Due to the advancements in sequencing technologies, genomic data are developing at an unmatched pace and at levels to foster translational research. Evidence from the Framingham Heart Study suggests that there is a genetic component related to CVDs including AF and HF. CVDs have a complex multifactorial etiology involving both genetic and environmental agents. Despite significant advancements in CVD diagnostics, prevention, and treatment, approximately half of the affected CVD patients reportedly die within five years of receiving a diagnosis. We are only in the developing stages of identifying causes of end-stage CVDs and providing personalized treatments with predictive analysis and deep phenotyping. Hypertension, diabetes, obesity, and valvular heart disease are among the known risk factors for AF and HF. AF is an arrhythmic disorder in the atrium of the heart, which can cause irregular heart rhythms, whereas HF is a chronic disorder, which weakens heart muscles and affects the regular function of the heart to pump enough oxygen-rich blood. Atrial fibrillation (AF) and heart failure (HF) are among the most common manifestations of CVDs. This difference in the manifestation of CVD between the sexes is accounted for by the roles that sex chromosomal mechanisms have in the control of diseases. Even though the lifetime risk is similar between the sexes, men tend to develop CVDs before women. Additionally, estrogens and androgens produced by gonadal hormones have been proven to play an important role for sex differences in the occurrence and progression of CVDs. In recently reported studies, the overall lifetime risk associated with CVD does not differ significantly between males and females as variable cardiovascular risk factors (e.g., systolic blood pressure, high-density lipoprotein cholesterol, hemoglobin A1c, and smoking behavior) were found to be similar. We listed our conclusion, which include detailed information about genes and SNPs associated with AF and HF.Ĭardiovascular disease (CVD) is one of the major contributors to morbidity and mortality in the USA and even around the globe. Seven genes had implications in both AF and HF, which are SYNPO2L, TTN, MTSS1, SCN5A, PITX2, KLH元, and AGAP5. We found 190 genes associated with AF and 26 genes linked to HF. While selecting relevant literature, we mainly focused on identifying genomic approaches involving the integration of genomic data analysis of common and rare genetic variants metadata and phenotypic details and multi-ethnic studies including individuals from ethnic minorities, and European, Asian, and American ancestries. We collected, reviewed, and compared high-quality scientific literature published between 20 and accessible through PubMed/NCBI. In this study, we examined and discussed variable genomic approaches investigating genes associated with AF, HF, and other CVDs. It can help in the identification of causal variants for AF, HF, and other CVDs by moving beyond the one-gene one-disease model through the integration of common and rare variant association, the expressed genome, and characterization of comorbidities and phenotypic traits derived from the clinical information. Correct application of bioinformatics using genomic data holds the potential to reveal the genetic underpinnings of various health conditions. With the advancements in sequencing technologies, genomic data have been generated at an unprecedented pace to foster translational research. To improve the deciphering of CVD mechanisms, we need to deeply investigate well-known and identify novel genes that are responsible for CVD development. Due to the complex nature, progression, inherent genetic makeup, and heterogeneity of CVDs, personalized treatments are believed to be critical. Atrial fibrillation (AF) and heart failure (HF) contribute to about 45% of all cardiovascular disease (CVD) deaths in the USA and around the globe.
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