Right Ventricle (right + ventricle)

Distribution by Scientific Domains
Distribution within Medical Sciences

Kinds of Right Ventricle

  • double outlet right ventricle
  • double-outlet right ventricle
  • outlet right ventricle


  • Selected Abstracts


    Stent Dilatation of a Right Ventricle to Pulmonary Artery Conduit in a Postoperative Patient with Hypoplastic Left Heart Syndrome

    CONGENITAL HEART DISEASE, Issue 2 2008
    Rowan Walsh MD
    ABSTRACT A 10-day-old child with hypoplastic left heart syndrome (HLHS) underwent first-stage palliation for HLHS, Norwood procedure with a Sano modification, i.e., placement of a right ventricular to pulmonary artery (RV-PA) conduit. The patient developed progressively worsening systemic oxygen desaturation in the immediate postoperative period. Stenosis of the proximal RV-PA conduit was diagnosed by echocardiography. In the catheterization laboratory stent placement in the conduit was performed. This resulted in increased systemic oxygen saturation. The patient was eventually discharged from the hospital with adequate oxygen saturations. [source]


    Large Apical Muscular Ventricular Septal Defect: Asymptomatic due to Anomalous Muscle Bundles in the Right Ventricle

    CONGENITAL HEART DISEASE, Issue 1 2007
    Anant Khositseth MD
    ABSTRACT This case report demonstrated an apical muscular ventricular septal defect (VSD) that was a large defect but behaved like a small defect because of the restrictive flow across the anomalous muscle bundles in the right ventricular (RV) apex. The anomalous muscle bundles separated the RV sinus into two parts: the RV apex connecting with the left ventricle through the apical muscular VSD on one side, and the rest of the RV sinus connecting with RV inflow and RV outflow on the other side. These findings explained why the 11-year-old girl in this study remained asymptomatic without evidence of volume load. Thus far, it was not necessary to close her defect because of the hemodynamic insignificance. [source]


    Rupture of a Right Sinus of Valsalva Aneurysm into the Right Ventricle During Vaginal Delivery: A Case Report

    ECHOCARDIOGRAPHY, Issue 10 2005
    F.E.S.C., Josip Vincelj M.D., Ph.D.
    A case is reported of a right sinus of Valsalva aneurysm rupture into the right ventricle during vaginal delivery in a 34-year-old healthy woman in her third pregnancy. Pregnancy was carried to term and a healthy baby was delivered vaginally. On day 7 following vaginal delivery she was admitted to hospital for dyspnea and cough, with clinical signs of severe heart failure. The diagnosis of the right sinus of Valsalva aneurysm rupture into the right ventricle was established by transthoracic and transesophageal echocardiography. Clinical recognition and early echocardiographic diagnosis followed by immediate surgical repair proved lifesaving in our patient. (ECHOCARDIOGRAPHY, Volume 22, November 2005) [source]


    Double Chambered Right Ventricle in 9 Cats

    JOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 1 2007
    H. Koffas
    Background: Double-chambered right ventricle (DCRV) is a frequently recognized cardiac congenital abnormality in humans. It has been described in dogs and in 1 cat. However systemic description of clinical and echocardiographic features of the disease in cats is currently lacking from the veterinary literature. Animals: Nine cats with DCRV are described. Results: The cats ranged from 4 months to 10 years of age. Eight cats at presentation were asymptomatic and 1 cat had chylothorax. In all cases echocardiography revealed abnormal fibromuscular bundles obstructing the mid-right ventricle, dividing the chamber into 2 compartments. The proximal right ventricular compartment was markedly hypertrophied, and right atrial dilation was usually present. The mean pressure gradient measured across the stenotic area was 130 ± 50 mm Hg. Concurrent abnormalities included a ventricular septal defect (n = 2); aortic malalignment, aortic insufficiency (n = 1); and congenital peritoneal-pericardial diaphragmatic hernia (n = 1). Two cats had systolic anterior motion of the mitral valve, one of which had concurrent left ventricular hypertrophy. Five cats have remained asymptomatic for a median period of 3.6 years (range, 3.3,5 years) and 3 cats have developed clinical signs associated with congestive heart failure (at 2, 3.3, and 9 years). One cat showed progressive lethargy and exercise intolerance and underwent partial ventriculectomy at the age of 2 years. This cat died during the operation with electromechanical dissociation. Conclusions: DCRV is a congenital cardiac abnormality that may be more common than previously recognized. [source]


    Phenotyping the Right Ventricle in Patients with Pulmonary Hypertension

    CLINICAL AND TRANSLATIONAL SCIENCE, Issue 4 2009
    M.S., Marc A. Simon M.D.
    Abstract Right ventricular (RV) failure is associated with poor outcomes in pulmonary hypertension (PH). We sought to phenotype the RV in PH patients with compensated and decompensated RV function by quantifying regional and global RV structural and functional changes. Twenty-two patients (age 51 ± 11, 14 females, mean pulmonary artery (PA) pressure range 13,79 mmHg) underwent right heart catheterization, echocardiography, and ECG-gated multislice computed tomography of the chest. Patients were divided into three groups: Normal, PH with hemodynamically compensated, and decompensated RV function (PH-C and PH-D, respectively). RV wall thickness (WT) was measured at end-diastole (ED) and end-systole (ES) in three regions: infundibulum, lateral free wall, and inferior free wall. Globally, RV volumes progressively increased from Normal to PH-C to PH-D and RV ejection fraction decreased. Regionally, WT increased and fractional wall thickening (FWT) decreased in a spatially heterogeneous manner. Infundibular wall stress was elevated and FWT was lower regardless of the status of global RV function. In PH, there are significant phenotypic abnormalities in the RV even in the absence of overt hemodynamic RV decompensation. Regional changes in RV structure and function may be early markers of patients at risk for developing RV failure. [source]


    Myocardial growth before and after birth: clinical implications,

    ACTA PAEDIATRICA, Issue 2 2000
    AM Rudolph
    Perinatal changes in myocardial growth have recently evoked considerable interest with regard to cardiac chamber development with congenital cardiac lesions and to myocardial development in preterm infants. It is suggested that cardiac chamber development is influenced by blood flow. Experimental pulmonary stenosis in fetal lambs may induce either greatly reduced or markedly increased right ventricular volume. Ventricular enlargement appears to be associated with a large ventricular volume load resulting from tricuspid valve regurgitation. A small competent tricuspid valve is associated with reduced flow through the ventricle due to outflow obstruction and a small right ventricle. Postnatal growth of the ventricles in congenital heart disease is discussed. Increase in myocardial mass prenatally is achieved by hyperplasia, both during normal development and when myocardial mass is increased by right ventricular outflow obstruction. Postnatally, increases in myocardial mass with normal growth, as well as with ventricular outflow obstruction, are largely due to hypertrophy of myocytes. Myocardial capillary numbers do not increase in proportion with myocyte numbers in ventricular myocardium in association with outflow obstruction. The postnatal effects of these changes in congenital heart lesions are considered. Studies in fetal lambs suggest that the late gestational increase in blood cortisol concentrations is responsible for the change in the pattern of myocardial growth after birth. The concern is raised that prenatal exposure of the premature infant to glucocorticoids, administered to the mother to attempt to prevent hyaline membrane disease in the infant, may inhibit myocyte proliferation and result in a heart with fewer than normal myocytes. This would necessitate that each myocyte would have to hypertrophy abnormally to achieve a normal cardiac mass postnatally. [source]


    Downregulation of oxytocin receptors in right ventricle of rats with monocrotaline-induced pulmonary hypertension

    ACTA PHYSIOLOGICA, Issue 2 2010
    T. L. Broderick
    Abstract Aim:, Pulmonary hypertension (PH) in the rat leads to right ventricular (RV) hypertrophy, inflammation and increased natriuretic peptide (NP) levels in plasma and RV. Because the release of nitric oxide (NO) and atrial natriuretic peptide (ANP) is a function of the oxytocin receptor (OTR), we examined the effect of PH on gene and protein expression of OTR, NP (A, atrial; B, brain) and receptors (NPRs), nitric oxide synthases (NOS), interleukin (IL)-1,, IL-6 and tumour necrosis factor-, in the hypertrophied RV in a model of PH. Methods:, RV hypertrophy was induced in male Sprague,Dawley rats with monocrotaline (MCT; 60 mg kg,1) and was confirmed by the presence of an increased RV weight and RV-to-[left ventricle (LV) and septum] ratio. Results:, In the RV of MCT-treated rats, a ,40% reduction in OTR mRNA and protein was observed compared with the RV of control rats. This reduction was associated with increased transcripts of ANP and BNP in both ventricles and a corresponding increase in NP receptor mRNA expression for receptors A, B and C. Protein expression of inducible NOS was increased in the RV, whereas endothelial NOS transcripts were increased only in the LV of MCT-treated rats. In the RV of MCT-treated rats, downregulation of OTR was also associated with increased mRNA expression of IL-1, and IL-6. Conclusion:, Our results show that downregulation of the OTR in the RV of MCT-treated rats is associated with increased expression of NP and their receptors as well as IL-1, and IL-6. This reduction in OTR in RV myocardium may have an impact on cardiac function in the MCT-induced model of PH. [source]


    Understanding heart development and congenital heart defects through developmental biology: A segmental approach

    CONGENITAL ANOMALIES, Issue 4 2005
    Masahide Sakabe
    ABSTRACT The heart is the first organ to form and function during development. In the pregastrula chick embryo, cells contributing to the heart are found in the postero-lateral epiblast. During the pregastrula stages, interaction between the posterior epiblast and hypoblast is required for the anterior lateral plate mesoderm (ALM) to form, from which the heart will later develop. This tissue interaction is replaced by an Activin-like signal in culture. During gastrulation, the ALM is committed to the heart lineage by endoderm-secreted BMP and subsequently differentiates into cardiomyocyte. The right and left precardiac mesoderms migrate toward the ventral midline to form the beating primitive heart tube. Then, the heart tube generates a right-side bend, and the d-loop and presumptive heart segments begin to appear segmentally: outflow tract (OT), right ventricle, left ventricle, atrioventricular (AV) canal, atrium and sinus venosus. T-box transcription factors are involved in the formation of the heart segments: Tbx5 identifies the left ventricle and Tbx20 the right ventricle. After the formation of the heart segments, endothelial cells in the OT and AV regions transform into mesenchyme and generate valvuloseptal endocardial cushion tissue. This phenomenon is called endocardial EMT (epithelial-mesenchymal transformation) and is regulated mainly by BMP and TGF,. Finally, heart septa that have developed in the OT, ventricle, AV canal and atrium come into alignment and fuse, resulting in the completion of the four-chambered heart. Altered development seen in the cardiogenetic process is involved in the pathogenesis of congenital heart defects. Therefore, understanding the molecular nature regulating the ,nodal point' during heart development is important in order to understand the etiology of congenital heart defects, as well as normal heart development. [source]


    Single Coronary Artery with Right Ventricular Fistula: Case Report and Literature Review

    CONGENITAL HEART DISEASE, Issue 1 2010
    Yoichiro Ishii MD
    ABSTRACT We report a rare case of a 6-year-old boy who was diagnosed with coronary artery fistulae communicating with the right ventricle and a left single coronary artery. Preoperative angiography showed a dilated and tortuous single coronary artery draining into the right ventricle. Two coronary artery fistulae draining into the right ventricle were detected at operation and both of these were ligated. Postoperative angiography showed that the single coronary artery diameter was almost normalized, although the vessel was still slightly tortuous. His clinical course was uneventful. In this report, we summarize cases of coronary artery fistula with single coronary artery that have been reported in the literature as well as our case. [source]


    Device Closure of a Secundum Atrial Septal Defect in a 4-Month-Old Infant with a Marginal Left Ventricle Following Coarctation Repair

    CONGENITAL HEART DISEASE, Issue 6 2007
    Emilie Jean-St-Michel BSc
    ABSTRACT A male infant presented at birth with severe coarctation of the aorta and marginal left ventricular and mitral valve dimensions associated with a large secundum atrial septal defect. Following successful arch repair, the left ventricle remained small with preferential left-to-right atrial shunting and a dilated right ventricle. Clinically, the infant continued with tachypnea, poor feeding, and failure to thrive. At 4 months of age, the defect was closed with an Amplatzer Atrial Septal Occluder which resulted in immediate left ventricular cavity enlargement and clinical improvement. [source]


    Evaluation of Right Ventricular Fibrosis in Adult Congenital Heart Disease Using Gadolinium-enhanced Magnetic Resonance Imaging: Initial Experience in Patients with Right Ventricular Loading Conditions

    CONGENITAL HEART DISEASE, Issue 5 2006
    Lopa P. Hartke MD
    ABSTRACT Objective., Gadolinium-enhanced cardiac magnetic resonance imaging has been used to show myocardial fibrosis, a finding that appears as late gadolinium enhancement. Its role in the evaluation of right ventricular fibrosis in congenital heart disease is unclear. The purpose of this study was to demonstrate late gadolinium enhancement of the right ventricle in adult and adolescent congenital heart disease and to investigate the relationship between this enhancement and clinical and pathophysiological data. Design., In total, 24 patients, 16 patients with congenital heart disease and right ventricular loading conditions and 8 controls, underwent gadolinium-enhanced viability imaging. Diagnoses varied and included repaired, palliated, and unrepaired lesions. The presence and extent of right ventricular late gadolinium enhancement was compared with patient clinical and hemodynamic data. Exact Wilcoxon tests, Fisher's exact tests, and Spearman's rank correlation were used to compare variables. Results., Nine of 16 patients (56%) were found to have right ventricular late gadolinium enhancement, ranging from 5% to 80% of right ventricular myocardium affected (mean 36.1%, SD 29.7). The combination of right ventricular systolic pressure ,98 mm Hg and systemic oxygen saturation ,93% strongly suggested the presence of right ventricular late gadolinium enhancement (positive predictive value 100%), but no single variable or combination of variables could reliably predict its absence (negative predictive values ,75%). Extent of right ventricular late gadolinium enhancement did not correlate with degree of either hypoxia or right ventricular hypertension. Conclusions., Gadolinium-enhanced cardiac magnetic resonance demonstrates right ventricular late gadolinium enhancement in some patients with congenital heart disease and right ventricular loading conditions. Clinical variables were associated with the presence of fibrosis but did not reliably predict severity. Myocardial preservation is likely a multifactorial process that may affect the right and left ventricles differently. [source]


    Protein kinase C mRNA and protein expressions in hypobaric hypoxia-induced cardiac hypertrophy in rats

    ACTA PHYSIOLOGICA, Issue 4 2010
    M. Uenoyama
    Abstract Aim:, Protein kinase C (PKC), cloned as a serine/threonine kinase, plays key roles in diverse intracellular signalling processes and in cardiovascular remodelling during pressure overload or volume overload. We looked for correlations between changes in PKC isoforms (levels and/or subcellular distributions) and cardiac remodelling during experimental hypobaric hypoxic environment (HHE)-induced pulmonary hypertension. Methods:, To study the PKC system in the heart during HHE, 148 male Wistar rats were housed for up to 21 days in a chamber at the equivalent of 5500 m altitude level (10% O2). Results:, At 14 or more days of exposure to HHE, pulmonary arterial pressure (PAP) was significantly increased. In the right ventricle (RV): (1) the expression of PKC-, protein in the cytosolic and membrane fractions was increased at 3,14 days and at 5,7 days of exposure respectively; (ii) the cytosolic expression of PKC-, protein was increased at 1,5, 14 and 21 days of exposure; (3) the membrane expressions of the proteins were decreased at 14,21 (PKC-,II), 14,21 (PKC-,), and 0.5,5 and 21 (PKC-,) days of exposure; (4) the expression of the active form of PKC-, protein on the plasma membrane was increased at 3 days of exposure (based on semiquantitative analysis of the immunohistochemistry). In the left ventricle, the expressions of the PKC mRNAs, and of their cytosolic and membrane proteins, were almost unchanged. The above changes in PKC-,, which were strongly evident in the RV, occurred alongside the increase in PAP. Conclusion:, PKC-, may help to modulate the right ventricular hypertrophy caused by pulmonary hypertension in HHE. [source]


    Effects of normobaric hyperoxia on water content in different organs in rats

    ACTA PHYSIOLOGICA, Issue 1 2002
    L. E. B. Stuhr
    ABSTRACT Pulmonary oxygen toxicity is a dose-dependent effect on alveolar epithelial and endothelial cells resulting in pulmonary oedema. Any concomitant effects on systemic capillary endothelium would be expected to result in capillary leakage and an increase in the tissues' water content. Total tissue water (TTW) in different organs was therefore studied in freely moving rats exposed to 100% O2 at normobaric pressure for 24 or 48 h, and compared to air-breathing control rats. The TTW for the following tissues was measured: Trachea, left bronchus, left lung, left and right ventricle, left kidney, skin (left paw-hindlimb), skin (back of the rat), left brain, left eye and thigh muscle left side. There was a significant increase in TTW of the lung accompanied by pleural effusion after 48 h of oxygen exposure as expected in all exposed animals. There was a small increase in TTW of the paw only, and a small decrease or no change in other tissues after 24 and 48 h of exposure. We conclude that there is no evidence of systemic capillary dysfunction as measured by tissue water content after exposure to hyperoxia in a dosage causing pulmonary oedema. [source]


    Right Ventricular Adaptations Along with Left Ventricular Remodeling in Older Athletes

    ECHOCARDIOGRAPHY, Issue 3 2009
    Oner Ozdogan M.D.
    Background: Afterload changes and anatomic interaction between the ventricles cause right ventricle (RV) adaptation along with left ventricle (LV) remodeling. This study was designed to evaluate RV adaptations along with LV remodeling and to determine the effect of aging on both ventricles in a population of older athletes. Methods: Echocardiographic characteristics of 48 endurance trained older athletes were examined by tissue Doppler imaging (TDI) and integrated backscatter (IBS). Results: Mean LV mass index was calculated as 107.8±17.0 g/m2. Twenty-two athletes were > 55 years old. Age was found to be a risk factor for diastolic dysfunction regarding lateral TDI velocities (Em < Am) (r = 0.385, P < 0.001). RV long-axis (LAX) diameters were associated with LA volumes and LV masses (r = 0.380, P < 0.01 and r = 0.307, P < 0.05). RV LAX diameters were correlated with RV TDI E-wave (r =,0.285, P < 0.05), RV LAX average, and peak IBS values (r = 0.36, P < 0.05 and r = 0.348, P < 0.05). Conclusions: TDI and IBS are applicable methods to evaluate the relationship between the two ventricles in athletes' heart. Increased RV LAX IBS values indicate increased LV mass and LA volume as a result of RV changes along with LV remodeling. Our data suggest that RV TDI E-wave and average RV IBS values reflect cardiac adaptations of both RV and LV in older athletes. [source]


    Biventricular Noncompaction: A Case Report

    ECHOCARDIOGRAPHY, Issue 9 2008
    Kursat Tigen M.D.
    Myocardial noncompaction is an extremely uncommon cardiomyopathy. It can present as an isolated cardiac malformation or in association with other congenital anomalies. The left ventricle is usually affected, but a biventricular involvement rarely occurs. A predominant right ventricular involvement has not been reported. Here, we report an 18-year-old woman with biventricular noncompaction that predominantly involves the right ventricle. [source]


    Detection of Subclinical Cardiac Involvement in Systemic Sclerosis by Echocardiographic Strain Imaging

    ECHOCARDIOGRAPHY, Issue 2 2008
    Alper Kepez M.D.
    Background: Cardiac involvement is one of the major problems in systemic sclerosis (SSc). Subclinical cardiac involvement has a higher frequency than thought previously. In this study we investigated whether subclinical cardiac involvement can be detected by using echocardiographic strain imaging in SSc patients without pulmonary hypertension. Methods: Echocardiographic examinations were performed to 27 SSc patients and 26 healthy controls. Left ventricular strain parameters were obtained from apical views and average strain value was calculated from these measurements. Results: There were no significant differences between patients and controls regarding two-dimensional (2D), conventional Doppler and tissue Doppler velocity measurements. Strain was reduced in 6 of 12 segments of the left ventricle (LV) and in 1 of 2 segments of the right ventricle (RV). Strain rate (SR) was reduced in 2 of 12 segments of the LV and 1 of 2 segments of the RV in SSc patients as compared to controls (P < 0.05 for all). These involvements did not match any particular coronary artery distribution. More important differences were detected by average strain and SR values of the LV between patients and controls (19.78 ± 3.00% vs 23.41 ± 2.73%, P < 0.001; 2.01 ± 0.41 vs 2.23 ± 0.27/sec, P = 0.026, respectively). Furthermore, carbon monoxide diffusion capacity (DLCO) in scleroderma patients significantly correlated with LV average strain (r = 0.59; P = 0.001). Conclusion: Evaluation of ventricular function by using echocardiographic strain imaging appears to be useful to detect subclinical cardiac involvement in SSc patients with normal standard echocardiographic and tissue Doppler velocity findings. [source]


    Right Coronary Artery Hepatic Vein Fistula: A Case Report

    ECHOCARDIOGRAPHY, Issue 10 2006
    Sevket Gorgulu M.D.
    There is a slight predominance for coronary artery fistulas that involve the right coronary artery, while multiple fistulas have also been reported. The usual site of termination is one or more of the low-pressure structures in the heart or the great vessels such as the right or left atria, right ventricle, coronary sinus, pulmonary artery, or superior vena cava. However, a coronary fistula that drains into a hepatic vein has not been reported in the literature. Therefore, this is the first case report indicating a right coronary artery fistula that drains into the middle hepatic vein. [source]


    Hepatopulmonary Syndrome and Right Ventricular Diastolic Functions: An Echocardiographic Examination

    ECHOCARDIOGRAPHY, Issue 4 2006
    Aziz Karabulut M.D.
    Aim: Liver functions are affected in the course of cardiac diseases, and similarly, liver diseases affect cardiac functions. Many studies in the literature have shown that left ventricular systolic and/or diastolic dysfunction may develop during chronic liver disease. However, there are limited studies investigating right ventricular functions during chronic liver diseases. Methods: A total of 84 patients who had no systolic and/or diastolic dysfunction in the left ventricle (LV) were evaluated; 46 patients with liver cirrhosis; 10 (21.74%) cirrhotic patients with hepatopulmonary syndrome (HPS) (group 1), 36 (78.26) cirrhotic patients without HPS (group 2), and 38 healthy individuals were treated as control. Results: Right ventricular diastolic dysfunction was determined in all patients of group 1 (100%), 26 of group 2 (72.22 %), and 4 of the controls (10.52%) (P < 0.05). Tricuspid deceleration time (dt) was significantly different between the groups (P < 0.05). In addition, right atrium (RA) diameters, right ventricle (RV) diameters, and RV wall thickness were significantly different between the groups (P < 0.05). Pulmonary artery pressure (P < 0.05) and pulmonary vascular resistance (P < 0.05) were also seen to be higher in group 1 than those in group 2 and control group. Conclusions: Right ventricular diastolic dysfunction rate is high in chronic liver diseases. In the presence of HPS, right ventricular diastolic dysfunction is more remarkable in patients than those without HPS. Right ventricular diastolic dysfunction may result in dilatation and hypertrophy in the right heart. [source]


    Real-Time Three-Dimensional Echocardiography in Diagnosis of Right Ventricular Pseudoaneurysm after Pacemaker Implantation

    ECHOCARDIOGRAPHY, Issue 3 2006
    Xuedong Shen M.D.
    Right ventricular rupture is a critical cardiac complication associated with cardiac tamponade and death. Occasionally, the site of rupture may be contained by the parietal pericardium and thrombus, thus forming a pseudoaneurysm. Cases of traumatic pseudoaneurysm of the right ventricle have been reported. However, right ventricular pseudoaneurysm following pacemaker implantation has not been previously reported. This case demonstrates two right ventricular pseudoaneurysms following perforation of the right ventricular wall using real-time three-dimensional echocardiography (3DE) after pacemaker implantation although only one definite pseudoaneurysm was diagnosed by routine two-dimensional echocardiography (2DE). We also found that color Doppler 3DE enhanced visualization of the connections between the right ventricle and the pseudoaneurysm. Color Doppler 3DE allowed us to peel away the myocardial tissue and rotate the image to study the jets from different angles. In summary, real-time 3DE and color Doppler 3DE provided excellent visualization of the right ventricular pseudoaneurysm, flow between the ventricle and the pseudoaneurysm, and additional information to that obtained by 2DE. [source]


    Rupture of a Right Sinus of Valsalva Aneurysm into the Right Ventricle During Vaginal Delivery: A Case Report

    ECHOCARDIOGRAPHY, Issue 10 2005
    F.E.S.C., Josip Vincelj M.D., Ph.D.
    A case is reported of a right sinus of Valsalva aneurysm rupture into the right ventricle during vaginal delivery in a 34-year-old healthy woman in her third pregnancy. Pregnancy was carried to term and a healthy baby was delivered vaginally. On day 7 following vaginal delivery she was admitted to hospital for dyspnea and cough, with clinical signs of severe heart failure. The diagnosis of the right sinus of Valsalva aneurysm rupture into the right ventricle was established by transthoracic and transesophageal echocardiography. Clinical recognition and early echocardiographic diagnosis followed by immediate surgical repair proved lifesaving in our patient. (ECHOCARDIOGRAPHY, Volume 22, November 2005) [source]


    Echocardiographic Features of Patients With Heart Failure Who May Benefit From Biventricular Pacing

    ECHOCARDIOGRAPHY, Issue 3 2003
    Amgad N. Makaryus
    Background: Recent studies suggest that cardiac resynchronization therapy through biventricular pacing (BVP) may be a promising new treatment for patients with advanced congestive heart failure (CHF). This method involves implantation of pacer leads into the right atrium (RA), right ventricle (RV), and coronary sinus (CS) in patients with ventricular dyssynchrony as evidenced by a bundle branch block pattern on electrocardiogram (ECG). Clinical trials are enrolling stable patients with ejection fractions (EF) , 35%, left ventricular end-diastolic diameters (LVIDd) , 54 mm, and QRS duration ,140 msec. We compared echocardiography features of these patients (group 1) with other patients with EF , 35%, LVIDd , 54 mm, and QRS < 140 msec (group 2 = presumably no dyssynchrony). Methods: Nine hundred fifty-one patients with CHF, LVID 54 mm, EF 35% by echocardiography were retrospectively evaluated. One hundred forty-five patients remained after those with primary valvular disease, prior pacing systems, or chronic atrial arrhythmias were excluded. From this group of 145 patients, a subset of 50 randomly selected patients were further studied (25 patients [7 females, 18 males] from group 1, and 25 patients [7 females, 18 males] from group 2). Mean age group 1 = 75 years old, mean age group 2 = 67 years old. Mean QRS group 1 = 161 msec, mean QRS group 2 = 110 msec. Each group was compared for presence of paradoxical septal motion, atrial and ventricular chamber sizes, LV mass, LVEF, and RV systolic function. Results: Of the initial group of 951 patients, 145 (15%) met inclusion criteria. In the substudy, 20/25 (80%) of group l and 7/25 (28%) of group 2 subjects had paradoxical septal motion on echo (Fisher's exact test, P = 0.0005). The t-tests performed on the other echocardiography variables demonstrated no differences in chamber size, function, or LV mass. Conclusions: Cardiac resynchronization therapy with BVP appears to target a relatively small population of our advanced CHF patients (15% or less). Although increasing QRS duration on ECG is associated with more frequent paradoxical septal motion on echo, it is not entirely predictive. Paradoxical septal motion on echo may therefore be more sensitive at identifying patients who respond to BVP. Further prospective studies are needed. (ECHOCARDIOGRAPHY, Volume 20, April 2003) [source]


    Assessment of Acute Right Ventricular Dysfunction Induced by Right Coronary Artery Occlusion Using Echocardiographic Atrioventricular Plane Displacement

    ECHOCARDIOGRAPHY, Issue 6 2000
    Alpesh R. Shah M.D.
    Right ventricular (RV) systolic function analysis by echocardiography has traditionally required RV endocardial border definition with subsequent tracing and is often inaccurate or impossible in technically poor studies. The atrioventricular plane displacement (AVPD) method attempts to use the descent of the tricuspid annular ring, a reflection of the longitudinal shortening of the right ventricle, as a surrogate marker for RV systolic function. We hypothesized that RV ischemia induced during right coronary artery occlusion proximal to the major right ventricular branches would result in severe right ventricular systolic dysfunction detectable by the AVPD method. During this pilot study, seven patients undergoing elective proximal RCA angioplasty had echocardiographic measurement of RV AVPD performed at baseline (i.e., immediately prior to RCA balloon inflation), during the last 30 seconds of first RCA balloon inflation, and at 1 minute after balloon deflation (recovery). Lateral and medial RV AVPD were significantly reduced from baseline values during intracoronary balloon inflation. (Lateral: 2.45 cm ± 0.22 vs 1.77 cm ± 0.13, P < 0.001; medial: 1.46 cm ± 0.37 vs 1.28 cm ± 0.32, P < 0.05). Additionally, lateral and medial RV AVPD significantly returned towards baseline values during recovery. (Lateral: 2.39 cm ± 0.20, P < 0.001; medial: 1.58 cm ± 0.27, P = 0.01). At baseline, all lateral RV AVPD values were > 2.0 cm, whereas during balloon inflation all were < 2.0 cm. No such clear distinction was found in medial RV AVPD values. Proximal RCA angioplasty is associated with a significant reduction in lateral and medial RV AVPD. Thus RV AVPD may serve as a marker for RV systolic dysfunction. [source]


    Reliability of Intraoperative Transesophageal Echocardiography During Tetralogy of Fallot Repair

    ECHOCARDIOGRAPHY, Issue 4 2000
    JAMES J. JOYCE M.D.
    There is limited information available concerning the accuracy of intraoperative transesophageal echocardiography (TEE) in predicting the extent of residual abnormalities after recovery from surgical repair of tetralogy of Fallot. Therefore, we investigated differences between the results of final postbypass TEE and those of postrecovery (mean, 6 days after surgery) transthoracic echocardiography in a total of 28 consecutive pediatric patients who underwent repair of tetralogy of Fallot with biplane or multiplane TEE. Both postbypass and postrecovery echocardiographic examinations included measurements of the right ventricle (RV)-main pulmonary artery (PA) and the main PA-branch PA peak instantaneous gradients, the degree of pulmonary valvar insufficiency, and color Doppler interrogation of the ventricular septum for residual defects. The RV-main PA gradient did not change significantly: 15 ± 13 vs 18 ± 14 mmHg (postbypass versus postrecovery, mean ± SD). None of the patients had a decrease of , 10 mmHg; and only one patient had an increase of ,: 15 mmHg. There also was no change in the degree of pulmonary insufficiency (3.0 ±1.2 versus 3.1 ± 1.1, using a scale of 0 to 4). Only one of the seven very small (, 2 mm) residual ventricular septal defects was not discovered during postbypass TEE. However, postrecovery transthoracic echocardiography detected significant branch PA stenosis (peak gradient, , 15 mmHg) in five patients (18%) that was not detected during postbypass TEE (P < 0.03). Of the branch PA stenoses that were not detected during TEE, four were left and one was right. Conclusions: Postbypass TEE after tetralogy of Fallot repair reliably predicts residual postrecovery hemodynamic abnormalities, except for branch PA stenosis. [source]


    Increased myocardial matrix metalloproteinases in hypoxic newborn pigs during resuscitation: effects of oxygen and carbon dioxide

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 7 2004
    W. B. Borke
    Abstract Background, Perinatal asphyxia is associated with cardiac dysfunction, and it is important to prevent further tissue injury during resuscitation. There is increasing evidence that myocardial matrix metalloproteinases (MMPs) are involved in myocardial hypoxaemia,reoxygenation injury. Objective, To assess MMPs and antioxidant capacity in newborn pigs after global ischaemia and subsequent resuscitation with ambient air or 100% O2 at different PaCO2 -levels. Methods, Newborn pigs (12,36 h of age) were resuscitated for 30 min by ventilation with 21% or 100% O2 at different PaCO2 levels after a hypoxic insult, and thereafter observed for 150 min. In myocardial tissue extracts, MMPs were analyzed by gelatin zymography and broad matrix-degrading capacity (total MMP). Total endogenous antioxidant capacity in myocardial tissue extracts was measured by the oxygen radical absorbance capacity (ORAC) assay. Results, Matrix metalloproteinase-2 more than doubled from baseline values (P < 0·001), and was higher in piglets resuscitated with 100% O2 than with ambient air (P = 0·012). The ORAC value was considerably decreased (P < 0·001). In piglets with elevated PaCO2, total MMP-activity in the right ventricle was more increased than in the left ventricle (P = 0·008). In the left ventricle, total MMPactivity was higher in the piglets with low PaCO2 than in the piglets with elevated PaCO2 (P = 0·013). Conclusion, In hypoxaemia-reoxygenation injury the MMP-2 level was highly increased and was most elevated in the piglets resuscitated with 100% O2. Antioxidant capacity was considerably decreased. Assessed by total MMP-activity, elevated PaCO2 during resuscitation might protect the left ventricle, and probably increase right ventricle injury of the myocardium. [source]


    Chamber-specific effects of hypokalaemia on ventricular arrhythmogenicity in isolated, perfused guinea-pig heart

    EXPERIMENTAL PHYSIOLOGY, Issue 4 2009
    Oleg E. Osadchii
    Diuretic-induced hypokalaemia has been shown to promote cardiac arrhythmias in hypertensive patients. The present study was designed to determine whether hypokalaemia increases arrhythmic susceptibility of the left ventricle (LV) or the right ventricle (RV), or both. Proarrhythmic effects of hypokalaemic perfusion (2.5 mm K+ for 30 min) were assessed in isolated guinea-pig heart preparations using simultaneous recordings of volume-conducted electrocardiogram and monophasic action potentials from six ventricular epicardial sites. Effective refractory periods, ventricular fibrillation thresholds and inducibility of tachyarrhythmias by programmed electrical stimulation and tachypacing were determined at the LV and the RV epicardial stimulation sites. Hypokalaemia promoted spontaneous ventricular ectopic activity, an effect attributed to non-uniform prolongation of ventricular repolarization resulting in increased RV-to-LV transepicardial dispersion of refractoriness and action potential duration. Furthermore, hypokalaemic perfusion was associated with reduced ventricular fibrillation threshold and increased inducibility of tachyarrhythmias by programmed electrical stimulation and tachypacing as determined at the LV stimulation site. In contrast, the RV stimulation revealed no change in arrhythmic susceptibility of the RV chamber. Consistently, hypokalaemia reduced the LV effective refractory period but had no effect on the RV refractoriness. This change enabled generation of premature propagating responses by extrastimulus application at earlier time points during LV repolarization. Increased prematurity of extrastimulus-evoked propagating responses was associated with exaggerated local inhomogeneities in intraventricular conduction and action potential duration in hypokalaemic LV, thus creating a favourable stage for re-entrant tachyarrhythmias. Taken together, these findings suggest that proarrhythmic effects of hypokalaemia are mostly attributed to increased LV arrhythmogenicity in the guinea-pig heart. [source]


    Remote myocardium gene expression after 30 and 120 min of ischaemia in the rat

    EXPERIMENTAL PHYSIOLOGY, Issue 2 2006
    Miguel S. Guerra
    The aim of the present study was to investigate how early the onset of ischaemia-induced changes in gene expression is in remote myocardium, and whether these changes would be different for left and right ventricles. Wistar rats (n= 27) were randomly assigned to left coronary artery (LCA) ligation for 30 or 120 min and sham groups. Evans Blue infusion revealed antero-apical left ventricle (LV) and left intraventricular (IV) septal ischaemia (35.5 ± 0.6% of LV mass). LCA ligation induced transient LV systolic dysfunction and sustained biventricular slowing of relaxation. Regarding mRNA levels, type B natriuretic peptide (BNP) was upregulated in the LV at 30 (+370 ± 191%) and 120 min (+221 ± 112%), whilst in the right ventricle (RV) this was only significant at 120 min (+128 ± 39%). Hipoxia-inducible factor 1, and interleukin 6 overexpression positively correlated with BNP. Inducible NO synthase upregulation was present in both ventricles at 120 min (LV, +327 ± 195%; RV, +311 ± 122%), but only in the RV at 30 min (+256 ± 88%). Insulin-like growth factor 1 increased in both ventricles at 30 (RV, +59 ± 18%; LV, +567 ± 192%) and 120 min (RV, +69 ± 33%; LV, +120 ± 24%). Prepro-endothelin-1 was upregulated in the RV at 120 min (+77 ± 25%). Ca2+ -handling proteins were selectively changed in the LV at 120 min (sarcoplasmic reticulum Ca2+ ATPase, 53 ± 7%; phospholamban, +31 ± 4%; Na+,Ca2+ exchanger, 31 ± 6%), while Na+,H+ exchanger was altered only in the RV (,79 ± 5%, 30 min; +155 ± 70%, 120 min). Tumour necrosis factor-, and angiotensin converting enzyme were not significantly altered. A very rapid modulation of remote myocardium gene expression takes place during myocardial ischaemia, involving not only the LV but also the RV. These changes are different in the two ventricles and in the same direction as those observed in heart failure. [source]


    Chronic Hypoxia Delays Myocardial Lactate Dehydrogenase Maturation in Young Rats

    EXPERIMENTAL PHYSIOLOGY, Issue 3 2003
    Z. Daneshrad
    The effect of exposure to hypobaric hypoxia for 4 weeks (oxygen pressure = 106 hPa), equivalent to 5500 m in altitude) on myocardial total lactate dehydrogenase (tLDH) activity and isoform (H and M) composition was comparatively studied in growing (4.5 weeks old) and in adult (4.5 months old) male rats. The consequences of the hypoxia-induced anorexia were checked in growing rats using a pair-fed group. Exposure to hypoxia induced a significant decrease in the H/tLDH ratio in the left (LV) and right ventricle (RV) of growing and adult rats. In adult rats this alteration was mainly a consequence of the significant increase in the specific activity of the M isomer, which resulted in an increase in the overall LDH activity. In contrast, in the LV of young rats exposed to hypoxia, the specific activity of the M isomer was similar to that of normoxic animals while the H isomer activity was significantly lower than in normoxic rats, and the overall LDH activity remained unchanged. These effects were specifically due to hypoxia per se since no significant alterations were observed in pair-fed animals. In the hypertrophied RV, the alteration of H and M isomers following hypoxia was similar to that observed in adults (i.e. no change in H and an increase in M isoform). We conclude that the well-known hypoxia-induced decrease in the H/tLDH ratio is governed by different age-dependent mechanisms. In adult rats, hypoxia may induce in both ventricles a stimulating effect on M isomer expression. In the LV of growing rats this stress could inhibit the H isomer maturation without any effect on the M isomer. In the RV of growing rats this effect could have been counteracted by the growth effect of the hypertrophying process. [source]


    Heat Shock Protein Expression is Increased in Cardiac and Skeletal Muscles of Fischer 344 Rats After Endurance Training

    EXPERIMENTAL PHYSIOLOGY, Issue 1 2000
    T. R. Samelman
    Heat shock proteins (HSPs) are expressed when cells are exposed to various types of stress and they may provide protection against cellular insult. Previous data have shown increases in HSP expression following acute exhaustive exercise in rats (Locke et al. 1990, 1995; Salo et al. 1991) and humans (Liu et al. 1999); however, it is not known if chronic exercise will increase resting levels of HSPs. The purpose of this study was to determine if basal protein levels of HSP 72/73 and HSP 60 are increased in cardiac and skeletal muscle of endurance trained Fischer 344 rats. Heart, soleus (SOL) and lateral gastrocnemius (LG) muscles were removed and hearts were sectioned into left ventricle (LV), right ventricle (RV) and atria (AT). Endurance training improved myocardial citrate synthase activity by 88, 90 and 77% and cytochrome c oxidase activity by 58, 51 and 89% in LV, RV and AT, respectively. LV and RV oxidative enzyme activities were greater when compared to AT for both trained and untrained rats (P < 0.05). HSP 72/73 expression was significantly greater (P < 0.05) in LV, RV and SOL from endurance trained versus from control rats (26, 45 and 67%, respectively). HSP 60 was also increased (P < 0.05) in LV, RV and SOL in trained relative to untrained rats. HSP 72/73 and HSP 60 were unchanged in AT and LG after training. These results indicate that endurance training increases the basal expression of stress proteins and this observation is consistent with the hypothesis that endurance training may activate a protective mechanism to stress. [source]


    Left ventricular hypertrophy in rats with biliary cirrhosis

    HEPATOLOGY, Issue 3 2003
    Javier Inserte
    Portal hypertension induces neuroendocrine activation and a hyperkinetic circulation state. This study investigated the consequences of portal hypertension on heart structure and function. Intrahepatic portal hypertension was induced in male Sprague-Dawley rats by chronic bile duct ligation (CBDL). Six weeks later, CBDL rats showed higher plasma angiotensin-II and endothelin-1 (P < .01), 56% reduction in peripheral resistance and 73% reduction in pulmonary resistance (P < .01), 87% increase in cardiac index and 30% increase in heart weight (P < .01), and increased myocardial nitric oxide (NO) synthesis. In CBDL rats, macroscopic analysis demonstrated a 30% (P < .01) increase in cross-sectional area of the left ventricular (LV) wall without changes in the LV cavity or in the right ventricle (RV). Histomorphometric analysis revealed increased cell width (12%, P < .01) of cardiomyocytes from the LV of CBDL rats, but no differences in myocardial collagen content. Myocytes isolated from the LV were wider (12%) and longer (8%) than right ventricular myocytes (P < .01) in CBDL rats but not in controls. CBDL rats showed an increased expression of ANF and CK-B genes (P < .01). Isolated perfused CBDL hearts showed pressure/end-diastolic pressure curves and response to isoproterenol identical to sham hearts, although generated wall tension was reduced because of the increased wall thickness. Coronary resistance was markedly reduced. This reduction was abolished by inhibition of NO synthesis with N -nitro-L-arginine. Expression of eNOS was increased in CBDL hearts. In conclusion, portal hypertension associated to biliary cirrhosis induces marked LV hypertrophy and increased myocardial NO synthesis without detectable fibrosis or functional impairment. This observation could be relevant to patients with cirrhosis. [source]


    Surgical Approach to the Management of Cardiovascular Echinococcosis

    JOURNAL OF CARDIAC SURGERY, Issue 3 2009
    Kutay Tasdemir M.D.
    Although cardiovascular hydatid cyst is rare, its early diagnosis and surgical management is important. Methods: We reviewed 10 patients with cardiovascular hydatid cyst who underwent surgery in our department between January 1982 and 2007. Standard cardiopulmonary bypass and antegrade cardioplegia with aortic cross-clamping were used in all but one patient. After the cysts were removed, the cavity was cleaned and then obliterated with purse-string sutures. Albendazole was used in all patients. The mean follow-up was 4.5 years. Results: The mean age was 27 years (range 12 to 76 years). Eight patients were men. The hydatid cysts were located on left ventricle (five patients), left atrium (two patients), right ventricle (three patients), right atrium (one patient), pericardium (one patient), and aorta (one patient). Except for two patients who died, all were discharged without postoperative complications. There was no late cardiac mortality or recurrence. Conclusions: Cardiac hydatid cyst should be treated surgically without delay. Although its surgical treatment carries a high complication rate, gentle handling of the heart during cardiopulmonary bypass minimizes operative risk. [source]