The Heart Health App That Finally Asks the Right Question

There are hundreds of heart health apps on the market today. Most of them do the same thing: they monitor your heart rateHeart rate is how many times your heart beats per minute., track your steps, measure your sleep, and tell you to eat more vegetables. Some of the more sophisticated ones connect to wearables and give you a real-time readout of your pulse. A few will even flag an irregular heartbeat.

These are useful tools. But they are all answering a different question.

Heart rate monitors tell you what your heart is doing right now. What they cannot tell you — what no wearable on your wrist can tell you — is what your heart is likely to do in ten, twenty, or thirty years based on the genetic blueprint you inherited from your family. That question requires a completely different kind of tool. And until now, no app has been built to answer it properly.

That changes today.

Introducing the Heart Risk Calculator

The Heart Risk CalculatorA risk calculator estimates your chance of a heart attack or stroke over the next ten years, using your age, cholesterol, blood pressure, and a few other inputs. is now available on Google Play, and it represents something genuinely new in the heart health app space. It is not a heart rate monitor. It is not a step counter. It is not a meditation timer or a blood pressureBlood pressure is the force of blood pushing against your artery walls. It is written as two numbers, like 120/80. The top number is the pressure when your heart squeezes, the bottom is when it relaxes. log. To our knowledge, it is among the first consumer apps designed specifically to quantify inherited cardiovascular risk using a weighted family-history framework — the Inherited Hazard Coefficient (IHC)The Inherited Hazard Coefficient is a proprietary quantitative formula (H = Σ(R × W) / A) that weights each family member's cardiac event by degree of biological relationship, severity of the event, and age at which it occurred, producing a single numerical index of a person's inherited cardiac risk load. — derived from principles established in peer-reviewed literature published in Circulation, JAMA, the European Heart Journal, and the Lancet. ^{[1],[2],[3],[4]}

The core insight behind this app is simple but profound: your family historyFamily history means whether your close relatives developed heart disease, and how young they were when it happened. is not a yes or no question.

Standard heart risk calculators — including the widely used Framingham Risk ScoreThe Framingham Risk Score is a specific ten-year heart-attack-risk calculator built from the Framingham Heart Study's decades of data — the original tool that turned "risk factors" into a number. — ask whether you have a family history of heart disease. ^[1] Yes or no. That’s it. A grandparent dying of a heart attackA heart attack happens when blood flow to part of the heart muscle is cut off and that muscle starts to die. at 82 and a sibling collapsing from sudden cardiac deathSudden cardiac death is when the heart abruptly stops and the person dies within minutes, often with no prior warning. at 39 both get the same checkbox. They are not the same thing. Not even close. And the research is unambiguous about this. ^[3],[5]

What Makes This App Different

It Asks Who, Not Just Whether

The Heart Risk Calculator organizes your family’s cardiac history by relationship, age at event, and severity of outcome. A fatal event in a first-degree relativeA biological family member who shares approximately 50 percent of an individual's genetic material, specifically parents, siblings, and children; cardiac events in first-degree relatives carry substantially more inherited risk signal than events in more distant relatives. at age 40 carries a fundamentally different inherited signal than a non-fatal event in a grandparent at age 75. The app captures that difference mathematically, using an evidence-informed weighting framework developed from published epidemiologic observations by Peter Megdal, PhD:

H = Σ (R × W) / A

Where R is the relation coefficientThe relation coefficient (R) is the numerical weight assigned to a family member in the Inherited Hazard Coefficient formula based on degree of biological relatedness: 0.5 for first-degree relatives such as parents and siblings, and 0.25 for second-degree relatives such as grandparents and aunts and uncles. (0.5 for parents and siblings, 0.25 for grandparents and aunts and uncles), W is the severity weightThe severity weight (W) is a numerical value assigned within the Inherited Hazard Coefficient formula to reflect how serious a relative's cardiac event was — for example, sudden cardiac death receiving a higher weight than a non-fatal, medically managed event. of the cardiac event, and A is the age at which the event occurred. The equation is an evidence-informed educational framework that combines established epidemiologic risk principles into a structured score — providing a structured estimate of inherited familial cardiac risk that no standard checkbox can capture.

It Reveals the Imaging TrapThe Imaging Trap is the clinical scenario in which a patient with significant inherited cardiac risk receives a zero Coronary Artery Calcium score and is falsely reassured, when in reality dangerous soft non-calcified plaque may already be present and detectable only by Coronary CT Angiography.

One of the most important — and most alarming — findings in recent cardiovascular research is what clinicians call the Imaging Trap. A standard Coronary ArteryAn artery is a blood vessel that carries blood away from the heart to the rest of the body. Calcium scan, one of the most commonly used screening tools in cardiology, can return a score of zero even while dangerous soft, non-calcified plaqueNon-calcified plaque is the soft, fatty portion of a plaque that has not hardened with calcium. It shows up dark on a CT scan. is actively building in your arteries. ^[6] For people with a significant inherited cardiac risk, a zero calcium scoreA zero calcium score means a CT scan found no hardened plaque in your heart's arteries at all. may provide false reassurance in selected patients.

The 2025 CAUGHT-CAD randomized trial confirmed that in patients with a family history of premature coronary artery diseasePremature coronary artery disease is coronary atherosclerosis that causes a clinically significant event — such as a heart attack or revascularization — before age 55 in men or age 65 in women; events in relatives at these ages are the primary signal used to define high inherited cardiac risk., Coronary CT AngiographyCoronary CT angiography, or CCTA, is a CT scan done with dye in your veins that produces detailed pictures of your heart's arteries. may identify non-calcified plaquePlaque is the buildup of cholesterol, immune cells, scar tissue, and calcium inside an artery wall. not detected by calcium scoring and may influence management in selected patients. ^[7] The Heart Risk Calculator is built around this research. It helps you understand whether your family history pattern may place you among people for whom additional discussion with a physician about imaging options could be appropriate.

It Captures What Wearables Completely Miss

Your Apple Watch knows your resting heart rate. It does not know that your brother had a fatal heart attack at 42. Your Fitbit tracks your sleep quality. It cannot tell you that a sibling with premature heart disease confers an odds ratio of 2.46 for your own cardiac risk — a figure documented in peer-reviewed research published in JAMA. ^[5] Your Garmin measures your VO2 maxVO2 max is the maximum amount of oxygen your body can use during all-out exercise. It is the standard measure of cardiorespiratory fitness.. It has no way of accounting for the additive inherited burden — what researchers call gene dosing — that occurs when multiple close relatives develop premature cardiovascular diseaseCardiovascular disease is the umbrella term for problems with the heart and blood vessels, including heart attacks, strokes, and blocked leg arteries., substantially increasing the probability of inherited genetic susceptibility. ^[3],[8]

Wearables measure what is happening in your body right now. The Heart Risk Calculator models the inherited familial signal reflected in your family history and what it suggests about your lifetime cardiac trajectory. Wearables and family-history tools provide complementary but different information — but only one of them helps identify people who may benefit from more intensive evaluation than standard screening provides.

It Gives You Something to Bring to Your Doctor

Every output from the Heart Risk Calculator is framed as a conversation starter, not a conclusion. The app generates a discussion-ready family history summary and a set of specific, clinically grounded questions you can bring to your next appointment. Questions like: given my family pattern, could I have soft plaqueNon-calcified, lipid-rich atherosclerotic plaque that does not appear bright on a standard calcium score scan but is detectable by CT angiography; it is considered higher risk for rupture than fully calcified plaque. that a standard calcium scan would miss? Should I be referred to a preventive cardiologistA preventive cardiologist is a physician subspecialist focused on identifying and modifying cardiovascular risk factors before a first event occurs, using advanced lipid testing, imaging, and genetic risk assessment rather than waiting for symptomatic disease. rather than managed in primary care? Does my family history change how standard risk tools should be interpreted in my case? ^[9]

These are the questions that can genuinely change the course of a clinical encounter. They are the questions that turn a routine annual physical into a meaningful cardiovascular conversation. And they are the questions that most people never know to ask — because no one has ever organized their family history in a way that makes those questions visible.

It Is Built on Real Science

The Heart Risk Calculator is not a wellness app built on general advice. The concepts incorporated into its framework are informed by more than 40 peer-reviewed publications spanning inherited cardiac risk, premature coronary artery diseaseCoronary artery disease is plaque buildup in the arteries feeding the heart muscle., family history epidemiologyEpidemiology is the study of health patterns in large groups of people — who gets sick, where, and what they had in common., and the geneticsGenetics is the study of what you inherit from your parents. of cardiovascular susceptibility. The gene dosing model underlying the Inherited Hazard Coefficient draws on foundational research in inherited cardiovascular disease published in Nature Reviews Cardiology, the Lancet, and the European Heart Journal. ^[4],[8] The parental and sibling risk data come from landmark studies in JAMA and Circulation. ^[3],[5] The clinical significance of early cardiac eventsClinically significant heart-related occurrences—including myocardial infarction, unstable angina, and cardiac death—used as outcome endpoints in cardiovascular trials. in close relatives — and the inadequacy of standard tools in capturing that significance — is documented across decades of cardiovascular epidemiology. ^[9]

This is not an algorithm someone built in a weekend. It is an evidence-informed educational framework, developed as an educational tool by Peter Megdal, PhD, that applies established epidemiologic principles to a problem that standard tools have never been designed to solve.

Why This Matters Right Now

Heart disease remains the number one cause of death in the United States. ^[10] Roughly half of all Americans have a family history of cardiac events. ^[11] And yet the tools available to most people for understanding their inherited risk remain remarkably primitive — a checkbox on an intake form, a Framingham score that was never designed to capture genetic loading, ^[1] and a calcium scan that may miss the most dangerous plaque entirely in younger, gene-dosed individuals. ^[6],[9]

For a 20-year-old whose sibling died of sudden cardiac death at 38, the Framingham Risk Score will often return a ten-year risk of under one percent — because the formula is driven by chronological age, not inherited biology. ^[1] That person’s inherited risk profile may warrant substantially more evaluation than suggested by conventional calculators. And without a tool that models the inherited familial signal in their family history, they will never know to ask the right questions until it is too late.

The Heart Risk app exists for that person. It exists for everyone who has sat in a doctor’s office and said “yes, there’s heart disease in my family” and watched that information disappear into a checkbox that changes nothing about their care.

Download It Today

The Heart Risk Calculator app is available now on Google Play for $4.99. It is an educational tool, not a medical device, and it does not replace clinical evaluation. But it may be the most important five dollars you spend on your heart health — not because it monitors your pulse, but because it finally asks the question that wearables and standard calculators have never been designed to answer.

Your family history is data. It’s time to use it.

This tool is for educational purposes only and does not constitute medical advice. The score has not been prospectively validated for predicting individual cardiovascular events and should not be used to diagnose disease. Always consult a qualified healthcare professional before making health decisions. Research by Peter Megdal, PhD — CuringHeartDisease.com

References

1. D’Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-753. doi:10.1161/CIRCULATIONAHA.107.699579.
2. Virani SS, Alonso A, Aparicio HJ, et al. Heart Disease and Stroke Statistics-2021 Update: A Report From the American Heart Association. Circulation. 2021;143(8):e254-e743. doi:10.1161/CIR.0000000000000950
3. Lloyd-Jones DM, Nam BH, D’Agostino RB Sr, et al. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA. 2004;291(18):2204-2211. doi:10.1001/jama.291.18.2204
4. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-2472. doi:10.1093/eurheartj/ehx144
5. Murabito JM, Pencina MJ, Nam BH, et al. Sibling cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults. JAMA. 2005;294(24):3117-3123. doi:10.1001/jama.294.24.3117
6. Villines TC, Hulten EA, Shaw LJ, et al. Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry. J Am Coll Cardiol. 2011;58(24):2533-2540. doi:10.1016/j.jacc.2011.10.851
7. Nerlekar N, Vasanthakumar SA, Whitmore K, et al. Effects of Combining Coronary Calcium Score With Treatment on Plaque Progression in Familial Coronary Artery Disease: A Randomized Clinical Trial. JAMA. 2025;333(16):1403-1412. doi:10.1001/jama.2025.0584
8. Bachmann JM, Willis BL, Ayers CR, Khera A, Berry JD. Association between family history and coronary heart disease death across long-term follow-up in men: the Cooper Center Longitudinal Study. Circulation. 2012;125(25):3092-3098. doi:10.1161/CIRCULATIONAHA.111.065490
9. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678
10. Martin SS, Aday AW, Allen NB, et al. 2025 Heart Disease and Stroke Statistics: A Report of US and Global Data From the American Heart Association. Circulation. 2025;151(8):e41-e660. doi:10.1161/CIR.0000000000001303
11. Moonesinghe R, Yang Q, Zhang Z, Khoury MJ. Prevalence and Cardiovascular Health Impact of Family History of Premature Heart Disease in the United States: Analysis of the National Health and Nutrition Examination Survey, 2007-2014. J Am Heart Assoc. 2019;8(14):e012364. doi:10.1161/JAHA.119.012364

Addendum

Evidentiary Basis for the Inherited Hazard Coefficient Algorithm

Companion document to: “The Heart Health App That Finally Asks the Right Question”

Overview

The Inherited Hazard Coefficient (IHC) is computed using the formula:

H = Σ (R × W) / A

Where R is the relation coefficient (0.5 for first-degree relatives: parents and siblings; 0.25 for second-degree relatives: grandparents, aunts, and uncles), W is the severity weight of the cardiac event, A is the age at which the event occurred, and Σ represents summation across all affected relatives in the family history.

Each structural element of this formula — the relation coefficient R, the severity weight W, the age denominator A, and the summation logic — is grounded in a specific body of peer-reviewed cardiovascular epidemiology. This addendum identifies the primary literature supporting each component and distinguishes that evidence from the design choices that represent the author’s own evidence-informed synthesis.

The R Term: Relation Coefficient

The R term encodes the degree of biological relatedness between the patient and the affected family member. First-degree relatives (parents, siblings) receive a coefficient of 0.5, reflecting the 50% shared genome. Second-degree relatives (grandparents, aunts, uncles) receive 0.25, reflecting 25% shared genome. The differential weighting of first- versus second-degree relatives is supported by two landmark Framingham-based studies.

Lloyd-Jones et al., JAMA 2004

^[1] This prospective Framingham offspring analysis was among the first to rigorously confirm parental cardiovascular disease as an independent predictorA variable that statistically forecasts an outcome—such as mortality—even after accounting for other known risk factors like age, BMI, and cholesterol through multivariable analysis. of offspring CVD after full adjustment for conventional risk factorsA risk factor is something that raises your chance of developing a disease — high cholesterol particles, high blood pressure, smoking, diabetes, family history.. Critically, the study demonstrated that risk compounded when both parents were affected — the conceptual foundation for the summation structure of the IHC. The paper directly supports the assignment of the 0.5 coefficient to parents and the differential weighting of first-degree versus second-degree relatives.

Murabito et al., JAMA 2005

^[2] This companion Framingham sibling analysis documented an unadjusted odds ratio of 2.46 for cardiovascular disease in individuals with an affected sibling — a magnitude comparable to or exceeding that of parental history in certain subgroups. This finding is the primary justification for assigning siblings the same R coefficient of 0.5 as parents, rather than a lower value. It also reinforced the core principle that first-degree relatives constitute a categorically different risk tier from second-degree relatives.

The A Term: Age at Event in the Denominator

The A term places the age at which the family member experienced their cardiac event in the denominator of the formula, so that younger events produce a higher IHC contribution. This is the most clinically consequential structural feature of the algorithm and is supported by consistent findings across multiple data sources.

Lloyd-Jones et al., JAMA 2004 and Murabito et al., JAMA 2005

^[1],[2] Both Framingham analyses stratified their findings by age at the family event and demonstrated substantially elevated risk when the cardiac event was premature — defined as occurring before age 55 in male relatives and before age 65 in female relatives. A family event at age 40 carries a fundamentally different inherited signal than the same event at age 78. The A term in the denominator is a direct mathematical encoding of this well-established epidemiologic principle.

D’Agostino et al., Circulation 2008 — Framingham Risk Score

^[3] Cited in the main article as the primary example of a risk calculator that does not account for age at the family event. The Framingham score uses the patient’s own chronological age as its dominant driver of 10-year risk, but incorporates no variable for the age at which family members experienced cardiac events. The A denominator in the IHC formula is specifically designed to correct for this gap — capturing what the Framingham score systematically omits.

The W Term: Severity Weight

The W term assigns differential weights to cardiac events based on their severity — with fatal events, sudden cardiac death, and early revascularizationRevascularization is a medical or surgical procedure—such as coronary artery bypass grafting or percutaneous coronary intervention—performed to restore blood flow through a blocked or narrowed coronary artery, addressing the physical obstruction rather than the underlying atherogenic process. receiving higher weights than medically managed non-fatal events. This reflects the well-documented relationship between event severity and underlying atherosclerotic burden.

Villines et al., JACC 2011 — CONFIRM Registry

^[4] This large multicenter CCTA registry demonstrated that even among patients with a CAC score of zero — conventionally considered low risk — a meaningful proportion harbored non-calcified, potentially obstructive plaque. The study provided strong evidence that event severity and plaque characteristics are not uniform across patients with nominally similar risk profiles. Fatal events in first-degree relatives imply a higher inherited plaque burdenPlaque burden is the total amount of plaque in your arteries, everywhere — not just at the single worst spot. and more aggressive disease trajectory than non-fatal, medically managed events — the epidemiologic rationale for the W severity weighting.

Nerlekar et al., JAMA 2025 — CAUGHT-CAD Trial

^[5] This 2025 randomized trial in patients with a family history of premature CAD demonstrated that non-calcified plaque burden varied substantially even among individuals within the same broad family history category. The trial used CCTA to quantify plaque progression as its primary endpoint, confirming that severity differentiation within the inherited risk spectrum has measurable clinical significance — and is not captured by binary family history classification or calcium scoring alone.

The Σ Term: Summation Across Relatives

The summation operator reflects the principle that inherited cardiac risk compounds with each additional affected relative. A patient with two affected first-degree relatives carries a meaningfully different inherited signal than a patient with one. The Σ structure encodes this dose-response relationshipA dose-response relationship describes how the magnitude of a biological effect changes as the amount of an exposure (such as weekly exercise minutes) increases; in this article, resistance training shows a non-linear dose-response for mortality, with benefits plateauing around 120 minutes per week and a J-shaped curve emerging at very high volumes in older women. mathematically.

Bachmann et al., Circulation 2012 — Cooper Center Longitudinal Study

^[6] This large prospective study of men followed over decades demonstrated that family history of coronary heart diseaseCoronary heart disease is the narrowing or blockage of the arteries that supply blood to the heart muscle, caused by the buildup of atherosclerotic plaque; it is the leading cause of heart attack and cardiac death worldwide. death was associated with significantly elevated long-term cardiovascular mortality, and that the risk accumulated across the follow-up period in a manner consistent with an underlying dose-responseA dose-response relationship means more of something produces more of an effect, in a consistent gradient. relationship. The study supports the logic of summing contributions across affected relatives rather than treating family history as a single binary flag.

Ference et al., European Heart Journal 2017

^[7] This Mendelian randomizationMendelian randomization is a clever research method that uses the genes people were born with as a natural experiment. analysis demonstrated that the atherogenic effect of LDL cholesterolLDL cholesterol, or LDL-C, is the amount of cholesterol sitting inside your LDL particles. It is the number on almost every standard lab report. — the primary driver of inherited lipid-related cardiac risk — is cumulative and time-dependent. Lifetime exposure to elevated LDLLDL, or low-density lipoprotein, is the main particle that carries cholesterol through your blood — and the main one that gets stuck in artery walls. produces atherosclerotic burden that is proportional to the integral of exposure over time, not simply to any single measurement. This biological framework supports the IHC summation structure: inherited cardiovascular risk is not a point estimate but a cumulative signal that should be aggregated across all affected relatives and weighted by the severity and timing of their events.

What the Literature Validates — and What It Does Not

What is validated

The peer-reviewed literature cited above establishes the following with high confidence:

• First-degree relatives confer greater inherited cardiac risk than second-degree relatives.
• Siblings carry risk comparable to parents, not intermediate between parents and grandparents.
• The age at which a family member experienced a cardiac event is a critical variable: premature events confer dramatically greater inherited signal than late-life events.
• Multiple affected relatives compound inherited risk in a dose-response fashion.
• Event severity correlates with underlying atherosclerotic burden and is not uniform across family history reports.
• Standard risk calculators systematically underutilize this information, particularly in younger patients with strong family histories.

What is not validated

The existing literature does not validate:

• The specific coefficient values chosen for R (0.5 and 0.25).
• The specific severity weight values assigned to W.
• The mathematical form of dividing by A rather than applying a categorical age-at-event modifier.
• The formula H = Σ(R×W)/A as a clinically calibrated predictive score for individual cardiovascular event risk.
• The IHC against any prospective outcome dataset.

The IHC formula is an evidence-informed educational framework that translates established epidemiologic principles into a structured, quantitative estimate of inherited familial cardiac risk. The inputs are grounded in landmark peer-reviewed literature. The specific mathematical implementation — the coefficient values, the weighting scheme, and the formula structure — represents the author’s synthesis of those principles and has not been independently validated. The ACC/AHA Primary PreventionPrimary prevention is treating someone who has never had a heart attack or stroke, to keep the first one from happening. Guideline ^[8] explicitly recognizes family history as a risk-enhancing factor that should modify clinical decision-making, but stops short of providing a quantitative formula for doing so. The IHC is designed to fill precisely that gap.

References

1. Lloyd-Jones DM, Nam BH, D’Agostino RB Sr, et al. Parental cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults: a prospective study of parents and offspring. JAMA. 2004;291(18):2204-2211. doi:10.1001/jama.291.18.2204
2. Murabito JM, Pencina MJ, Nam BH, et al. Sibling cardiovascular disease as a risk factor for cardiovascular disease in middle-aged adults. JAMA. 2005;294(24):3117-3123. doi:10.1001/jama.294.24.3117
3. D’Agostino RB Sr, Vasan RS, Pencina MJ, et al. General cardiovascular risk profile for use in primary care: the Framingham Heart Study. Circulation. 2008;117(6):743-753. doi:10.1161/CIRCULATIONAHA.107.699579
4. Villines TC, Hulten EA, Shaw LJ, et al. Prevalence and severity of coronary artery disease and adverse events among symptomatic patients with coronary artery calcification scores of zero undergoing coronary computed tomography angiography: results from the CONFIRM (Coronary CT Angiography Evaluation for Clinical Outcomes: An International Multicenter) registry. J Am Coll Cardiol. 2011;58(24):2533-2540. doi:10.1016/j.jacc.2011.10.851
5. Nerlekar N, Vasanthakumar SA, Whitmore K, et al. Effects of Combining Coronary Calcium Score With Treatment on Plaque Progression in Familial Coronary Artery Disease: A Randomized Clinical Trial. JAMA. 2025;333(16):1403-1412. doi:10.1001/jama.2025.0584
6. Bachmann JM, Willis BL, Ayers CR, Khera A, Berry JD. Association between family history and coronary heart disease death across long-term follow-up in men: the Cooper Center Longitudinal Study. Circulation. 2012;125(25):3092-3098. doi:10.1161/CIRCULATIONAHA.111.065490
7. Ference BA, Ginsberg HN, Graham I, et al. Low-density lipoproteins cause atherosclerotic cardiovascular disease. 1. Evidence from genetic, epidemiologic, and clinical studies. A consensus statement from the European Atherosclerosis Society Consensus Panel. Eur Heart J. 2017;38(32):2459-2472. doi:10.1093/eurheartj/ehx144
8. Arnett DK, Blumenthal RS, Albert MA, et al. 2019 ACC/AHA Guideline on the Primary Prevention of Cardiovascular Disease: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019;140(11):e596-e646. doi:10.1161/CIR.0000000000000678