Cardiovascular Diseases. Genetic Susceptibility, by Nikolaos Papageorgiou

By Nikolaos Papageorgiou

Cardiovascular illnesses: Genetic Susceptibility, Environmental components and Their interplay covers the specified heritability features and picking genetic and environmental contributions to cardiovascular future health. this significant reference presents an outline of the genetic foundation of heart problems and its probability factors.

Included are very important issues, starting from way of life offerings, possibility elements, and publicity, to pollution and chemical substances. additionally coated are the impacts of Mendelian features and familial aggregation and the interactions and interrelationships among genetics and environmental components which, compared, offer a legitimate figuring out of the interaction among inherited and purchased threat factors.

The e-book offers a miles wanted reference for this speedily turning out to be box of analysis. by way of combining the most recent study in the based chapters of this reference, a greater realizing of genetic and environmental contribution to heart problems is located, aiding to verify extra investigations within the box and layout prevention and remedy strategies.

  • Provides an outline of the genetic foundation of heart problems and its probability factors
  • Reviews numerous huge population-based stories which point out that publicity to numerous environmental components may well bring up CVD morbidity and mortality, exploring the plausibility of this organization by means of information from animal studies
  • Reflects on destiny stories to aid knowing the position of genes and environmental elements within the improvement and development of cardiovascular disease

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Extra resources for Cardiovascular Diseases. Genetic Susceptibility, Environmental Factors and their Interaction

Sample text

02). In contrast, in a study of 94 healthy volunteers, the intronic IVS10 + 12G > A polymorphism was not associated with differential ADP-induced platelet aggregation [43]. CYP1A2 The CYP1A2 enzyme that comprises 10% of the liver P450 enzymes has gained considerable attention for an enhanced clopidogrel response in smokers, thought to be mediated by induction of this enzyme [44]. In the CHARISMA study, current smokers on clopidogrel had lower all-cause and cardiovascular mortality compared with former smokers or never smokers [45].

In the Omeprazole Clopidogrel Aspirin (OCLA) double-blind placebo-controlled randomized trial, 124 PCI patients received omeprazole or placebo along with clopidogrel and aspirin [81]. 0001). The COGENT trial randomized 3873 patients to receive a fixed-dose combination of clopidogrel 75 mg and omeprazole 20 mg or clopidogrel and placebo in patients with an indication for DAPT [82]. 96). However the study was underpowered precluding definitive conclusions in this regard. In a subanalysis of an observational genotyping study, no difference was found in platelet aggregation at 24 h in clopidogrel-treated patients receiving rabeprazole vs placebo [83].

Moreover no difference was noted in cardiovascular events at 18 months. In 95 CAD patients, platelet reactivity was lower in CYP2C19*2 carrier patients by the VASP assay, but no difference was observed in patients treated with or without PPI. Neither CYP2C19*2 allele carriage nor PPI treatment was associated with adverse clinical outcomes [84]. Chen et al. conducted a systematic review of eight studies [85]. 14). However analysis of 314 patients from three randomized studies demonstrated no differences in the incidence of MACE.

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