Association between 22 cytokine gene polymorphisms and dilated cardiomyopathy in Macedonian patients.

BACKGROUND: Inflammation is an important component in the pathogenesis of many cardiovascular diseases and one of the commonest mechanisms in cardiomyopathy. There have been several studies on the cytokine polymorphism and dilated cardiomyopathy (DCM), but the results obtained were contradictory. AIM: To examine a possible role of 22 cytokine gene polymorphisms in host susceptibility to or protection against DCM in Macedonians. METHODS: In this study 301 healthy unrelated individuals and 52 patients with DCM were studied. Cytokine genotyping was performed by PCR with sequence-specific priming (PCR-SSP) (Heidelberg kit). RESULTS: After the Bonferroni adjustment, the IL-4 -1098/T, IL-4 -1098/T:T, IL-4/TCC, and IL-4/TCC:TTC cytokine genes were positively associated with DCM, while a negative association was identified for IL-4 -1098/G, IL-4 -1098/G:T, IL-1B +3962/C:C, IL-4/GCC, and IL-4/GCC:TTC. CONCLUSIONS: These results suggest that some cytokine gene polymorphisms are significantly associated and affect host susceptibility/resistance to DCM in Macedonians.

Heart Failure with Preserved Ejection Fraction - Concept, Pathophysiology, Diagnosis and Challenges for Treatment.

Heart failure (HF) with preserved left ventricular (LV) ejection fraction (HFpEF) occurs in 40 to 60% of the patients with HF, with a prognosis which is similar to HF with reduced ejection fraction (HFrEF). HFpEF pathophysiology is different from that of HFrEF, and has been characterized with diastolic dysfunction. Diastolic dysfunction has been defined with elevated left ventricular stiffness, prolonged iso-volumetric LV relaxation, slow LV filing and elevated LV end-diastolic pressure. Arterial hypertension occurs in majority cases with HFpEF worldwide. Patients are mostly older and obese. Diabetes mellitus and atrial fibrillation appear proportionally in a high frequency of patients with HFpEF. The HFpEF diagnosis is based on existence of symptoms and signs of heart failure, normal or approximately normal ejection and diagnosing of LV diastolic dysfunction by means of heart catheterization or Doppler echocardiography and/or elevated concentration of plasma natriuretic peptide. The present recommendations for HFpEF treatment include blood pressure control, heart chamber frequency control when atrial fibrillation exists, in some situations even coronary revascularization and an attempt for sinus rhythm reestablishment. Up to now, it is considered that no medication or a group of medications improve the survival of HFpEF patients. Due to these causes and the bad prognosis of the disorder, rigorous control is recommended of the previously mentioned precipitating factors for this disorder. This paper presents a universal review of the most important parameters which determine this disorder.

Recurrence of left ventricular hypertrophy following cessation of erythropoietin therapy.

The high cardiac output state is considered a major factor for occurrence of left ventricular hypertrophy (LVH). Increased left ventricular mass is a powerful predictor of morbidity and mortality. We analyzed morphologic changes of the heart in dialysis patients during treatment with erythropoietin (EPO) and after cessation of therapy. Fourteen hemodialysis patients were treated with EPO for 1 year. They were above age 18, dialyzed 3 times per week, and with a hematocrit below 28 vol%. EPO was given subcutaneously, at a dose of 20 U/kg body weight 3 times per week, before each hemodialysis session. Anemia was corrected and hematocrit maintained between 30 and 35 vol%. When this part of the study was completed, EPO was stopped in all 14 patients. Echocardiography was performed three times: at baseline, at 12 months of therapy, and 1 year after EPO cessation. Mean hematocrit of the group at these 3 time intervals was 23.78 +/- 2.11 vol%; 33.14 +/- 1.95 vol%; and 25.93 +/- 5.23 vol%, respectively (mean +/- SD). The following echocardiographic changes occurred. End-diastolic volume decreased from 134.8 +/- 25.4 to 113.2 +/- 26.4 ml and increased back to 136.2 +/- 46.2 ml. Left ventricular mass decreased from 296.6 +/- 62.4 to 225.2 +/- 52.7 g and increased again to 311.7 +/- 106 g. Cardiac output decreased from 7,295.8 +/- 2,166.9 to 5,816.4 +/- 1,216.2 ml/min and increased to 6,803.2 +/- 1,646.5 ml/min. Total peripheral resistance increased from 1,360.8 +/- 428 to 1,691.3 +/- 326 and decreased again to 1,242.8 +/- 303.3 dyne x s/cm5. All these changes were significant. Mean arterial pressure increased from 114.7 +/- 13.9 to 119.3 +/- 13.8 mm Hg and decreased to 100.5 +/- 9.3 mm Hg. LVH could be affected severely by the degree of anemia in uremics and was reversible.