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PubMed1998

Controlling perioperative morbidity and mortality after lung transplantation for pulmonary hypertension.

Lung transplantation for pulmonary hypertension now accounts for more than 18% of all transplantations performed with 1-year survival rates for primary pulmonary hypertension approximating 65%. Patients have NYHA class III or IV symptoms and typically have marked right ventricular dysfunction. Accelerated or acute decompensation can occur. A decline in status leads to a patient with severe right heart failure, hepatic dysfunction and severe malnutrition, conditions that increase perioperative morbidity and mortality. Immediate right ventricular dysfunction may be related to allograft injury with persistent elevation of pulmonary artery pressures or to intrinsic right ventricular disease; this can be supported with inotropic medications. Single-lung transplantation results in postoperative physiology that can require aggressive therapy to limit mortality. When allograft dysfunction occurs, significant hypoxemia results to a greater degree than that observed with single-lung transplantations for other diseases or following double-lung transplantation. As a result, careful donor selection for a single lung transplantation is crucial. The most common reason for prolonged ventilation is allograft reperfusion injury with ventilation-perfusion mismatching. Neuromuscular blockade can decrease oxygen utilization and improve chest wall compliance, whereas lateral positioning with the native lung down can be crucial to improving V/Q matching. Differential lung ventilation allows the application of larger quantities of positive end-expiratory pressure to the injured allograft. The use of exogenous nitrates has been advocated to reduce pulmonary vascular resistance. Nitric oxide has attractive potential benefits because it can be delivered directly to the lungs and functions to dilate the pulmonary vascular bed. All else having failed, we and others have successfully used extracorporeal membrane oxygenation to support cardiopulmonary function.

Humans↗
PubMed2005

Cardiac troponin I release in acute pulmonary embolism in relation to the duration of symptoms.

PURPOSE: To evaluate the release of cardiac troponin I in normotensive patients with acute pulmonary embolism in relation to the duration of symptoms. METHODS: Fifty-seven normotensive patients with acute pulmonary embolism were included in the study. Patients were divided into two groups based on the duration of symptoms at presentation: symptoms of < or =72 h, group A; symptoms of >72 h, group B. Serum cardiac troponin I levels were measured at presentation. RESULTS: Mean age was 63+/-18 years and 23 (40%) patients were males. Thirty-three (58%) patients had symptoms of < or =72 h (group A) and 24 (42%) had symptoms of >72 h (group B). Both groups had similar prevalence of right ventricular dysfunction on echocardiography (55% [n=18] in group A vs. 42% [n=10] in group B, p=NS). Sixteen patients had elevated serum cardiac troponin I (mean+/-S.D. 3.3+/-2.3 ng/ml, range 0.6-8.3 ng/ml). Elevated serum cardiac troponin I was strongly associated with right ventricular dysfunction (p=0.015). All patients with elevated serum cardiac troponin I (n=16) were in group A (p<0.0001). Twelve of 18 (67%) patients with (p=0.0005) and 4 of 15 (27%) patients without (p=NS) right ventricular dysfunction had elevated serum cardiac troponin I. Thirteen of 16 (81%) patients with elevated serum cardiac troponin I had duration of symptoms < or =24 h at presentation. CONCLUSIONS: The dynamics of cardiac troponin I release in acute pulmonary embolism in patients who present with symptoms of < or =72 h duration could be different from those who present with longer duration of symptoms. Therefore, the use of cardiac troponin I in risk stratification of acute pulmonary embolism might be limited to the patients presenting within 72 h of the onset of symptoms.

Acute Disease↗
PubMed1998

Mechanical valves in the pulmonary position: a reappraisal.

OBJECTIVES: To evaluate midterm results of mechanical valves in pulmonary position in patients with pulmonary regurgitation and right ventricular dysfunction as an alternative to bioprostheses. PATIENTS: Mechanical valves (six tilting disc valves and two bileaflet valves) were implanted in eight patients previously operated on for tetralogy of Fallot (n = 7) and truncus arteriosus (n = 1), with severe right ventricular dysfunction caused by massive pulmonary regurgitation. RESULTS: All patients survived prosthesis implantation and are currently well. At follow-up (3 months to 9 years), they do not show signs of valve failure, and right ventricular function has dramatically improved in all but one, who still shows moderate ventricular hypokinesia. CONCLUSION: After operative correction of congenital heart defects in selected patients who show severe dysfunction of the right ventricle caused by pulmonary regurgitation/stenosis, mechanical valves may represent an alternative to bioprosthetic valves. The selection of the valve type is still a matter of debate. However, according to literature data, complications seem to have occurred only in patients with bileaflet mechanical valves in the pulmonary position, whereas no thromboembolic episodes or valve failure is reported in subjects with tilting disc valves in the right ventricular outflow. Tilting disc valves might perform better in the right ventricular outflow than bileaflet valves.

Adolescent↗
PubMed2006

Percutaneous pulmonary valve implantation.

Percutaneous implantation of valves is a fast evolving field in interventional cardiology. Acquired pulmonary valve disease is uncommon; however, right ventricular outflow tract dysfunction is one of the common indications of reoperations during late follow-up of repaired congenital heart disease. The impact of pulmonary valvular dysfunction on right ventricular function during late follow-up of patients with adult congenital heart disease has led to earlier intervention. The importance of a technique with lower morbidity and mortality, good patient acceptance, and efficacy that is comparable with surgery cannot be underestimated. Percutaneous pulmonary valve implantation uses a valved-stent assembly implanted by means of a double balloon catheter delivery system. The device is a bovine jugular venous valve sutured inside a platinum-iridium. In a series of 58 consecutive patients, we implanted this valve successfully with good clinical and hemodynamic results and no mortality on long-term follow-up. Early device designs led to reintervention by surgical explantation in the early experience, and a second percutaneous pulmonary valve implantation during latter experience. This exciting new technique will lead to review of the current indications and timing of intervention for right ventricular outflow tract dysfunction in late follow-up of congenital heart disease.

Adolescent↗
PubMedDate not supplied

Clinical and echocardiographic evidence suggesting afterload reduction as a mechanism of action of tolazoline in neonatal hypoxemia.

The effect of tolazoline was assessed in 29 hypoxic neonates. Tolazoline was given in a bolus starting at 1 mg/kg and repeated or infused for 5-134 hours. A "good clinical response," defined as a rise in PaO2 of more than 20 mm Hg, was obtained in 23 (79%), 20 of this group were weaned from the respirator, and three died. Six infants did not respond initially and four died. Failure to respond to tolazoline or to be weaned from the ventilator was usually associated with severe additional pathology. Urine output (greater than 1 ml/kg/h) was adequate in most neonates during therapy. In those with preexisting oliguria (less than 1 ml/kg/h), output improved during therapy. Blood pressure monitoring showed a fall in blood pressure in 19 patients during tolazoline administration, but true hypotension only occurred in four; in seven there was no fall and in three there was a rise in blood pressure. Echocardiography was performed prior to therapy in 19 patients and repeated in 12 patients after 24 h. Additional "tracking" was performed at 10 min, 1 h, and 4 h in seven patients. Prior to therapy, right ventricular dysfunction was demonstrated by abnormal right ventricular systolic time intervals (RVSTIs) in 17 of the patients tested. A rapid improvement was evident during therapy especially with "tracking." Left ventricular dysfunction, assessed by left ventricular systolic time intervals (LVSTIs), ejection fraction (EF), shortening fraction (SF), and velocity of circumferential fiber shortening (VCF), was also evident prior to therapy and improved, though more gradually than the RVSTIs.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Pressure↗
PubMed1987

Factors that exaggerate the deleterious effects of pulmonary insufficiency on the right ventricle after tetralogy repair. Surgical implications.

Postoperative cardiac catheterization data of 74 patients with pulmonary insufficiency after tetralogy repair were analyzed. Two groups were identified: Group A, 26 patients with normal right ventricular function (ejection fraction 95% +/- 5.5%, end-systolic volume 110% +/- 17% of predicted normal) and Group B, 48 patients with right ventricular dysfunction (ejection fraction 80% +/- 18% [p less than 0.001], and end-systolic volume 218% +/- 75% of predicted normal [p less than 0.001]). There was no significant difference between the two groups with respect to frequency of previous palliative procedures, age at operative repair, operative techniques, methods of myocardial protection, and follow-up period. Right ventricular dysfunction in Group B was associated with significant distal pulmonary stenosis (right ventricle-pulmonary artery pressure gradient 28 +/- 13 torr in Group A versus 55 +/- 20 torr in Group B, p less than 0.001), moderate pulmonary regurgitation (regurgitant fraction 18% +/- 11% in Group A versus 32% +/- 10% in Group B, p less than 0.001), and large transannular outflow patch (ratio of patch diameter to descending aorta diameter 1.31 +/- 0.16 in Group A versus 2.50 +/- 0.28 in Group B, p less than 0.001). Pulmonary valve insertion was performed in 42 patients in Group B. Eighteen had subsequent cardiac catheterization. Right ventricular function recovered completely (end-systolic volume 122% +/- 24%, and ejection fraction 92% +/- 7% of predicted) in five of six patients (83%) who had valve insertion within the first 2 years after tetralogy repair. In contrast, right ventricular function remained abnormal in all 12 patients who had valve insertion later than 2 years after tetralogy repair (p less than 0.05). Patients with residual pulmonary stenosis and/or a large transannular outflow patch are at risk for the development of right ventricular dysfunction from pulmonary insufficiency after tetralogy repair. Early correction of these residual lesions and control of pulmonary insufficiency may prevent long-term deterioration in right ventricular function.

Adolescent↗
PubMed2001

Right ventricular diastolic dysfunction in patients with anticardiolipin antibodies and antiphospholipid syndrome.

OBJECTIVE: To evaluate the prevalence of diastolic dysfunction in patients with anticardiolipin antibodies (aCL) and to examine whether the antiphospholipid syndrome (APS) is associated with diastolic dysfunction independently of valvular abnormalities and systolic dysfunction. METHODS: Pulsed, continuous, colour Doppler echocardiography was performed in 179 subjects, of whom 15 were excluded from the analysis because of systolic dysfunction or severe valvular disease. The remaining 164 subjects included 29 patients with primary APS, 26 patients with secondary APS (APS in the presence of systemic lupus erythematosus (SLE)), and 30 patients with SLE and aCL but without APS; 43 patients with SLE without aCL and 36 normal volunteers served as control groups. RESULTS: The groups compared differed significantly in all measures of right ventricular function. There was a gradation of increasing diastolic function impairment as manifested by prolonged deceleration time (DT) and isovolumic relaxation time (IVRT) across the groups of patients with SLE without aCL, SLE with aCL, secondary APS, and primary APS. Differences in left ventricular diastolic function measures were less prominent. In regression analysis, DT increased by 19.6 ms (p=0.002) in the presence of primary APS and by 20.1 ms (p=0.038) in the presence of pulmonary hypertension. The titre of IgG aCL was the strongest predictor of a prolonged IVRT. CONCLUSION: Diastolic dysfunction, in particular of the right ventricle-that is, independent of valvular disease and systolic dysfunction, is a prominent feature of APS and may be related to the pathogenesis of the syndrome.

Adult↗
PubMed1986

[Evaluation of coronary lesions in biventricular inferoposterior infarction].

Fifty-two patients with primary transmural infero-posterior infarcts underwent right heart catheterisation on admission to hospital and coronary angiography between the 7th day and 4th month after onset of symptoms. The patients were divided into two groups A (N = 34) with signs of right ventricular dysfunction on admission indicating biventricular infarction, and B (N = 18) without right ventricular dysfunction classified as isolated LV infarction. No significant differences were observed between the two groups with respect to: global and regional LV function; the incidence of single, double and triple vessel disease; the incidence and location of right coronary artery thrombosis; the incidence and location of lesions of the left coronary tree (LCA, LAD, Cx); the extent of coronary disease (Gensini score); the dominant artery (right coronary/circumflex), the frequency and quality of revascularisation of distal vessels. The only significant differences were the higher incidence of severe lesions (90 p. 100) of the right coronary and circumflex arteries and of stenosis of the first large septal branch of the LAD artery in Group A (p less than 0.05). These results show that the indications for coronary angiography in biventricular inferior infarction are no greater than those in mono LV inferior infarction. This supports experimental data on the physiopathology of RV infarction which demonstrates that except in cases of proximal thrombosis of the right coronary artery, the possibilities of revascularisation from the left coronary tree are limited.

Adult↗
PubMed2003

QR in V1--an ECG sign associated with right ventricular strain and adverse clinical outcome in pulmonary embolism.

AIMS: To test the hypothesis that Qr in V(1)is a predictor of pulmonary embolism, right ventricular strain, and adverse clinical outcome. METHODS AND RESULTS: ECG's from 151 patients with suspected pulmonary embolism were blindly interpreted by two observers. Echocardiography, troponin I, and pro-brain natriuretic peptide levels were obtained in 75 patients with pulmonary embolism. Qr in V(1)(14 vs 0 in controls; p<0.0001) and ST elevation in V(1)> or =1 mV (15 vs 1 in controls; p=0.0002) were more frequently present in patients with pulmonary embolism. Sensitivity and specificity of Qr in V(1)and T wave inversion in V(2)for predicting right ventricular dysfunction were 31/97% and 45/94%, respectively. Three of five patients who died in-hospital and 11 of 20 patients with a complicated course, presented with Qr in V(1). After adjustment for right ventricular strain including ECG, echocardiography, pro-brain natriuretic peptide and troponin I levels, Qr in V(1)(OR 8.7, 95%CI 1.4-56.7; p=0.02) remained an independent predictor of adverse outcome. CONCLUSIONS: Among the ECG signs seen in patients with acute pulmonary embolism, Qr in V(1)is closely related to the presence of right ventricular dysfunction, and is an independent predictor of adverse clinical outcome.

Arrhythmias, Cardiac↗
PubMed1996

Spontaneous closure of the human fetal ductus arteriosus--A cause of fetal congestive heart failure.

OBJECTIVE: Closure of the fetal ductus arteriosus, which is usually due to nonsteroidal antiinflammatory agents, may be detrimental. Therefore prenatal and postnatal clinical and echocardiographic findings in four human fetuses with spontaneous ductus arteriosus occlusion are reported. STUDY DESIGN: Echocardiographic and clinical data were retrospectively analyzed. RESULTS: Spontaneous closure of the ductus arterious was discovered in four fetuses (gestational age 34 to 38 weeks). No mother had received nonsteroidal antiinflammatory agents. Enlargement of the right heart and pulmonary arteries and tricuspid and pulmonary regurgitation were present in all cases. Two fetuses had right ventricular hypertension. Postnatally their right ventricular function recovered promptly. The others had severe right heart failure with abnormal umbilical venous pulsations. After immediate delivery none had signs of persistent pulmonary hypertension. However, they have echocardiographic evidence of right ventricular dysfunction 2 to 6 months after delivery. CONCLUSIONS: Occlusion of the fetal ductus arteriosus may also occur in the absence of treatment with nonsteroidal antiinflammatory agents. Immediate delivery resulted in good clinical outcome, although right ventricular dysfunction may persist.

Constriction, Pathologic↗
PubMed2006

Age- and training-dependent development of arrhythmogenic right ventricular cardiomyopathy in heterozygous plakoglobin-deficient mice.

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is an inherited disorder that causes sudden death and right ventricular heart failure in the young. Clinical data suggest that competitive sports may provoke ARVC in susceptible persons. Genetically, loss-of-function mutations in desmosomal proteins (plakophilin, desmoplakin, or plakoglobin) have been associated with ARVC. To test the hypothesis that reduced desmosomal protein expression causes ARVC, we studied the cardiac effects of heterozygous plakoglobin deficiency in mice. METHODS AND RESULTS: Ten-month-old heterozygous plakoglobin-deficient mice (plakoglobin+/-) had increased right ventricular volume, reduced right ventricular function, and spontaneous ventricular ectopy (all P<0.05). Left ventricular size and function were not altered. Isolated, perfused plakoglobin+/- hearts had spontaneous ventricular tachycardia of right ventricular origin and prolonged right ventricular conduction times compared with wild-type hearts. Endurance training accelerated the development of right ventricular dysfunction and arrhythmias in plakoglobin+/- mice. Histology and electron microscopy did not identify right ventricular abnormalities in affected animals. CONCLUSIONS: Heterozygous plakoglobin deficiency provokes ARVC. Manifestation of the phenotype is accelerated by endurance training. This suggests a functional role for plakoglobin and training in the development of ARVC.

Aging↗
PubMed2002

Right ventricular cardiomyopathy in beta-thalassaemia major.

AIMS: To evaluate right ventricular function in patients with beta-thalassaemia major and congestive heart failure. Background In patients with beta-thalassaemia major a high incidence of cardiac involvement still exists despite improved prognosis with chelation therapy. Development of severe right heart failure is common and has been attributed to pulmonary hypertension secondary to lung haemochromatosis. However, the possibility of direct right ventricular myocardial involvement in the absence of significant pulmonary hypertension has not been adequately investigated. METHODS: Twenty-nine consecutively screened patients with beta-thalassaemia major and congestive heart failure were investigated by Doppler echocardiography, right ventricular first-pass radionuclide examination and cardiac catheterization. Haemodynamic data were obtained both before and after volume loading. A control group of 39 patients with beta-thalassaemia major, free from cardiac disease, and matched for age, gender, body surface area and heart rate was used for comparison. A subset of the control thalassaemic group (n=15) underwent both radionuclide and haemodynamic assessment. RESULTS: The majority of patients were on non-optimal chelation therapy. Only two of 29 patients were found to have cor pulmonale. One other patient suffered from constrictive pericarditis. A restrictive filling pattern in both ventricles and left ventricular systolic dysfunction were evident in the other 26 patients. Pulmonary artery pressure (systolic, 33+/-8 vs 27+/-5 mmHg, P<0.05) and pulmonary vascular resistance (114+/-56 vs 65+/-29 dynes. s. cm(-5), P<0.01) were only mildly elevated in the heart failure group. After volume challenge, cardiac output remained unchanged although the increments of ventricular filling pressures were significant (Deltaright atrial: 4.8+/-2.2 mmHg, P<0.05; Deltapulmonary capillary wedge: 5.6+/-2.9 mmHg, P<0.05) and correlated with each other (r=0.69;P<0.001) in heart failure patients, suggesting pericardial constraint and ventricular interaction. In these patients compared with the control thalassaemic group, a lower right ventricular ejection fraction (29%+/-9 vs 59%+/-6, P<0.0001) without correlation with pulmonary artery pressures was found. Haemodynamically significant right ventricular dysfunction defined as mean right atrial pressure >10 mmHg and ratio of mean right atrial-to-capillary wedge pressure >0.8 was evident in 15 of the 26 patients (58%), all with severe symptoms, representing three fourths of the patients in functional class III and IV. Simultaneous pressure recordings in six of these 15 patients showed equalization of ventricular end-diastolic pressures within 5 mmHg. CONCLUSION: The majority of patients with beta-thalassaemia major and severe congestive heart failure demonstrated a unique haemodynamic pattern similar to that described in predominant right ventricular infarction, indicating severe right ventricular cardiomyopathy in addition to left ventricular dysfunction. The incidence of cor pulmonale as a cause of right heart failure seems to be much lower than previously hypothesized.

Adult↗
PubMed2004

Echocardiographic visualization of acute pulmonary embolus and thrombolysis in the ED.

Echocardiography has been used to diagnose acute right-sided dysfunction arising from pulmonary embolism (PE). Rarely, it can visualize the embolic material in the right heart cavities. We report a case of acute PE that was seen in the right ventricle and right pulmonary artery using bedside transthoracic echocardiography in the ED. As a result of the prompt diagnosis of a massive embolus and associated right ventricular dysfunction, the patient was treated with thrombolytics. Serial echocardiographs confirmed the response to therapy and the dissolution of thrombi. In this report, echocardiographic findings of acute PE and indications of thrombolytics in PE are also reviewed from the literature. Based on available evidence, those patients who present with cardiogenic shock from PE, and young patients with acute PE leading to right ventricular dysfunction benefit the most from early thrombolytic therapy.

Adult↗
PubMed1994

Life-threatening arrhythmias and RV dysfunction after surgical repair of tetralogy of Fallot. Comparison between transventricular and transatrial approaches.

BACKGROUND: Late postoperative arrhythmias and right ventricular dysfunction may occur after classic repair of tetralogy of Fallot. METHODS AND RESULTS: During a mean follow-up of 8.9 years (range, 5 to 14 years), 24-hour ambulatory electrocardiographic studies were done in 107 patients after repair of tetralogy of Fallot. Radionuclide angiography was performed in 97, and 78 patients also underwent postoperative heart catheterization. The patients were divided into two groups: group A consisted of 71 patients aged 2 months to 61 years (mean, 6.8 years) in whom the right ventricular approach was used; group B included 36 patients aged 8 months to 39 years (mean, 7.9 years) whose repair was through the right atrium. A transannular patch was employed in 42 (59.2%) patients in group A and in 23 (63.9%) patients in group B. Eighteen patients were adults (> 18 years old) at the time of surgery: 13 (18.3%) in group A and 5 (13.8%) in group B. During a mean follow-up of 9.7 years, 57 (80.3%) group A patients were in New York Heart Association (NYHA) functional class I. Atrial flutter was present in 3 (4.2%) patients, and 28 (39.4%) had significant ventricular arrhythmias (> or = Lown grade 2). Postoperative heart catheterization showed good hemodynamic results in 36 of 54 group A patients studied (12 of whom had ventricular arrhythmias); moderate-to-severe pulmonary regurgitation was present in 14 (25.9%) patients; only 2 (3.7%) patients had right ventricular hypertension. On electrophysiological study, 8 of 28 (28.6%) patients in group A had inducible sustained ventricular tachycardia. Despite antiarrhythmic therapy, 2 of these patients died suddenly, presumably from ventricular arrhythmias. Two other late deaths in group A were caused by heart failure. During a mean follow-up of 7.2 years, 33 of 36 (91.7%) patients in group B were in NYHA functional class I. Atrial flutter was not found in any patient in this group. Only 1 (2.8%) patient, who had moderate-to-severe pulmonary regurgitation, had significant ventricular arrhythmias (> or = Lown grade 2). Postoperative catheterization showed good hemodynamic results in 20 of 24 patients; 3 (12.5%) had moderate-to-severe pulmonary regurgitation, and 1 (4.2%) patient had right ventricular hypertension. Sustained ventricular tachycardia could not be induced in any of the 5 adult patients who underwent electrophysiological studies. One late death (caused by endocarditis) occurred in group B. CONCLUSIONS: The right atrial approach significantly reduced the risk of life-threatening ventricular arrhythmias after repair of tetralogy of Fallot (P < .001) without increasing the incidence of supraventricular arrhythmias. Right ventricular dysfunction and severe pulmonary regurgitation were also more prevalent (P < .01) when the right ventricular approach was used.

Arrhythmias, Cardiac↗
PubMed2000

Five-minute recording of heart rate variability in severe chronic heart failure: correlates with right ventricular function and prognostic implications.

BACKGROUND: In advanced chronic heart failure (CHF), correlation between heart rate variability (HRV) and parameters of disease severity is still unclear. A reduced HRV has been related to left but not to right ventricular function parameters. Moreover, the prognostic role of spectral measures is not fully defined. We sought to assess HRV by using a short electrocardiographic recording in ambulatory patients with severe CHF to investigate the relation of HRV with clinical neurohormonal and hemodynamic parameters and to determine its predictive prognostic power. METHODS AND RESULTS: HRV was obtained from 5-minute electrocardiographic recordings in 75 ambulatory patients with CHF referred for heart transplantation screening. Standard frequency-domain parameters (total power, low-frequency power, and high-frequency power) were calculated. Prognostic value of these autonomic markers and their correlation with clinical and instrumental parameters were also assessed. A low low-frequency/high-frequency ratio was an independent predictor of cardiac events (P =.015). No correlation was found between New York Heart Association class and HRV, whereas significant correlations were identified between norepinephrine plasma levels, several hemodynamic parameters, and spectral measures (P < or =.03). A reduced HRV, particularly a low-frequency power reduction (P =.000), was highly related to indexes of right ventricular dysfunction. CONCLUSIONS: The current data indicate that spectral analysis of HRV, calculated from short electrocardiographic recordings, may represent a simple but effective means contributing to risk stratification of patients with severe CHF. Autonomic information obtained from this analysis suggests that right ventricular dysfunction may be a critical element determining autonomic imbalance in patients with severe CHF.

Biomarkers↗
PubMed2005

Modern surgical treatment of massive pulmonary embolism: results in 47 consecutive patients after rapid diagnosis and aggressive surgical approach.

OBJECTIVES: This study retrospectively reviews an aggressive multidisciplinary approach to the treatment of massive pulmonary embolism, centering on rapid diagnosis with contrast-enhanced computed tomography of the chest to define the location and degree of clot burden and transthoracic echocardiography to document right ventricular strain followed by immediate surgical intervention when appropriate. METHODS: Between October 1999 through February 2004, 47 patients (30 men and 17 women; median age, 58 years; age range, 24-86 years) underwent emergency surgical embolectomy for massive central pulmonary embolism. The indications for surgical intervention were (1) contraindications to thrombolysis (21/47 [45%]), (2) failed medical treatment (5/47 [10%]), and (3) right ventricular dysfunction (15/47 [32%]). Preoperatively, 12 (26%) of 47 patients were in cardiogenic shock, and 6 (11%) of 47 were in cardiac arrest. RESULTS: There were 3 (6%) operative deaths, 2 with preoperative cardiac arrest; 2 of these 3 patients required a right ventricular assist device. In 38 (81%) patients a caval filter was placed intraoperatively. Median length of stay was 11 days (range, 3-75 days). Median follow-up was 27 months (range, 2-50 months); follow-up was 100% complete in surviving patients. There were 6 (12%) late deaths, 5 of which were from metastatic cancer. Actuarial survival at 1 and 3 years' follow-up was 86% and 83%, respectively. CONCLUSION: An aggressive approach to large pulmonary embolus, including rapid diagnosis and prompt surgical intervention, has improved results with surgical embolectomy. We now perform surgical pulmonary embolectomy not only in patients with large central clot burden and hemodynamic compromise but also in hemodynamically stable patients with right ventricular dysfunction documented by means of echocardiography.

Actuarial Analysis↗
PubMed2003

Atelectasis causes vascular leak and lethal right ventricular failure in uninjured rat lungs.

During mechanical ventilation, lung recruitment attenuates injury caused by high VT, improves oxygenation, and may optimize pulmonary vascular resistance (PVR). We hypothesized that ventilation without recruitment would induce injury in otherwise healthy lungs. Anesthetized rats were ventilated with conventional mechanical ventilation (VT 8 ml/kg; respiratory frequency 40 per minute) and 21% inspired oxygen, with or without a recruitment strategy consisting of recruitment maneuvers plus positive end-expiratory pressure, in the presence or absence of a laparotomy. Additional experiments examined the impact of atelectasis on right ventricular function using echocardiography, as well as functional residual capacity and PVR. Lack of recruitment resulted in reduced overall survival (59% nonrecruited vs. 100% recruited, p < 0.05), increased microvascular leak, greater impairment of oxygenation and lung compliance, increased PVR, and elevated plasma lactate. Echocardiography demonstrated that right ventricular dysfunction occurred in the absence of recruitment. Finally, samples from nonrecruited lungs demonstrated ultrastructural evidence of microvascular endothelial disruption. Although such effects clearly do not occur with comparable magnitude in the clinical context, the current data suggest novel mechanisms (microvascular leak, right ventricular dysfunction) whereby derecruitment may contribute to development of lung injury and adverse systemic outcome.

Animals↗
PubMed2004

Right ventricular targeted gene transfer of a beta-adrenergic receptor kinase inhibitor improves ventricular performance after pulmonary artery banding.

OBJECTIVE: Abrupt increases in right ventricular afterload occur after cardiac transplantation and pulmonary artery banding, which can result in right ventricular hypertrophy and dilatation. Right ventricular dysfunction is also accompanied by beta-adrenergic receptor desensitization. We sought to determine whether selective right ventricular expression of a transgene encoding a beta-adrenergic receptor kinase inhibitor can improve right ventricular remodeling early after pulmonary artery banding. METHODS: Rabbits underwent pulmonary artery banding 3 days after percutaneous right coronary artery injection of empty adenovirus (n = 19), a control adenovirus containing the beta-galactosidase transgene (n = 10), or an adenovirus containing the beta-adrenergic receptor kinase inhibitor transgene (n = 14). Sham-operated animals (n = 7) underwent instrumentation without deployment of the pulmonary artery band. Right ventricular function was assessed in each rabbit before and 7 days after pulmonary artery banding. Right ventricular mass and dimensions (surface area and volume) were obtained, and biochemical analysis was performed to confirm transgene expression and to characterize beta-adrenergic receptor signaling. RESULTS: Right ventricular mass was increased in animals treated with adenovirus containing the beta-adrenergic receptor kinase inhibitor transgene, adenovirus containing the beta-galactosidase transgene, and empty adenovirus after banding when compared with results in sham-operated animals. However, right ventricular volume and surface area, as measures of dilatation, were significantly lower in pulmonary artery banded rabbits pretreated with adenovirus containing the beta-adrenergic receptor kinase inhibitor transgene when compared with those treated with empty adenovirus or adenovirus containing the beta-galactosidase transgene. Right ventricular contractility and defective beta-adrenergic receptor signaling were significantly enhanced in rabbits expressing the beta-adrenergic receptor kinase inhibitor after pulmonary artery banding. CONCLUSIONS: Right ventricular preconditioning with the beta-adrenergic receptor kinase inhibitor transgene can attenuate the early right ventricular dilatation and dysfunction associated with pulmonary artery banding. Thus beta-adrenergic receptor kinase inhibition might represent a novel target for limiting ventricular remodeling after increased right ventricular afterload.

Adenoviridae↗