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Biomedical subjects

George I Varughese

Publications and source records attributed to George I Varughese.

17 recordsLinked to original sources
PubMed2006

Effects of blood pressure on the prothrombotic risk in 1235 patients with non-valvular atrial fibrillation.

BACKGROUND: Increased levels of plasma von Willebrand factor (vWf, an index of endothelial damage/dysfunction) and soluble P-selectin (sP-sel, an index of platelet activation) concentrations have been reported as indices of the prothrombotic state in both non-valvular atrial fibrillation and hypertension separately. However, the effect of hypertension on the levels of these indices in the setting of atrial fibrillation, and whether increasing severity of hypertension presents an additive prothrombotic risk, is unclear. METHODS: Plasma concentrations of vWf and sP-sel were measured by ELISA in 1235 patients with atrial fibrillation, and levels related to a history of hypertension and rising quartiles of systolic, diastolic and pulse pressure in those with and without diabetes mellitus and prior vascular events. RESULTS: Mean plasma vWf was higher among patients with atrial fibrillation with a history of hypertension (149 vs 145 IU/dl, p = 0.005). Also, an increase in the levels of vWf with increasing quartiles of pulse pressure (p = 0.042) was noticed. However, on multivariate analysis, after adjusting for potential confounders, the effects of both hypertension and pulse pressure became non-significant (p = 0.261 and p = 0.5, respectively). Levels of sP-sel were unaffected by a history of hypertension and rising quartiles of systolic and diastolic blood pressure, or pulse pressure. CONCLUSION: Among patients with atrial fibrillation, patients with hypertension have higher vWf levels, indicating endothelial damage/dysfunction, which is associated with increasing pulse pressure. However, these associations are probably owing to the presence of other associated cardiovascular disease, rather than hypertension itself. Furthermore, platelet activation (sP-sel) was unrelated to hypertension or blood pressure in this atrial fibrillation cohort. Hypertension or blood pressure levels do not seem to have an independent additive affect on the prothrombotic state in atrial fibrillation.

Aged↗
PubMed2006

Novel concepts of statin therapy for cardiovascular risk reduction in hypertension.

Hypertension is associated with an increase in cardiovascular events. Pathophysiological mechanisms of this include endothelial damage/dysfunction, inflammatory activation, insulin resistance, platelet activation and alterations in the coagulation cascade leading to a prothrombotic state. Dyslipidaemia acts synergistically with hypertension in increasing cardiovascular risk. HMG CoA reductase inhibitors (statins) are lipid-lowering drugs and more recently have been shown to have a significant pleiotropic effect on endothelial function, inflammation, platelet activation and coagulation. Statins affect the whole pathophysiology of atherogenesis from deposition to plaque rupture and thrombogenesis because of its pleiotropic effects. Therefore it is intuitive that statins may be of benefit in hypertensive patients with conventionally normal lipid levels by preventing the pathological effects of hypertension. There is an increasing clinical evidence base for statins use in patients with hypertension. In this article, the novel pleiotropic and conventional mechanisms of statins, and clinical data of statin therapy in patients with hypertension are reviewed.

Blood Coagulation↗
PubMed2006

Under pressure.

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Antihypertensive Agents↗
PubMed2005

Diabetes mellitus and atrial fibrillation: perspectives on epidemiological and pathophysiological links.

Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia, which is also associated with a substantial risk of mortality and morbidity from stroke, thromboembolism, heart failure and hospitalisations. On a epidemiological basis, diabetes mellitus is commonly associated with AF. Nonetheless, AF is also associated with vascular disease and hypertension, which are themselves intimately linked to diabetes. Indeed, the precise pathophysiological and clinical relationships between AF and diabetes mellitus are not completely understood. What we do know is that both diabetes and AF are individually bad for our patients, and the presence of both requires aggressive management strategies.

Atrial Fibrillation↗
PubMed2005

Is hypertension a prothrombotic state?

Hypertension is complicated by thrombosis-related events (such as myocardial infarction and stroke), and despite the high vascular pressures, these thrombotic occlusive events paradoxically occur more often than hemorrhagic episodes. The predisposition for thrombogenesis is increased in hypertension, which leads to changes in the platelets, endothelium, and matrix metalloproteinases and their inhibitors, as well as the coagulation and fibrinolytic pathways, which help promote the induction and the maintenance of this prothrombotic or hypercoagulable state. Other cardiovascular diseases, such as atrial fibrillation, congestive heart failure, and left ventricular hypertrophy, which may occur as a result of untreated hypertension, can also activate the prothrombotic state. These changes can, to a certain degree, be reversed by the treatment of hypertension, although the effects may be inconsistent. The evidence for antithrombotic therapy is less consistent, but in "high risk" hypertensive patients, antiplatelet therapy is useful.

Antihypertensive Agents↗
PubMed2005

Targeting the renin-angiotensin-aldosterone-system in atrial fibrillation: a shift from electrical to structural therapy?

Despite its increasing incidence and prevalence, treatment options in atrial fibrillation (AF) are far from ideal and often limited. After decades of focus on the electrical aspects of AF with unsatisfactory results, recent research is focusing increasingly on the atrial structural remodelling that underlies the development of AF in different pathological conditions, such as hypertension, heart failure, diabetes mellitus and coronary artery disease. The aim of this review is to provide a comprehensive overview of the role of the renin-angiotensin-aldosterone-system in AF and to highlight the clinical evidence on renin-angiotensin-aldosterone-system blockade as a therapeutic option in AF.

Angiotensin II Type 1 Receptor Blockers↗