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PubMed1998

Use of Echocardiography in Patients with Congestive Heart Failure.

Echocardiography is used widely to evaluate patients presenting with congestive heart failure (CHF). Because of its unique ability to evaluate left ventricular (LV) size and geometry, LV systolic and diastolic function, right ventricular size and function, heart valves, pericardium, and congenital abnormalities, echocardiography is valuable in establishing a specific cardiac diagnosis, guiding therapy, and assessing prognosis in CHF. Stress echocardiography can be useful in diagnosing underlying coronary artery disease or myocardial viability. Newer techniques such as contrast echocardiography and 3D reconstruction can improve the ability of echocardiography to accurately provide quantitative assessments of chamber sizes, geometry, and function. This review discusses the strengths and limitations of echocardiography in patients with CHF.

Journal Article↗

PubMed2004

Assessment of left ventricular cardiac output by arterial thermodilution technique via a left atrial catheter in a patient on a right ventricular assist device.

Following heart transplantation (HTx) in a 49-year old male, the patient's haemodynamic situation deteriorated in the early postoperative period despite increasing doses of catecholamines. When transoesophageal echocardiography (TEE) showed a dilated right ventricle, but adequate left ventricular (LV) function, a right ventricular assist device (RVAD) was implanted to support the right ventricle of the failing graft. Evaluation of the resulting cardiac output (CO) of the left ventricle and, thus, assessment of the remaining right ventricular function in patients supported by a RVAD is of great clinical interest. In this situation, continuous measurement of LV function, enabling assessment of the remaining right ventricular function, can be performed by pulse contour analysis following initial calibration of the system by arterial thermodilution CO measurement via a left atrial catheter.

Arteries↗

PubMed2001

Right ventricular diastolic function in beta-thalassemia major: echocardiographic and clinical correlates.

BACKGROUND: Cardiac hemochromatosis remains the most frequent cause of death in beta-thalassemia major. Previous studies suggest an important right ventricular (RV) contribution to cardiac morbidity and mortality. Studies with Doppler echocardiography have shown contradictory results regarding left ventricular (LV) filling, whereas the RV filling characteristics have not been studied yet. We prospectively studied the pattern of RV filling and investigated echocardiographic and clinical correlates during baseline and follow-up examinations in patients with beta-thalassemia major. METHODS AND RESULTS: The study included 79 patients, aged 24.2 +/- 8.0 years, with homozygous beta-thalassemia major without symptoms of heart failure with normal LV function and 51 healthy control subjects, matched for age, sex, and body surface area. Doppler echocardiographic indexes of systolic and diastolic ventricular function were assessed. Hemodynamic measurements were obtained in 8 patients by right heart catheterization. An abnormal RV relaxation pattern was evident in the patient group. The LV filling characteristics indicated increased preload without abnormal alteration, whereas catheterization findings were consistent with a high cardiac output state. Short tricuspid deceleration time (DT) had the best predictive value for subsequent cardiac events. Repeat echocardiographic study in 35 asymptomatic patients at 19 +/- 7 months demonstrated deterioration of LV systolic function, chamber enlargement, and shortening of DT of tricuspid and mitral inflow. CONCLUSIONS: In patients with homozygous beta-thalassemia major without cardiac disease, the pattern of RV filling is abnormally altered, indicating impaired relaxation. In contrast, the LV filling is compatible with increased preload, as in chronic anemia. Short DT of early tricuspid inflow carries important prognostic value. LV remodeling occurs over time along with transition toward a restrictive ventricular filling pattern.

Adolescent↗

PubMed1985

Prostaglandin E1. A new therapy for refractory right heart failure and pulmonary hypertension after mitral valve replacement.

Patients undergoing mitral valve replacement, particularly those with severe pulmonary hypertension and/or congestive heart failure, may develop life-threatening right heart failure in the immediate postbypass period. We have observed that such patients have intense pulmonary vasoconstriction. The markedly increased pulmonary impedance may aggravate the right heart failure and prevent recovery of right ventricular function in this setting. Therefore, we studied the effects of high-dose prostaglandin E1 (30 to 150 ng/kg/min), a potent pulmonary vasodilator, in combination with massive infusion of norepinephrine (up to 1 microgram/kg/min) into the left atrium in five consecutive patients with refractory right heart failure and pulmonary hypertension after mitral valve replacement. This pharmacologic approach takes advantage of the pulmonary vasodilating effects of prostaglandin E1, while offsetting associated systemic vasodilation and resulting hypotension. All five patients had rapid pulmonary vasodilator responses followed by marked improvement in right ventricular function. All survived the operation and none had right ventricular infarction or chronic right heart failure postoperatively.

Adult↗

PubMed1979

Relationships between hemodynamic profiles and topography of acute myocardial infarction.

Initial hemodynamics were studied in 101 patients with acute myocardial infarction complicated by shock or left heart failure. 59 had anterior myocardial infarction (AMI); 42 had inferior myocardial infarction (IMI). Data were processed by univariate analysis and correspondence analysis. AMIs and IMIs were significantly different on conduction disturbances, heart rate, left ventricular filling pressure, mean pulmonary artery pressure and right ventricular function indices. Both patients and parameters were projected on the most meaningful factorial plane generated by correspondence analysis. This two-dimensional graphical representation showed that all the information was roughly distributed along the 2 orthogonal axes defining this plane. Survivors and nonsurvivors were fairly well separated along the first factorial axis (prognostic axis) which was highly correlated with both outcome and left ventricular function parameters. AMIs and IMIs were grossly separated along the second factorial axis (topographical axis) which was rather well correlated with location and right ventricular function parameters. These studies suggest that AMI and IMI hemodynamic profiles are modulated by the presence or absence of right ventricular dysfunction. Moreover right ventricular dysfunction may be held responsible of some lack of information about left ventricular function status.

Acute Disease↗

PubMed1995

Right ventricular diastolic function 15 to 35 years after repair of tetralogy of Fallot. Restrictive physiology predicts superior exercise performance.

BACKGROUND: We have shown previously that transient right ventricular restriction after tetralogy of Fallot repair prolongs postoperative course. This is a prospective study of right ventricular diastolic performance in late follow-up patients. METHODS AND RESULTS: We studied biventricular function, using Doppler echocardiographic examination. Pulmonary arterial, tricuspid, and mitral valves and superior vena cava Doppler spectrals were obtained in 41 patients (mean age, 28.8 years), 15 to 35 years (mean, 23.6) after complete repair of tetralogy of Fallot. Patients were considered to have evidence of right ventricular restriction if antegrade diastolic flow was detected in the main pulmonary artery, coinciding with atrial systole (A wave), throughout the respiratory cycle. Exercise function was measured by graded treadmill testing with respiratory mass spectrometry. Three patients were excluded because of pulmonary outflow obstruction (Doppler gradient > 40 mm Hg) or residual intracardiac shunts. Of the 38 patients, 37 were in sinus rhythm. Twenty (52.6%) had definite evidence of restriction with an A wave in the pulmonary artery, augmented during inspiration. In all 20 cases, there was superior vena caval flow reversal with atrial systole. Both inspiratory and expiratory transtricuspid E-wave deceleration time was significantly shorter in the restrictive group (P < .003 and P < .03, respectively). All patients had Doppler evidence of pulmonary regurgitation, but its duration was shorter in the restrictive group (P < .01) during inspiration. Cardiothoracic ratio was significantly lower in the restrictive group (P < .01), suggesting less severe pulmonary regurgitation. Both restrictive and nonrestrictive groups had reduced exercise MVO2 compared with healthy age- and sex-matched control subjects, but those with restrictive physiology had significantly better maximum oxygen uptake than the nonrestrictive group (P < .001). CONCLUSIONS: Isolated right ventricular restriction late after tetralogy of Fallot repair is common. Although it reflects abnormal hemodynamics, the A wave contributes to forward pulmonary arterial flow and shortens the duration of pulmonary regurgitation. Consequently, there is less cardiomegaly and improved exercise performance in those patients.

Adolescent↗

PubMed1991

Single-lung transplantation for pulmonary hypertension. Three-month hemodynamic follow-up.

BACKGROUND: Shorter waiting times, relative technical simplicity, and satisfactory application to a broad spectrum of patients has made single-lung transplantation an attractive option in the treatment of patients with end-stage pulmonary hypertension. METHODS AND RESULTS: Seven patients with pulmonary hypertension underwent single-lung transplantation. Simultaneous closure of associated atrial septal defects was accomplished in two patients. Despite severely compromised pretransplant right ventricular function in all patients, there was no early or late mortality. Right ventricular functional recovery as characterized by hemodynamic assessment before and at a mean of 13 weeks posttransplant was nearly uniform and characterized by a drop in 1) pulmonary arterial systolic pressure from 92 +/- 7 mm Hg to 29 +/- 6 mm Hg (p = 0.001), 2) central venous pressure from 10 +/- 6 mm Hg to 1 +/- 2 mm Hg (p = 0.02), and 3) pulmonary vascular resistance index from 1,924 +/- 663 to 232 +/- 73 dyne.sec.cm-9 (p = 0.001). Radionuclide ventriculography before and at a mean of 17 weeks posttransplant documented a significant (p = 0.006) increase in right ventricular ejection fraction from 22 +/- 15% to 51 +/- 11%. Quantitative pulmonary perfusion scintigraphy at a mean of 17 weeks posttransplant demonstrated a significant (p = 0.001) increase in perfusion to the transplanted lung from 56 +/- 6% to 89 +/- 7%. There was a concomitant, slight but significant (p = 0.004) decrease in ventilation to the transplanted side from 56 +/- 6% to 49 +/- 8%. After transplantation, all patients returned to New York Heart Association functional class I or II from their preoperative levels of class III or IV. CONCLUSIONS: These early follow-up data cautiously support the option of single-lung transplantation in patients with pulmonary hypertension, although long-term durability of these hemodynamic changes deserves documentation before widespread application.

Follow-Up Studies↗

PubMed1987

Right ventricular dysfunction and the exercise limitation of chronic obstructive pulmonary disease.

This study examined right ventricular function during exercise in patients with chronic obstructive pulmonary disease to answer the following questions: Is there a significant correlation between oxygen consumption at maximal exercise and exercise right ventricular ejection fraction? Does the right ventricular ejection fraction response to exercise correlate with exercise changes in pulmonary artery pressure, total pulmonary resistance or pulmonary vascular resistance? Which combinations of cardiac, ventilatory and blood gas variables are the best predictors of oxygen consumption at maximal exercise? Twenty-six patients with stable chronic obstructive pulmonary disease performed symptom-limited supine bicycle exercise with simultaneous hemodynamic and radionuclide ventriculographic measurements. The oxygen consumption at maximal exercise correlated with the exercise right ventricular ejection fraction (n = 21, r = 0.66; p less than 0.005), exercise stroke volume (r = 0.68; p less than 0.001), exercise cardiac output (r = 0.77; p less than 0.00005) and exercise ventilation (r = 0.85; p less than 0.00001). The change in right ventricular ejection fraction from rest to exercise correlated inversely with the change from rest to exercise in total pulmonary resistance (r = -0.51; p less than 0.05) but not with the change in mean pulmonary pressure (r = -0.37) or in pulmonary vascular resistance (r = 0.09). Multivariate analysis showed that the variables giving the highest combined correlation with oxygen consumption were ventilation and right ventricular ejection fraction (r = 0.95, adjusted r2 = 0.88). These results suggest that exercise oxygen consumption of patients with chronic obstructive pulmonary disease is related to right ventricular systolic function, exercise right ventricular dysfunction is related, in part, to abnormal exercise total pulmonary resistance, and exercise limitation in chronic obstructive pulmonary disease occurs as a result of the dynamic interaction between disordered right heart function and ventilation.

Adult↗

PubMed1984

[Left ventricular function in patients with right ventricular overload evaluated by exercise echocardiography: comparison of pulmonary hypertension and atrial septal defects].

To evaluate left ventricular function in patients (pts) with right ventricular overload, exercise echocardiographic studies using a bicycle ergometer were performed for seven pts with pulmonary hypertension (PH), two with cor pulmonale (CP) and 16 with atrial septal defects (ASD), and the results were compared with those of 10 (control I) and 27 (control II) normal persons. These subjects were categorized in two study groups; study I consisting of PH, CP and control group I with an exercise workload of 25 watts for 3 min; and study II consisting of ASD and control group II with an exercise workload of 50 watts for 3 min. The results were as follows: M-mode echocardiography revealed that: During exercise, the stroke volume (SV) was increased with a significant decrease of left ventricular end-systolic dimension (LVDs), but without a change in left ventricular end-diastolic dimension (LVDd) in control groups I and II, with a marked increase of LVDd and a slight decrease of LVDs in the ASD group. By contrast, the SV in the PH group tended to decrease during exercise with a slight decrease of LVDd, but without a significant change in LVDs. Right ventricular dimension (RVD) was significantly increased during exercise in the PH group, but was decreased in the ASD group. In control groups I and II, RVD did not change during exercise. In ASD, and control groups I and II, the peak velocity of circumferential fiber shortening (Vcf) was increased during exercise, and the peak negative Vcf was significantly decreased. However, these parameters exhibited impaired responses during exercise in the PH group. Abnormal interventricular septal (IVS) motion at rest tended to become normal during exercise in 12 of 16 pts with ASD. In all pts with PH, however, IVS motion did not change substantially during exercise. There were similar parameter responses between the PH and CP groups. Two-dimensional echocardiography showed that: The left ventricular short-axis view demonstrated a diastolic left ventricular configuration which changed from oblique to relatively circular orientation during exercise in the ASD group. In four of five pts with PH, the diastolic configuration of the left ventricle was oblique because of a loss of the normal curvature of the IVS at rest and during exercise. The diastolic left ventricular configuration improved during exercise in only one pt with PH, with slightly elevated pulmonary arterial systolic pressure as in the ASD group.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗

PubMed2005

The right ventricle in pulmonary hypertension.

Pulmonary arterial hypertension (PAH) is a term used to classify a variety of conditions that share in common an injury to the pulmonary vasculature that produces elevations in pulmonary arterial pressure. However, it is the integrity of right ventricular function, rather than the degree of vascular injury, that is the major determinant of symptoms and survival in PAH. The article will review the normal structure and function of the right ventricle and summarize the impact of PAH and its treatments on right ventricular function.

Bosentan↗

PubMed1989

Right ventricular performance after monocrotaline-induced pulmonary hypertension.

Chronic pulmonary hypertension leads to a compensatory hypertrophy of the right ventricle (RV). Performance of the hypertrophied heart has been shown to vary depending on the type and severity of the overload, the species, age, and sex of the animal in which the hypertrophy is induced and the ventricle to which the overload is applied (left ventricle vs. right ventricle). In this study we employed two novel approaches to examine the performance of the hypertrophied right ventricle in male Sprague-Dawley rats. First, monocrotaline (MCT), a pyrrolizidine alkaloid isolated from the plant Crotalaria spectabilis, was used to noninvasively induce chronic pulmonary hypertension, RV pressure overload, and RV hypertrophy. After 5 wk the RV-to-(left ventricle + septum) ratio was increased by 94% over control. The volume of isolated right ventricular myocytes from MCT-treated rats was increased due primarily to an increase in cell cross-sectional area. Second, a stable, isolated, working heart preparation, normally used to study left ventricular function, was modified to study right ventricular function. In vitro ventricular performance of severely hypertrophied hearts was elevated compared with control hearts at all preloads. Significant elevations in positive and negative maximum pressure development (dP/dtmax) suggested that both the rate of pressure development and the rate of relaxation were enhanced. Coronary flow and RV-diastolic pressure were similar in the MCT and control group. Thus RV hypertrophy caused by a chronic pressure overload induced by MCT resulted in enhanced ventricular performance with no evidence of failure.

Animals↗

PubMed2004

[MR imaging and arrhythmogenic right ventricular dysplasia (ARVD)].

Arrhythmogenic right ventricular dysplasia (ARVD) is a cardiomyopathy of unknown etiology responsible for 20% of cases of sudden death in young adults secondary to arrhythmia. It is characterized histologically by fatty or fibro-fatty infiltration of the right ventricular myocardium. Diagnostic criteria have been proposed for diagnosing ARVD. Imaging, especially MRI, plays an important role. MR imaging must be performed using cardiac gating, and should include both cine-MR sequences for evaluation of segmental and global right ventricular function or any morphological change of the right ventricular shape, and anatomic sequences to detect fatty or fibro-fatty infiltration of the right ventricular myocardium.

Adult↗

PubMed2002

Quantification of regional right and left ventricular function by ultrasonic strain rate and strain indexes after surgical repair of tetralogy of Fallot.

The quantification of regional myocardial function in tetralogy of Fallot (TOF) by conventional M-mode and 2-dimensional echocardiography is difficult because of the complex right ventricular (RV) and altered left ventricular (LV) geometry. In 30 asymptomatic postoperative TOF patients (aged 4 to 16 years) with a low pressure in the right ventricle and with varying degrees of pulmonary regurgitation and in 30 aged-matched healthy children, the ultrasonic-derived regional deformation parameters peak systolic strain rate (SR) and systolic strain (epsilon) were acquired from ventricles and compared. In TOF RV free walls, SR, and epsilon were reduced in the basal, mid-, and apical segments and averaged -1.5 +/- 0.6 second(-1) for SR and -22 +/- 8% for epsilon, respectively (p <0.001 vs normals). Peak systolic SR of the basal RV free wall correlated significantly with the QRS duration of the electrocardiogram (r = 0.81, p <0.0001). Abnormalities in RV deformation were more marked in patients with transannular patches versus infundibular patches. In the septum there was a homogeneous reduction in SR and epsilon in the basal, mid-, and apical segments. These averaged -1.4 +/- 0.3 second(-1) for SR and -19 +/- 4% for epsilon, respectively (p <0.01 vs normals). Longitudinal SR and epsilon values of the 3 LV lateral wall segments (averaged SR = -1.6 +/- 0.4 second(-1), averaged epsilon = -20 +/- 5%; p <0.05 vs normals), and radial SR and epsilon of the LV posterior wall (SR = 3.3 +/- 0.9 second(-1); epsilon = 51 +/- 14%; p <0.05 vs normals) were significantly reduced. Thus, abnormalities in regional RV and LV systolic myocardial function in asymptomatic postoperative TOF patients were quantified by the deformation parameters SR and epsilon. RV deformation abnormalities are associated with electrical depolarization abnormalities.

Adolescent↗

PubMed2003

[The arrhythmogenic right ventricular cardiomyopathy (ARVC)].

The following report illustrates the case of a 40-year old patient, who was transferred to our hospital because of a symptomatic sustained ventricular tachycardia (VT). The documented VT showed typical left bundle branch block morphology with an inferior axis, which was accompanied by repolarization abnormalities in the right precordial leads, as revealed by the surface ECG. While coronary angiography allowed the exclusion of an obstructive coronary heart disease and confirmed an intact left ventricular function, the right ventricular angiography as well as the MRI demonstrated not only reduced right ventricular function but also regional abnormalities of contraction in the inferior and diaphragmal regions and typical "outpouchings" and "bulgings". The MRI also provided evidence for sporadic fatty infiltrations of the right ventricle. In the electrophysiological study, sustained VT could be reproducibly induced, while showing the typical RVOT configuration, which corresponded to the clinically apparent VT. Since these examination results matched with the criteria of McKenna et al., arrhythmogenic right ventricular cardiomyopathy was diagnosed. The patient underwent implantation of a cardioverter-defibrillator (ICD) and medical treatment with metoprolol. This particular case report was selected because it shows a typical presentation of an ARVC. Furthermore, the present example offers the possibility of demonstrating that in the case of an ARVC in the regions of the right ventricle, arrhythmogenic areals can also be found which seem morphologically inconspicuous.

Adult↗

PubMed1996

[Hemodynamic changes induced by apnea test in patients with brain death].

OBJECTIVE: In France, an apnoea test is compulsory to confirm brain death. This test results in a major hypercarbia and respiratory acidosis. This study aimed to assess haemodynamic changes elicited by the apnoea test. STUDY DESIGN: Prospective clinical study. PATIENTS: Fifteen patients with brain death METHODS: Before the apnoea test, the lungs were ventilated with pure oxygen for 20 minutes. Thereafter, the test was conducted with continuous oxygen flow through the endotracheal tube, and SpO2 monitoring. Blood gases and haemodynamic parameters, including systemic arterial pressure, pulmonary artery pressure, pulmonary artery occlusion pressure, cardiac index and right ventricular function parameters were assessed before, during and 20 minutes after the apnoea test. Mean values at the various times were compared. RESULTS: Hypercarbia and acidosis induced a major pulmonary hypertension and an increase in cardiac output, associated with a decrease in systemic vascular resistances. Despite pulmonary hypertension and acidosis, right ventricular function was maintained. All haemodynamic modifications were reversed by reventilation. CONCLUSION: Apnoea test induces a reversible pulmonary hypertension that is seemingly not deleterious for right ventricular function. Apnoea test probably does not alter viability of the donor's organs.

Acidosis, Respiratory↗

PubMed2005

Assessment of right and left ventricular function by tissue Doppler echocardiography in patients after biventricular repair of pulmonary atresia with intact ventricular septum.

BACKGROUND: Survival of patients with PAIVS has improved significantly with adoption of a selective management approach based on RV and coronary arterial anatomy. We sought to determine the right (RV) and left ventricular (LV) function of patients with pulmonary atresia and intact ventricular septum (PAIVS) long-term after biventricular repair. METHODS: The regional ventricular function of 22 patients (11 males) aged 12.8+/-5.6 years with PAIVS after biventricular repair was assessed by tissue Doppler echocardiography (TDE). The results were compared to those of 22 age-matched controls. RESULTS: When compared with controls, patients had significantly reduced myocardial tissue velocities, systolic and diastolic strain rate, and peak systolic strain in the basal, mid-, and apical segments of the RV free wall, interventricular septum and LV lateral wall (all with p<0.01). Heterogeneity of systolic and diastolic strain rate was observed in the RV free wall and interventricular septum in patients but not in controls. CONCLUSION: Impairment of RV and LV regional longitudinal myocardial function occurs in patients with PAIVS late after biventricular repair.

Adolescent↗

PubMed2004

Regional right and left ventricular function after the Senning operation: an ultrasonic study of strain rate and strain.

BACKGROUND: Systemic right ventricular dysfunction is a major concern in the follow-up of patients who underwent an atrial redirection procedure for transposition (concordant atrio-ventricular and discordant ventriculo-arterial connections). No good non-invasive method is currently available for quantifying right ventricular function. AIMS: We have used ultrasonically based imaging of strain rate and strain to quantify regional deformation in the right ventricle after the Senning operation, comparing properties of regional deformation of the right ventricle with right ventricular ejection fraction as measured using magnetic resonance imaging. METHODS: In 20 asymptomatic patients who had undergone the Senning procedure, we measured peak systolic strain rate and systolic strain values in the right ventricular free wall, the septum and the left ventricular lateral wall using colour Doppler myocardial imaging, comparing the data with findings obtained in 30 healthy subjects. Global right ventricular ejection fraction was assessed using magnetic resonance imaging. RESULTS: Properties of deformation of the right ventricular free wall were reduced and homogeneous after the Senning procedure compared to normals, with significantly lower values for peak systolic strain rate and systolic strain (-1.1 +/- 0.4 vs. -2.5 +/- 0.9 s(-1); p < 0.05 and -16 +/- 7% vs. -38 +/- 13%; p < 0.05, respectively). There was a significant correlation between regional longitudinal right ventricular systolic strain values and right ventricular ejection fraction (r = -0.87, p < 0.001). In the septum, peak systolic strain rate was again reduced and homogeneous (-1.2 +/- 0.4 vs. -1.8 +/- 0.5 s(-1); p < 0.05 vs. normals). Also in the left ventricle, the lateral wall peak systolic strain rate and systolic strain values were reduced (-1.5 +/- 0.5 vs. -2.1 +/- 0.9 s(-1); p < 0.05 and -20 +/- 6% vs.-25 +/- 9%; p < 0.05, vs. normals, respectively). CONCLUSIONS: Properties of regional longitudinal deformation of the systemic right ventricle are reduced after the Senning procedure compared to normal controls, and correlate well with global right ventricular performance. These findings suggest that ultrasonic strain rate and strain imaging could be used in the non-invasive follow-up of ventricular function in these patients.

Adolescent↗

PubMed2002

Improved right heart function after myocardial preservation with 2,3-butanedione 2-monoxime in a porcine model of allogenic heart transplantation.

BACKGROUND: Right heart dysfunction is a major cause for early morbidity and mortality after heart transplantation. Experiments were designed to evaluate the influence of the calcium-desensitizing drug 2,3-butanedione 2-monoxime (BDM) on right heart function in a porcine model of heart transplantation. METHODS: Donor hearts of domestic pigs were arrested with BDM in Krebs solution (n = 7) and with BDM in Bretschneider's histidine-tryptophan-ketoglutarate (HTK) solution (n = 6). There were 2 control groups: University of Wisconsin (UW, n = 6) and HTK (n = 6). An isovolumic model was used in which the right ventricular volume was precisely controlled in vivo with an intracavitary high-compliance balloon. After 4 hours of ischemia, hearts were transplanted into recipients. After 1 and 2 hours of reperfusion, the right ventricular balloon volume was increased in 10-mL increments until right ventricular failure occurred and the developed pressures were recorded. RESULTS: Maximal right ventricular developed pressures were significantly different after 2 hours of reperfusion (UW: 35 +/- 13 mm Hg; HTK: 47 +/- 8 mm Hg; Krebs+BDM: 49 +/- 9 mm Hg; HTK+BDM: 50 +/- 6 mm Hg; P =.04). Hearts subjected to BDM could be loaded with a significantly increased volume after 1 hour and after 2 hours (UW: 57 +/- 10 mL vs HTK: 43 +/- 8 mL vs Krebs+BDM: 70 +/- 10 mL vs HTK+BDM: 67 +/- 15 mL; P =.002). Postischemic right ventricular enddiastolic compliance was significantly increased in groups treated with BDM after 1 hour (P =.02) and after 2 hours (P =.039). CONCLUSIONS: The drug BDM significantly improves right ventricular function in a heart transplantation model. The increase in volume load and developed right ventricular pressure achieved by BDM application would translate into a decreased risk of right ventricular failure after clinical transplantation.

Adenosine↗