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antiarrhythmic/upala

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Considering the cardioprotective and anti-inflammatory properties of clofibrate, the aim of the present experiment was to investigate the involvement of local and systemic inflammatory cytokines in possible antiarrhythmic effects of clofibrate in ouabain-induced arrhythmia in rats. Rats were orally
Persistent myocardial ischemia post-myocardial infarction can lead to fatal ventricular arrhythmias such as ventricular tachycardia and fibrillation, both of which carry high mortality rates. Dexmedetomidine (Dex) is a highly selective α2-agonist used in surgery for congenital cardiac

Pro- and anti-arrhythmic effects of anti-inflammatory drugs.

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Inflammatory process is strongly associated with cardiac arrhythmia, either as a cause or a consequence. Antiinflammatory drugs are widely prescribed, and some of them have been associated with an increased cardiovascular risk. Then, the eventual pro- or anti-arrhythmic effect of these drugs is of
Lowering plasma low density lipoprotein-cholesterol (LDL-C), blood pressure, homocysteine, and preventing platelet aggregation using a combination of a statin, three blood pressure lowering drugs such as a thiazide, a beta blocker, and an angiotensin converting enzyme (ACE) inhibitor each at half

Anti-Inflammatory and Antiarrhythmic Effects of Beta Blocker in a Rat Model of Rheumatoid Arthritis

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Background Patients with rheumatoid arthritis are at twice the risk of ventricular arrhythmia and sudden cardiac death as the general population. We hypothesize that β-blocker treatment of rheumatoid arthritis is antiarrhythmic by producing synergistic anticatecholaminergic and anti-inflammatory
OBJECTIVE Patients with rheumatoid arthritis (RA) are twice as likely to experience sudden cardiac death compared with individuals without RA. Although the underlying mechanisms of this have not been clarified, evidence points to the effects of systemic inflammation on ventricular repolarization.
The aim of this study was to verify whether exaggerated arrhythmogenesis is attributed to inflammatory factors actively involving an excess of reactive oxygen species (ROS), transforming growth factor (TGF)-beta and endothelin (ET). We hypothesized that CPU86017, derived from berberine, which

Colchicine after pulmonary vein isolation: is inflammation the new anti-arrhythmic target.

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Current treatment options in (peri)myocarditis and inflammatory cardiomyopathy.

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In inflammatory dilated cardiomyopathy and myocarditis there is--apart from heart failure and antiarrhythmic therapies--no alternative to an aetiologically driven specific treatment. Prerequisite are noninvasive and invasive biomarkers including endomyocardial biopsy and PCR on cardiotropic agents.

Treatment options in myocarditis and inflammatory cardiomyopathy : Focus on i. v. immunoglobulins.

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For myocarditis and inflammatory cardiomyopathy, an etiologically driven treatment is today the best option beyond heart failure therapy. Prerequisites for this are noninvasive and invasive biomarkers including endomyocardial biopsy and polymerase chain reaction on cardiotropic agents. Imaging by

Inflammatory cytokines and atrial fibrillation: current and prospective views.

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Atrial fibrillation (AF) is the most common sustained arrhythmia and a challenging clinical problem encountered in daily clinical practice. There is an increasing body of evidence linking inflammation to a broad spectrum of cardiovascular conditions including AF. Historical evidence supports an

[Role of non antiarrhythmic medications in the prevention of atrial fribrillation].

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After cardioversion of atrial fibrillation, structural and electrophysiologic remodelling of the atria is implicated in the arrhythmia recurrences despite antiarrhythmic drug treatment. Strategies targeting this substrate have therefore been proposed. In this view, Renin angiotensin system
Sepsis is a serious medical condition that is characterized by a whole-body inflammatory state and the presence of a known or suspected infection. Amiodarone is a class III antiarrhythmic agent, a multichannel blocker (Ca++, Na+, and K+), and a noncompetitive α- and β-adrenergic blocker in cardiac
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