Where your DNA places you among other people, and the studies behind it.
Not tailored to your result, and not medical advice
Address High Blood Pressure Early: In the Framingham cohort, hypertension preceded 91% of new heart failure cases and accounted for an estimated 39% of cases in men and 59% in women. Compared with people who had normal pressure, the adjusted hazard of heart failure was about twofold in men and threefold in women. The usual route is chronic pressure overload driving left ventricular hypertrophy and stiffening, which surfaces years later as heart failure. JAMA (PubMed)
Build Up Weekly Aerobic Activity: A meta-analysis of 12 prospective cohorts covering 370,460 people and 20,203 heart failure events found an inverse dose-response between physical activity and incident heart failure. At about 500 MET-minutes a week, the guideline minimum of roughly 150 minutes of moderate activity, pooled risk was 10% lower (hazard ratio 0.90); at double that it was 19% lower, and at quadruple that 35% lower (hazard ratio 0.65). The curve kept falling past the guideline floor rather than flattening, so extra activity was associated with further reduction. Circulation (PubMed)
Keep Midlife Weight Gain In Check: Among 5,881 Framingham participants, each 1-unit rise in body mass index was associated with 5% higher heart failure risk in men and 7% in women, and obesity roughly doubled risk (hazard ratio 1.90 in men, 2.12 in women). Risk climbed steadily across weight categories rather than only at the extreme, so this is a gradient and not a threshold effect. Excess weight is thought to act partly through added cardiac workload and partly through the hypertension and diabetes that travel with it. New England Journal of Medicine (PubMed)
Keep Alcohol Intake Low: Ethanol is directly toxic to heart muscle in a dose-dependent way, producing myocyte loss, fibrosis and chamber dilation independently of any nutritional or vitamin deficiency. Alcohol is one of the main causes of nonischemic dilated cardiomyopathy, around a third of cases in published series, with risk described in reviews at sustained intakes near 90 g a day, roughly six to seven US standard drinks, for more than five years. Recovery of heart function is reported in the majority of cases after drinking stops, including in some people whose ejection fraction was severely reduced. Nutrients (PMC)
Treat Salt Advice With Caution: Lower sodium intake reduces blood pressure, which is why it appears in general prevention advice, but the randomized evidence for strict salt restriction in people who already have heart failure is neutral. The honest reading is that sodium remains a reasonable lever for blood pressure in prevention, while in that trial population tighter restriction did not change hard outcomes. Anyone already following a sodium plan set with their clinician should settle changes to it with them. The Lancet (PubMed)
How much of this is genetic?
Genetics explains 26% of why people differ in this trait. The rest is environment, daily habits and chance.
Heritability estimate: Swedish nationwide adoption study, Falconer heritability ~26% (Lindgren et al. 2018, JAMA Cardiology); common-variant architecture from the HERMES GWAS (Shah et al. 2020, Nature Communications)
Background and further reading
Heart failure is a chronic syndrome in which the heart cannot pump or fill with blood efficiently enough to meet the body's needs. It is the shared end point of many underlying conditions, most often coronary artery disease, long-standing high blood pressure, diabetes, valve disease, and cardiomyopathy. It affects an estimated 64 million people worldwide, and its prevalence rises steeply with age. Common symptoms include breathlessness (especially on exertion or when lying flat), fatigue, reduced exercise tolerance, and swelling in the legs, ankles, or abdomen. Because heart failure is a syndrome with many causes, a genetic predisposition score captures only part of the overall picture.
Genetic Basis: Family and adoption studies place the heritability of heart failure at roughly a quarter, lower than many single-gene cardiac conditions because so much of the risk flows through modifiable and acquired diseases such as hypertension and coronary artery disease. The largest genome-wide meta-analysis, from the HERMES consortium (about 47,000 cases and 930,000 controls), identified around a dozen common-variant loci and found that much of the signal acts indirectly, through established risk factors like atrial fibrillation, coronary disease, and left ventricular function. Implicated genes include PITX2, BAG3, CDKN1A, and KLHL3, several of which also feature in cardiac development, protein-quality-control, and blood-pressure biology. Rarer, high-impact variants in cardiomyopathy genes such as TTN and LMNA can cause inherited forms of heart failure, but those are assessed separately and are not what a common-variant polygenic score measures.
Environmental and Lifestyle Factors: Most of what shapes heart-failure risk lies outside the genome. High blood pressure, coronary artery disease, type 2 diabetes, obesity, smoking, excess alcohol, and physical inactivity are the dominant contributors, and each is modifiable. Managing blood pressure, staying physically active, not smoking, moderating alcohol, and maintaining a healthy weight all support long-term heart health regardless of genetic score. Because these factors carry far more day-to-day weight than common genetic variants, a higher polygenic score is best read as one more reason to attend to heart-healthy habits rather than as a forecast.
The published research behind your score, and the variants it draws on.
28 published scores from 7 studies
The heart failure score combines 28 polygenic scores drawn from 7 published studies.
These traits are influenced by some of the same genes and variants as this one
Content updated August 2026.
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