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Dive into the research topics where Kewal K. Talwar is active.

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Featured researches published by Kewal K. Talwar.


European Journal of Echocardiography | 2009

Unusual cause of rapidly progressive right-sided heart failure: aortic sinus of Valsalva aneurysm causing ball valve obstruction of the tricuspid valve

Shiv Bagga; Prashant Nanasaheb Mohite; Sreenivas Reddy; Shyam Kumar Singh Thingnam; Kewal K. Talwar

A rare presentation with rapidly progressive right heart failure due to tricuspid inflow obstruction (simulating right-sided valvular heart disease) caused by a non-coronary cusp sinus of Valsalva aneurysm with small perforation is reported. The aneurysm was causing ball valve obstruction at the tricuspid valve, leading to dilated right atrium and back pressure changes which were relieved after successful aneurysectomy.


Pacing and Clinical Electrophysiology | 2010

A Limitation of Tachycardia Discrimination Algorithm in a Patient with Hypertrophic Cardiomyopathy and Intermittent Complete Heart Block

Rajiv Mahajan; Manoj Kumar Rohit; Ajay Bahl; Kewal K. Talwar

A 30-year-old man presented to the outpatient department in early 2004 with history of three episodes of syncope. He had a family history of sudden cardiac death. His father and paternal uncle had died suddenly at the age of 38 and 40 years, respectively. An electrocardiogram revealed left ventricular hypertrophy. On evaluation, he was found to have nonobstructive hypertrophic cardiomyopathy. He had two brothers, aged 25 and 32 years. They were both asymptomatic. On echocardiographic screening, they were found to be normal. They are on regular follow-up. He underwent single-lead implantable cardioverter defibrillator (ICD) (Gem 7227, Medtronic Inc., Minneapolis, MN, USA) in 2004. He received both appropriate and inappropriate shocks over the next 3 years. There was only one episode of ventricular tachycardia (VT) at a cycle length of 370 ms, which had received appropriate therapy. There were two episodes when he received inappropriate therapy for sinus tachycardia (ST). In 2007, he had significant exertional fatigue and was noted to have intermittent complete heart block and the device started to pace at the backup rate of 40/minute. The patient was receiving metoprolol 25 mg twice a day which was stopped and his ventricular pacing rate was increased from 40 to 60/minute. Subsequent electrocardiogram revealed left bundle branch block with prolonged PR of 240 ms. An echocardiogram at this time revealed a left ventricular outflow tract obstruction (LVOTO) of 20 mmHg at rest with no provokable increase in gradient. In view of the inappropriate shocks and intermittent complete heart block, the device was upgraded, in 2007, to a dual


Pacing and Clinical Electrophysiology | 2009

V-Sense Episode in a Biventricular Pacemaker Device: What Is the Likely Mechanism?

Rajiv Mahajan; Manoj Kumar Rohit; Kewal K. Talwar

A 61-year-old man with dilated cardiomyopathy (DCM), severe left ventricular dysfunction, left bundle branch block (LBBB), normal sinus rhythm, and New York Heart Association class III as optimal pharmacological therapy underwent biventricular pacemaker (INSYNC III, Medtronic Inc., Minneapolis, MN, USA) implantation in January 2008. He had previously undergone angiography that had revealed normal coronaries and an endomyocardial biopsy that was consistent with DCM. Baseline electrocardiogram (ECG) revealed PR interval 240 ms and LBBB with QRS duration 140 ms. Echocardiography had revealed significant mechanical dyssynchrony. Pacing was programmed to DDD mode with lower rate of 60 beats/min and upper rate of 130 beats/min. The sensed atrioventricular (AV) delay and paced AV delay were programmed to 120 and 140 ms,


Journal of Cardiovascular Electrophysiology | 2009

Activation sequence change during left free wall pathway ablation: what is the mechanism?

Rajiv Mahajan; Manoj Kumar Rohit; Kewal K. Talwar

A 35-year-old male with a 6-year history of recurrent palpitation and documented paroxysmal supraventricular tachycardia was referred to us for catheter ablation. He had several episodes of supraventricular tachycardia despite being on adequate drug therapy. A standard 12-lead electrocardiogram (ECG) during sinus rhythm revealed no abnormalities. Echocardiogram revealed a structurally normal heart. The patient was taken up for electrophysiology study and catheter ablation. The electrophysiology study was performed in postabsorptive state. Three quadripolar catheters were inserted via femoral venous access and advanced to the high right atrium, His bundle, and right ventricle under fluoroscopic control. A decapolar catheter was inserted via the right internal jugular vein and advanced into the coronary sinus (CS) with the proximal bipole at the ostium (os). Programmed atrial stimulation revealed a continuous atrioventricular (AV) node function curve. Incremental right ventricular pacing revealed nondecremental ventriculoatrial (VA) conduction, with the earliest atrial activation at the distal bipole CS (1–2). Programmed ventricular stimulation easily and repeatedly induced a regular narrow QRS complex tachycardia with a cycle length (CL) of 280 ms. The activation sequence on the CS during tachycardia was eccentric (Fig. 1A). A diagnosis of orthodromic A V reentrant tachycardia (AVRT) using a left-sided free-wall accessory pathway (AP) was made. The retrograde transaortal approach was used for ablation. The ablation catheter was positioned above the mitral valve at the left AV annulus. Radiofrequency (RF) energy was delivered to the earliest atrial activation site just above the CS12 catheter electrode at the mitral annulus. The RF energy was applied during tachycardia. Figure 1B and C shows the intracardiac tracings after the second and third burn, respectively. What has happened?


Molecular and Cellular Biochemistry | 2008

ACE I/D polymorphism in Indian patients with hypertrophic cardiomyopathy and dilated cardiomyopathy

Taranjit Singh Rai; Perundurai S. Dhandapany; Tarunveer Singh Ahluwalia; Monica Bhardwaj; Ajay Bahl; Kewal K. Talwar; Krishnakumar Nair; Andiappan Rathinavel; Madhu Khullar


Molecular and Cellular Biochemistry | 2009

Genetic and clinical profile of Indian patients of idiopathic restrictive cardiomyopathy with and without hypertrophy

Taranjit Singh Rai; Shamim Ahmad; Tarunveer Singh Ahluwalia; Monica Ahuja; Ajay Bahl; Uma Nahar Saikia; Balvinder Singh; Kewal K. Talwar; Madhu Khullar


Molecular and Cellular Biochemistry | 2012

Risk of obesity and type 2 diabetes with tumor necrosis factor-α 308G/A gene polymorphism in metabolic syndrome and coronary artery disease subjects

Ranbir Chander Sobti; Rupinder Kler; Yash Paul Sharma; Kewal K. Talwar; Neha Singh


Molecular and Cellular Biochemistry | 2012

Proteomic analysis of circulating human monocytes in coronary artery disease

Aruna Poduri; Ajay Bahl; Kewal K. Talwar; Madhu Khullar


Molecular and Cellular Biochemistry | 2009

Circulating proinflammatory cytokines and N-terminal pro-brain natriuretic peptide significantly decrease with recovery of left ventricular function in patients with dilated cardiomyopathy

Shamim Ahmad; Parminder Singh Otaal; Taranjit Singh Rai; Ajay Bahl; Uma Nahar Saikia; Rohit Manoj; M. Thungapathra; Kewal K. Talwar; Madhu Khullar


Cvd Prevention and Control | 2009

P-347 TNF-α Modulates Gene Expression of Cardiac Dystrophin and Titin Proteins through NF-Kappa B Pathway

Madhu Khullar; Shamim Ahmad; Ajay Bahl; Rohit Manoj Kumar; Rajiv Mahajan; Kewal K. Talwar

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Ajay Bahl

Post Graduate Institute of Medical Education and Research

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Madhu Khullar

Post Graduate Institute of Medical Education and Research

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Taranjit Singh Rai

Post Graduate Institute of Medical Education and Research

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Manoj Kumar Rohit

Post Graduate Institute of Medical Education and Research

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Shamim Ahmad

Post Graduate Institute of Medical Education and Research

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Uma Nahar Saikia

Post Graduate Institute of Medical Education and Research

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Balvinder Singh

Council of Scientific and Industrial Research

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Tarunveer Singh Ahluwalia

Post Graduate Institute of Medical Education and Research

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