Atrial fibrillation (AF) is a complex condition with several possible contributing factors. The rapid and irregular heartbeat produced by AF increases the risk of blood clot formation inside the heart. These clots may eventually become dislodged, causing embolism, stroke and other disorders. AF occurs in up to 15% of patients with hyperthyroidism compared to 4% of people in the general population and is more common in men and in patients with triiodothyronine (T3) toxicosis. The incidence of AF increases with advancing age. Also, subclinical hyperthyroidism is a risk factor associated with a 3-fold increase in development of AF. Thyrotoxicosis exerts marked influences on electrical impulse generation (chronotropic effect) and conduction (dromotropic effect). Several potential mechanisms could be invoked for the effect of thyroid hormones on AF risk, including elevation of left atrial pressure secondary to increased left ventricular mass and impaired ventricular relaxation, ischemia resulting from increased resting heart rate, and increased atrial eopic activity. Reentry has been postulated as one of the main mechanisms leading to AF. AF is more likely if effective refractory periods are short and conduction is slow. Hyperthyroidism is associated with shortening of action potential duration which may also contribute to AF.

The last several years have seen increasing interest in understanding cachexia, muscle wasting, and physical frailty across the broad spectrum of patients with cardiovascular illnesses. This interest originally started in the field of heart failure, but has recently been extended to other areas such as atrial fibrillation, coronary artery disease, peripheral artery disease as well as to patients after cardiac surgery or transcatheter aortic valve implantation. Tissue wasting and frailty are prevalent among many of the affected patients. The ageing process itself and concomitant cardiovascular illness decrease lean mass while fat mass is relatively preserved, making elderly patients particularly prone to develop wasting syndromes and frailty. The aim of this review is to provide an overview of the available knowledge of body wasting and physical frailty in patients with cardiovascular illness, particularly focussing on patients with heart failure in whom most of the available data have been gathered. In addition, mechanisms of wasting and possible therapeutic targets are discussed.

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BackgroundWe assessed the influence of atorvastatin on selected indicators of an inflammatory condition, left ventricular function, hospitalizations and mortality in patients with dilated cardiomyopathy (DCM).MethodsWe included 68 DCM patients with left ventricular ejection fraction (LVEF) ≤40% treated optimally in a prospective, randomized study. They were observed for 5 years. Patients were divided into two groups: patients who were commenced on atorvastatin 40 mg daily for two months followed by an individually matched dose of 10 or 20 mg/day (group A), and patients who were treated according to current recommendations without statin therapy (group B).ResultsAfter 5-year follow-up we assessed 45 patients of mean age 59 ± 11 years - 22 patients in group A (77% male) and 23 patients in group B (82% male). Interleukin-6, tumor necrosis factor alpha, and uric acid concentrations were significantly lower in the statin group than in group B (14.96 ± 4.76 vs. 19.02 ± 3.94 pg/ml, p = 0.012; 19.10 ± 6.39 vs. 27.53 ± 7.39 pg/ml, p = 0.001, and 5.28 ± 0.48 vs. 6.53 ± 0.46 mg/dl, p = 0.001, respectively). In patients on statin therapy a reduction of N-terminal pro-brain natriuretic peptide concentration (from 1425.28 ± 1264.48 to 1098.01 ± 1483.86 pg/ml, p = 0.045), decrease in left ventricular diastolic (from 7.15 ± 0.90 to 6.67 ± 0.88 cm, p = 0.001) and systolic diameters (from 5.87 ± 0.92 to 5.17 ± 0.97, p = 0.001) in comparison to initial values were observed. We also showed the significant increase of LVEF in patients after statin therapy (from 32.0 ± 6.4 to 38.8 ± 8.8%, p = 0.016). Based on a comparison of curves using the log-rank test, the probability of survival to 5 years was significantly higher in patients receiving statins (p = 0.005).ConclusionsAtorvastatin in a small dose significantly reduce levels of inflammatory cytokines and uric acid, improve hemodynamic parameters and improve 5-year survival in patients with DCM.

Hypertension is a progressive cardiovascular syndrome that arises from many differing, but interrelated, etiologies. Hypertension is the most prevalent cardiovascular disorder, affecting 20% to 50% of the adult population in developed countries. Arterial hypertension is a major risk factor for cardiovascular diseases and death. Epidemiologic data have shown that control of hypertension is achieved in only a small percentage of hypertensive patients. Findings from the World Health Organization project Monitoring Trends and Determinants in Cardiovascular Diseases (MONICA) showed a remarkably high prevalence (about 65%) of hypertension in Eastern Europeans. There is virtually no difference however, between the success rate in controlling hypertension when comparing Eastern and Western European populations. Diagnosing hypertension depends on both population awareness of the dangers of hypertension and medical interventions aimed at the detecting elevated blood pressure, even in asymptomatic patients. Medical compliance with guidelines for the treatment of hypertension is variable throughout Eastern Europe. Prevalence of hypertension increases with age, and the management of hypertension in elderly is a significant problem. The treatment of hypertension demands a comprehensive approach to the patient with regard to cardiovascular risk and individualization of hypertensive therapy.

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Biomarkers should have high sensitivity, specificity, reproducibility, be cost-effective, and provide incremental predictive or diagnostic utility over standard risk factors or tests. Despite numerous studies investigating biomarkers in heart failure (HF), there are only a few that predict HF in hypertensive patients. This article summarizes data from numerous studies concerning possible biomarkers of HF in hypertensive patients such as: serum uric acid (SUA), interleukins, monocyte chemoattractant protein one (MCP-1), cardiotrophin-1 (CT-1), carboxy-terminal propeptide of procollagen type I (PICP), type I collagen telopeptide (CITP) and N-terminal propeptide of type III procollagen (PIIINP), metalloproteinases (MMPs), B-type natriuretic peptide (BNP) and its derivatives, glycoprotein CA125 and cystatin C. Early detection of patients of increased risk of hypertensive heart disease may result in early implementation of effective preventive strategies. Therefore, there is need to identify newer biomarkers, if they can improve risk prediction, identifying patients, in which earlier or more aggressive intervention will improve clinical outcomes.