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Right Ventricular Hypertrophy (right + ventricular_hypertrophy)
Selected AbstractsLate Presentation of Pulmonary Valve Stenosis Confirmed by Cardiovascular Magnetic ResonanceCONGENITAL HEART DISEASE, Issue 3 2008Didier Locca MD ABSTRACT We describe the case of a 70-year-old man who presented with increasing exertional dyspnea. He was found to have an ejection systolic murmur and evidence of right ventricular outflow tract obstruction, with a peak velocity of 4.5 m/s recorded by transthoracic Doppler echocardiography. Cardiovascular magnetic resonance showed right ventricular hypertrophy, pulmonary valve stenosis, peak recorded velocity 4.2 m/s, with thickened pulmonary valve leaflets of reduced mobility, and poststenotic dilatation of the main pulmonary artery. The case illustrates that severe pulmonary valve stenosis can present late in life and that cardiovascular magnetic resonance can be useful in clarifying nature and level of right ventricular outflow tract obstruction in an adult. [source] Protein kinase C mRNA and protein expressions in hypobaric hypoxia-induced cardiac hypertrophy in ratsACTA PHYSIOLOGICA, Issue 4 2010M. 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] Results of balloon valvuloplasty in 40 dogs with pulmonic stenosisJOURNAL OF SMALL ANIMAL PRACTICE, Issue 3 2004M. Stafford Johnson The records of 43 dogs presenting with severe pulmonic stenosis in which balloon valvuloplasty was attempted were reviewed. Thirty-four dogs (79 per cent) were symptomatic at initial presentation. All patients were selected for balloon valvuloplasty on the basis of a Doppler-derived trans-stenotic pressure gradient of over 80 mmHg and concurrent evidence of mild to severe right ventricular hypertrophy. Forty dogs underwent balloon valvuloplasty; the procedure was not performed in three dogs because of an aberrant coronary artery in two cases and because catheterisation of the pulmonary artery was not possible in the third. Overall, 37 out of the 40 dogs (93 per cent) were successfully ballooned, resulting in a mean reduction in the pressure gradient of 46 per cent, with a mean pressure gradient of 124 mmHg on presentation and 67 mmHg six months after the procedure. Three dogs died during balloon valvuloplasty (all of which had a concurrent defect) and three dogs showed a poor clinical response to the procedure. Thus balloon valvuloplasty was successful and resulted in a sustained clinical improvement in 80 per cent of previously symptomatic cases. This study was undertaken to document the results of balloon valvuloplasty in a larger population of dogs than has previously been published. [source] Right ventricular noncompaction associated with long QT in a fetus with right ventricular hypertrophy and cardiac arrhythmiasPRENATAL DIAGNOSIS, Issue 6 2008Ruben J. Acherman No abstract is available for this article. [source] Isolated congenital spleen agenesis: A rare cause of chronic thromboembolic pulmonary hypertension in an adultRESPIROLOGY, Issue 6 2008Fumiyuki TAKAHASHI Abstract: This report describes a case of isolated congenital spleen agenesis complicated by chronic thromboembolic pulmonary hypertension (CTPH) in a 44-year-old female patient. The patient had increasing exertional dyspnoea and thrombocytosis. An echocardiogram showed severe pulmonary hypertension and right ventricular hypertrophy, and contrast-enhanced chest CT revealed multiple thromboemboli within both pulmonary arteries. A perfusion lung scan demonstrated multiple segmental defects and no spleen was detected by abdominal CT, ultrasonography or scintigraphy. Comprehensive clinical examinations disclosed no evidence of a thrombus elsewhere or of an associated malformation such as a cardiac anomaly. Anticoagulation therapy was started, and a perfusion lung scan revealed partial improvement of the hypoperfusion in the right lower lobe. However, repeat echocardiography showed the pulmonary hypertension persisting for 1 year. The multiple segmental defects in the perfusion lung scans were also persistent. Collectively, a diagnosis of CTPH with isolated congenital spleen agenesis was established. This is the first documented case of CTPH in an adult with isolated congenital asplenia. Although congenital spleen agenesis is a rare condition, this case report suggests that this possibility should be considered when a diagnosis of CTPH and thrombocytosis is made. [source] The Extracellular Signal-Regulated Kinase Is Involved in the Effects of Sildenafil on Pulmonary Vascular RemodelingCARDIOVASCULAR THERAPEUTICS, Issue 1 2010Zhen Zeng Pulmonary hypertension is a group of diseases comprising vascular constriction and obstructive changes of the pulmonary vasculature. Phosphodiesterase type 5 inhibitors, for example, sildenafil, can alleviate vascular remodeling in the monocrotaline pulmonary hypertension model in rats. We investigate the mechanisms of sildenafil on the pulmonary vascular remodeling of pulmonary hypertension induced by monocrotaline (MCT) in rats. Thirty Sprague-Dawley rats (weighing 200,220 g) were administered with MCT abdominal cavity injection or equivalent volume of normal saline (NS) (which were treated as C group n = 10) to induce pulmonary hypertension model. Fourteen days later, 20 MCT treated rats were randomly fed with sildenafil (25mg/kg/day) or placebo as S, P group (10 rats for each group), respectively. Another 6 weeks later, mean pulmonary artery pressure (mPAP), index of right ventricular hypertrophy (RV/LV+S) of all animals were measured under general anesthesia. Pulmonary tissue was collected to investigate pathological features of pulmonary arteries and to measure protein expression of ERK1/ERK2 and MKP1. After 6 weeks, there were significant elevated mPAP and RV/LV+S in both P and S groups. The ratio of wall thickness to vessel diameter in pulmonary arteries with diameters <200 ,m were increased in both P and S groups. But the ratio of wall thickness to vessel diameter was smaller in S group than that in P group. The phosphorylation level of ERK1/ERK2 were elevated in both P and S groups, but the level of phosphorlation ERK1/ERK2 were lower in S group than that in P group. Intriguingly, the expression level of MKP1 was significantly increased in both S and P groups, while it was higher in S group than that in P group. The Sildenafil can decrease mPAP and inhibit the progress of pulmonary vascular remodeling in pulmonary hypertension rats. The ERK-MAP kinase signaling pathway might play a role during this process. [source] | |||||||||||||