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Results for “Ventricular Dysfunction, Right”

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At least 1,225 records · Page 68Linked to original sources
PubMed1997

Comparison of mortality rates and progression of left ventricular dysfunction in patients with idiopathic dilated cardiomyopathy and dilated versus nondilated right ventricular cavities.

This study assesses the influence of right ventricular (RV) dilation on the progression of left ventricular (LV) dysfunction and survival in patients with idiopathic dilated cardiomyopathy (IDC). Using transthoracic echocardiography, we studied 100 patients with IDC aged 20 to 80 years (mean 55 +/- 14); 67% were men. In the apical 4-chamber view, diastolic LV and RV chamber area measurements classified patients into 2 groups: group RV enlargement+ (RV area/LV area > 0.5) included 54 patients; group RV enlargement- (no RV enlargement) had RV area/LV area < or = 0.5. Echocardiographic studies were repeated in all patients after a mean of 33 +/- 16 months. At the time of the initial study, the 2 groups did not differ in age, gender, incidence of atrial fibrillation and diabetes, left ventricular mass, and LV ejection fraction, but the RV enlargement+ group had more severe tricuspid regurgitation and less LV enlargement. After 47 +/- 22 months (range 12 to 96), patients in group RV enlargement+ had lower LV ejection fraction (29% vs 34%, p = 0.006) than patients with initial RV enlargement-. At clinical follow-up, mortality was higher (43%) in patients with initial RV enlargement+ than the RV enlargement- patients (15%), p = 0.002. For survivors, the mitral deceleration time averaged 157 +/- 36 ms; for nonsurvivors or patients who required transplant, the mitral deceleration time averaged 97 +/- 12 ms (p < 0.0001). With use of a multivariate Cox model adjusting for LV ejection fraction, LV size, and age, the relative risk ratio of mortality from initial RV enlargement+ was 4.4 (95% confidence limits 1.7 to 11.1) (p = 0.002). Thus, patients with significant RV dilation had nearly triple the mortality over 4 years and more rapidly deteriorating LV function than patients with less initial RV dilation. In IDC, RV enlargement is a strong marker for adverse prognosis that may represent a different morphologic subset.

Adult↗
PubMed1998

Left ventricular diastolic collapse in low-pressure cardiac tamponade.

A case of systemic hypotension with volume depletion not responding to intravenous fluids was found to have features of cardiac tamponade on two-dimensional (2-D) echocardiography. Intracardiac pressures were normal on cardiac catheterization. An interesting observation was the presence of left ventricular (LV) collapse on 2-D echocardiography. To the authors' best knowledge, such a case of low pressure cardiac tamponade with LV collapse has not been reported earlier.

Adolescent↗
PubMed2006

Usefulness of magnetic resonance imaging for the diagnosis of right ventricular dysplasia in children.

Cardiac magnetic resonance (CMR) has been helpful in adults in the diagnosis of arrhythmogenic right ventricular dysplasia. Short of direct surgical observation or autopsy, no gold standard exists. CMR diagnostic criteria include right atrial and ventricular dilation, regional right ventricular (RV) wall motion abnormalities, outflow tract ectasia, and myocardial fatty infiltration. To determine whether adult diagnostic criteria are useful in children referred for CMR for this diagnosis, the images and records of 81 patients (aged 11.5 +/- 5.5 years) over an 8-year period were reviewed. Histories included ventricular tachycardia, palpitations, dilated right ventricle, syncope, near sudden death, or family history of RV dysplasia. Four families were studied with parents who had RV dysplasia diagnosed by surgery, explanted heart, or CMR. CMR imaging included T1-weighted imaging, cine, 1-dimensional RV myocardial tagging, and phase-encoded velocity mapping, and 2 patients underwent delayed-enhancement CMR. Only 1 of the 81 patients met 5 of the criteria. None of the others met >2 of the criteria, and only 2 patients met 1 or 2 criteria. For questionable regional wall motion abnormalities, RV myocardial tagging was helpful. In conclusion, CMR of patients with a history suspicious for the diagnosis of RV dysplasia is a low-yield test in children. This may be due to the evolving nature of the disease, which does not manifest itself from a morphologic or ventricular-function standpoint until later in development. Follow-up studies as patients age may be advantageous.

Cardiomyopathy, Dilated↗
PubMed2001

Normal myocardial function in severe right ventricular volume overload hypertrophy.

Severe left ventricular volume overloading causes myocardial and cellular contractile dysfunction. Whether this is also true for severe right ventricular volume overloading was unknown. We therefore created severe tricuspid regurgitation percutaneously in seven dogs and then observed them for 3.5-4.0 yr. All five surviving operated dogs had severe tricuspid regurgitation and right heart failure, including massive ascites, but they did not have left heart failure. Right ventricular cardiocytes were isolated from these and from normal dogs, and sarcomere mechanics were assessed via laser diffraction. Right ventricular cardiocytes from the tricuspid regurgitation dogs were 20% longer than control cells, but neither the extent (0.171 +/- 0.005 microm) nor the velocity (2.92 +/- 0.12 microm/s) of sarcomere shortening differed from controls (0.179 +/- 0.005 microm and 3.09 +/- 0.11 microm/s, respectively). Thus, despite massive tricuspid regurgitation causing overt right heart failure, intrinsic right ventricular contractile function was normal. This finding for the severely volume-overloaded right ventricle stands in distinct contrast to our finding for the left ventricle severely volume overloaded by mitral regurgitation, wherein intrinsic contractile function is depressed.

Animals↗
PubMed2004

Decreased right ventricular function after coronary artery bypass grafting and its relation to exercise capacity: a tricuspid annular motion-based study.

BACKGROUND: Decreased right ventricular (RV) function is a known echocardiographic finding after coronary artery bypass grafting (CABG). For patients with heart failure, RV dysfunction is a predictor of poor exercise capacity. The significance and time course of RV dysfunction and its relation to exercise capacity after CABG have not been elucidated, however. OBJECTIVES: In this prospective study, we assessed RV function measured from echocardiographic tricuspid annular motion (TAM) before and after CABG and its relation to exercise capacity. METHODS: In 99 patients accepted for CABG, we did a baseline echocardiographic investigation before operation, followed by repeated echocardiograms 3 months and 1 year after CABG. RV function was assessed using the magnitude of TAM measured at the RV free wall. An exercise stress test and coronary angiography were performed before and 3 months after CABG. RESULTS: RV function assessed by TAM was significantly reduced 3 months after CABG (22.4 vs 14.5 mm, P <.001) compared with preoperative measurements and remained so after 1 year (14.7 mm, P <.001). Left ventricular systolic function was unchanged 3 months after CABG. The 1-year echocardiographic follow-up showed paradoxical septal movement in 96% of the patients. Exercise capacity improved significantly 3 months after CABG compared with before (1.6 vs 1.83 W/kg, P <.001). These finding are independent of the state of the right coronary artery. CONCLUSIONS: One year after CABG, RV function remained depressed and septal motion remained paradoxical compared with the preoperative investigation, suggesting that these postoperative findings might be permanent in the majority of patients. Despite the reduced RV function, exercise performance 3 months after CABG was improved. The depressed RV function, measured from TAM after CABG, probably lacks clinical significance.

Aged↗
PubMed1997

Causes of death after the modified Norwood procedure: a study of 122 postmortem cases.

BACKGROUND: Although the results of the modified Norwood procedure as palliation for the hypoplastic left heart syndrome have improved considerably, in-hospital mortality remains high (28% to 46%). METHODS: To establish the causes of death and consider their therapeutic applications, we reviewed our pathology experience from 1980 to 1995, inclusive, regarding 122 patients who died after undergoing the Norwood procedure. RESULTS: The most important causes of death were found to be impairment of coronary perfusion (33 patients, 27%), excessive pulmonary blood flow (23 patients, 19%), obstruction of pulmonary arterial blood flow (21 patients, 17%), neoaortic obstruction (17 patients, 14%), right ventricular failure (16 patients, 13%), bleeding (9 patients, 7%), infection (6 patients, 5%), tricuspid or common atrioventricular valve dysfunction (6 patients, 5%), sudden death from presumed arrhythmias (6 patients, 5%), and necrotizing enterocolitis (3 patients, 3%). In 26 patients (21%), more than one factor appeared responsible for death. CONCLUSIONS: The leading causes of death after the Norwood procedure were found to be largely correctable surgical technical problems associated with perfusion of the lungs (36%), of the myocardium (27%), and of the systemic organs (14%).

Aortic Diseases↗
PubMed1998

Electrocardiographic and morphometric features in patients with ventricular tachycardia of right ventricular origin.

OBJECTIVE: To study differences between repetitive monomorphic ventricular tachycardia (RMVT) of right ventricular origin, and ventricular tachycardia in arrhythmogenic right ventricular dysplasia (ARVD). PATIENTS: Consecutive groups with RMVT (n = 15) or ARVD (n = 12), comparable for age and function. METHODS: Analysis of baseline, tachycardia, and signal averaged ECGs, clinical data, and right endomyocardial biopsies. Pathological findings were related to regional depolarisation (QRS width) and repolarisation (QT interval, QT dispersion). RESULTS: There was no difference in age, ejection fraction, QRS width in leads I, V1, and V6, and QT indices. During ventricular tachycardia, more patients with ARVD had a QS wave in V1 (p < 0.05). There were significant differences for unfiltered QRS, filtered QRS, low amplitude signal duration, and the root mean square voltage content. In the absence of bundle branch block, differences became non-significant for unfiltered and filtered QRS duration. Mean (SD) percentage of biopsy surface differed between RMVT and ARVD: normal myocytes (74(3.4)% v 64.5(9.3)%; p < 0.05); fibrosis (3(1.7)% v 8.9(5.2)%; p < 0.05). When all patients were included, there were significant correlations between fibrosis and age (r = 0.6761), and fibrosis and QRS width (r = 0.5524 for lead I; r = 0.5254 for lead V1; and r = 0.6017 for lead V6). CONCLUSIONS: The ECG during tachycardia and signal averaging are helpful in discriminating between ARVD and RMVT patients. There are differences in the proportions of normal myocytes and fibrosis. The QRS duration is correlated with the amount of fibrous tissue in patients with ventricular tachycardia of right ventricular origin.

Adult↗
PubMed1978

Right ventricular ejection fraction in patients with acute anterior and inferior myocardial infarction assessed by radionuclide angiography.

We measured right and left ventricular ejection fracttion (EF) from high frequency time-activity curves obtained during the initial passage of an intravenous bolus of 99mTc (Sn) pyrophosphate. In 22 normal controls right ventricular EF averaged 0.52 +/- 0.04 (SD). In 24 acute anterior or lateral infarction patients right ventricular EF was normal (0.56 +/- 0.10), while left ventricular EF was reduced (0.45 +/- 0.10, P less than 0.001 vs controls). In 19 acute inferior infarction patients left ventricular EF also was depressed (0.51 +/- 0.09, P less than 0.001 vs controls). Among 7 of 19 inferior infarction patients with right ventricular by scintigraphy, right ventricular EF was reduced (0.39 +/- 0.05; P less than 0.001 vs normals; P less than 0.01 vs inferior infarction patients without right ventricular involvement). In the latter group right ventricular EF averaged 0.51 +/- 0.10 (NS vs normals). We conclude 1) a single injection of 99mTc (Sn) pyrophosphate can identify right and left ventricular dysfunction and infarct location in acute myocardial infarction, 2) right ventricular EF is well-preserved except when inferior infarction involves the right ventricle.

Acute Disease↗
PubMed2002

[Arrhythmogenic right ventricular cardiomyopathy versus fatty replacement of the right ventricle. An autopsy case report].

We report an autopsy case of a cardiomyopathy characterized by fatty replacement of the right ventricular myocardium and compare its clinical and histologic characteristics with those of the arrhythmogenic right ventricular cardiomyopathy. A 39-year old male died suddenly in a hospital room. He had an alcoholic cirrhosis with ascitis, but the clinical examination and the biology showed no abnormalities explaining the death. Histologically, in the right ventricle, large areas of cardiomyocytes were replaced by fat, but there was no fibrosis. In contrast, fibrosis is present in association with fat in arrhythmogenic right ventricular cardiomyopathy. Fatty replacement of the right ventricle is likely to be a distinct entity. Right ventricular failure has been shown to be a possible complication. Sudden death is probably rare and is likely to occur when other arrhythmogenic factors are associated.

Adipose Tissue↗
PubMed1999

Altered cardiac histology following apical right ventricular pacing in patients with congenital atrioventricular block.

Previous studies have demonstrated that right ventricular apical pacing inherently alters ventricular contraction, regional blood flow, wall stress, and predisposes to diminished function. However, histological consequences of chronic apical pacing potentially contributing to the observed ventricular dysfunction remain conjectural. Previous canine studies have demonstrated histopathological cellular abnormalities with apically initiated ventricular pacing that may result in the observed diminished ventricular function. To determine if comparable adverse changes also occur in the clinical setting, 16 endomyocardial biopsies were obtained from 14 age-matched patients with congenital complete atrioventricular block (CCAVB) and otherwise normal anatomy, divided into two groups: eight biopsies (median patient age 15.5 years) from patients prior to pacemaker implant and another eight biopsies (median patient age 16 years) from patients following 3-12 years (median 5.5) of chronic ventricular pacing. In one patient, biopsy samples were obtained before and after pacing. Results demonstrated a significant (P<0.05) increase in histopathological alterations among the patient biopsy samples following pacing, consisting of myofiber size variation, fibrosis, fat deposition, sclerosis, and mitochondrial morphological changes. These findings indicate that chronic apical right heart ventricular pacing may adversely alter myocellular growth, especially among the young, on the cellular and subcellular level, potentially contributing to the diminished function observed clinically.

Adolescent↗