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Coronary Artery Disease: HELP
Articles by Chetan Varma
Based on 6 articles published since 2010
(Why 6 articles?)

Between 2010 and 2020, Chetan Varma wrote the following 6 articles about Coronary Artery Disease.
+ Citations + Abstracts
1 Review Current Understanding of Atherogenesis. 2017

Brown, Richard A / Shantsila, Eduard / Varma, Chetan / Lip, Gregory Y H. ·Department of Medicine, University of Birmingham Institute of Cardiovascular Sciences, City Hospital, United Kingdom. · Department of Medicine, University of Birmingham Institute of Cardiovascular Sciences, City Hospital, United Kingdom; Cardiology Department at Sandwell and West Birmingham Hospitals NHS Trust, City Hospital and Sandwell Hospital, West Bromwich, United Kingdom. · Cardiology Department at Sandwell and West Birmingham Hospitals NHS Trust, City Hospital and Sandwell Hospital, West Bromwich, United Kingdom. · Department of Medicine, University of Birmingham Institute of Cardiovascular Sciences, City Hospital, United Kingdom; Cardiology Department at Sandwell and West Birmingham Hospitals NHS Trust, City Hospital and Sandwell Hospital, West Bromwich, United Kingdom. Electronic address: g.y.h.lip@bham.ac.uk. ·Am J Med · Pubmed #27888053.

ABSTRACT: Scientific understanding of atherogenesis is constantly developing. From Virchow's observations 160 years ago we now recognize the endothelial response to injury as inflammatory, involved in all stages of atherosclerosis. Endothelial activation may cause reversible injury or dysfunction, or lead to irreparable damage. Indeed, early atherosclerosis is reversible. The introduction of genome-wide association testing has furthered the identification of potentially important genetic variants that help explain the heritability of coronary artery disease as well as spontaneous cases of severe coronary artery disease in patients with otherwise minimal risk factors. However, the mechanisms by which many of the newer variants exert their influence remain unknown.

2 Review Epidemiology and pathogenesis of diffuse obstructive coronary artery disease: the role of arterial stiffness, shear stress, monocyte subsets and circulating microparticles. 2016

Brown, Richard A / Shantsila, Eduard / Varma, Chetan / Lip, Gregory Y H. ·a University of Birmingham Institute of Cardiovascular Sciences, City Hospital , Birmingham , UK. · b Cardiology Department, City Hospital , Birmingham , UK. ·Ann Med · Pubmed #27282244.

ABSTRACT: Despite falling age-adjusted mortality rates coronary artery disease (CAD) remains the leading cause of death worldwide. Advanced diffuse CAD is becoming an important entity of modern cardiology as more patients with historical revascularisation no longer have suitable anatomy for additional procedures. Advances in the treatment of diffuse obstructive CAD are hampered by a poor understanding of its development. Although the likelihood of developing clinically significant (obstructive) CAD is linked to traditional risk factors, the morphology of obstructive CAD among individuals is highly variable - some patients have diffuse stenotic disease, while others have a focal stenosis. This is challenging to explain in mechanistic terms as vascular endothelium is equally exposed to injury stimulants. Patients with diffuse disease are at high risk of adverse outcomes, particularly if unsuitable for revascularisation. We searched multiple electronic databases (MEDLINE, EMBASE and the Cochrane Database) and reviewed the epidemiology, pathogenesis and prognosis relating to advanced diffuse CAD with particular focus on the role of endothelial shear stress, large artery stiffness, monocyte subsets and circulating microparticles. Key messages Although traditional CAD risk factors correlate strongly with disease severity, significant individual variation in disease morphology exists. Advanced, diffuse CAD is difficult to treat effectively and can significantly impair quality of life and increases mortality. The pathophysiology associated with the progression of CAD is the result of complex maladaptive interaction between the endothelium, cells of the immune system and patterns of blood flow.

3 Review Lessons from primary PCI practice for the next decade. 2014

Lee, Leong / Varma, Chetan. ·Department of Cardiology, City Hospital, Birmingham, UK. ·Heart · Pubmed #25028411.

ABSTRACT: Primary percutaneous coronary intervention (PPCI) is the reperfusion treatment of choice for acute ST-elevation myocardial infarction with studies having demonstrated improved outcomes with PPCI over thrombolysis. Its use has increased substantially over the last decade, overtaking thrombolytic therapy in many countries. This has been paralleled with advances in adjunctive technology and pharmacological therapy to further improve outcome, but challenges remain for PPCI practitioners. The evidence behind PPCI is reviewed at every stage of the patient's journey.

4 Article Impact of Mon2 monocyte-platelet aggregates on human coronary artery disease. 2018

Brown, Richard A / Lip, Gregory Y H / Varma, Chetan / Shantsila, Eduard. ·Institute of Cardiovascular Sciences, City Hospital, University of Birmingham, Birmingham, UK. · Hull and East Yorkshire Hospitals NHS Trust, Castle Hill Hospital, Cottingham, UK. · Sandwell and West Birmingham Hospitals NHS Trust, City Hospital, Birmingham, UK. ·Eur J Clin Invest · Pubmed #29423944.

ABSTRACT: BACKGROUND: Monocyte-platelet aggregates (MPAs) form when Mon1, Mon2 or Mon3 monocyte subsets adhere to platelets. They are pathophysiologically linked to coronary artery disease (CAD). However, their individual roles in the occurrence of diffuse CAD remain unknown. MATERIALS AND METHODS: Peripheral blood from 50 patients with diffuse CAD, 40 patients with focal CAD and 50 age-matched patients with normal coronary arteries was analysed by flow cytometry to quantify MPAs associated with individual monocyte subsets. Cutaneous forearm microcirculation was assessed using laser Doppler flowmetry at rest and after iontophoresis of acetylcholine (endothelium-dependent vasodilation) and sodium nitroprusside (endothelium-independent vasodilation) at 100 μA for 60 seconds. Patients with CAD had repeat assessment at 6 and 12 months. RESULTS: Baseline counts of MPAs with Mon2 subset (CD14++CD16+CC2+ monocytes) were significantly higher in patients with diffuse CAD compared to focal CAD (P = .001) and patients without CAD (P = .006). On multivariate regression, MPAs with Mon2 independently predicted diffuse CAD (odds ratio 1.10, 95% confidence interval 1.02-1.19, P = .01) and correlated negatively with endothelium-dependent microvascular vasodilation (r = -.37, P = .008), an association which persisted after adjustment for covariates. Longitudinal observation confirmed the persistence of an inverse relationship between MPAs with Mon2 and endothelium-dependent microvascular function. CONCLUSION: Monocyte-platelet aggregates with Mon2 are increased in patients with diffuse CAD and therefore could represent an important contributor to accelerated coronary atherosclerotic progression by a mechanism involving microvascular endothelial dysfunction.

5 Article Eosinophil count predicts mortality following percutaneous coronary intervention. 2012

Toor, Iqbal S / Jaumdally, Rumi / Lip, Gregory Y H / Millane, Teri / Varma, Chetan. ·Department of Cardiology, City Hospital, Birmingham B18 7QH, UK. ·Thromb Res · Pubmed #22771073.

ABSTRACT: INTRODUCTION: Several inflammatory markers have been shown to be independent predictors for both the development of clinically significant atherosclerosis and for adverse outcome in patients with symptomatic coronary artery disease (CAD). We investigated the prognostic role of eosinophil count in low to intermediate risk patients with CAD. METHODS: We studied 909 patients admitted for elective or urgent percutaneous coronary intervention (PCI) from April 2002 to December 2004, and measured pre-procedural total and differential white blood cell (WBC) counts. Inter-tertile WBC differences in short (6months) and long term (up to 74months) mortality were analysed after adjusting for differences in baseline characteristics. RESULTS: Over a median period of 54months (inter-quartile range 47-65), a total of 138 deaths (15.2%) occurred, of which 24 were in the first 6months of follow-up. Cox regression analysis showed that high pre-procedural eosinophil count (top tertile) was associated with improved outcome within the first 6months (OR=0.23 [0.06-0.84]; p=0.03) but after this period there was an increased risk of mortality (OR=2.21, [1.26-3.88]; p=0.006). CONCLUSIONS: Eosinophil count is a novel biomarker for risk stratification of CAD patients, which was associated initially with reduced mortality, but after 6months with increased mortality.

6 Article 1-year outcome of TRIAS HR (TRI-stent adjudication study-high risk of restenosis) a multicenter, randomized trial comparing genous endothelial progenitor cell capturing stents with drug-eluting stents. 2011

Klomp, Margo / Beijk, Marcel A / Varma, Chetan / Koolen, Jacques J / Teiger, Emmanuel / Richardt, Gert / Bea, Florian / van Geloven, Nan / Verouden, Niels J / Chan, Yu Kwan / Woudstra, Pier / Damman, Peter / Tijssen, Jan G / de Winter, Robbert J. ·Department of Cardiology, Academic Medical Center-University of Amsterdam, Amsterdam, the Netherlands. ·JACC Cardiovasc Interv · Pubmed #21851905.

ABSTRACT: OBJECTIVES: This study sought to demonstrate the noninferiority of endothelial progenitor cell capturing stents (ECS) relative to drug-eluting stents (DES) regarding target lesion failure (TLF) and the composite of cardiac death, myocardial infarction, and target lesion repeat revascularization within 1 year. BACKGROUND: A "pro-healing" approach for prevention of in-stent restenosis is theoretically favorable over the use of cytotoxic/cytostatic drugs released from DES to treat coronary artery disease. Promoting accelerated endothelialization of the stent, ECS have shown promising results in studies with patients carrying noncomplex lesions. METHODS: We undertook an international, clinical trial in 26 centers planning to randomize 1,300 patients with stable coronary artery disease and with a high risk of restenosis between treatment, with either ECS or DES. After a routine review with 50% of the patients enrolled, early cessation of the trial was recommended by the data and safety monitoring board when TLF in the ECS population was higher and treatment of new patients with an ECS would be unreasonable. RESULTS: At 1 year evaluating 304 patients receiving ECS and 318 receiving DES, TLF occurred in 17.4% of the ECS-treated patients and in 7.0% of the DES-treated patients (p = 0.98 for noninferiority). CONCLUSIONS: Within 1 year, inhibition of intimal hyperplasia by the ECS is not sufficiently strong to compete with DES in terms of restenosis prevention in patients/lesions with a high risk of restenosis. Furthermore, long-term follow-up is pivotal to fully appreciate the clinical value of ECS, including the effect on late intimal hyperplasia regression.