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PubMed2004

Right ventricular systolic function and the manner of transformation of the right ventricle in patients with dilated cardiomyopathy.

BACKGROUND: Dilated cardiomyopathy (DCM) is generally considered to be accompanied by both left and right ventricular dysfunction, but most studies only analyze the left ventricular function. METHODS AND RESULTS: Biplane right ventriculography was performed in 13 control subjects and 13 patients with DCM and New York Heart Association functional class II. Three dimensions of the right ventricle (RV) (the long axis dimension (LA), the anterior - posterior dimension (AP), and the septum -free wall dimension (SF)) and 2 dimensions of the left ventricle (LV) (LA and AP) were examined to assess regional function. The group with DCM had a lower stroke volume index and RV ejection fraction. In the RV dimensional analysis, the group with DCM had a smaller SF and a larger AP at end-diastole, and larger AP and LA at end-systole. There was a significant linear negative correlation between SF of RV and AP of LV at end-diastole. CONCLUSION: In clinically well-controlled cases of DCM, RV systolic function is depressed, and the RV is compressed by the LV, becoming less thick than in the controls. This transformation results from some parallel interaction between the RV and a markedly enlarged LV.

Adolescent↗
PubMed2000

Role of the etiology of cardiomyopathies on exercise capacity and oxygen consumption in patients with severe congestive heart failure.

Peak oxygen consumption is of great importance for the decision of heart transplantation in congestive heart failure. Moreover, the level of exercise capacity seems to depend on the etiology of congestive heart failure. This study compared 14 heart failure patients with idiopathic dilated cardiomyopathy (group 1) to 14 heart failure patients with cardiomyopathy due to ischemic heart disease (group 2), matched for sex (13 male, one female in each group), age +/-10 years, left ventricular ejection fraction +/-5% and pulmonary artery mean pressure +/-5 mm Hg, to assess exercise capacity and oxygen consumption independently of the age, sex and the level of left ventricular dysfunction. Right ventricular function was also assessed. No difference existed in terms of right ventricular parameters. Maximal exercise parameters were significantly higher in group 1 than in group 2. Peak oxygen consumption was statistically higher in group 1 than in group 2. In the whole population, a significant correlation was found between peak oxygen consumption and right ventricular ejection fraction (r=0. 44, P<0.02) but not between peak oxygen consumption and left ventricular ejection fraction. For similar levels of left ventricular dysfunction, exercise capacity and oxygen consumption appear to be better in idiopathic dilated cardiomyopathy than in ischemic cardiomyopathy, thereby suggesting that functional tolerance of left ventricular dysfunction might depend on the etiology of severe congestive heart failure.

Cardiomyopathies↗
PubMed2000

Early effects of right ventricular volume overload on ventricular performance and beta-adrenergic signaling.

OBJECTIVE: Right ventricular dysfunction is a poorly understood but persistent clinical problem. This study was undertaken to evaluate ventricular performance and beta-adrenergic receptor signaling in a tricuspid regurgitation model of right ventricular overload. METHODS: Seventeen dogs were chronically instrumented with epicardial dimension transducers. By means of the shell-subtraction model, right ventricular pressure-volume relationships were evaluated in normal and right ventricular overload states. Right ventricular chamber performance was quantified by the stroke work at an end-diastolic volume relationship. RESULTS: Right ventricular volume overload caused a 28% +/- 11% and 31% +/- 9% decline in chamber performance acutely and at 1 week, respectively, whereas end-diastolic volume increased from 45 +/- 21 to 60 +/- 30 mL (P =. 019). beta-Adrenergic receptor signaling in myocardial samples was assessed, examining adenylyl cyclase and G-protein-coupled receptor kinase activity. Stimulated adenylyl cyclase activity significantly decreased, and G-protein-coupled receptor kinase activity significantly increased in both left and right ventricular samples caused by increased levels of beta-adrenergic receptor kinase 1. No change in beta-adrenergic receptor density was seen at 1 week. CONCLUSIONS: Early right ventricular overload is associated with impaired right ventricular chamber contractility, dilation, and, importantly, a biventricular alteration of beta-adrenergic receptor signaling.

Adenylyl Cyclases↗
PubMed1996

[Echocardiographic analysis of cardiac size and function in patients with severe obstructive sleep apnea].

The purpose of this study was to determine usefulness of non invasive echocardiographic measurements in patients with severe obstructive sleep apnea (OSA). Diagnosis of OSA was established by polysomnography. We investigated 18 patients (16M, 2F), mean age 45 +/- 10 years, mean weight 114 +/- 16 kg and mean apnea/hypopnea index 69 +/- 23. Two-dimensional (2D) and Doppler echocardiography (DOP) was used to assess: 1. Systolic function of left ventricle by determination of cardiac output (CO), ejection fraction (EF), 2. Diastolic function of left ventricle by calculation of mitral early diastolic velocity to arterial velocity ratio (Ev/Av) and atrial flow to total mitral flow ratio (AF/Tf), 3. Right ventricle thickness in systole (RVWS) and diastole (RVWD), and its diastolic diameter (RVD), 4. Pulmonary arterial pressure (PAP) by evaluation of acceleration time in the pulmonary artery (ACT) and tricuspid regurgitation jet velocity (TR). Results (mean +/- SD): Co 6.67 +/- 2.0 L/min, EF 44 +/- 5.6%, RVWS 10.9 +/- 1.3 mm, RVWD 6.7 +/- 1.1 mm, RVD 30.3 +/- 2.8 mm, Ev/Av 1.22 +/- 0.39, Af/Tf 0.38 +/- 0.11, AcT 121.4 +/- 20.3 ms. These data confirm that intermittent hypoxia and increased ventricular afterload cause both systolic and diastolic left ventricular dysfunction. Right ventricular hypertrophy found despite normal resting, wake, PAP could be probably attributed to transient pulmonary hypertension during repeatable nocturnal hypoxic episodes.

Adult↗
PubMed1999

Late results of Senning operation.

OBJECTIVES: Few data exist for long-term results after the Senning operation for transposition of the great arteries. Sinus node dysfunction and systemic ventricular dysfunction have been the main problems. We evaluated risk factors for late death and the incidence of late death, sinus node dysfunction, and right ventricular dysfunction in 100 patients. METHODS: The study was a retrospective analysis with a mean follow-up time of 12.8 +/- 3.1 years. No patients were lost to follow-up. Patients were divided in 2 groups according to ventricular septal defect (73 simple, 27 complex). The electrocardiogram, ambulatory electrocardiogram, echocardiogram, and chest radiograph were reviewed for each patient. RESULTS: The overall mortality rate was 10%. The actuarial survival was 90% (simple) and 78% (complex); the probability of staying in sinus rhythm was 34% and 7%, and the probability of normal right ventricular function was 52% and 39%, respectively, 15 years after operation. The incidence of sinus node dysfunction increased gradually over time, although the incidence of right ventricular dysfunction increased rapidly after 10 years of follow-up. Late deaths, arrhythmias, and right ventricular dysfunction were significantly more frequent in the complex group. Right ventricular dysfunction and active arrhythmias were risk factors for late death. CONCLUSION: Long-term follow-up after the Senning operation shows increasing incidence of sinus node dysfunction and right ventricular dysfunction over time. Deteriorating right ventricular function is a major concern. Its early recognition and initiation of appropriate management to preserve cardiac function is an important follow-up goal.

Actuarial Analysis↗
PubMed1999

Echocardiographic features of primary, secondary and familial amyloidosis.

BACKGROUND: Currently recognized types of amyloidosis include primary, familial and secondary, each of which may affect the heart. There may be differences in the heart response to the deposition of amyloid fibrils in these three forms of the disease. MATERIALS AND METHODS: Over a period of 10 years (1985-95), 28 consecutive patients with primary, 11 with secondary and 17 with familial amyloidosis were studied at the Departments of Cardiology of Laiko and Hammersmith Hospitals. The diagnosis of amyloidosis was confirmed by biopsies of subcutaneous fat, rectum, kidney, bone marrow, gum or sural nerve. Diagnosis of cardiac involvement was based on typical electrocardiographic and echocardiographic findings. RESULTS: The left ventricular fractional shortening (%) was reduced in primary compared with familial or secondary amyloidosis (29.8 +/- 10.2 vs. 36.2 +/- 6.5 vs. 36 +/- 5.9, P < 0.05). The transmitral flow velocity pattern was compatible with abnormal relaxation in most patients in the three groups [primary 16 (57%), familial 11 (64. 7%), secondary 6 (54.5%), P = NS]. Right ventricular systolic dysfunction (right ventricular dP/dt < 220 mmHg s-1 or tricuspid annulus systolic excursion < 10 mm) was present in 8 (28.6%), 2 (11. 8%) and 0 patients. Patients with primary amyloidosis were followed up for 15 +/- 6 months. There were 12 deaths, and repeat echocardiography in the survivors revealed a significant deterioration of left ventricular systolic function (fractional shortening = 23.6% +/- 8.8%, P < 0.05 vs. baseline). CONCLUSION: Primary amyloidosis is characterized by more severe cardiac involvement than the familial or secondary amyloidosis and has an ominous course.

Adult↗
PubMed1993

Cardiac involvement in Becker muscular dystrophy.

OBJECTIVES: The purpose of this study was to assess the incidence of myocardial involvement and the relation of cardiac disease to the molecular defect at the deoxyribonucleic acid (DNA) or protein level in Becker muscular dystrophy. BACKGROUND: Dystrophin gene mutations produce clinical manifestations of disease in the heart and skeletal muscle of patients with Becker muscular dystrophy. METHODS: Thirty-one patients underwent electrocardiographic and echocardiographic examination and 24-h Holter monitoring. The diagnosis was established by neurologic examination, dystrophin immunohistochemical assays or Western blot on muscle biopsy, or both, and DNA analysis. RESULTS: Electrocardiographic and echocardiographic findings were abnormal in 68% and 62% of the patients, respectively. Right ventricular involvement was detected in 52%. Left ventricular impairment was observed either as an isolated phenomenon (10%) or in association with right ventricular dysfunction (29%). Right ventricular disease was manifested in the teenagers, and an impairment of the left ventricle was observed in older patients. Right ventricular end-diastolic volumes were significantly increased compared with those in a control group. The left ventricular ejection fraction was significantly lower in older patients than in control subjects or younger patients. Life-threatening ventricular arrhythmias were detected in four patients. No correlations were found between skeletal muscle disease, cardiac involvement and dystrophin abnormalities. In our patients, exon 49 deletion was invariably associated with cardiac involvement. Exon 48 deletion was associated with cardiac disease in all but two patients. CONCLUSIONS: The cardiac manifestation of Becker muscular dystrophy is characterized by early right ventricular involvement associated or not with left ventricular impairment. Exon 49 deletion is associated with cardiac disease.

Adolescent↗
PubMed2005

Transthoracic echocardiographic predictors of left atrial appendage thrombus.

Transesophageal echocardiography (TEE) is commonly performed to detect the presence of a left atrial appendage (LAA) thrombus in the setting of an embolic event or before an anticipated electrical cardioversion for atrial fibrillation. The predictive value of transthoracic echocardiographic (TTE) findings in these patients has not been well defined. This study evaluated whether TTE findings can predict LAA thrombi using TEE as the gold standard for the identification of LAA thrombi. From November 1995 to March 2003, 10,753 patients underwent TEE to exclude LAA thrombi after embolic events or before cardioversion. Of these, 3,768 patients had complete TTE examinations performed <2 weeks before undergoing TEE. Demographics, TTE, and cardiac rhythm variables were analyzed using univariate and multivariate logistic regression to identify predictors of LAA thrombi diagnosed on subsequent TEE. LAA thrombi were identified by TEE in 199 patients (5.3%). Several TTE variables predicted LAA thrombi by TEE, including mitral stenosis, atrial fibrillation, tricuspid regurgitation, valvular prosthesis, left ventricular dysfunction, and right ventricular dysfunction. Mitral regurgitation was associated with a reduced risk for LAA thrombi (odds ratio 0.61, p = 0.003). A structurally normal heart in sinus rhythm (n = 247, 6.9%) had a 100% negative predictive value for LAA thrombi. In conclusion, several TTE variables were found to be predictive of LAA thrombi. The likelihood of LAA thrombi being found on TEE was infinitely small in the absence of these variables and the presence of sinus rhythm.

Aged↗
PubMed2002

Usefulness of B-type natriuretic peptide levels in predicting hemodynamic perturbations after heart transplantation despite preserved left ventricular systolic function.

The aim of this prospective study was to evaluate the association of peripheral B-type natriuretic peptide (BNP) levels with clinical symptoms and central hemodynamic and echocardiographic measures in cardiac transplantation. BNP reflects ventricular wall stress and correlates with severity of heart failure. No previous investigation has comprehensively assessed the rapid bedside BNP assay for predicting hemodynamic measures of cardiac allograft function in heart transplantation. We evaluated BNP levels using a rapid point-of-care assay in 87 stable cardiac transplant recipients who had 237 consecutive measurements along with endomyocardial biopsy, right-sided cardiac catheterization, and echocardiography. Using median tendencies, 2 groups were identified: the low BNP group (n = 116, BNP <150 pg/ml) and the high BNP group (n = 121, BNP >/=150 pg/ml). The high BNP group had increased right atrial pressures, higher pulmonary artery systolic pressures, pulmonary capillary wedge pressures, and lower cardiac index. Besides hemodynamic variables, the presence of right ventricular dysfunction (p = 0.05) and significant tricuspid regurgitation (p = 0.003) were associated with higher BNP levels. Independent predictors of BNP levels on multivariate analysis included elevated pulmonary capillary wedge pressure, lower cardiac index, and symptoms of dyspnea and fatigue. This initial investigation establishes the accuracy of a point-of-care BNP assay in predicting cardiopulmonary hemodynamic aberrations despite preserved left ventricular systolic function in heart transplant recipients. Rapid bedside BNP analysis may provide a noninvasive surrogate method for the comprehensive assessment of cardiac allograft function and hemodynamics in heart transplantation.

Adult↗
PubMed2002

Right ventricular diastolic relaxation in conscious dog models of pressure overload, volume overload, and ischemia.

OBJECTIVE: Limitations in clinical understanding of right ventricular relaxation can be attributed to the paucity of information from basic studies in animal models of right ventricular disease. This study examined, in the conscious state, right ventricular relaxation dynamics under normal conditions (n = 15) and in subacute (2-5 weeks) canine models of right ventricular pressure overload (n = 6), volume overload (n = 7), and free wall ischemia (n = 7). METHODS: Right-heart micromanometric measurements were obtained by using multisensor catheters. A new algorithm was developed to obtain representative ensemble averages of hemodynamic waveform data sets. Right ventricular relaxation was analyzed by using an exponential model with 3 parameters: P(0), tau, and P(b). Significant changes versus control values were determined by means of analysis of variance and the Student unpaired t test with Bonferroni's adjustment. RESULTS: In the state of pressure overload, right ventricular pressure decay exhibits an increased P(0) (56.2 +/- 19.1 vs 13.1 +/- 5.1 mm Hg [mean +/- SD]) and prolonged tau (57.1 +/- 2.8 vs 27.8 +/- 3.9 ms); there is also a decreased P(b) (-7.9 +/- 1.5 vs 0.28 +/- 1.8 mm Hg). The only significant change in volume overload is an increased asymptote, P(b) (5.3 +/- 2.9 mm Hg). In right ventricular ischemia, prolongation of tau (41.4 +/- 13.0 ms) and decreased P(b) (-1.95 +/- 1.1 mm Hg) attain high significance. CONCLUSIONS: Distinctive abnormalities in right ventricular relaxation dynamics accompany pressure overload, volume overload, and ischemia and may contribute to clinical right ventricular dysfunction.

Animals↗
PubMed2003

Combined arterial switch and Senning operation for congenitally corrected transposition of the great arteries: patient selection and intermediate results.

OBJECTIVE: Late results after traditional methods of repair of congenitally corrected transposition of the great arteries are poor. The combined arterial switch and Senning (double switch) operation may improve outcomes by using the morphologically left ventricle and mitral valve in the systemic circulation. In this report we review patient selection and intermediate results after the double switch operation for congenitally corrected transposition of the great arteries. METHODS: Since 1993, a total of 35 patients with congenitally corrected transposition of the great arteries with two ventricles of adequate size and no valvular pulmonary stenosis were potential candidates for a double switch operation. Eleven were not yet in need of further treatment, and 1 died during evaluation. The remaining 23 patients were entered into a protocol leading to anatomic repair. Their hospital records were reviewed, and follow-up data were obtained to evaluate early and intermediate outcomes. RESULTS: The 23 patients were candidates for anatomic repair because of right ventricular dysfunction or tricuspid regurgitation (n = 15) or associated uncorrected defects (n = 8). Pulmonary artery banding was performed in a total of 15 patients, either for left ventricular retraining (n = 11) or for congestive heart failure (n = 4). In 2 patients, aged 12 and 14 years, retraining was unsuccessful because of left ventricular dysfunction. Four patients with banding are currently awaiting repair. Eight patients proceeded to undergo double switch operations without preliminary pulmonary artery banding. To date, 17 patients have undergone double switch operations, with no early or late mortality. One patient required cardiac transplantation for progressive left ventricular failure after a preliminary banding and double switch operation done at 7 years of age. Ventricular function and tricuspid regurgitation remained stable or improved in all other cases. No patient has surgically acquired arrhythmias or significant residual hemodynamic conditions. All patients are alive and clinically well at a mean follow-up of 36 months (range 1 month-8 years). CONCLUSIONS: Congenitally corrected transposition of the great arteries with a normal pulmonary valve and two adequate ventricles can be managed with combined arterial switch and Senning operation with excellent intermediate results. Reconditioning the left ventricle may not be suitable for older patients. Late follow-up will be necessary to determine whether this management strategy provides a survival advantage for these patients.

Algorithms↗
PubMed2006

Primary myocardial involvement in systemic sclerosis.

Systemic sclerosis (SSc) is a connective tissue disease characterized by diffuse vascular lesions and fibrosis. Primary myocardial involvement is common in SSc and, when clinically evident, appears as a poor prognostic factor. An increasing body of evidence suggests that myocardial involvement is due, at least in part, to microcirculation impairment with abnormal vasoreactivity, with or without associated structural abnormalities of the small coronary arteries or arterioles. Using conventional methods, myocardial perfusion impairment, systolic and diastolic left ventricular dysfunction and right ventricular dysfunction have been reported in SSc. Recently, tissue Doppler echocardiography and magnetic resonance imaging have confirmed these results. Vasodilators, such as calcium channel blockers and angiotensin converting enzyme inhibitors, improve both myocardial perfusion and function abnormalities.

Arterioles↗
PubMed1995

Effects of dynamic cardiomyoplasty on right ventricular function.

This study was planned to document the right ventricular function immediately after cardiomyoplasty. Right ventricular volumes were calculated with the use of fast response thermistor. Right ventricular end-diastolic volume was reduced from 91 +/- 8 mL/M2 to 75 +/- 7 mL/M2 (p < 0.05) and right ventricular end-systolic volumes increased from 51 +/- 5 mL/M2 to 59 +/- 4 mL/M2 24 hours after the operation. Central venous pressure was raised from 2 +/- 1 to 9 +/- 3 mm H2O. These changes were interpreted as impairment of the right ventricular diastolic function. Cardiac index raised from 1.8 +/- 0.5 L/M2 per minute to 2.7 +/- 0.3 L/m2 per minute within a period of 7 days (p < 0.05). As a result of this study, we concluded that preoperatively normal right ventricular function deteriorates after the cardiomyoplasty. In the intensive care unit volume balance must be carefully monitored to avoid creating right ventricular dysfunction.

Adult↗
PubMed1995

Left ventricular impairment in arrhythmogenic right ventricular dysplasia: what we can learn from angiography.

Left ventricular impairment of arrhythmogenic right ventricular dysplasia is a common feature. Angiographic left ventricular contraction abnormalities can be found in more than 20% of patients with arrhythmogenic right ventricular dysplasia. Left ventricular impairment appears at all functional and morphological stages of the disease, even in cases with only slight or moderate right ventricular dysfunction. An event of aborted sudden cardiac death with documented ventricular fibrillation can be found in 56% of patients with left ventricular impairment. Left ventricular abnormalities seem to be an independent risk factor of sudden cardiac death; this is particularly true in patients with cardiac arrest as the first manifestation of the disease.

Adult↗
PubMed1996

[Prostaglandin E1 at low-doses improved right ventricular ejection fraction in anesthetic management for CABG].

A 52-year-old male for CABG developed a severe right heart failure, because of the direct injury to the right ventricular wall, after cardiopulmonary bypass. The volume loading therapy could not improve the cardiac function, then we used an infusion of low-dose prostaglandin E1 (0.02-0.04 micrograms.kg-1.min-1) for the acute right heart failure with increased pulmonary vascular resistance. After continuous infusion of this dose, the pulmonary vascular resistance decreased quickly, the right ventricular ejection fraction increased, and the stroke volume index also improved. These hemodynamic changes are the result of the potent vasodilating effect of PGE1, that especially could decrease selectively the pulmonary vascular resistance, and increase the preload of the left ventricle. This dose of PGE1, did not cause a severe systemic hypertension that is a serious complication during vasodilating therapy with any vasoactive drugs. In the present case, we speculated that the low-dose PGE1, is effective to improve the right ventricular function during the acute right heart failure which resulted from the intrinsic right ventricular dysfunction.

Alprostadil↗
PubMed1998

Hemodynamic and inotropic effects of milrinone after heart transplantation in the setting of recipient pulmonary hypertension.

BACKGROUND: Right ventricular failure remains an important cause of early morbidity and death after heart transplantation and is commonly related to preexistent recipient chronic pulmonary hypertension, which occurs as a result of long-standing congestive heart failure. In this study, the hemodynamic and inotropic effects of milrinone were assessed after bicaval heart transplantation in the setting of monocrotaline pyrrole-induced recipient chronic pulmonary hypertension. METHODS: Twenty dogs were used for 10 successfully completed transplantation experiments. Recipient animals underwent right atrial injection of 3 mg/kg monocrotaline pyrrole 4 months before transplantation. Hemodynamic and functional data were taken 1 hour after termination of cardiopulmonary bypass and after milrinone infusion. Myocardial function was assessed with load-insensitive means (preload-recruitable stroke work) and pulmonary vascular impedance was calculated with Fourier analysis. RESULTS: At the time of transplantation, before cardiopulmonary bypass, pulmonary hemodynamic indexes in recipient animals were significantly increased when compared with donors and were further significantly increased after cardiopulmonary bypass. Two animals died after transplantation as a result of acute right ventricular failure. In surviving animals milrinone infusion led to significant increases in right ventricular function, which occurred in association with significant improvements in pulmonary vascular impedance and transpulmonary efficiency. CONCLUSIONS: In the setting of monocrotaline pyrrole-induced recipient pulmonary hypertension, milrinone was associated with significant improvements in pulmonary vascular impedance, right ventricular function, and transpulmonary efficiency. These data suggest that milrinone is an effective means to improve right ventricular dysfunction and pulmonary vascular efficiency after bicaval heart transplantation in the setting of recipient chronic pulmonary hypertension.

Animals↗
PubMed1988

Differential ventricular ischemic injury: an experimental model of right ventricular failure with a variable degree of left ventricular dysfunction.

The hemodynamic manifestations of right ventricular dysfunction after ischemic injury depend not only on the severity of injury but also on the degree of coexistent left ventricular dysfunction. A better understanding of right ventricular failure and of optimal therapies has been hindered in part by lack of suitable experimental models of selective and differential ventricular injury. Therefore, we developed a technique of differential ventricular myocardial protection during a period of global cardiac ischemia and examined the effect of such an injury on intrinsic right and left ventricular myocardial function, metabolism, and regional blood flow. Twenty-six dogs were subjected to 30 minutes of ischemia while being supported by cardiopulmonary bypass. During ischemia, right and left ventricular myocardial temperatures were independently varied by selective ventricular endomyocardial thermal regulation. Nine dogs underwent right and left ventricular normothermic ischemia, eight underwent right and left ventricular hypothermic ischemia, and nine underwent right ventricular normothermic and left ventricular hypothermic ischemia. In both ventricles, normothermic ischemia resulted in greater depression of ventricular ability to generate stroke work as a function of end-diastolic dimension (p less than 0.05), greater depletion of myocardial adenine nucleotide content (p less than 0.05), and greater subendocardial reperfusion hyperemia (p less than 0.05). Myocardial temperature of the contralateral ventricle during ischemia had no effect (p = not significant) on intrinsic ventricular functional, metabolic, or regional blood flow response to injury. For a given degree of right ventricular injury assessed by these parameters, the degree of left ventricular injury could be independently varied by as much as 50%. This is a particularly suitable model for the investigation of acute right ventricular failure.

Adenine Nucleotides↗
PubMed2001

Modified Glenn connection for acutely ischemic right ventricular failure reverses secondary left ventricular dysfunction.

BACKGROUND: Right heart failure after cardiopulmonary bypass can result in severe hemodynamic compromise with high mortality, but the underlying mechanisms remain poorly understood. After ischemia-induced right ventricular failure, alterations in the interventricular septal position decrease left ventricular compliance and limit filling but may also distort left ventricular geometry and compromise contractility and relaxation. This study investigated the effect of acute isolated right ventricular ischemia on biventricular performance and interaction and the response of subsequent right ventricular unloading by use of a modified Glenn shunt. METHODS: In 8 pigs isolated right ventricular ischemic failure was induced by means of selective coronary ligation. A modified Glenn circuit was then established by a superior vena cava-pulmonary artery connection. Ventricular performance was determined by conductance catheter-derived right ventricular pressure-volume loops and left ventricular pressure-segment length loops. Hemodynamic data at baseline, after right ventricular ischemia, and after institution of the Glenn circuit were obtained during inflow occlusion, and the load-independent contractile indices were derived. RESULTS: Right ventricular free-wall ischemia resulted in acute right ventricular dilation (118 +/- 81 mL vs 169 +/- 70 mL, P =.0008) and impairment of left ventricular contractility indicated by the reduced end-systolic pressure-volume relation slope (50.0 +/- 19 mm Hg/mm vs 18.9 +/- 8 mm Hg/mm, P =.002) and preload recruitable stroke work index slope (69.6 +/- 26 erg x cm(-3) x 10(3) vs 39.7 +/- 13 erg x cm(-3) x 10(3), P =.003). In addition, left ventricular relaxation (tau) was significantly prolonged (33.3 +/- 10 ms vs 53.0 +/- 16 ms, P =.012). Right ventricular unloading with the Glenn shunt reduced right ventricular dilation and significantly improved left ventricular contraction, end-systolic pressure-volume relation slope (18.9 +/- 8 mm Hg/mm vs 35.8 +/- 18 mm Hg/mm, P =.002), preload recruitable stroke work index slope (39.7 +/- 26 erg x cm(-3) x 10(3) vs 63.0 +/- 22 erg x cm(-3) x 10(3), P =.003), and diastolic performance (tau 53.0 +/- 16 ms vs 43.5 +/- 13 ms, P =.001). CONCLUSIONS: Right ventricular ischemia-induced dilation resulted in acute impairment of left ventricular contractility and relaxation. A modified Glenn shunt attenuated the left ventricular dysfunction by limiting right ventricular dilation and restoring left ventricular cavity geometry.

Animals↗