right sided obstructive lesion. Ventricular assist devices were used in three other patients: a centrifugal left ventricular assist device in Patient 1 (10 months, 5.7 kg) after repair of the anomalous left coronary artery, and a pneumatic biventricular assist device (stroke volume 12 ml) in Patient 2 (6 months, 7.0 kg) for cardiac arrest after closure of ventricular septal defect and in Patient 3 (10 months, 7.8 kg) for post transplant graft failure. Duration of extracorporeal membrane oxygenation duration ranged from 26 to 192 hr (mean, 88 hr). Three patients were weaned from extracorporeal membrane oxygenation and two survived. Two others were separated from extracorporeal membrane oxygenation because of bleeding, but both subsequently died. Patient 1 was weaned from the left ventricular assist device after 192 hr and discharged from the hospital. Support was discontinued after 45 hr in Patient 2 who exhibited irreversible brain damage. Patient 3 was weaned from a biventricular assist device after 174 hr, but suffered recurrent graft failure. Our results show that an appropriate circulatory support system should be selected according to the cardiac anatomy in infants.     

Temporary mechanical left heart support. Recovery of heart function in patients with end-stage idiopathic dilated cardiomyopathy

BACKGROUND: Implantation of a mechanical cardiac support system (MCSS) in patients with idiopathic dilated cardiomyopathy (IDC) may improve cardiac function and allow explantation of the device. Our experience now includes 13 patients who have been "weaned" from MCSS and we report about the overall results of this treatment as well as the effects of ventricular unloading on cardiac function, anti-beta 1-adrenoceptor-autoantibody (A-beta 1-AAB) level and the degree of myocardial fibrosis. METHODS: 13 patients with non-ischemic IDC who had been admitted here in cardiogenic shock (CI < 1.61.min-1.m2, left ventricular ejection fraction [LVEF] < 16% and left ventricular internal diameter in diastole [LVIDd] > 68 mm) and who all tested positive for A-beta 1-AABs were implanted with an uni-(12 patients) or a biventricular (1 patient) mechanical assist device. Echocardiographic evaluation and A-beta 1-AAB-level-monitoring was routinely performed after implantation and explantation of the MCSS and the degree of myocardial fibrosis was assessed at the time of implantation and after explantation. RESULTS: During a mean duration of mechanical support of 236 +/- 201 days (range: 30 to 794 days), LV-EF improved to a mean of 46% and LVIDd decreased to a mean value of 56 mm in these 13 patients. A-beta 1-AABs decreased and disappeared 11.7 weeks after implantation of the device and did not reincrease thereafter. The highly pathologic degree of fibrosis at the time of implantation diminished to normal values about 1 year after explantation. One patient died of anesthesiologic complications and another patient shortly presented with a new episode of cardiac insufficiency 6 months after explantation. He was implanted again with an univentricular assist device was successfully transplanted 3 weeks later. Mean observation period of the remaining 11 patients now amounts to 12.6 +/- 9.77 (range: 3 to 26) months after explantation of the device--as of May, 31, 1997--with a cumulative observation period of 139 patient months. CONCLUSION: Temporary implantation of a MCSS may normalize cardiac function in selected patients with IDC. The striking degree of myocardial fibrosis can reduce to normal values after explantation of the device. A-beta 1-AABs disappear during ventricular unloading and do not increase thereafter. "Weaning" from mechanical device may constitute an alternative treatment to cardiac transplantation in selected patients.     

Halasz syndrome revealed in the newborn infant by pulmonary arterial hypertension. Study of 4 cases

In the 4 studied patients presenting with an Halasz's syndrome, the disease was complicated since the neonatal period by pulmonary arterial hypertension and heart failure. Three out of the 4 infants rapidly died, one after pneumonectomy. The fourth is surviving and benefitted solely from medical cardiotonic treatment. The pathogenesis of early pulmonary arterial hypertension in Halasz's syndrome is complex. The possibly associated cardiac malformations, the persistance of fetal obstructive hypertension due to the increase of the flow in the left pulmonary artery, the left to right shunt induced by the abnormal venous return and predominantly by the systemic blood supply to the right lung, are responsible, at various degrees, for pulmonary hypertension. Among surgical procedures to be proposed, the simple ligation of abnormal arteries which take their origin from the aorta seems to be preferable to pneumonectomy.     

Biphasic graft preservation for lung transplantation

The standard, most widely applied way of preserving a lung for transplantation is infusion through the pulmonary artery (PA) of a pulmonaryplegic solution. In this prospective study, we analyzed the initial function of the pulmonary and cardiac graft after biphasic infusion of a solution introduced retrograde through the left auricle and antegrade through the PA. Twenty-six heart and lung grafts (9 unilateral and 17 bilateral) were preserved by cardioplegia and pulmonaryplegia (biphasic) between January 1996 and March 1997. Indicators of graft viability recorded were the ratio of arterial oxygen pressure (PaO2) to inspired fraction (FiO2), mean systemic pressure (MSP), mean pulmonary artery pressure (MPAP) cardiac output, pulmonary vascular resistance (PVR) and systemic vascular resistance (SVR). The variables were recorded upon arrival of the grafts in the intensive care unit and in the first 24 h. Morbidity and mortality after heart transplants were recorded throughout a follow-up period of one month. After transplantation, most patients had a oxygenation coefficient (PaO2/FiO2) greater than 252 mmHg in the first 48 h. Hemodynamic parameters were also kept within normal ranges immediately after surgery and 24 h later. Mean ischemic time was 245 min for unilateral transplants, 215 for the first lung in double lung transplants, and 300 min for the second lung. In the early postoperative period, 3 patients suffered lung graft dysfunction, which was treated satisfactorily with nitric oxide (NO). No heart transplant patient suffered primary heart failure or left ventricular dilatation. We conclude that biphasic pulmonary preservation achieves satisfactory initial functional viability of the graft. Heart grafts removed simultaneously functioned successfully in the transplanted patient without additional pharmacological or mechanical support.     

Determinants of the pulmonary artery pressure rise in left ventricular dysfunction

Pulmonary artery hypertension in patients with left ventricular dysfunction is related to poor outcome but the role of cardiac functional abnormalities in the genesis of pulmonary hypertension remains unknown. The aim of this prospective study was to identify the determinants of pulmonary hypertension in 102 consecutive patients with primary left ventricular dysfunction (ejection fraction < 50%). Systolic pulmonary artery pressure was measured by continuous wave Doppler. Left ventricular systolic and diastolic function, severity of functional mitral regurgitation, cardiac output, and left atrial volume were assessed using Doppler echocardiography. In patients with left ventricular dysfunction, systolic pulmonary artery pressure was increased (51 +/- 14 mmHg, range 23 to 87 mmHg). Mitral deceleration time (r = -0.61; p = 0.0001) and mitral effective regurgitant orifice (r = 0.50; p = 0.0001) were the strongest parameters related to systolic pulmonary artery pressure. Multivariate analysis identified these two variables as the strongest predictors of systolic pulmonary artery pressure in association with the mitral E/A ratio (p = 0.006) and age (p = 0.005). In conclusion, pulmonary hypertension is common and variable in patients with left ventricular dysfunction. It is closely related to diastolic dysfunction and severity of functional mitral regurgitation but not independently to the degree of left ventricular systolic dysfunction. These findings underline the importance of assessing diastolic function and quantifying mitral regurgitation in patients with left ventricular dysfunction.