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BACKGROUND: Right heart failure remains the leading early cause of mortality after heart transplantation, especially with antecedent pulmonary hypertension. Paradoxically, the discarded recipient right heart, acclimated to pulmonary hypertension, is often stronger than its nonconditioned donor replacement. Heterotopic ("piggyback") transplantation is plagued by problems related to the retained, dilated, hypocontractile left ventricle (lung compression, systemic emboli, arrhythmias). Were it possible to retain the recipient's right heart, excising only the left ventricle, this could have important advantages, especially in severe pulmonary hypertension. This report describes such a technique. METHODS AND RESULTS: In four transplantation experiments (dogs), right ventricular-sparing transplantation proved technically feasible and hemodynamically successful. Bleeding after excision of the left ventricle was easily controlled. Back-bleeding from the native aortic valve (now open into the pericardial space) was not problematic. All atrial, aortic, and pulmonary arterial connections proved feasible. The preserved recipient right heart of all animals remained in stable sinus rhythm. All recipients were easily weaned from cardiopulmonary bypass, maintaining mean arterial pressures 60 to 110 mm Hg. CONCLUSIONS: This investigation develops a technique for donor right ventricle sparing in cardiac transplantation, demonstrating technical and hemodynamic feasibility. This method holds promise for the unsolved clinical problem of right heart failure after orthotopic heart transplantation with antecedent pulmonary hypertension.
The effects of an enoximone monotherapy on left-ventricular and especially on right-ventricular haemodynamics were investigated in fourteen patients with impaired left-ventricular function secondary to coronary artery disease. Anaesthesia was induced and maintained with fentanyl and flunitrazepam. After reaching steady state, a bolus of 0.5 mg/kg enoximone was administered, followed by an infusion of 0.5 microgram/kg/min. Besides the common haemodynamic parameters particulary the right-ventricular ejection fraction (RVEF) was measured using a special thermodilution technique. The predefined time points were: before administration of enoximone (baseline) and 5 min, 10 min, 15 min, 20 min, and 30 min after bolus injection of enoximone. Compared to the baseline the maximum effects of enoximone were a 28% increase of cardiac index accompanied by a 39% decline of systemic vascular resistance and an unchanged left-ventricular stroke-work index. While central venous pressure and mean pulmonary artery pressure remained unchanged. RVEF (+20%) and right-ventricular stroke-work index (+30%) were significantly augmented, augmented, indicating improved right-ventricular performance. No adverse effects of the enoximone administration were observed perioperatively. We conclude that an enoximone monotherapy is beneficial for patients with impaired myocardial function undergoing cardiac surgery.
A 40-year-old man with Down syndrome presented with right heart failure. He was markedly obese and had severe developmental delay. There was marked edema and an early diastolic sound. Transthoracic echocardiography suggested a right heart mass. Transesophageal echocardiography revealed an unruptured balloon-like sinus of Valsalva aneurysm within the right atrium that obstructed the tricuspid orifice. The patient died in hospital of mixed obstructive and/or septic shock.
We evaluated the effects of deep inspiration, expiration, and the Valsalva maneuver on composite cardiac (left and right ventricular) and pulmonary volumes using equilibrium radionuclide angiography in 15 adult males without left or right ventricular dysfunction. The additional effects of nitroglycerin during these maneuvers were also examined. Midexpiration was used as the control point and data analyzed as a ratio (e.g., inspiration counts divided by midexpiration counts). Left ventricular volume (LVV) declined with inspiration (0.90 +/- 0.08 inspiratory/midexpiration) and with the Valsalva maneuver (0.89 +/- 0.08 Valsalva/midexpiration). Similar changes occurred after nitroglycerin, although the effects of the Valsalva maneuver on LVV were exaggerated when compared to the initial control intervention (0.79 +/- 0.09, vs 0.88 +/- 0.07, p less than .05). Right ventricular volume (RVV) increased with inspiration and decreased with the Valsalva maneuver; these changes were similar after nitroglycerin. Pulmonary blood volume (PBV) was greater with inspiration than expiration (1.02 +/- 0.10 vs 0.95 +/- 0.05, p less than .05), and was reduced with the Valsalva maneuver. Nitroglycerin reduced significantly all volumes and the reduction was similar for each compartment when respiratory interventions were compared. We conclude that blood pool imaging can be used to characterize abrupt fluxes in central circulatory volumes. Blood pool imaging of the heart and lungs should be considered a technique for monitoring the distribution of blood volume during acute pharmacologic and physiologic alterations.
Pulmonary arterial hypertension, defined as a mean pulmonary artery pressure exceeding 20 mmHg has been observed both in experimental animal and human sepsis, even before development of the adult respiratory distress syndrome. In this article we review several mechanisms that have been invoked for the pulmonary arterial hypertension associated with sepsis (and the adult respiratory distress syndrome): obstruction of the pulmonary microcirculation with microthrombi composed of platelets and leukocytes, and active pulmonary vasoconstriction induced by the autonomous nervous system, hypoxia or vasoactive humoral factors ("mediators"). Some of these mediators, in particular serotonin and arachidonic acid metabolites have been the subject of substantial research and therapeutic manipulation. Since pulmonary arterial hypertension imposes an increased afterload to the right ventricle and because right ventricular dysfunction appears to be a major determinant of the outcome of sepsis, the study of the mechanisms involved in pulmonary arterial hypertension may lead to improved management of sepsis and septic shock.
OBJECTIVE: The single-indicator transpulmonary thermodilution technique (PiCCO system) provides two derived indices of cardiac systolic function: the cardiac function index and the global ejection fraction. We used transesophageal echocardiography to compare theses indices with left ventricular fractional area of change only for patients with no isolated right ventricular dysfunction. (The global cardiac systolic function may be decreased despite preserved left ventricular function in this situation.) DESIGN: Prospective, open, clinical study. SETTING: Intensive care unit (ICU) in a university hospital. PATIENTS: Thirty-three mechanically ventilated patients. INTERVENTION: Left ventricular fractional area of change (LVFAC) was measured using transesophageal echocardiography. The cardiac function index (CFI) and the global ejection fraction (GEF) were determined from transpulmonary thermodilution-derived cardiac output and thoracic volumes. MEASUREMENTS AND MAIN RESULTS: Transesophageal echocardiography identified 3 patients with isolated right ventricular failure (PiCCO underestimated LVFAC in this situation). Significant correlations were established between LVFAC and CFI (r=0.87, n=30, p<0.0001) or GEF (r=0.82, n=30, p<0.0001). The mean differences between measured LVFAC and LVFAC estimated with CFI or GEF were 0.8+/-8.5% (range: -17 to 14%) and 0.8+/-9.0% (range: -21 to 19%), respectively. Area under the receiver operating characteristics curves for the estimation of LVFAC >/=40% using CFI or GEF was 0.92. CFI >4 and GEF >18% estimated LVFAC >/=40% with respective sensitivities of 86 and 88% and specificities of 88 and 79%. Significant correlations were established between changes of LVFAC and CFI/GEF over time. CONCLUSIONS: In mechanically ventilated ICU patients, PiCCO-derived cardiac function index and global ejection fraction provide reliable estimations of LV systolic function but may underestimate it in the cases of isolated right ventricular failure.
One year after total correction of tetralogy of Fallot, reoperation was performed in a 2-year-old infant because of an aneurysm of the right ventricular outflow tract. After removal of the aneurysm, massive right ventricular failure occurred. Maximal medical inotropic support could not reestablish sufficient right ventricular function. Therefore, it was decided to implant the new HIA-Medos system as a right ventricular assist. In the postoperative period, echocardiographic controls showed increasing contractility of the right ventricle. The assist system was removed after 3 days and the infant was discharged in good condition on the 22nd postoperative day.
A 25-year-old male asylum-seeker presented with chest pain, exertional dyspnea, and orthopnea 20 years after the surgical repair of a pentalogy of Fallot. An extracardiac mass compressing the right ventricle was subsequently detected and surgical decompression was performed to relieve the resulting right intraventricular hypertension. At operation, the mass proved to be a coagulase-negative, staphylococcal abscess. In addition, the removal of the mass unmasked a previously nonrecognized pulmonary outflow stenosis that required balloon dilatation and beta-blocker therapy. While infections are known to occur after sternotomy, the formation of an abscess in the anterior mediastinum several years after the intervention appears to be exceptional; this diagnosis came to mind only after the more common complications had been considered, e.g., pseudoaneurysm or pericardial hematoma. To our knowledge, this is the first report of an abscess in the anterior mediastinum that had probably formed over many years following a sternotomy, compressed the right ventricle and masked a pulmonary stenosis.
OBJECTIVE: Intraindividual comparison of right ventricular volumes and function using electron beam computed tomography (EBT) and magnetic resonance imaging (MRI). METHODS: Twenty-seven patients with a known cardiac history were referred for evaluation of ventricular function parameters. The following standardized protocols were used: contrast-enhanced multislice mode EBT and gradient echo sequence MRI. Right ventricular end-diastolic volume (EDV), end-systolic volume (ESV), stroke volume (SV), and ejection fraction (EF) were calculated using a slice summation method. Interobserver variability was calculated. RESULTS: The correlation between the 2 methods was: r = 0.901 for EDV, r = 0.938 for ESV, r = 0.823 for SV, and r = 0.953 for EF. Electron beam computed tomography overestimated EDV and ESV slightly when compared with MRI (P < 0.05). No significant differences (P > 0.05) were found between SV and EF. Mean values determined by EBT and MRI were as follows: 168.6 +/- 62.3 mL and 153.7 +/- 59.1 mL for EDV, 104.7 +/- 60.4 mL and 95.1 +/- 54.8 mL for ESV, 63.2 +/- 19.3 mL and 58.7 +/- 19.8 mL for SV, and 40.2% +/- 14.1% and 40.2% +/- 13.6% for EF, respectively. Interobserver variability ranged between 1.0% and 3.2%. CONCLUSION: Electron beam computed tomography shows good agreement with a close correlation and an acceptable interobserver variability for right ventricular volumes and global function, with a small but significant overestimation of EDV and ESV when compared with MRI.
Long-standing pulmonary insufficiency after repair of tetralogy of Fallot may adversely affect ventricular function. We evaluated 20 patients postoperatively by radionuclide ventriculography and clinical findings after total correction of tetralogy of Fallot. Patients were divided into two groups as follows: Group I patients (10) had no pulmonary insufficiency; Group II patients (10) had moderate or severe pulmonary insufficiency. Preoperatively, there was no difference between groups in terms of age, functional capacity according to the New York Heart Association criteria, hemoglobin and hematocrit level, cardiothoracic ratio, McGoon ratio, left and right ventricular ejection fraction, cardiac output or cardiac index. Postoperatively, right ventricular ejection fraction was 40.10 +/- 2.28 in Group I and 29.5 +/- 2.86 in Group II, p < 0.01. Left ventricular ejection fraction was 59.3 +/- 2.90 in Group I and 50.9 +/- 4.19 in Group II, p < 0.01. Radionuclide ventriculography is a useful means of identifying right ventricular dysfunction following repair of tetralogy of Fallot. The dysfunction appears significantly worse in patients with pulmonary insufficiency.
Right ventricular pressure volume cycles from patients with coronary artery disease were created in order to assess their characteristics and the effects of peak ventricular pressure and right and left artery coronary disease. Thirty-three patients undergoing diagnostic catheterisation for ischaemic heart disease underwent right ventricular catheterisation with a micromanometer and a conductance catheter. Simultaneous pressure and volume signals were recorded and analysed as functions of time, and of each other, forming pressure volume cycles. A total of 19/33 (58%) patients had an abnormal pressure volume loop with a clear end systolic shoulder, and an isovolumic relaxation phase. The mean peak ventricular pressure for all patients was raised (35.2 S.D. 11.8 mmHg), but there was no correlation between indices of shape and peak systolic pressure. Values of dP/dtmax were also raised, but there was no significant difference in this or any other index between patients with left or right coronary artery disease. Thus, in patients with coronary artery disease, the right ventricular pressure volume loop is frequently abnormal in a pattern that is recognised as a feature of an increased ventricular afterload.
BACKGROUND: In patients with the tetralogy of Fallot, QRS prolongation predicts malignant ventricular arrhythmias. QRS prolongation may result from right ventricular dilatation. The relation of ECG markers to biventricular wall mass and volumes has not been assessed. OBJECTIVE: To investigate the relations of surface ECG markers of depolarisation and repolarisation to right and left ventricular volume and biventricular wall mass. METHODS: 37 Fallot patients (mean (SD) age 17 (9) years) were studied 14 (8) years after surgical repair; 34 had important pulmonary regurgitation. Left and right ventricular size was assessed from tomographic magnetic resonance imaging (MRI), and the amount of pulmonary regurgitation by velocity mapping MRI. QT, QRS, and JT duration and interlead dispersion markers were derived from a standard 12 lead ECG. RESULTS: Mean QRS duration was significantly prolonged (133 (31) v 91 (11) ms in controls), as were dispersion of QRS (36 (17) v 20 (6) ms), QT interval (87 (48) v 42 (20) ms), and JT interval (93 (48) v 42 (19) ms). Biventricular volumes were increased (right ventricular end diastolic volume, 129 (41) v 70 (9) ml/m(2); left ventricular end diastolic volume, 83 (16) v 69 (10) ml/m(2)), as was right ventricular wall mass (24 (7) v 17 (2) g/m(2)). QRS duration correlated best with right ventricular mass (r = 0.55, p < 0.01). CONCLUSIONS: In patients operated on for tetralogy of Fallot and with pulmonary regurgitation, ECG predictors of ventricular arrhythmias are influenced by several mechanical factors that may occur simultaneously. These include increased right ventricular volume, but also increases in left ventricular volume and in right and left ventricular wall mass.
To determine whether the overload associated with myocardial infarction and ventricular failure in rats is coupled with activation of DNA synthesis in the remaining left and right ventricular myocytes, flow cytometric analysis was performed on myocyte nuclei prepared from both ventricles 7 and 30 days after coronary occlusion. In addition, oral captopril was administered in separate groups of control and experimental rats to establish whether a relation existed between attenuation of ventricular loading and magnitude of DNA synthesis in myocytes. Results demonstrated that left ventricular failure and right ventricular dysfunction at 7 days after infarction were biventricularly associated with marked increases in the number of myocyte nuclei in the G2M phase of the cell cycle. In contrast, the fraction of nuclei in the G0+G1 phase decreased. In comparison with the earlier time point, the 30-day interval was characterized by a significant magnitude of cardiac hypertrophy, a moderate amelioration of ventricular pump function, and a decrease in the percentage of myocyte nuclei in the G2M phase in both ventricles. However, 30 days after infarction, the number of right ventricular myocyte nuclei in the S and G2M phases remained elevated with respect to control animals. Captopril therapy reduced the extent of ventricular loading and the population of myocyte nuclei in the cell cycle at 7 days. In conclusion, DNA synthesis in myocyte nuclei may represent an important adaptive component of the myocardial response to infarction.
There is a need for a small, simple, and versatile intracorporeal ventricular assist device (IVAD) as an alternative to the large implantable electromechanical LVAD systems in current use. Because the basic design of the Thoratec paracorporeal VAD has been demonstrated in over 1,000 patients, weighing from 17 to 144 kg, and for durations up to 515 days including patient discharge (by using the portable driver), we are developing a new intracorporeal version of our VAD. This IVAD has a smooth contoured, polished titanium housing, and maintains the same blood flow path and Thoralon polyurethane blood pumping sac as the paracorporeal VAD. The IVAD is controlled with the Thoratec TLC-II Portable VAD Driver, which is a small briefcase sized, battery powered, pneumatic control unit. Intracorporeal LVADs and/or RVADs are implanted in a preperitoneal position, with a single small (9 mm OD) percutaneous pneumatic driveline for each VAD. The major advantages of the new IVAD design are size and simplicity. The IVAD weight (339 g) and implanted volume (252 ml) are substantially smaller than current implantable electromechanical LVAD systems. Only the small blood pump is implanted, leaving the more complex control unit external, where it can be serviced and replaced. The versatile design is intended for left and/or right heart support in large or small patients. The IVAD in combination with the TLC-II portable driver will be a viable and attractive alternative to large, implanted electromechanical systems.
OBJECTIVES: Our aim was to determine mechanisms underlying abnormalities of right ventricular (RV) diastolic function seen in heart failure. BACKGROUND: It is not clear whether these right-sided abnormalities are due to primary RV disease or are secondary to restrictive physiology on the left side of the heart. The latter regresses with angiotensin-converting enzyme inhibition (ACE-I). METHODS: Transthoracic echo-Doppler measurements of left- and right-ventricular function in 17 patients with systolic left ventricular (LV) disease and restrictive filling before and 3 weeks after the institution of ACE-I were compared with those in 21 controls. RESULTS: Before ACE-I, LV filling was restrictive, with isovolumic relaxation time short and transmitral E wave acceleration and deceleration rates increased (p < 0.001). Right ventricular long axis amplitude and rates of change were all reduced (p < 0.001), the onset of transtricuspid Doppler was delayed by 160 ms after the pulmonary second sound versus 40 ms in normals (p < 0.001) and overall RV filling time reduced to 59% of total diastole. Right ventricular relaxation was very incoordinate and peak E wave velocity was reduced. Peak RV to right atrial (RA) pressure drop, estimated from tricuspid regurgitation, was 45+/-6 mm Hg, and peak pulmonary stroke distance was 40% lower than normal (p < 0.001). With ACE-I, LV isovolumic relaxation time lengthened, E wave acceleration and deceleration rates decreased and RV to RA pressure drop fell to 30+/-5 mm Hg (p < 0.001) versus pre-ACE-I. Right ventricular long axis dynamics did not change, but tricuspid flow started 85 ms earlier to occupy 85% of total diastole; E wave amplitude increased but acceleration and deceleration rates were unaltered. Values of long axis systolic and diastolic measurements did not change. Peak pulmonary artery velocity increased (p < 0.01). CONCLUSIONS: Abnormalities of RV filling in patients with heart failure normalize with ACE-I as restrictive filling regresses on the left. This was not due to altered right ventricular relaxation or to a fall in pulmonary artery pressure or tricuspid pressure gradient, but appears to reflect direct ventricular interaction during early diastole.
In a 52-year-old man with new onset atrial fibrillation, transthoracic echocardiography showed an isolated, considerably dilated right ventricle. Frequent causes of right ventricular dilatation were ruled out. The image-forming investigation showed an isolated dilation of the ventral part of the heart, which, in combination with a blunt chest trauma 30 years previously, led to a previous cardiac contusion being suspected. In accordance with this hypothesis myocardial scintigraphy showed asymmetric hypertrophy of the right ventricular wall, which is consistent with the remodeling that occurs in response to injured cardiac tissue. After electrical cardioversion sinus rhythm was obtained; the patient remained symptom free.
Operations for certain congenital cardiac lesions can produce pulmonary regurgitation. Pulmonary regurgitation contributes to right ventricular dysfunction, which may cause early postoperative morbidity and mortality. To ameliorate the problems of pulmonary regurgitation during the early postoperative period, we evaluated a method for its acute control. Complete pulmonary valvectomy was performed utilizing inflow occlusion in eight sheep. A catheter with a 15 ml spherical balloon was positioned in the pulmonary arterial trunk; its inflation and deflation were regulated by an intra-aortic balloon pump unit. Blood flow from the pulmonary arterial trunk and forward and regurgitant fraction were determined from electromagnetic flow transducer recordings. The regurgitant fraction with uncontrolled pulmonary regurgitation was 38% +/- 3% (forward flow = 42 +/- 5 ml/beat and regurgitant flow = 16 +/- 2 ml/beat). Inflation of the balloon during diastole was timed to completely eliminate pulmonary regurgitation. This balloon control of pulmonary regurgitation increased pulmonary arterial diastolic pressure from 12 +/- 1 to 17 +/- 1 mm Hg (p less than 0.0001) and decreased pulmonary arterial systolic pressure from 31 +/- 3 to 27 +/- 1 mm Hg (p = 0.06). Pulmonary arterial pulse pressure decreased from 19 +/- 3 to 9 +/- 1 mm Hg (p less than 0.003). Elimination of pulmonary regurgitation decreased right ventricular stroke volume (25 +/- 3 versus 42 +/- 5 ml/beat, p less than 0.0002) and resulted in a 46% reduction in right ventricular stroke work (5.0 +/- 0.6 versus 9.4 +/- 1.0 gm-m/beat, p less than 0.001) with no change in net forward pulmonary artery flow. Thus, acute pulmonary regurgitation can be controlled and this control improves overall hemodynamic status and decreases right ventricular work.