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At least 1,207 records · Page 67Linked to original sources
PubMed2004

Timing and type of surgery for severe pulmonary regurgitation after repair of tetralogy of Fallot.

Repaired tetralogy of Fallot (rTOF) has an excellent long-term prognosis; however, survival is somewhat less than normal. Of all the residual lesions and sequellae after rTOF, pulmonary regurgitation (PR) is the most important, correlating with right ventricular (RV) size, exercise intolerance and serious ventricular arrhythmias. Pulmonary valve replacement (PVR) has beneficial effects on RV size and function, provided it is performed early, before irreversible RV dysfunction ensues. Moreover, PVR is associated with an improvement in patients' symptoms and exercise tolerance and combined with arrhythmia surgery (cryoablation) it leads to a dramatic decrease in the incidence of fatal ventricular arrhythmias. Associated lesions, especially branch pulmonary artery stenosis, which aggravates PR, and tricuspid regurgitation, which further impacts on RV size and function, need addressing. Large right ventricular outflow (RVOT) akinetic and aneurysmal regions are frequent and further compromise RV function; therefore, resection during PVR should be attempted. Despite excellent mid-term results, homografts and xenografts, usually used for RVOT reconstruction, suffer late dysfunction and failure, committing patients and surgeons to further operations. Therefore, the decision to operate should be based on the balance between progressive RV dilatation, exercise intolerance, symptoms, arrhythmias and the fact that further reoperations will be needed. Research on the ideal valve for RVOT reconstruction is ongoing. Prospective follow-up of patients with rTOF with exercise testing and assessment of RV size and function, preferably with magnetic resonance, will define better the natural history of the disease and will probably provide firm guidelines for PVR timing especially in asymptomatic patients.

Arrhythmias, Cardiac↗
PubMed2005

Late outcome of Senning and Mustard procedures for correction of transposition of the great arteries.

OBJECTIVES: To evaluate late mortality and morbidity after an atrial switch procedure for correction of transposition of the great arteries (TGA) and to assess predictive factors for adverse outcome. SETTING: Tertiary referral centre. DESIGN AND PATIENTS: Retrospective follow up study of 137 patients surviving hospitalisation for TGA atrial switch procedure (Mustard or Senning) in a single institution and divided into two groups (simple and complex) depending on presurgical anatomy. Several surgical and follow up factors were evaluated during 16.7 (5.6) years' follow up. RESULTS: Late mortality was 5.1% (95% confidence interval 1.37% to 8.84%) with sudden death as the most common cause. No significant difference was found between Mustard and Senning procedures and between the complex and simple groups in terms of mortality. Independent predictive factors for late mortality were a history of supraventricular tachyarrhythmias and advanced New York Heart Association (NYHA) functional class during follow up. A very common finding was development of sinus node dysfunction (47.6%), which had no influence on mortality. There was little need for reintervention (5.1%) and relatively few cases of right ventricular systolic dysfunction (14.6%). During follow up, most patients (96.2%) were in NYHA functional class I-II. CONCLUSIONS: Overall long term outcomes of patients with atrial repair of TGA in the present era are encouraging in terms of late mortality and quality of life. Nevertheless, better outcomes may be offered through improved diagnostic methods for right ventricular function and better management of supraventricular tachyarrhythmias.

Adolescent↗
PubMed1997

Detection of pulmonary emboli and associated right heart dysfunction by combining ventilation perfusion lung scanning and xenon ventriculography.

PURPOSE: The authors sought to determine if the right ventricular ejection fraction (RVEF), as measured by xenon ventriculography, is depressed in patients with pulmonary emboli. The authors also sought to correlate any decrement in RVEF with the extent of lung perfusion defects. MATERIALS AND METHODS: The authors identified all patients who had lung ventilation-perfusion (V/Q) scans between January 1994 and December 1996, that were interpreted as high probability for pulmonary embolism. From these patients, the authors selected those who had undergone concurrent xenon ventriculography (XV) (n = 23), and then reprocessed the initial ventriculography data for confirmation. The authors also reviewed original V/Q scans, chest radiographs, and clinical data. A control group was drawn from patients with normal V/Q scans who had undergone XV. RESULTS: Fifteen patients (65%) with high probability V/Q scans had an abnormally low RVEF (< .32). Patients with high probability V/Q scans also had a significantly lower mean RVEF (0.28 +/- .08) than patients with normal V/Q scans (.39 +/- .08 SD). The degree of RVEF decline correlated poorly with the number of segmental perfusion defects (r = -.39). CONCLUSIONS: RVEF is often depressed in patients with high probability V/Q scans. XV can identify these patients, while routine lung V/Q scans cannot.

Adult↗
PubMed2005

Magnetic resonance imaging in experimental Chagas disease: a brief review of the utility of the method for monitoring right ventricular chamber dilatation.

Chagas' disease caused by infection with Trypanosoma cruzi leads to a myocardiopathy that evolves from the acute to the chronic phase. Magnetic resonance imaging (MRI) is an important tool for monitoring cardiac morphology and function both in humans and in animals. In the present work, we present a brief review of MRI applications for the study of ventricular hypertrophy and dilatation of the right ventricle in murine models of Chagas' disease. Studies using MRI demonstrate an increase in right ventricular chamber dimension during both phases of infection, indicating that increase of the right ventricle is a marker for experimental chagasic myocardiopathy. Based on previous studies using MRI in these models we propose that this technique is an excellent approach for monitoring heart functionality from the acute through the chronic phase of infection in different parasite-host pairs and for monitoring the efficacy of cardioprotective or immune-therapeutic agents.

Animals↗
PubMed2001

Right ventricular cardiomyopathy accompanied by protein-losing enteropathy and chylous effusion.

Severe right-side heart failure developed in a 47-year-old Japanese woman who suffered from hypoalbuminemia and a massive right side chylous pleural effusion. She had been diagnosed as having protein-losing enteropathy with right ventricular cardiomyopathy. Autopsy showed congenital anomalies of the lymph ducts and abnormal deposition of fibrous and fatty tissue in the right ventricular myocardium. The clinical and pathological findings are consistent with the nonarrythmogenic form of the arrythmogenic right ventricular dysplasia.

Adult↗
PubMed1995

[Outcome of arrhythmogenic right ventricular dysplasia. Apropos of 4 cases].

The authors propose a classification of the outcome of arrhythmogenic right ventricular dysplasia with reference to 4 selected cases with a follow-up period of over 9 years. In type I, the left ventricular ejection fraction is normal (EF > 50%) and the risk, exclusively arrhythmic, can be controlled by appropriate antiarrhythmic therapy. This is the commonest form of arrhythmogenic right ventricular dysplasia with different varieties according to the degree of dilatation of the right ventricle. In type II, there is a variable degree of left ventricular involvement (30 < EF < 50%) either by extension of a comparable disease process as observed in the right ventricle or by an isolated or superimposed phenomenon of myocarditis. This form is stable and may remain stable for many years providing the arrhythmias are correctly treated. In type III, progressive degradation of the myocardium is observed over a period of about 10 years with a clinical presentation comparable to that of certain arrhythmogenic dilated cardiomyopathies which are often hereditary. In this case, the patients have an arrhythmic risk associated with that of cardiac failure which becomes progressively irreversible. The histology shows interstitial fibrosis with biventricular lymphocytic infiltration suggesting an autoimmune phenomenon. Therefore, the classification of cases of arrhythmogenic right ventricular dysplasia depends on the potential evolutivity of the lesions. When the patient is seen in the early stages of the disease, the prognosis should be garded, especially in a hereditary form.

Adult↗
PubMedDate not supplied

Right ventricular myocardial infarction: presentation and acute outcomes.

Acute inferior wall myocardial infarction can be complicated by right ventricular myocardial infarction (RVMI), and the excess mortality cannot be fully explained by mechanical reasons. The authors try to systematically assess the incidence, clinical presentation and early outcomes of right ventricular infarction in a tertiary-care setup. Their study was a prospective observational series of consecutive patients with RVMI. All patients with acute inferior myocardial infarction (n=135) were enlisted. RVMI was diagnosed by > or = 1 mm ST elevation in lead V(4R) in a right-sided electrocardiogram. Right ventricular (RV) infarction occurred in 37% (n=50) of patients with acute inferior infarctions. Patients with isolated inferior infarction served as controls (n=85). Echocardiography was performed within 24 hours of admission. From both groups, 66% qualified for thrombolysis. The incidence of hypotension-bradycardia and heart blocks requiring pacing support was much higher in right ventricular infarction (n=21) than in inferior infarction (n=13). Clinically manifest RV dysfunction (raised jugular venous pulse [JVP], hypotension, tricuspid regurgitation) and right ventricular dilation detected by echocardiography were seen in only 13 patients. The in-hospital mortality rate was significantly higher (n=8, 16%) in right ventricular infarction group than in inferior infarction group (n=3, 3.5%). Right ventricular infarction was seen in a third of inferior myocardial infarctions (IMIs), but hemodynamically evident right ventricular dysfunction occurred in only a tenth of acute IMIs. Nevertheless, the acute in-hospital mortality rate of patients with right ventricular infarction was much higher than in those with inferior infarction owing to arrhythmic and mechanical complications.

Female↗
PubMed1993

Right ventricular thallium-201 kinetics in pulmonary hypertension: relation to right ventricular size and function.

Right ventricular ischemia occurs in experimental models of pulmonary hypertension. We analyzed right ventricular size and function and 201Tl uptake to determine if there was a relationship between 201Tl uptake and systolic function in 19 patients with pulmonary artery hypertension who were being evaluated for heart-lung transplantation. All patients had dipyridamole stress 201Tl scintigraphy, radionuclide angiography and echocardiography. In nine patients (Group 1), right ventricular ejection fraction was < 30% (mean 22% +/- 8%). In 10 patients (Group 2) it was > 30% (mean 45% +/- 11%). In Group 1, right ventricular 201Tl uptake in the lateral wall after dipyridamole was increased compared to Group 2 (40% +/- 7% versus 28% +/- 15% counts/pixel, p < 0.05) while left ventricular free wall uptake was similar. The ratio of right to left ventricular 201Tl uptake was increased in Group 1 versus Group 2 (0.81% +/- 0.30% versus 0.49% +/- 0.18%, p < 0.05). At 4 hr, right ventricular free wall 201Tl clearance was comparable, 51% +/- 13% versus 51% +/- 18% in Groups 1 and 2, respectively. No patient had perfusion abnormalities. Right ventricular ejection fraction was inversely related to dipyridamole stress right ventricular 201Tl uptake, r = -0.49, p < 0.03, s.e.e. = 13.6. Right ventricular 201Tl uptake was directly related to right ventricular wall thickness (r = 0.56, p = 0.18, s.e.e. = 10.4). Therefore, patients with more severe right ventricular systolic dysfunction have greater 201Tl uptake after dipyridamole stress, suggesting increased myocardial mass and possibly blood flow in response to hypertrophy. Patients with the most marked hypertrophy have impairment of right ventricular systolic function, independent of ischemia.

Adult↗
PubMed1996

Cytoskeletal role in the contractile dysfunction of cardiocytes from hypertrophied and failing right ventricular myocardium.

We have shown on the levels of the sarcomere and the cardiocyte that increased microtubule density accounts, to a remarkable degree, for the contractile dysfunction characteristic of pressure-overload right ventricular hypertrophy. In this study, we have asked whether these linked phenotypic and contractile abnormalities persist during the transition to right heart failure in this model and whether, following this transition, microtubule depolymerization remains effective in restoring normal cellular contractile function when characterized in terms of sarcomere mechanics. The feline right ventricle was pressure overloaded by pulmonary artery banding. The quantity of microtubules was estimated from immunoblots and immunofluorescent micrographs, and their mechanical effects were assessed by measuring sarcomere motion during microtubule depolymerization. These measurements were made in control cats and in operated cats having right ventricular hypertrophy alone or hypertrophy with associated right heart failure; the left ventricle from each heart served as a normally loaded same-animal control. We show here both that alterations in microtubule density and sarcomere mechanics are a persistent and progressive feature of the hypertrophied and then failing cat right ventricle and that the ratio of polymerized to free tubulin is selectively increased in the failing right ventricle. The mechanical defect, though more severe in failing than in hypertrophied right ventricles, was normalized by microtubule depolymerization. Because we find persistent and progressive increases both in microtubules and in the functional consequence of aberrant sarcomere mechanics during the transition from hypertrophy to failure when right ventricular pressure overloading is severe, this cytoskeletal abnormality may well contribute to the contractile dysfunction characteristic of right heart failure in this model.

Animals↗