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Circulation: HeartFailure, Ahead of Print. About 3% to 4% of patients with African ancestry carry this geneticpredisposition to develop signs and symptoms of hATTR-CA. Nevertheless, clinical manifestations of hATTR-CA appear only late in the fifth and sixth decades of life, despite its clear genetic background.
Journal of the American Heart Association, Ahead of Print. BackgroundObservational studies have shown a significant association between immune cells and heartfailure (HF).
Geneticpredisposition to ventricular scarring is associated with heartfailure and ventricular arrhythmia. Although many pathogenic variants have been shown to predispose patients to poor outcomes, the impact of many VUS remains uncharacterized.
Results Our study identified a geneticpredisposition associated with an additional 3.6 years of education, which significantly reduced the risk of various CVDs. However, the impact of education on pulmonary embolism remains inconclusive.
The Need for Personalization in Cardiology Cardiovascular health is inherently complex, with conditions ranging from hypertension to heartfailure requiring specific treatment plans. Given the vast array of patient profiles and varying conditions, more than a one-size-fits-all approach is needed.
Studies show that repeated binge drinking can contribute to spikes in blood pressure, increasing the likelihood of stroke, heart attack, and heartfailure. Heart Muscle Damage and HeartFailure The impact of drinking alcohol on the heart muscle is another critical area of concern.
It encompasses a range of conditions, including coronary artery disease, heartfailure and arrhythmias. While lifestyle factors such as diet, exercise and smoking play a significant role in the development of heart disease, genetics also contribute substantially.
The female-specific positive association of PGSMDwith CAD risk was replicated in BioVU.CONCLUSIONS:Genetic predisposition to MD confers a greater risk of CVDs in females versus males, even in the absence of any depression diagnosis.
The aim is to assess the prevalence, clinical consequences, and geneticpredisposition of reduced EF in athletes.METHODS:Young endurance athletes were recruited from elite training programs and underwent cardiac phenotyping, genetic analyses and clinical events were recorded over a mean of 4.4
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