Framingham Risk Score Calculator

How to Use This Calculator

1. Enter age (30-74), sex, cholesterol values, systolic BP, BP treatment status, and smoking.
2. Framingham 10-year CHD risk and category update instantly.
3. Use the CVD Framingham tab for the broader CVD endpoint version.
4. Use the Framingham vs ASCVD tab to understand when to prefer each tool.

Formula

Example

Frequently Asked Questions

• What is the Framingham Risk Score? ▼
  The Framingham Risk Score is a sex-specific algorithm that estimates an individual's 10-year probability of developing coronary heart disease (CHD). It was derived from the Framingham Heart Study, the longest-running cardiovascular cohort study in the world, started in 1948 by the National Heart, Lung, and Blood Institute (NHLBI) in Framingham, Massachusetts. The CHD risk score, formalized by Wilson et al. in Circulation in 1998, uses six variables: age, total cholesterol, HDL cholesterol, systolic blood pressure, blood pressure treatment status, and smoking. The original 1998 version used age-binned point scores; a continuous logistic regression version was published subsequently and is used in most modern calculators. Risk categories are: low (< 10%), intermediate (10-20%), and high (≥ 20%). A 2008 update by D'Agostino et al. expanded the Framingham approach to predict broader CVD events (stroke, heart failure, PAD, and CHD combined), providing a single composite CVD risk score and introducing the concept of "cardiovascular age" (the age of someone with average risk factors that matches the subject's estimated risk).
• Why is Framingham still used despite being old? ▼
  The Framingham Heart Study remains influential for several reasons. First, it is the longest-running and most extensively validated cardiovascular risk cohort study in medical history, providing over 70 years of follow-up data that have generated more than 3,000 scientific publications. The risk equations derived from Framingham data have been tested in hundreds of external validation studies across multiple populations, giving clinicians confidence in their behavior and calibration, even if that calibration is not perfect in all populations. Second, the Framingham approach introduced the conceptual framework of multivariable cardiovascular risk prediction that underpins all modern risk calculators — without Framingham there would be no ACC/AHA Pooled Cohort Equations or ESC SCORE2. Third, in some clinical contexts (particularly in countries outside the US without locally derived risk equations), Framingham remains the best available tool. Fourth, the Framingham cardiovascular age concept is highly effective for patient communication — telling a 45-year-old that their cardiovascular age is 58 based on modifiable risk factors can motivate lifestyle change more effectively than abstract probability numbers.
• How does Framingham compare to the ACC/AHA ASCVD calculator? ▼
  The ACC/AHA Pooled Cohort Equations (2013), which power the ASCVD risk calculator, supersede Framingham for clinical decision-making in the United States for several important reasons. First, endpoint: Framingham CHD includes coronary heart disease events only, while ASCVD Pooled Cohort includes both CHD and stroke (plus peripheral arterial disease in some formulations), providing a more comprehensive cardiovascular event estimate. Second, derivation population: the Pooled Cohort Equations were derived from a more ethnically diverse set of US cohorts (ARIC, CHS, CARDIA) and include race-specific equations for African Americans, making them more applicable to the current US population than the predominantly White Framingham cohort. Third, validation: multiple studies have shown that Framingham systematically overestimates CHD risk in lower-risk populations (such as European and Asian populations) by 50-100%, while the Pooled Cohort Equations, though also criticized for overestimation, show better calibration in contemporary US cohorts. Fourth, guideline endorsement: ACC/AHA 2018/2019 guidelines specifically require use of the Pooled Cohort Equations for statin therapy decisions.
• What are the limitations of Framingham for diverse populations? ▼
  The Framingham Heart Study's limitations for diverse populations are well-documented and represent one of the most significant criticisms of the original risk score. The study was conducted in Framingham, Massachusetts, and the derivation cohort was almost entirely White European-descent Americans from a small, relatively affluent, predominantly working-class town. This demographic homogeneity means: the equations systematically overestimate CHD risk in Japanese, Chinese, Korean, and other East Asian populations (whose CHD rates at similar risk factor burdens are substantially lower than US White populations); they may underestimate risk in South Asian populations (Indians, Pakistanis, Bangladeshis) who have higher-than-expected CHD rates for their traditional risk factor burden; and for African Americans, the equations underestimate risk, which is why the ACC/AHA Pooled Cohort Equations included separate Black-specific equations. Multiple country-specific calibrations of Framingham have been developed for the UK (QRISK), Europe (ESC SCORE, now SCORE2), New Zealand, and other regions, substantially improving local accuracy by recalibrating the equations to match observed local event rates. The core variables of the Framingham model remain valid across populations; what varies is the background risk and the precise coefficients.
• Is the Reynolds Risk Score better than Framingham? ▼
  The Reynolds Risk Score, developed by Ridker et al. and published in 2007 (for women) and 2008 (for men), was specifically designed to improve on Framingham by adding two novel variables: high-sensitivity C-reactive protein (hsCRP) and family history of premature myocardial infarction. The score was derived from the Women's Health Study (90,000 women) and Physicians' Health Study II (10,000 men). In the derivation and validation studies, Reynolds correctly reclassified approximately 20-40% of intermediate-risk patients compared to Framingham — some to higher risk (prompting earlier treatment) and some to lower risk (avoiding unnecessary treatment). Patients with elevated hsCRP ≥ 2.0 mg/L and a Framingham intermediate risk consistently showed higher actual event rates than Framingham predicted, supporting the use of hsCRP to upgrade risk. The JUPITER trial (Ridker et al. NEJM 2008) demonstrated that rosuvastatin reduced cardiovascular events in apparently healthy patients with elevated hsCRP, providing direct evidence that hsCRP-driven risk reclassification can inform effective treatment decisions. However, Reynolds never achieved wide guideline adoption in part because hsCRP testing adds cost, the reclassification benefit is modest in absolute terms, and other risk enhancers (Lp(a), CAC score) have since emerged as arguably more useful refinement tools.

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