Background:In acute decompensated heart failure (ADHF), diuretic use, the mainstay therapy for congestion, is associated with electrolyte abnormalities and worsening renal function. Vasopressin mediates fluid retention in heart failure. In contrast to diuretics, the vasopressin antagonist tolvaptan may increase net volume loss in heart failure without adversely affecting electrolytes and renal function. Hyponatremia (serum sodium concentration, <135 mEq/L) is a predictor of death among patients with heart failure.Objective:We prospectively observed the short term efficacy and safety of low dose (15 mg) tolvaptan in admitted patients with hyponatremia and ADHF in Indian population.Methodology:A total of 40 patients with ADHF along with hyponatremia (<125 mEq/L) on standard therapy were treated with 15 mg of tolvaptan at a single oral dose for 7 days.Results:Serum sodium concentrations increased significantly after treatment with tolvaptan from baseline (P < 0.02). There was a significant improvement in symptoms and New York Heart Association (NYHA) class after starting tolvaptan (P ≤ 0.05). Total diuretic dose and mean body weight was reduced non-significantly at 7th day from the baseline. Side-effects associated with tolvaptan included increased thirst, dry mouth and increased urination. Few patients had worsening renal function. However, several patients developed hypernatremia.Conclusion:In this small observational study, tolvaptan initiation in patients with ADHF with hyponatremia in addition to standard therapy may hold promise in improvement in NYHA class and serum sodium. At the same time, we observed that serious adverse events such as renal function deterioration and hypernatremia developed after tolvaptan treatment, which needs to be addressed in future by randomized study with larger sample size.
a b s t r a c tVentricular noncompaction has been recognized as a distinct form of rare cardiomyopathy characterized by numerous, prominent ventricular trabeculations and deep intertrabecular recesses and is caused by a disorder of endomyocardial morphogenesis. Concomitance of either valvular pathologies or complete atrioventricular block with biventricular noncompaction has rarely been reported. Herein, we present a case of 67 years old male presented with syncopal attack and congestive heart failure due to biventricular noncompaction with significant left ventricular dysfunction associated with complete atrioventricular block. He was formerly diagnosed as dilated cardiomyopathy for last 2 years. Review of literatures of all reported cases has been discussed.
We are reporting the first case of rare association between multiple congenital cardiac malformations with severe rheumatic mitral stenosis which is an acquired structural cardiac disease. A 16 years old female patient presented with progressive dyspnoea & cyanosis for the last one month with past history of recurrent pneumonia since infancy. Physical examination revealed presence of cyanosis, grade I clubbing, radio-radial & radio-femoral delay, loud & single second heart sound, apical long mid diastolic murmur and left parasternal ejection systolic murmur. Transthoracic echocardiography revealed severe rheumatic mitral stenosis, multiple ventricular septal defects (VSD) with bidirectional shunt, hypoplastic aortic arch, Coarctation of aorta and severe pulmonary hypertension. Transesophageal echocardiography revealed the same findings along with the presence of moderate mitral regurgitation and 9 mm perimembranous VSD extending into muscular septum. Cardiac catheterization study confirmed the echocardiographic findings and demonstrated large patent ductus arteriosus (PDA). We have planned for high-risk percutaneous transmitral commissurotomy (PTMC) for this patient to decrease the back pressure on pulmonary vasculature. So that right to left shunt will be decreased and cyanosis will also improve. But parents refused to give consent for PTMC. She was on treatment with regular penicillin prophylaxis, diuretics, sildenafil and infective endocarditic prophylaxis. We should be aware of this kind of complex association between congenital and acquired structure heart disease. Eisenmenger syndrome could also be a presentation of juvenile severe rheumatic mitral stenosis when it is associated with congenital shunt lesion like VSD/PDA in our case.
Percutaneous transvenous mitral commissurotomy (PTMC) using Inoue/Accura balloon is an effective procedure for management of patients with rheumatic mitral stenosis. Inability to cross the mitral valve is one of the pertinent reasons for procedural failure. We describe a series of three patients who were tackled with successful PTMC using a novel technique of veno-arterial looping and in the fourth patient we used double loop entry into left ventricle with veno-arterial rail and peripheral balloon dilatation for completing the PTMC. This is first such reported case series in literature to our knowledge.
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