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1.  Association of BNP and Troponin Levels with Outcome among Cardiac Resynchronization Therapy Recipients 
We conducted a prospective multicenter study to assess the prognostic value of combined baseline pre-implant plasma levels of the biomarkers cardiac troponin T (TnT) and BNP among CRT-D recipients.
At CRT-D implant, patients were stratified based on detectable TnT (≥0.01 ng/ml) and elevated BNP (predefined as >440 pg/ml) levels. Patients were classified into 3 groups high (both detectable TnT and high BNP), intermediate (either detectable TnT or high BNP), or low (non-detectable TnT and low BNP). Patients were followed for 12 months. Survival curves free from mortality or HFH were assessed. To assess the predictive value of biomarker category, we constructed a multivariate Cox regression model, including the covariates of age, NYHA class, LVEF, and QRS duration.
A total of 267 patients (age 66 ± 12 years, males 80%, LVEF 25% ± 8%, ischemic CM 52%, QRSd 155 ± 26 ms) were studied. After one year, there were 13 deaths and 25 HFH events. A significant difference in event free survival among the 3 groups was observed, with high and intermediate categories having worse survival than low (log-rank test, p <0.001). In the multivariate model, risk category was a significant predictor of outcome: Hazard ratios were 7.34 (95% CI: 2.48 to 21.69) and 2.50 (95% CI: 1.04 to 6.04) for high and intermediate risk groups respectively (p<0.0001).
Among CRT-D recipients, baseline TnT and BNP values alone or in combination provide significant prognostic value for the outcome of mortality or HFH.
PMCID: PMC4414915  PMID: 25677851
Biomarkers; BNP; Cardiac Resynchronization Therapy; Congestive Heart Failure; Troponin
2.  Genetic Variation in the Alternative Splicing Regulator, RBM20, is associated with Dilated Cardiomyopathy 
Dilated cardiomyopathy (DCM) is a leading cause of heart failure and death. The etiology of DCM is genetically heterogeneous.
We sought to define the prevalence of mutations in the RNA splicing protein, RBM20, in a large cohort with DCM, and to determine if genetic variation in RBM20 is associated with clinical outcomes.
Subjects included in the GRADE (Genetic Risk Assessment of Defibrillator Events) study were at least 18 years of age, had an ejection fraction of ≤ 30%, and an implantable cardioverter-defibrillator (ICD). The coding region and splice junctions of RBM20 were screened in DCM subjects; two common polymorphisms in RBM20, rs942077 and rs35141404, were genotyped in all GRADE subjects.
1465 subjects were enrolled in the GRADE study and 283 with DCM were screened for RBM20 mutations. The mean age of subjects with DCM was 58 ± 13 years, 64% were male and the mean follow up was 24.2 ± 17.1 months after ICD placement. RBM20 mutations were identified in eight subjects with DCM (2.8%). Mutation carriers had a similar survival, transplantation rate, and frequency of ICD therapy compared to non-mutation carriers. Three of eight subjects (37.5%) with RBM20 mutations had atrial fibrillation (AF) whereas 19 (7.4%) subjects without mutations had AF (p= 0.02). Among all GRADE subjects, rs35141404 was associated with AF (minor allele OR 0.62, 95% CI 0.44–0.86, p=0.006). In the subset of GRADE subjects with DCM, rs35141404 was associated with AF (minor allele OR 0.58, p=0.047).
Mutations in RBM20 were observed in approximately 3% of subjects with DCM. There were no differences in survival, transplantation rate, and frequency of ICD therapy in mutation carriers.
PMCID: PMC3516872  PMID: 22004663
dilated cardiomyopathy; genetics; mutation; single nucleotide polymorphism; RBM20
3.  Association of TNF-α –308G/A, SP-B 1580 C/T, IL-13 –1055 C/T gene polymorphisms and latent adenoviral infection with chronic obstructive pulmonary disease in an Egyptian population 
Chronic obstructive pulmonary disease (COPD) is a leading cause of disability and death. The most common cause of COPD is smoking. There is evidence suggesting that genetic factors influence COPD susceptibility and variants in several candidate genes have been significantly associated with COPD. In this study, we aimed to investigate the possible association of the TNF-α –308, SPB+1580, IL-13 –1055 gene polymorphisms and latent adenovirus C infection with COPD in an Egyptian population.
Material and methods
Our study included 115 subjects (75 smokers with COPD, 25 resistant smokers and 15 non-smokers) who were subjected to spirometric measurements, identification of adenovirus C and genotyping of TNF-α –308G/A, SP-B+1580 C/T and IL-13 –1055 C/T polymorphisms by real-time PCR.
The adenovirus C gene was identified in all subjects. The distribution of TNF-α genotypes showed no significant differences between different groups. However, homozygous A genotype was associated with a significant decrease in FEV1, FEV1/FVC and FEF25/75% of predicted in COPD (p < 0.05). As regards SP-B genotypes, resistant smokers had a significantly higher homozygous T genotype frequency compared to COPD and non smokers (p = 0.005). Interleukin 13 genotypes showed no significant difference between different groups. There was a significant decrease in FEF25/75% of predicted in T allele carriers in COPD patients (p = 0.001).
The COPD is a disease caused by the interaction of combined genes and environmental influences, in the presence of smoking and latent adenovirus C infection, TNF-α –308A, SPB +1580 T and IL-13 –1055 T polymorphisms predispose to the development of COPD.
PMCID: PMC3361041  PMID: 22662002
single nucleotide polymorphism; smoking; adenovirus C; chronic obstructive pulmonary disease

Results 1-3 (3)