Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ventricular Function, Right”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,477 records · Page 82Linked to original sources
PubMed2000

Failure of stroke volume augmentation during exercise and dobutamine stress is unrelated to load-independent indexes of right ventricular performance after the Mustard operation.

BACKGROUND: Impaired right ventricular function has been implicated as a cause of reduced maximal exercise capacity after the Mustard operation for transposition of the great arteries. METHODS AND RESULTS: Fourteen asymptomatic survivors of the Mustard operation were studied. Each underwent conventional cardiac catheterization, and after satisfactory hemodynamics were confirmed, load-independent indexes of ventricular function were derived by conductance catheter during dobutamine infusion (0, 5, and 10 microg x kg(-1) x min(-1)). Seven patients also underwent upright exercise testing on a bicycle ergometer with analysis of respiratory gas exchange by continuous mass spectrometry. Accessible pulmonary blood flow was measured at each workload with an automated acetylene rebreathing technique. All patients exercised to a satisfactory end point (respiratory quotient >1.1). Maximum oxygen consumption during exercise was impaired compared with predicted values (mean, 77%; P:<0.02). Both exercise and dobutamine infusion were associated with an increase in cardiac index and heart rate and a reduced stroke volume index response. This was despite significantly improved indexes of myocardial contraction (end-systolic pressure volume relation, P:<0.001), preload recruitable stroke work index (P:<0.01), VA coupling (P:<0.001), and isovolumic relaxation (P:<0.001) during dobutamine infusion. There were no changes observed in end-diastolic pressure-volume relations, but there was failure to augment ventricular filling manifest by absence of change in dV/dt (P:=NS). CONCLUSIONS: The stroke volume response to exercise stress is reduced in patients after the Mustard operation. A similar failure to augment stroke volume occurs during dobutamine stress despite appropriate responses in load-independent indexes of contraction and relaxation. This is due to failure to augment right ventricular filling rates during tachycardia, presumably as a result of impaired AV transport, consequent to the abnormal intra-atrial pathways.

Cardiac Surgical Procedures↗
PubMed2001

Use of peak Doppler gradient across ventricular septal defects leads to underestimation of right-sided pressures in patients with "sloped" Doppler signals.

In patients with "sloped" appearance of the Doppler signal across a ventricular septal defect (VSD), the peak Doppler velocity seems to overestimate the catheterization-derived peak-to-peak gradient, resulting in underestimation of right-sided heart pressures. In 11 patients with sloped Doppler signals across the VSD, ventricular pressure tracings were compared with simultaneous recordings of the Doppler signal. The average peak Doppler gradient (40.2 +/- 19.2 mm Hg) overestimated the catheterization-derived peak-to-peak gradient (20.2 +/- 13.6 mm Hg) significantly (P < or =.001). Doppler mean gradient (20.2 +/- 11.3 mm Hg; P = ns) and end-systolic gradient (17.0 +/- 12.5 mm Hg; P < or =.05) were closer estimates of the catheterization peak-to-peak gradient. All Doppler gradients showed good correlation to the catheterization peak-to-peak gradient with r2 values of 0.77, 0.73, and 0.91. We conclude that Doppler mean or end-systolic gradients should be used for calculation of right-sided heart pressures in this patient population.

Cardiac Catheterization↗
PubMed1994

The optimal cardioplegic temperature.

Seventy-two patients undergoing coronary artery bypass grafting were randomized to receive cold (8 degrees C) antegrade or retrograde, tepid (29 degrees C) antegrade or retrograde, or warm (37 degrees C) antegrade or retrograde blood cardioplegia (n = 12 in each group). Myocardial oxygen utilization as well as lactate and acid metabolism were assessed intraoperatively and cardiac function was assessed postoperatively. Myocardial oxygen consumption and anaerobic lactate release were greatest during warm, intermediate during tepid, and least during cold cardioplegic arrest. Myocardial oxygen consumption and lactate release were underestimated during retrograde cardioplegia because of contamination of aortic root samples. Warm retrograde and tepid retrograde cardioplegia resulted in greater lactate and acid washout with reperfusion. Left ventricular stroke work indices were greater after warm antegrade and tepid antegrade cardioplegia than after cold antegrade cardioplegia, and right ventricular stroke work indices were greatest after warm antegrade cardioplegia. Warm antegrade cardioplegia increased aerobic metabolism during and after cardioplegia and preserved left and right ventricular function. Tepid antegrade cardioplegia reduced anaerobic lactate and acid release during arrest and preserved cardiac function.

Adult↗
PubMed2004

Prognostic implications of echocardiography in advanced heart failure.

PURPOSE OF REVIEW: The growing epidemic of systolic congestive heart failure mandates strategies to identify accurately people with high morbidity and mortality. Echocardiography remains the most widely available noninvasive tool for the assessment of cardiac structure, function, and hemodynamics. Clinical data paired with echocardiographic analysis in patients with systolic heart failure obtained from a variety of investigations have allowed for the evaluation of this modality as a prognostic tool. RECENT FINDINGS: Detailed appraisal of the literature has revealed five distinct, easy-to-evaluate echocardiographic parameters that may assist clinicians to segregate high-risk patients. The presence of or the inability to modify a left ventricular ejection fraction less than 25%, impaired right ventricular function (assessed by any of four methods), left ventricular end-diastolic dimension greater than 6.5 to 7 cm, a restrictive mitral inflow, or pulmonary hypertension (peak tricuspid regurgitant velocity >2.5 m/s) should alert clinicians of patients with high morbidity (recurrent congestive heart failure admission, arrhythmia, impaired functional capacity) and mortality. Particularly important among these variables is the presence of a restrictive mitral inflow pattern. SUMMARY: Detailed analysis of two-dimensional and Doppler data routinely obtained from echocardiograms has established prognostic implications among patients with systolic heart failure. Although prospective clinical trials are lacking, the use of echocardiography to segregate risk should be incorporated into current strategies to treat congestive heart failure and influence clinical listing for cardiac transplantation.

Cardiac Output↗
PubMed1995

Measurement of pulmonary artery diastolic pressure from the right ventricle.

OBJECTIVES: This study evaluated the feasibility of estimating pulmonary artery end-diastolic pressure from within the right ventricle. If feasible, this could have important implications for long-term hemodynamic monitoring. BACKGROUND: Right ventricular pressure at the time of pulmonary valve opening closely approximates pulmonary artery end-diastolic pressure. Because maximal first derivative of right ventricular pressure (dP/dt) can be easily measured, if it occurs at or very near pulmonary valve opening, right ventricular pressure at maximal right ventricular dP/dt would be an estimation of pulmonary artery end-diastolic pressure. METHODS: In 10 patients undergoing routine right and left heart catheterization, simultaneous measurements were made using micromanometers in the right ventricle and pulmonary artery at baseline, during isometric work and Valsalva maneuver. Right ventricular pressure at maximal right ventricular dP/dt was considered the estimated pulmonary artery end-diastolic pressure and was compared with the actual pulmonary artery end-diastolic pressure. RESULTS: At baseline, estimated and actual pulmonary artery end-diastolic pressures were (mean +/- SD) 17.7 +/- 6.6 and 16.7 +/- 6.7 mm Hg, respectively (p = NS). During isometric stress, estimated and actual pulmonary artery end-diastolic pressures were 30.4 +/- 12.7 and 28.4 +/- 10.1 mm Hg, respectively (p = NS). During Valsalva maneuvers, estimated and actual pulmonary artery end-diastolic pressures were 36.5 +/- 17.8 and 38.0 +/- 16.1 mm Hg, respectively (p = NS). CONCLUSIONS: Although more extensive testing is necessary to evaluate validity in different physiologic and pathologic situations, it appears that right ventricular pressure at maximal right ventricular dP/dt can provide accurate estimation of pulmonary artery end-diastolic pressure.

Cardiac Catheterization↗
PubMed2001

Current management of primary pulmonary hypertension.

Primary pulmonary hypertension (PPH) is a rare disorder with an annual incidence of 1 to 2 per million people. The aetiology of this disorder is unknown, but it appears to result from an abnormal interaction of environmental and genetic factors leading to a vasculopathy. The pulmonary arteries in these patients exhibit a spectrum of pathological lesions ranging from the early medial hypertrophy to the end-stage fibrotic plexiform lesions. This characteristic pathology is also observed in pulmonary hypertension resulting from connective tissue disease (particularly systemic sclerosis), HIV infection, portal hypertension and certain toxins. PPH is a condition that is difficult to diagnose and treat, with a median survival of 2.8 years in historical studies. One of the difficulties in treating patients with PHH is that the subacute nature of disease presentation often prevents an accurate diagnosis during the early stages of the illness. Progressive dyspnoea on exertion is the most common presenting symptom. Diagnostic evaluation should include electrocardiography, chest radiograph and echocardiography, and laboratory and other studies to evaluate for secondary causes (e.g. pulmonary function tests, chest computed tomography and ventilation/perfusion scans, pulmonary arteriogram, cardiopulmonary testing, right heart catherisation). PHH is a disorder for which there is no known cure. Current medical and surgical treatment options for patients with PHH include anticoagulation, vasodilators and transplantation. Calcium channel antagonists are currently the oral drugs of choice for the treatment of patients with New York Heart Association (NYHA) Class II disease. These agents, in particular the dihydropyridine compounds, have beneficial effects on haemodynamics and right ventricular function, and possibly increased survival. Epoprostenol is administered by intravenous infusion, and studies have demonstrated short- and long-term improvements in symptoms, haemodynamics and survival. It is well tolerated and has become the treatment of choice for patients with NYHA Class III and IV disease. Inotropic agents are used as a bridge to transplant, which is indicated in patients who do not respond to maximal medical therapy. Experience has shown that single lung, double lung and heart-lung transplantation are approximately of equal efficacy. Currently, single lung transplant appears to be the procedure of choice. Newer agents, such as sildenafil, beraprost and bosentan, are presently being evaluated for the treatment of this disorder. Future study should include elucidation of the pathogenic mechanisms in the development of this vasculopathy, which will hopefully lead to the development of improved treatment options for patients with PHH.

Anticoagulants↗
PubMed2026

Severe Suprasystemic Refractory Pulmonary Hypertension in a Neonate with St&#xfc;ve-Wiedemann Syndrome Associated with Biallelic LIFR Variants: Molecular Insights and a Neonatal Case Report.

St&#xfc;ve-Wiedemann syndrome (SWS) is an ultra-rare autosomal recessive skeletal dysplasia caused by loss-of-function variants in the leukemia inhibitory factor receptor (LIFR) gene. While characterized by bone deformities and dysautonomia, severe persistent pulmonary hypertension of the newborn (PPHN) significantly contributes to high early mortality. We report a neonate with genetically confirmed SWS who presented with severe, suprasystemic PPHN refractory to standard pulmonary vasodilators, including inhaled nitric oxide. This case provides a detailed longitudinal hemodynamic characterization of severe suprasystemic PPHN in genetically confirmed SWS, including serial assessment of pulmonary pressures, shunt direction, and right ventricular function during treatment. Rather than identifying PPHN as a novel manifestation of SWS, it extends the phenotypic and hemodynamic characterization of pulmonary vascular involvement in this rare disorder.

Humans↗
PubMed1993

[Are central hemodynamics the decisive factor in the manifestation of chronic heart failure?].

In the past some authors revealed that data assembled during examinations of the central haemodynamics, echocardiography, subjective complaints, physical findings and load tolerance in patients with chronic heart failure are not mutually consistent. The authors examined therefore comprehensively 40 patients with different grades of cardiac failure. They revealed very loose relations between the grade of functional classification, echocardiographic and invasive haemodynamic parameters at rest on the one hand and spiroergometric indicators on the other hand. Closer relations with spiroergometric findings were obtained with values of invasive haemodynamic parameters after a load, in particular values of the cardiac index, and systemic vascular resistance. The authors conclude that for clinical manifestations of chronic cardiac failure the peripheral circulation and tissue metabolism is at least equally important as changes of central haemodynamics. Moreover, the importance of the right ventricular function and diastolic cardiac function is not sufficiently appreciated.

Adult↗
PubMed2005

Early detection of cardiac dysfunction in thalassemic patients by radionuclide angiography and heart rate variability analysis.

BACKGROUND: Cardiac dysfunction remains the major cause of death in beta-thalassemia. Aim of this study was to assess early myocardial damage in thalassemic patients with no symptoms or echocardiographic evidence of dysfunction at routine monitoring. METHODS: Twenty patients (seven females; median 25 yr [first quartile 22,third quartile 28]) with beta-thalassemia underwent radionuclide angiography (RNA) at rest and during low-dose dobutamine infusion (5-10 gamma/kg/min). Right and left ventricular ejection fractions (EF) were determined by first-pass method and gated equilibrium acquisition, respectively. Twenty-four-hour Holter monitoring with time-domain heart rate variability (HRV) assessment and echocardiographic follow-up (21 months [5,27]) were performed. RESULTS: Eleven patients showed regional wall motion abnormalities at RNA; left ventricular EF, HR and diastolic measurements significantly increased after dobutamine infusion. Patients with abnormal RNA right ventricular EF (n = 8, <0.45) showed lower echocardiographic left ventricular EF at the enrollment (0.54 [0.50,0.61] vs. 0.62 [0.56,0.67], P = 0.02) than those with a normal right ventricular EF. Patients with reduced standard deviation of the averages of RR intervals in all 5-minute periods of entire recording (SDANN) (n = 6, <100 ms), a measure of HRV, had lower echocardiographic left ventricular EF (0.53 [0.49,0.62] vs. 0.62 [0.56,0.66], P = 0.03) and lower fractional shortening (0.28 [0.25,0.32] vs. 0.36 [0.30,0.39], P = 0.003) at the enrollment than those with normal SDANN. No significant association was found between RNA and HRV measurements and follow-up left ventricular function. CONCLUSIONS: Right ventricular dysfunction and abnormal HRV may represent the early features of cardiac disease in thalassemic patients with no evidence of ventricular dysfunction at routine evaluation.

Adult↗
PubMed2004

Goal-oriented thrombolytic therapy for venous thromboembolic disease.

The goal of a therapeutic intervention should be to positively impact a meaningful patient outcome. Too often, though, efficacy of a treatment is based on a surrogate endpoint. Thrombolytic therapy for venous thromboembolic disease is an example of a treatment whose success is primarily based on radiographic or echocardiographic endpoints and not endpoints such as symptom relief, functional capacity, quality of life, thrombosis recurrence, and survival. Thrombolysis for lower-extremity deep venous thrombosis does not reduce the incidence of pulmonary embolism, has unclear impact on the rates of post-thrombotic syndrome, and is associated with increased rates of major hemorrhage compared to conventional anticoagulation. Reserving thrombolysis for limb-threatening thrombosis especially in the young seems prudent. Currently available evidence does not support the routine use of thrombolytic therapy in patients with hemodynamically stable pulmonary embolism regardless of right ventricular function status. Risks, benefits, and alternative therapies must always be considered, and therapy must be guided by individual case circumstances and the best available scientific evidence.

Endpoint Determination↗
PubMedDate not supplied

[Prevention of negative hemodynamic effects of protamine sulfate by simultaneous infusion of microdoses of adrenaline].

Two groups of coronary patients subjected to revascularization of the myocardium were examined in order to detect the negative hemodynamic effects of protamine sulfate (PS) and the possibility of their correction by simultaneous infusion of adrenaline microdoses. In group 1 (27 pts.) heparin was neutralized by infusion of PS alone (6 mg/kg) and in group 2 (27 pts.) by simultaneous infusion of PS and adrenaline (15 ng/kg/min). The functions of the right and left ventricles were evaluated by catheterization of the pulmonary artery by a Swan-Ganz catheter and transesophageal Doppler echocardiography. These methods provided volume and velocity characteristics of the right and left compartments of the heart. PS deteriorated the systolic function of the right ventricle, particularly in patients with initial dysfunction of the right heart. Infusion of adrenaline simultaneously with PS leveled its negative effects, thus preventing myocardial dysfunction.

Adrenergic Agonists↗
PubMed1997

Human fetal right ventricular ejection force under abnormal loading conditions during the second half of pregnancy.

Our objective was to determine whether abnormal loading conditions can modify human fetal right ventricular ejection force during the second half of pregnancy. By Doppler echocardiography, we studied 73 normal fetuses between 19 and 41 weeks of gestation, 27 fetuses with hypoplastic left heart syndrome (chronic volume overload) between 18 and 38 weeks of gestation, 14 fetuses with mild to moderate constriction of the ductus arteriosus (pulsatility index (PI) between 1.0 and 1.9) and seven fetuses with severe constriction (PI < 1.0) or occlusion of the ductus arteriosus (relatively acute pressure overload) between 28 and 34 weeks of gestation. In the normal and ductal constriction/occlusion groups, blood velocity waveforms were recorded at the level of the aortic and pulmonary valves, and in the group with hypoplastic left heart syndrome at the level of the pulmonary valve. The ventricular ejection forces were calculated. In the normal group, right (RVEF; r = 0.91, p < 0.0001) and left (LVEF; r = 0.86, p < 0.0001) ventricular ejection forces increased and were equal during the second half of gestation. In the group with hypoplastic left heart syndrome the RVEF increased (r = 0.76, p < 0.0001) with advancing gestation. The RVEF (p < 0.0005) and its average weekly increase (p < 0.0001) were greater in the hypoplastic left heart syndrome group than in the normal group. In the group with mild to moderate ductal constriction, both ventricular ejection forces were similar to those of the normal group. The RVEF (p < 0.003) and its average weekly increase (p < 0.03) were lower in the group with severe ductal constriction or occlusion than in the normal group. The LVEF did not differ from that of the normal group We conclude that chronic volume overload increases and relatively acute pressure overload decreases human fetal RVEF. The right ventricular performance is modified by abnormal loading conditions.

Blood Flow Velocity↗
PubMed1999

Bi-directional cavopulmonary shunt: is accessory pulsatile flow, good or bad?

OBJECTIVE: Evaluation of the effect and long-term outcome of accessory pulsatile blood flow versus classical bi-directional cavopulmonary connection (BCPC). METHODS: Retrospective review of the medical and surgical records. RESULTS: Two-hundred and five patients (119 boys, 86 girls) underwent BCPC from 1990 to 1996. Accessory pulsatile flow was present in 68%, flow being maintained through the pulmonary trunc in 46%, systemic-to-pulmonary artery shunt in 13% and mixed in 7%, or patent ductus arteriosus in 2%. Patients with accessory pulsatile flow had lower hospital mortality (3% versus 5%), while mean pulmonary artery pressure (14.1 versus 12.6 mmHg P = 0.050) and increase of oxygen saturation (12.4 versus 8.7, P = 0.034) were significantly higher. The period of artificial ventilation (1.9 day) and ICU stay (6 days) did not differ for both groups. Late mortality was higher following accessory pulsatile flow (6% versus 1%). At late follow-up patients with accessory pulsatile flow had significantly higher oxygen saturation (mean 85 +/- 4%, versus 79 +/- 4%; P < or = 0.005). If subsequent completion of Fontan is considered the optimal palliation and subsequent systemic to pulmonary artery shunt, arteriovenous fistula and transplantation is considered a failure, patients with accessory pulsatile flow had significantly more and earlier completion of the Fontan procedure (mean 1.7 +/- 2.4 years, versus 2.7 +/- 4.4 years; P = 0.008). Survival is not influenced by age at bi-directional cavopulmonary shunt surgery, left or right functional ventricular anatomy or previous palliative surgery. One patient with accessory pulsatile flow developed systemic-to-pulmonary collateral's eventually requiring lobectomy. CONCLUSION: Despite two different initial palliative techniques the outcome was not significantly different. Accessory pulsatile blood flow appeared not to be a contra-indication for a completion Fontan procedure. Moreover, the data suggest that after accessory pulsatile flow can safely be performed, at late follow-up oxygen saturation is higher, while, significantly more and earlier completion of Fontan occurred. Age at bi-directional cavopulmonary shunt, basic left or right ventricular anatomy or previous palliative surgery did not influence survival.

Adolescent↗
PubMed2005

Inhaled iloprost to control residual pulmonary hypertension following pulmonary endarterectomy.

OBJECTIVE: Pulmonary endarterectomy (PEA) is the standard therapy for patients with chronic thromboembolic pulmonary hypertension (CTEPH). In the immediate postoperative period, persistent pulmonary hypertension increases the risk of acute respiratory or right heart failure. In pulmonary arterial hypertension, prostanoid inhalation has been found to improve pulmonary hemodynamics, right ventricular function, gas exchange, and clinical outcome. We report the results of a double-blinded randomized trial with the aerosolized prostacyclin analogue iloprost in patients with residual pulmonary hypertension after PEA. METHODS: Twenty-two patients (age, 55+/-13 years; 8 females; propofol- and sufentanil-based anesthesia; pressure-controlled mechanical ventilation) were randomized to receive either a single dose of 25 microg aerosolized iloprost (iloprost group; n=11) or normal saline (placebo group; n=11) immediately after postoperative ICU admission. Primary endpoints were changes in gas exchange, pulmonary and systemic hemodynamics, and clinical outcome. RESULTS: Iloprost significantly enhanced cardiac index (CI) and reduced mean pulmonary arterial pressure (mPAP) and pulmonary vascular resistance [PVR (dynscm(-5))] in contrast to placebo. Placebo: pre-inhalation 413+/-195 versus post-inhalation 404+/-196 at 30 min (p=0.051), 415+/-189 at 90 min (p=0.929). Iloprost: pre-inhalation 503+/-238 versus post-inhalation 328+/-215 at 30 min (p=0.001), 353+/-156 at 90 min (p=0.003). Blood oxygenation remained unchanged. CONCLUSION: In addition to the effect of PEA, iloprost reduces residual postoperative pulmonary hypertension, decreases right ventricular afterload and may facilitate the early postoperative management after PEA.

Administration, Inhalation↗
PubMed2005

Differential exercise performance on ventricular assist device support.

BACKGROUND: Ventricular assist devices (VADs) are approved for destination therapy because they improve survival in end-stage heart failure (HF). VADs are powered pneumatically or electrically. Pneumatic and electric left ventricular assist devices (LVADs) and biventricular assist devices (BiVADs) provide excellent hemodynamic support at rest, but differences in their effects on exercise tolerance are unclear. We sought to evaluate the effect of devices with varying operating parameters on exercise capacity. METHODS: Exercise physiology data obtained during maximal exercise with on-line gas-exchange analysis were collected for 38 consecutive VAD-implanted HF patients referred for exercise testing. RESULTS: Electric LVADs were implanted in 18 patients, and pneumatic LVADs in 10 patients. Percent of predicted peak exercise oxygen consumption (VO2%) was significantly greater in pneumatic LVAD patients (52.1 +/- 11.1% vs 38.2 +/- 11.3%, p < 0.05). The 10 patients implanted with a pneumatically powered LVAD were compared to 10 patients implanted with a pneumatically powered BiVAD. LVAD-supported patients had a higher VO2% (52.1 +/- 11.1% vs 36.5 +/- 17.7%, p < 0.05). CONCLUSIONS: HF patients supported with a pneumatic LVAD appear to have better exercise tolerance than those receiving an electric LVAD. Patients on LVAD support have better exercise tolerance than BiVAD-supported patients. This highlights the importance of right ventricular function to exercise tolerance in HF patients, and may have implications for future VAD design.

Adult↗
PubMedDate not supplied

Surgical therapy for congestive heart failure: indications for transplantation versus cardiomyoplasty.

Heart transplantation is the procedure of choice for patients with severe congestive heart failure, but many patients are not candidates because of associated medical problems and the lack of donor hearts. Since 1988 we have performed 36 heart transplantations. One and 2-year actuarial survival rates have been 82% and 73%. Sixteen patients who were not candidates for heart transplantation have undergone cardiomyoplasty, a procedure in which the left latissimus dorsi is transposed to the myocardium and paced synchronously with the heart to augment cardiac function. The average age was 55 years (range, 39 to 65 years). Preoperative left and right ejection fractions were 24.9% +/- 2.1% and 43% +/- 4.5%. Eleven patients were in the New York Heart Association class IV, and five patients were in class III. Four operative deaths occurred, and three additional deaths occurred within 6 months of surgery. Nine patients became long-term survivors, and seven of nine patients are alive at a mean follow-up of 29 months. All patients are in New York Heart Association class I or II. In long-term survivors, mean left ventricular ejection fraction increased from 24.9% +/- 2.1% to 31.8% +/- 3.5% (p less than 0.01). All but one of the operative and early deaths occurred in patients with biventricular failure (n = 6). One operative death and no early deaths occurred in patients with normal right ventricular ejection fraction. This initial experience suggests that cardiomyoplasty may be helpful for heart failure patients with preserved right ventricular function, but heart transplantation should be the therapy of choice for biventricular failure.

Assisted Circulation↗
PubMedDate not supplied

Radiographic evaluation of caudal vena cava size in dogs.

Dilation of the caudal vena cava (CVC) on lateral thoracic radiographs is often interpreted as suggestive of right-sided congestive heart failure. To quantitate the clinical utility of evaluating CVC size as an indicator of right-sided heart disease, we compared the ratio of the diameter of the CVC as measured on a left lateral thoracic radiograph to the descending aorta (Ao), length of the thoracic vertebra above the tracheal bifurcation (VL), and width of the right fourth rib (R4) in 35 dogs with right heart disease and 35 control dogs. Each CVC ratio (CVC/Ao, CVC/VL, CVC/R4) was statistically larger in dogs with right heart disease. Response operating characteristic curves and likelihood ratios were used to determine ratios helpful in identifying dogs with right heart disease. A CVC/Ao > 1.50, CVC/VL > 1.30, or CVC/R4 > 3.50 are strongly suggestive of a right-sided heart abnormality in a patient.

Animals↗
PubMed1995

Importance of angiotensin-converting enzyme in pulmonary hypertension.

Angiotensin II causes pulmonary vasoconstriction in man and in animals, and angiotensin-converting enzyme (ACE) inhibitors have prevented the development of chronic pulmonary hypertension in animals models. Angiotensin II may contribute to lung vascular remodeling in pulmonary hypertensive disease, since cilazapril, an inhibitor of ACE, reduces pulmonary vascular medical thickening in chronically hypoxic rats with established pulmonary hypertension. Furthermore, the ACE DD genotype, which has been associated with increased circulating and tissue ACE activity, has been associated with left ventricular hypertrophy in human hypertensive disorders. The ACE DD genotype may also 'permit' a greater hypertrophic adaptation of the pressure-over-loaded right ventricle. In fact, we have shown that pulmonary hypertension patients with maintained cardiac output and less right-heart failure fall into the group with the DD genotype and that patients with a low cardiac output and more severe right-heart failure fall into the group with the non-DD genotype, supporting the hypothesis. We assessed cardiopulmonary hemodynamics in patients with primary (unexplained) pulmonary hypertension and segregated the patients based on their ACE genotype. For similar mean pulmonary artery pressures in the DD and non-DD groups, the cardiac output was substantially lower in the patients with the non-DD genotype, whereas the values for mean right atrial pressure and pulmonary vascular resistance were double when compared with the DD group. Our data show that the ACE DD genotype is prevalent in patients with severe pulmonary hypertension and is a marker of maintained right ventricular function.

Animals↗