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83 ±0.6) and CS group (2.1 ±0.7). One-year survival was 34.8% in the MC group and 54.8% in the CS group (
= 0.663). Median long-term survival was 1.66 years in the MC group and 3.92 years in the CS group, log rank
= 0.001.
Initially, the degree of FMR was reduced in the MC group from 2.9 ±0.3 to 1.7 ±0.7 and from 2.7 ±0.5 to 2.1 ±0.7 in the CS group, p within and between groups less then 0.01. Within 6 months, FMR remained reduced in the MC group (1.83 ±0.6) and CS group (2.1 ±0.7). Immunology inhibitor One-year survival was 34.8% in the MC group and 54.8% in the CS group (p = 0.663). Median long-term survival was 1.66 years in the MC group and 3.92 years in the CS group, log rank p = 0.001.Since their formal introduction in 1980, implantable cardioverter defibrillators (ICDs) have undergone innumerable design modifications through several generations. They are indispensable today in successfully managing fatal ventricular arrhythmias. Their role in averting sudden cardiac death is recognized beyond doubt. Their applications and indications have continuously expanded over the last two decades. This article reviews the salient features in the evolution of ICDs, their current indications, recent advances and future directions. With more advanced detection algorithms, the potential integration with leadless pacing, and the possibility to serve as a remote monitoring device to recognize atrial fibrillation, acute ischemia, or electrolyte imbalance, the application of ICDs is rapidly evolving.
Vitamin D (VD) deficiency is a common disease that occurs in all stages of life. A growing number of studies call attention to the relationship between VD deficiency and cardiovascular disease. The aim of this study was to investigate the effect of VD on subclinical left ventricular (LV) function in diabetic and non-diabetic patients with no significant coronary artery disease.

We recruited 140 patients (80 diabetics and 60 non-diabetics) with symptoms of stable ischemic heart disease who underwent coronary angiography and who had no significant coronary artery disease in our clinic. The 25(OH)D
levels were measured and patients who had 25-(OH)D
levels below 20 ng/dl were defined as the VD deficient group. In addition to conventional echocardiographic parameters, tissue Doppler echocardiography was used for LV diastolic functions and 2D speckle tracking strain echocardiography (2D STE) for evaluating the longitudinal deformation indices of the LV myocardium.

In all groups, LV global longitudinal strain (GLS) was significantly impaired in patients with VD deficiency (
< 0.001) compared to patients without VD deficiency. LV global longitudinal strain rate (GLSR) was significantly impaired in patients with VD deficiency (
= 0.003). The GLS was negatively associated with 25-(OH)D
in the VD deficiency group (
= -0.52623,
< 0.001). Conversely, GLS was positively associated with 25-(OH)D
levels in the normal VD group (
= 0.28,
= 0.048).

VD deficiency is associated with impaired myocardial GLS. The present study demonstrated that VD deficiency may be the cause of subclinical myocardial dysfunction in patients with or without diabetes mellitus and no history of significant coronary artery disease.
VD deficiency is associated with impaired myocardial GLS. The present study demonstrated that VD deficiency may be the cause of subclinical myocardial dysfunction in patients with or without diabetes mellitus and no history of significant coronary artery disease.
Lipoprotein(a) (Lp[a]) is a risk factor of cardiovascular disease (CVD). Familial hypercholesterolemia (FH), which exhibits high low-density lipoprotein cholesterol (LDL-C) levels, is a risk factor of CVD. The relationship of Lp(a) with CVD has been characterized in populations specific to FH.

Studies reporting on the relationship of Lp(a) with CVD among FH subjects via PubMed up to 2020 were reviewed.

Eight studies were identified as eligible. In the meta-analyses, a high Lp(a) level was significantly and predictively associated with CVD compared to a low Lp(a) level in 2 cross-sectional studies (odds ratio = 2.57; 95% confidence interval (CI) 1.16-5.73) and 6 cohort studies (risk/hazard ratio = 1.91; 95% CI 1.50-2.43). The totally integrated relative risk of these studies was 1.97 (95% CI 1.57-2.46).

FH subjects with high Lp(a) levels can have a high CVD risk, and besides LDL-C, attention should be paid to Lp(a) levels in FH subjects.
FH subjects with high Lp(a) levels can have a high CVD risk, and besides LDL-C, attention should be paid to Lp(a) levels in FH subjects.
Paroxysmal atrial fibrillation (PAF) is a well-documented prothrombotic state that carries significant embolic risk. However, precise hemostatic changes in the very early stage of the disease are not completely studied. The aim of the study was to study von Willebrand factor (vWF) and coagulation factor VIII (FVIII) plasma levels and activity in the first hours (up to 24 h) of PAF clinical manifestation.

We selected consecutively 51 non-anticoagulated patients (26 men, 25 women, mean age 59.84 ±1.60) with PAF and 52 controls (26 men, 26 women, mean age 59.50 ±1.46 years) corresponding in gender, accompanying diseases and conducted treatment. The indicators were examined using enzyme-linked immunoassays and photometric tests.

All patients were hospitalized between the 2
and 24
h after the onset of arrhythmia (mean 8.14 ±0.74 h). Higher FVIII levels (107.52 ±3.48% vs. 93.85 ±2.93%,
< 0.05) and activity (200.03 ±11.11% vs. 109.73 ±4.90%,
< 0.001) were found in the PAF group. vWF levels (178.40 ±12.95% vs. 119.53 ±6.12%,
< 0.001) and activity (200.92 ±12.45% vs. 110.80 ±5.14%,
< 0.001) were also higher. These changes did not depend on age, sex, body mass index or CHA
DS
-VASc score in the PAF group (
> 0.05). PAF duration was a significant predictor of increased FVIII levels and activity. Increased PAF duration was followed by increased values of the factors (
= 0.85,
< 0.001;
= 0.83,
< 0.001).

The results presented an activated coagulation cascade and endothelial injury, suggesting hypercoagulability still in the early hours of PAF. These changes in PAF did not correlate with CHA
DS
-VASc score risk factors, outlining PAF as a possible independent embolic risk factor.
The results presented an activated coagulation cascade and endothelial injury, suggesting hypercoagulability still in the early hours of PAF. These changes in PAF did not correlate with CHA2DS2-VASc score risk factors, outlining PAF as a possible independent embolic risk factor.
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