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Purpose: In patients with cirrhosis, the Model for End-Stage Liver Disease Sodium (MELD-Na) score is a validated predictor of outcomes after transplant and non-transplant surgical procedures. This study investigates the association of MELD-Na score with complications following elective ventral hernia repair in non-cirrhotic patients.Methods: The ACS NSQIP database was queried (2005-2016) for all elective laparoscopic and open ventral hernia procedures in patients without ascites or esophageal varices. Postoperative outcomes were compared by MELD-Na score using Chi-square tests. Multivariate logistic regression was used to control for potentially confounding variables.Results: A total of 48,955 elective hernia repairs were identified; 68.7% were open repairs. The overall complication rate (Clavien-Dindo ≥ 1) was 14.3%, with a wound complication rate of 5.5%, and major complication rate (Clavien-Dindo ≥ 3) of 4.3%. A preoperative MELD-Na score ≥ 10 was present in 29.4%. Incremental increases in MELD-Na score (10-14, 15-19, and ≥ 20) were associated with increased overall complications (OR 1.25, CI 1.31-1.37; OR 1.53, CI 1.30-1.80; OR 1.70, CI 1.24-2.31, respectively), major complications (OR 1.42, CI 1.20-1.69; OR 1.85, CI 1.43-2.39; OR 2.13, CI 1.35-3.38, respectively), 30-day mortality (OR 1.58, CI 1.05-2.37; OR 2.34, CI 1.39-3.96; OR 3.16, CI 1.37-7.28, respectively), and return to the operating room (OR 1.19, CI 1.01-1.41; OR 1.38, CI 1.05-1.81; OR 1.78, CI 1.10-2.90, respectively).Conclusion: MELD-Na score is independently associated with postoperative complications in ventral hernia repair. As an objective and simple predictive model, it may be useful in preoperative risk calculations for complex patients. [ABSTRACT FROM AUTHOR]

Nearly one-third of adults in the United States have hypertension, which is associated with increased cardiovascular disease (CVD) morbidity and mortality. The goal of antihypertensive pharmacogenetic research is to enhance understanding of drug response based on the interaction of individual genetic architecture and antihypertensive therapy to improve blood pressure control and ultimately prevent CVD outcomes. In the context of the Genetics of Hypertension Associated Treatment study and using a case-only design, we examined whether single-nucleotide polymorphisms in RYR3 interact with four classes of antihypertensive drugs, particularly the calcium channel blocker amlodipine versus other classes, to modify the risk of coronary heart disease (CHD; fatal CHD and non-fatal myocardial infarction combined) and heart failure (HF) in high-risk hypertensive individuals. RYR3 mediates the mobilization of stored Ca+2 in cardiac and skeletal muscle to initiate muscle contraction. There was suggestive evidence of pharmacogenetic effects on HF, the strongest of which was for rs877087, with the smallest P-value=0.0005 for the codominant model when comparing amlodipine versus all other treatments. There were no pharmacogenetic effects observed for CHD. The findings reported here for the case-only analysis of the antihypertensive pharmacogenetic effect of RYR3 among 3058 CHD cases and 1940 HF cases show that a hypertensive patient's genetic profile may help predict which medication(s) might better lower CVD risk. [ABSTRACT FROM AUTHOR]

In a double-blind, outcome trial conducted in hypertensive patients randomized to chlorthalidone (C), amlodipine (A), lisinopril (L), or doxazosin (D), the α-adducin Gly460Trp polymorphism was typed (n=36 913). Mean follow-up was 4.9 years. Relative risks (RRs) of chlorthalidone versus other treatments were compared between genotypes (Gly/Gly+Gly/Trp versus Trp/Trp). Primary outcome was coronary heart disease (CHD). Coronary heart disease incidence did not differ among treatments or genotypes nor was there any interaction between treatment and genotype (P=0.660). Subgroup analyses indicated that Trp allele carriers had greater CHD risk with C versus A+L in women (RR=1.31) but not men (RR=0.91) with no RR gender differences for non-carriers (gender–gene–treatment interaction, P=0.002). The α-adducin gene is not an important modifier of antihypertensive treatment on cardiovascular risk, but women Trp allele carriers may have increased CHD risk if treated with C versus A or L. This must be confirmed to have implications for hypertension treatment.The Pharmacogenomics Journal (2007) 7, 112–122. doi:10.1038/sj.tpj.6500395; published online 16 May 2006 [ABSTRACT FROM AUTHOR]

Discusses the design and rationale of Genetics of Hypertension Associated Treatment (GenHAT) study which aims to determine whether variants in hypertension susceptibility genes interact with antihypertensive medication to modify coronary heart disease risk in hypertensives. Objectives of GenHAT study; Methods of genotyping; Anonymization of DNA samples.