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Results for “Ventricular Dysfunction, Right”

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At least 1,441 records · Page 80Linked to original sources
PubMed2002

Analysis of atrioventricular plane movements by Doppler tissue imaging and M-mode in children with atrial septal defects before and after surgical and device closure.

Our objective was to compare the effects of surgical and device closure of atrial septal defects (ASDs) on atrioventricular plane function. In healthy individuals, both short- and long-axis motion contribute to ventricular pump function. Short-axis function (i.e., the amplitude and velocity of atrioventricular plane movements) may be evaluated by M-mode and Doppler tissue imaging. The study group consisted of 19 children with ASD of the secundum type before and after surgical (n = 12) or device (n = 7) closure and 10 healthy controls. Surgical and device closures were uncomplicated and all defects were completely closed. Registrations of atrioventricular plane systolic and diastolic amplitude and velocity were made from the tricuspid and the mitral annulus and from the septum in the apical four-chamber view. Comparisons were made between examinations before and after closure, between the two subgroups of patients treated by surgical and device closure, respectively, and between the patient group and the control groups. Before ASD closure, all measurements were normal or near normal. After surgery, systolic amplitudes and velocities of the tricuspid annulus and in the septum decreased significantly, whereas no changes were seen in the device group. Less marked changes were seen in diastolic measurements. However, in the surgical group significant decrease to subnormal values were found in the tricuspid annulus and in the septum, which may indicate a decreased diastolic function postoperatively. Mitral valve annulus amplitude and velocity were not affected by the treatment. Atrioventricular function is normal in children with right ventricular volume overload. The decrease to subnormal values after open-heart surgery is not seen after device closure of the ASD, indicating that surgery affects right ventricular function.

Adolescent↗
PubMed2003

Right ventricular involvement in myocardial infarction and cardiogenic shock.

CONTEXT: Right ventricular involvement in acute myocardial infarction and cardiogenic shock has received little attention by clinicians and researchers, although its pathophysiology, clinical presentation, and natural history are distinctly different from those of left ventricular infarction and associated cardiogenic shock. Right ventricular shock has important therapeutic implications for the management of patients, which need to be recognised. STARTING POINT: Investigators at the SHOCK Registry (Alice Jacobs and colleagues, J Am Coll Cardiol 2003; 341: 1273-79) evaluated 49 patients with cardiogenic shock predominantly due to right ventricular infarction and compared them with 884 patients with cardiogenic shock and predominantly left ventricular failure. Perhaps surprisingly, these investigators found that the in-hospital mortality of patients with right ventricular shock was not significantly lower than that of patients with left ventricular shock (53% vs 61%, p=0.296), despite the fact that patients with right ventricular shock were younger, with a lower prevalence of previous infarctions, fewer anterior infarct locations, and less multivessel disease. There was a shorter median time between index infarction and diagnosis of shock in patients with right ventricular shock. In multivariate analysis, right ventricular shock was not an independent predictor of lower in-hospital mortality. WHERE NEXT? The unexpectedly high mortality of patients with cardiogenic shock due to predominantly right ventricular infarction challenges the general notion that right ventricular involvement in myocardial infarction has only little relevance for patient's outcome. Therefore, more attention should be given to the detection of right ventricular involvement in acute myocardial infarction and particularly in cardiogenic shock. If right ventricular shock is diagnosed, urgent reperfusion of the infarct related artery and appropriate circulatory support are required.

Adult↗
PubMed2001

Transient but marked ST elevation in precordial leads caused by ischemia of the isolated right ventricular branch.

The present case is a 64 year-old man in whom transient but marked ST elevation was confirmed in the contralateral precordial leads (V1-3) during percutaneous transluminal coronary angioplasty (PTCA) of the proximal right coronary artery, suggesting that the patient had anteroseptal ischemia. The ST elevation persisted even after the balloon was deflated, and no changes in the left coronary artery were detected. In addition, blood flow in the affected area of the right coronary artery was favorable and there was a transient delay only in the right ventricular branch. Once blood flow in the right ventricular branch improved, ST returned to baseline, and when the right ventricular branch was again occluded by the balloon, ST elevation occurred in a reproducible manner. Hence, the electrocardiographic changes in the precordial leads were caused by occlusion of the right ventricular branch. It is rare to observe ST elevation caused by isolated right ventricular branch ischemia.

Angioplasty, Balloon, Coronary↗
PubMed1995

[Arrhythmogenic right ventricular dysplasia. Report of a familial case].

Arrhythmogenic right ventricular dysplasia is a pathologic condition of unknown origin that primarily affects the right ventricle free wall characterized by progressive atrophy with fibrous-fatty substitution of the myocardium. The patient affected may present in childhood or as an adult with cardiomegaly or/and ventricular arrhythmias with a left bundle branch block configuration. The reports of familial occurrence suggest the etiologic role of a genetic defect with autosomal dominance and variable expression and penetrance, an alternative, myocarditis (toxic or infectious) is a possible cause. The aim of the present study is an non-invasive instrumental evaluation of the family of a young patient affected by arrhythmogenic right ventricle dysplasia. The authors evaluated 10 patients, 7 women and 3 men, all asymptomatic, with electrocardiography, exercise stress test on a bicycle ergometer, 24-hour Holter monitoring and two-dimensional echocardiography. A patient had certain ARVD diagnosis, while in the other 9 patients all the instrumental investigations were normal. This observation seem to confirm that ARVD may be familial and justify a systematic in-depth familial study in all demonstrated cases of ARVD and the follow-up of all patients identified who had arrhythmias or isolated right ventricular morphologic anomalies.

Adolescent↗
PubMed2005

Left heart lesions in patients with Ebstein anomaly.

OBJECTIVE: To identify the incidence of left heart abnormalities in patients with Ebstein anomaly, recognizing that left-sided lesions in this patient group have been overlooked. PATIENTS AND METHODS: According to the echocardiography database at the Mayo Clinic in Rochester, Minn, 106 consecutive patients with Ebstein anomaly underwent echocardiography between July 1, 2001, and February 28, 2003. Clinical data as well as electrocardiographic and echocardiographic reports and images were reviewed. RESULTS: Ebstein anomaly was severe in 76 patients (72%). Previous tricuspid valve surgery was reported in 46 patients (43%), and previous closure of an atrial septal defect or patent foramen ovale was reported in 34 patients (32%). Left ventricular (LV) myocardial changes resembling noncompaction occurred in 19 patients (17.9%), LV systolic dysfunction in 7 patients (7%), LV diastolic dysfunction in 34 (36%) of 95 patients, and LV dilatation in 4 patients (4%). Additional left-sided cardiac lesions included mitral valve prolapse in 16 patients (15%), bicuspid aortic valve in 8 (8%), mitral valve dysplasia in 4 (4%), and ventricular septal defect in 8 (8%). Wolff-Parkinson-White syndrome occurred in 22 patients (21%). The QRS axis tended to be different in LV noncompaction with a mean +/- SD axis of 12 degrees +/- 74 degrees vs 36 degrees +/- 66 degrees overall (P=.08). Otherwise, there were no differences in clinical or surgical data between the groups with normal and abnormal LV myocardium. CONCLUSIONS: In patients with Ebstein anomaly, left heart abnormalities involving the myocardium or valves were observed in 39% of patients. Ebstein anomaly should not be regarded as a disease confined to the right side of the heart.

Adolescent↗
PubMed2001

Right ventricular dysplasia in an asymptomatic young man: an uncommon case with biventricular involvement and no known family history.

A 33-year-old man had cardiomegaly on a routine x-ray examination. He was asymptomatic with no history of infarction, syncope, or palpitations. There was no family history of congenital heart disease or sudden death. Two-dimensional transthoracic echocardiography demonstrated marked enlargement of the right atrium and ventricle with severely depressed right and left ventricular function that was consistent with right ventricular dysplasia. The patient was treated with an angiotensin-converting enzyme inhibitor and did well for 6 months, but then developed symptomatic left-sided congestive heart failure. Short-term improvement was obtained with intravenous inotropic therapy, but he continued to have progressive symptoms of heart failure. Approximately 7 months after his initial presentation, the patient underwent orthotopic heart transplantation for intractable congestive heart failure. Pathologic examination of the explanted heart established the diagnosis of right ventricular dysplasia with left ventricular involvement. This is an uncommon presentation of right ventricular dysplasia with biventricular involvement and no known family history.

Adult↗
PubMed2002

Pure right ventricular infarction.

A 76-year-old man with chest pain was admitted to hospital where electrocardiography (ECG) showed ST-segment elevation in leads V1-4, indicative of acute anterior myocardial infarction. ST-segment elevation was also present in the right precordial leads V4R-6R. Emergency coronary angiography revealed that the left coronary artery was dominant and did not have significant stenosis. Aortography showed ostial occlusion of the right coronary artery (RCA). Left ventriculography showed normal function and right ventriculography showed a dilated right ventricle and severe hypokinesis of the right ventricular free wall. Conservative treatment was selected because the patient's symptoms soon ameliorated and his hemodynamics was stable. 99mTc-pyrophosphate and 201Tl dual single-photon emission computed tomography showed uptake of 99mTc-pyrophosphate in only the right ventricular free wall, but no uptake of 99mTc-pyrophosphate and no perfusion defect of 201Tl in the left ventricle. The peak creatine kinase (CK) and CK-MB were 1,381 IU/L and 127 IU/L, respectively. His natural course was favorable and the chest pain disappeared under medication. Two months after the onset, the ECG showed poor R progression in leads V1-4 indicating an old anterior infarction. Coronary angiography confirmed the ostial stenosis of the hypoplastic RCA. This was a case of pure right ventricular free wall infarction because of the occlusion of the ostium of the hypoplastic RCA, but not of the right ventricular branch. Because the electrocardiographic findings resemble those of an acute anterior infarction, it is important to consider pure right ventricular infarction in the differential diagnosis.

Aged↗
PubMed1999

Right ventricular ischemia mimicking acute anterior myocardial infarction.

Isolated right ventricular ischemia in combination with myocardial infarction (MI) is uncommon, accounting for fewer than 3% of all MI cases. A young man who presented with acute right ventricular ischemia from occlusion of a codominant right coronary artery proximal to an acute marginal branch is presented. His presenting electrocardiogram (ECG) showed ST segment elevation in V1 to V4 mimicking acute anterior MI. ECG criteria for isolated right ventricular ischemia are discussed.

Acute Disease↗
PubMed2004

[Right ventricle in arterial hypertension].

Left ventricular hypertrophy is the best known and most evident cardiac organ manifestation of arterial hypertension. However, only limited findings are available on function and structure of the right ventricle. The published studies show that the right ventricle is also affected in the course of hypertensive heart disease. Particularly hypertrophy of the right ventricular free wall, impaired right ventricular diastolic filling, elevated right ventricular filling pressure as well as impairment of right ventricular ejection fraction in the late phase of arterial hypertension were reported. Possible causes of these structural and functional changes of the right ventricle are (1) translation of the increased left ventricular filling pressure in the pulmonary circulation, (2) interaction of the right and left ventricle, and (3) systemic circulation of cytokines and growth hormones such as angiotensin II, aldosterone, and others.

Arteries↗
PubMed2003

A new right ventricular assist device for right ventricular support.

Right ventricular support by mechanical devices for postcardiotomy right heart failure is still associated with a high mortality. We report on the first use of a new paracardiac microaxial blood pump for postcardiotomy right heart failure in two patients undergoing emergency coronary artery bypass grafting (the first patient for a myocardial infarction complicated by a left ventricular wall rupture, the second patient for a dissection of the right coronary artery after an interventional procedure).

Coronary Artery Bypass↗
PubMed1997

Right side implant of the unipolar single lead defibrillation system.

The active can defibrillator has been designed for implantation in the left prepectoral region. Whether this system can be successfully implanted on the right side is unknown. We describe six cases in which placement of the unipolar single lead defibrillation system was successfully attempted in the right prepectoral region due to impediments on the left side. The mean age of the patients was 62 +/- 12 years. Five patients had ischemic heart disease and one idiopathic dilated cardiomyopathy. The endocardial defibrillation electrode was placed in the right ventricle through the right subclavian vein and positioned at the apex in two patients and in the septal position in four patients. Defibrillation threshold testing was performed using a step-up/step-down protocol beginning at 12 J with 3-J increments or decrements. Defibrillation threshold was defined as the lowest energy of the first shock able to terminate ventricular fibrillation. The generator models used were the Medtronic 7218C in 1 patient, the Medtronic 7219C in 3 patients, and the Ventritex Cadet 115 AC in 2 patients. The mean defibrillation threshold was 15 +/- 3 J. The defibrillation thresholds were retested at 1, 3, and 6 months, and showed no significant change in five patients but decreased from 15 J to 12 J in one patient. The presence of impediments on the left side should not preclude attempts to place the unipolar active can system in the right prepectoral region.

Aged↗
PubMed1998

Progressive tricuspid valve disease in patients with congenitally corrected transposition of the great arteries.

BACKGROUND: The outcome of patients with corrected transposition of the great arteries (CTGA) is variably affected by associated intracardiac defects, tricuspid valve competence, and systemic right ventricular (RV) function. The relative importance of these factors in long-term outcome has not been evaluated. METHODS AND RESULTS: Since 1958, 40 patients with CTGA were studied to determine risk factors for poor outcome, including age, open heart surgery, tricuspid insufficiency (TI), cardiac rhythm, pulmonary overcirculation, and RV dysfunction. Follow-up ranged from 7 to 36 years (mean 20 years). Intracardiac repair was performed in 21 patients; 19 were unoperated or had closed heart procedures. For the purposes of this study the designation TI(S) refers to at least moderately severe TI as delineated by echocardiogram and/or angiography. TI(s) was the only independently significant factor for death (P=0.01), and in turn, only the presence of a morphologically abnormal TV predicted TI(s)(P=0.03). Twenty-year survival without TI(S)was 93%, but only 49% with TI(S). Poor long-term postoperative outcome was due to TI(S) in all but 1 patient; 20-year survival rates for operated patients with and without TI(s)were 34% and 90%, respectively (P=0.002). Similarly, 20-year survival rates for unoperated patients with and without TI(s)were 60% and 100%, respectively, whether or not attempts to repair the TI were made (P=0.08). CONCLUSIONS: TI(S)represents the major risk factor for CTGA patients; RV dysfunction appears to be almost always secondary to long-standing TI. Decisions related to surgical interventions with or without associated lesions must be strongly influenced by the status of the tricuspid valve.

Adolescent↗
PubMed2006

[Pulmonary hypertension].

Pulmonary hypertension can arise in the presence of acute cardiopulmonary decompensation or develop as a chronic and progressive disease in association with connective tissue diseases, infectious diseases, or metabolic diseases, or in the form of idiopathic pulmonary hypertension. Impaired regulation of endogenous vasoactive mediators, growth factors, and thrombotic factors leads to pulmonary artery vasoconstriction, endothelial and epithelial proliferation, and thrombotic vascular obstruction, with resulting right heart failure. There is no curative treatment for chronic pulmonary hypertension, and the immediate objective of palliative treatment is to relieve right heart stress by reducing pulmonary arterial pressure with the aid of pulmonary vasodilators. Depending on the severity of the illness, perioperative mortality is high, which must be borne in mind by both anesthetists and intensivists. Chronic medical treatment for these patients must be optimized before any surgery is undertaken. In the perioperative period, it is essential that anything that could lead to worsening of pulmonary hypertension is avoided, or at least recognized and treated at an early stage. Intraoperatively, imminent acute right heart decompensation is treated by improving right-ventricular contractility and reducing right-ventricular afterload. In the postoperative period, monitoring and optimization of the cardiopulmonary status, adequate analgesia and sedation, and careful anticoagulation must be ensured.

Anesthesia↗