Publications by authors named "Tarvinder S Dhanjal"

Background: Atrial arrhythmias (AA) commonly affect patients with cardiac amyloidosis (CA) and are a contributing risk factor for the development of heart failure (HF). This study sought to investigate the long-term efficacy and impact of catheter ablation on HF progression in patients with CA and AA.

Methods: Thirty-one patients with CA and AA undergoing catheter ablation were retrospectively included (transthyretin-ATTR CA 61% and light chain-AL CA 39%).

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Aims: Since the introduction of direct oral anticoagulant (DOAC) for atrial fibrillation (AF) therapy, inappropriate and/or underdosing of these drugs has been a major clinical challenge. We evaluated the characteristics of patients with AF treated with inappropriate and low-dose DOACs.

Methods And Results: Patients with AF treated with inappropriate and low-dose DOACs from October 2021 to December 2021 were evaluated from the French National Prospective Registry (PAFF).

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Background: The DiamondTemp ablation (DTA) system is a novel temperature-controlled irrigated radiofrequency (RF) ablation system that accurately measures tip-tissue temperatures for real-time power modulation. Lesion morphologies from longer RF durations with the DTA system have not been previously described. We sought to evaluate lesion characteristics of the DTA system when varying the application durations.

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Aims: Atrial fibrillation (AF)/atrial flutter is common during cardiac amyloidosis (CA). Electrical cardioversion (EC) is a strategy to restore sinus rhythm (SR). However, left atrial thrombus (LAT) represents a contraindication for EC.

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Aims: This study sought to describe and evaluate the impact of a routine in-hospital cardiac resynchronization therapy (CRT) programme, including comprehensive heart failure (HF) evaluation and systematic echo-guided CRT optimization.

Methods And Results: CRT implanted patients were referred for optimization programme at 3 to 12 months from implantation. The program included clinical and biological status, standardized screening for potential cause of CRT non-response and systematic echo-guided atrioventricular and interventricular delays (AVd and VVd) optimization.

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Objectives: In this study the authors determined the extent of cellular infiltration and dispersion, and regional vascularization in electrophysiologically (EP) defined zones in post-myocardial infarction (MI) swine ventricle.

Background: The critical isthmus (CI) in post-MI re-entrant ventricular tachycardia (VT) is a target for catheter ablation. In vitro evidence suggests that myofibroblasts (MFB) within the scar border zone (BZ) may increase the susceptibility to slow conduction and VT, but whether this occurs in vivo remains unproven.

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Introduction: Reversible premature ventricular complexes-induced cardiomyopathy (PVC-CMP) is a well-described, multi-factorial entity. Single predictors, such as PVC burden or QRS duration, may not apply equally to all patients in contemporary unselected populations including patients with structural heart disease (SHD) or with particular origin such as epicardial (EPI) PVC. We sought to evaluate clinical criteria associated with PVC-CMP notably focusing on the EPI origin impact and ECG recognition and the value of a new composite predictor of PVC-CMP, the PVC-CMP-Index.

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Background: We tested the hypothesis that ischemia-induced ventricular fibrillation (VF) is facilitated by platelets, trapped regionally in the ischemic zone and activated to release arrhythmogenic secretome.

Methods And Results: In a randomized study in blood-free, buffer-perfused isolated rat hearts, ischemic zone territory (34±1% of left ventricle) was selected so that ischemia evoked VF in only 42% of controls. VF incidence was increased to 91% (P<0.

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Migration of megakaryocytes (MKs) from the proliferative osteoblastic niche to the capillary-rich vascular niche is essential for proplatelet formation and platelet release. In this study, we explore the role of surface glycoprotein receptors and signaling proteins in regulating MK migration and platelet recovery after immune-induced thrombocytopenia. We show that spreading and migration of mouse primary bone marrow-derived MKs on a fibronectin matrix are abolished by the Src family kinases inhibitor PP1, the Syk kinase inhibitor R406 and the integrin alphaIIbbeta3 antagonist lotrafiban.

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Dextrocardia is a rare cardiac anomaly in which the heart is located in the right hemithorax. This developmental irregularity can occur in isolation as situs solitus, or in association with situs inversus or situs ambiguous. Although there are reports of coronary angiography in patients with dextrocardia, there are very few reported cases of mechanical intervention.

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We report a patient with Crohn's disease and end-stage renal failure, which resulted in severe vitamin D deficiency and hyperparathyroidism. This resulted in the development of calciphylaxis, which initially manifested as pulmonary vasculature calcification; however, the diagnosis was not clear until the classic skin lesions had developed. Calciphylaxis is a rare condition, which is increasing in incidence, and a high index of suspicion is essential for early diagnosis and treatment.

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Although the expression of PECAM-1 (CD31) on vascular and haematopoietic cells within the bone marrow microenvironment has been recognized for some time, its physiological role within this niche remains unexplored. In this study we show that PECAM-1 influences steady state hematopoietic stem cell (HSC) progenitor numbers in the peripheral blood but not the bone marrow compartment. PECAM-1(-/-) mice have higher levels of HSC progenitors in the blood compared to their littermate controls.

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PECAM-1 is a member of the superfamily of immunoglobulins (Ig) and is expressed on platelets at moderate level. PECAM-1 has been reported to have contrasting effects on platelet activation by the collagen receptor GPVI and the integrin, alphaIIbbeta3, even though both receptors signal through Src-kinase regulation of PLCgamma2. The present study compares the role of PECAM-1 on platelet activation by these two receptors and by the lectin receptor, CLEC-2, which also signals via PLCgamma2.

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During thrombopoiesis, maturing megakaryocytes (MKs) migrate within the complex bone marrow stromal microenvironment from the proliferative osteoblastic niche to the capillary-rich vascular niche where proplatelet formation and platelet release occurs. This physiologic process involves proliferation, differentiation, migration, and maturation of MKs before platelet production occurs. In this study, we report a role for the glycoprotein PECAM-1 in thrombopoiesis.

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