Coronary heart disease

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Muhammad Saad, M.B.B.S.[2]

Coronary heart disease (CHD), also called coronary artery disease (CAD), ischaemic heart disease, atherosclerotic heart disease, is a narrowing of the small blood vessels that supply blood and oxygen to the heart. This is usually the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart) with oxygen and nutrients. While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a “sudden” heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle.

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries. These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. The streaks increase in size and lead to the formation of plaque within the arteries. When the plaque obstruct the passage of blood within the coronary arteries, it causes ischemia, or lack of oxygen, within the heart muscle.

There are a large number of causes of chest pain that coronary heart disease must be distinguished from.

Coronary heart disease is the most common cause of sudden death,^[1] and is also the most common reason for death of men and women over 20 years of age. According to present trends in the United States, half of healthy 40-year-old males will develop CHD in the future, and one in three healthy 40-year-old women.^[2] According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CHD.

There are many risk factors and risk equivalents associated with coronary heart disease. Risk factors include cigarette smoking, hypertension, a family history of premature coronary artery disease, high LDL cholesterol, low HDL cholesterol, and older age. Some of these risk factors are modifiable, and are good targets for primary prevention in the health care setting.

Risk stratification among patients with and at risk for coronary artery disease is critical so that the level of aggressiveness of management can match the risk of future events. The magnitude of risk is often clearer in the patient who has had a vascular event than in the assessment of primary risk assessment (who will have a future event who does not yet have evidence of CHD). Patients at low to intermediate risk by history and physical examination account for 75% of cardiovascular events. There is therefore the need for improved risk stratification tools to reclassify those patients deemed to be at low risk on history and physical examination into a higher risk category. In select populations, coronary artery calcium scoring, carotid intima-media thickness (CIMT) assessment and C reactive protein (CRP) assessment may offer addition improvements in risk stratification.

Pretest probability of coronary artery disease is assessed basing upon the age, gender and the symptoms. Patients are stratified into very low, low, intermediate, and high risk for CAD.^[3]

Coronary heart disease may be asymptomatic, or have symptoms such as chest pain, shortness of breath, fatigue, weakness and lightheadedness.

Stress testing is used for risk stratification and diagnosis of coronary artery disease.

Coronary angiography is useful in evaluating the whole length of the vessel from its origin to its branches. It is useful in identifying any thrombus, stenosis or dissections in coronary vessels.

Goals for treating coronary artery disease include lowering blood pressure, managing diabetes with cardiovascular-risk-reducing agents such as SGLT2 inhibitors and GLP-1 receptor agonists, independent of HbA1c target^[4], and lowering LDL cholesterol. Long-term treatment will generally depend on the symptoms and severity of disease, and include aspirin, ACE inhibitors, and other ani-coagulant and anti-platelet regimens.Low-dose colchicine (0.5 mg daily) should also be considered as an adjunctive anti-inflammatory therapy for long-term management. ^[5] The mainstay of treatment for stable angina which occurs with exertion, includes nitroglycerin. When unstable angina causes symptoms at rest, or in the setting of an acute myocardial infarction, the immediate therapy is morphine, supplemental oxygen (only if SpO₂ <90%), nitrate, and aspirin. Angioplasty may also be required in cases of acute coronary syndrome.Beta-blockers should be used selectively: they are indicated when LVEF is <50%, or in the presence of angina, arrhythmias, or hypertension, but are no longer routinely recommended for all patients with chronic coronary disease.^[6]

The LDL target in primary prevention depends upon the patient’s risk factors. LDL targets in primary prevention should be guided by estimated 10-year ASCVD risk using the PREVENT™ equations^[7]. Statin therapy is recommended for those with intermediate risk (5–<10%) and reasonable for those with borderline risk (3–<5%) after shared decision-making, with the goal of achieving at least a 50% LDL-C reduction from baseline^[7].Non-statin therapies — including ezetimibe, bempedoic acid, and PCSK9 inhibitors should be considered when statin therapy alone is insufficient.^[7] Attempts should be made to reduce triglyceride levels and to increase HDL levels.Coronary artery calcium (CAC) scoring and Lp(a) measurement should be considered to further refine cardiovascular risk and guide treatment intensity.^[7] The underlying causes for existing dyslipidemias should be identified and appropriately managed. Drugs that cause dyslipidemias should be avoided. Patients should be evaluated reguarly for the presence of risk factors for coronary heart disease, and those with increased risk should be counseled on the beneficial effects of daily aspirin therapy. Patients should also regularly be counseled about modifying risk factors such as obesity, hypertension, smoking, and the benefits of an exercise plan.

Patients who should be treated with secondary prevention are those with established atherosclerosis including peripheral artery disease; carotid artery disease; atherosclerotic aortic disease; diabetes and those with a 10-year ASCVD risk >20% by contemporary risk calculators (e.g., PREVENT™ equations or SCORE2).^[8] There are 13 aspects of secondary prevention: Smoking cessation; blood pressure control; lipid-lowering; increasing physical activity; weight loss; diabetes control; antiplatelet agents/anticoagulants; RAS blockers; beta-blockers; depression management; cardiac rehabilitation, influenza vaccine and low-dose colchicine (0.5 mg/day) for anti-inflammatory residual risk reduction.^[9] Please note that secondary prevention guidelines, especially, those involving medication, may differ between UA/NSTEMI; STEMI; and Chronic Stable Angina.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries. These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. The streaks increase in size and lead to the formation of plaque within the arteries. When the plaque obstruct the passage of blood within the coronary arteries, it causes ischemia, or lack of oxygen, within the heart muscle.

Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth.

Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the coronary artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.

CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.

Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in caliber.

Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, recent evidence suggests that the gradual buildup may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.

Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.

As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.

A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood.

A 2006 study by the Cleveland Clinic found a region on Chromosome 17 was confined to families with multiple cases of myocardial infarction.^[1]

Periodontal disease may contribute to this inflammation.^[2][3] Poor oral hygiene is associated with elevated C-reactive protein and fibrinogen.^[3]

A more controversial link is that between Chlamydophila pneumoniae infection and atherosclerosis.^[4] While this intracellular organism has been demonstrated in atherosclerotic plaques, evidence is inconclusive as to whether it can be considered a causative factor. Treatment with antibiotics in patients with proven atherosclerosis has not demonstrated a decreased risk of heart attacks or other coronary vascular diseases.^[5]

Cardiac syndrome X is the presence of typical angina, abnormal exercise-test results, and normal coronary arteries (including no vasospasm).^[6] Syndrome X may be caused by subendocardial hypoperfusion that can be demonstrated by cardiovascular magnetic resonance imaging during the administration of adenosine.^[6]

An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack). Surprisingly, more fatal ruptures occur on plaques that are not severely stenosed^[7][8][9]

Approximately 15% of NSTEMI and 2% of STEMI patients have no obstruction of coronary arteries and in about half of these patients, spasm of a coronary artery can be induced.^[10]

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

There are a large number of causes of chest pain that coronary heart disease must be distinguished from.

• Air embolism
• Anomalous origin of coronary artery
• Aortic dissection
• Aortic stenosis
• Atrial myxoma
• Chest trauma
• Cocaine
• Collagen vascular disease
• Coronary artery dissection
• Endocarditis
• Hypercoagulable state
• Hypertrophic cardiomyopathy
• Hypotension
• Luetic aortitis
• Nitrate withdrawal
• Raynaud’s Disease
• Takayasu’s Disease
• Thrombi from:

  • Catheter
  • Left atrium
  • Left ventricle
  • Prosthetic valves

• Variant angina

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Coronary heart disease is the most common cause of sudden death,^[1] and is also the most common reason for death of men and women over 20 years of age. According to present trends in the United States, half of healthy 40-year-old males will develop CHD in the future, and one in three healthy 40-year-old women.^[2] According to the Guinness Book of Records, Northern Ireland is the country with the most occurrences of CHD.

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Synonyms and keywords: CAD risk factors; risk factors for CAD

There are many risk factors and risk equivalents associated with coronary heart disease. Risk factors include cigarette smoking, hypertension, a family history of premature coronary artery disease, high LDL cholesterol, low HDL cholesterol, and older age. Some of these risk factors are modifiable, and are good targets for primary prevention in the health care setting.

“

Category I: Risk factors for which interventions have proved to reduce the incidence of coronary artery disease events such as cigarette smoking, LDL cholesterol, dietary modification, hypertension and thrombogenic factors. Category II: Risk factors for which interventions are likely, based on our current pathophysiologic understanding and on epidemiologic and clinical trial evidence, to reduce the incidence of coronary artery disease events such as diabetes, physical inactivity, HDL cholesterol, obesity and postmenopausal status. Category III: Risk factors clearly associated with an increase in coronary artery disease risk and which, if modified, might lower the incidence of coronary artery disease events such as psychosocial factors, triglycerides, Lp(a), homocysteine, oxidative stress and alcohol consumption. Category IV: Risk factors associated with increased risk but which cannot be modified or whose modification would be unlikely to change the incidence of coronary artery disease events such as age, gender, family history and many others.

”

You are essentially considered to have the equivalent of coronary heart disease if you have any of the following:

• Aortic aneurysm
• Diabetes
• Framingham Risk Score (FRS) of > 20%
• Peripheral vascular disease (PVD) (defined as claudication, an Ankle Brachial Index (ABI) of < 0.9)
• Symptomatic carotid artery disease (defined as prior stroke or TIA)

• Cigarette smoking
• Family history of premature coronary artery disease (CAD)
• High LDL (defined as LDL > 130 mg /dl)
• Hypertension ( defined as a BP ≥140/90 mm Hg or if the patient is on antihypertensive drugs)
• Low HDL (defined as HDL < 40 mg/dL males, < 50 mg/dL in females)
• Older Age (men ≥45 years old; women ≥55 years old)

• The SCORE project, assembled a pool of datasets from 12 European cohort studies, representing 2.7 million person years of follow-up to predict any kind of fatal cardiovascular event over a ten-year period.
• This system includes both non-modifiable and modifiable coronary risk factors such as:

• Age
• Gender
• Systolic blood pressure
• Smoking
• Total cholesterol and/or cholesterol:HDL ratio

to estimate a person’s total ten-year risk of cardiovascular death.

• Patients with established coronary artery disease, diabetics with microalbuminuria, asymptomatic patients with multiple risk factors are considered high-risk for the development of fatal coronary event.

• The threshold for being at high-risk according to the SCORE system is defined as greater than or equal to 5% since it estimates the fatal events and not the composite primary end-point. This system is shown to be most helpful in the decision-making process to intensify secondary prevention strategies. Hence, the SCORE risk estimation system offers direct estimation of total fatal cardiovascular risk in a format suited to the constraints of clinical practice.

In alphabetical order: ^{[3] [4]}

• ACE DD genotype
• Age

  • Men > 45
  • Women > 45 (early menopause)
  • Women > 55 (normal onset menopause)

• Chronic Renal Failure
• Cigarette smoking
• Decreased apolipoprotein A1
• Decreased serum folate
• Diabetes Mellitus
• Family history of premature coronary artery disease
• HDL cholesterol < 40 mg/dl
• Hyperhomocysteinemia
• Hypertension
• Hypertriglyceridemia
• Immunosuppressive posttransplant
• Increased apolipoprotein B
• Increased C-reactive protein
• Increased fibrinogen
• Infections
• Insulin resistance syndrome
• Lack of supportive primary relationship
• LDL cholesterol > 130 mg/dl
• Low birth weight
• Metabolic syndrome
• Obesity
• Oral contraceptive use
• Sedentary living
• Syndrome X
• Type A personality

Class I

“1. Primary care providers should evaluate the presence and status of control of major risk factors for CHD for all patients at regular intervals (approximately every 3 to 5 years). (Level of Evidence: C)”

“2. Ten-year risk (National Cholesterol Education Program [NCEP] global risk) of developing symptomatic CHD should be calculated for all patients who have 2 or more major risk factors to assess the need for primary prevention strategies.[6][7] (Level of Evidence: B)”

“3. Patients with established CHD should be identified for secondary prevention efforts, and patients with a CHD risk equivalent (e.g., atherosclerosis in other vascular beds, diabetes mellitus, chronic kidney disease, or 10-year risk greater than 20% as calculated by Framingham equations) should receive equally intensive risk factor intervention as those with clinically apparent CHD. (Level of Evidence: A)”

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Risk stratification among patients with and at risk for coronary artery disease is critical so that the level of aggressiveness of management can match the risk of future events. The magnitude of risk is often clearer in the patient who has had a vascular event than in the assessment of primary risk assessment (who will have a future event who does not yet have evidence of CHD). Patients at low to intermediate risk by history and physical examination account for 75% of cardiovascular events. There is therefore the need for improved risk stratification tools to reclassify those patients deemed to be at low risk on history and physical examination into a higher risk category. In select populations, coronary artery calcium scoring, carotid intima-media thickness (CIMT) assessment and C reactive protein (CRP) assessment may offer addition improvements in risk stratification.

You are essentially considered to have the equivalent of coronary heart disease if you have any of the following:

• Aortic aneurysm
• Diabetes
• Framingham Risk Score (FRS) of > 20%
• Peripheral vascular disease (PVD) (defined as claudication, an Ankle Brachial Index (ABI) of < 0.9)
• Symptomatic carotid artery disease (defined as prior stroke or TIA)

• Cigarette smoking
• Family history of premature coronary artery disease (CAD)
• High LDL (defined as LDL > 130 mg /dl)
• Hypertension ( defined as a BP ≥140/90 mm Hg or if the patient is on antihypertensive drugs)
• Low HDL (defined as HDL < 40 mg/dL males, < 50 mg/dL in females)
• Older Age (men ≥45 years old; women ≥55 years old)

The Framingham Risk Score is used to estimate the 10-year cardiovascular risk of an individual. The Framingham Risk Score is based on data obtained from the Framingham Heart Study. There are two Framingham Risk Scores, one for men and one for women.

– Low Risk is less than 10%

– Intermediate Risk is 10 – 20%

– High Risk is more than 20%

Duke treadmill score (DTS) = Treadmill time (Bruce) – 5 x ST deviation (no. mm) – 4 x Angina index (0,1,2)

Low Risk Score	≥ 5	Treat medically
Intermediate Score	10 to 4	Stress Imaging
High Risk Score	≤ 11	Cath/PCI/CABG

Stress imaging is induction of reversible ischemia in a patient using drugs which can can cause increased contraction of heart muscle like dobutamine or drugs which cause vasodilatation and decrease blood supply to heart. Both these mechanisms cause stress on heart.

Class I

” 1. Symptomatic, able to exercise, uninterpretable ECG.”

” 2. Symptomatic, unable to exercise.”

” 3. Symptomatic prior coronary revascularization.”

” 4. Functionally significant lesion.”

” 5. Intermediate risk on Duke Treadmill Score.”

Low risk findings

• It has normal or near normal MPI
• Normal stress echo
• The annual mortality rate in these patients will be < 1%

Intermediate risk findings

• Mild to moderate dysfunction of left ventricle. (resting ejection fraction of 35- 49%)
• Moderate stress induced perfusion defect without LV dilatation or increased uptake into pulmonary vessels.
• Mild to moderate stress induced regional wall motion abnormalities in echocardiogram seen in upto 4 segments.
• The annual mortality rate of these patients will be 1 – 3%.

High risk findings

• Significant LV dysfuntion. (resting ejection fraction of <40%%)
• Abnormal left ventricular end systolic volume.
• Extensive ischemic regional wall motion abnormality in more than 5 segments.
• Low ischemic threshold during stress echo.
• Multi-vessel regional wall motion abnormality.
• The annual mortality rate in these patients will be > 3%.

Class I

“1. Global risk scores (such as the Framingham Risk Score) that use multiple traditional cardiovascular risk factors should be obtained for risk assessment in all asymptomatic adults without a clinical history of CHD. These scores are useful for combining individual risk factor measurements into a single quantitative estimate of risk that can be used to target preventive interventions.[2] (Level of Evidence: B)”

Class I

“1. Family history of atherothrombotic CVD should be obtained for cardiovascular risk assessment in all asymptomatic adults.[3][4] (Level of Evidence: B)”

Class III: No Benefit

“1. Genotype testing for CHD risk assessment in asymptomatic adults is not recommended.[5][6] (Level of Evidence: B)”

Class III: No Benefit

“1. Measurement of lipid parameters, including lipoproteins, apolipoproteins, particle size, and density, beyond a standard fasting lipid profile is not recommended for cardiovascular risk assessment in asymptomatic adults.[7] (Level of Evidence: C)”

Class III: No Benefit

“1. Measurement of natriuretic peptides is not recommended for CHD risk assessment in asymptomatic adults.[8] (Level of Evidence: B)”

Class III: No Benefit

“1. In asymptomatic high-risk adults, measurement of CRP is not recommended for cardiovascular risk assessment.[9] (Level of Evidence: B)”

“2. In low-risk men younger than 50 years of age or women 60 years of age or younger, measurement of CRP is not recommended for cardiovascular risk assessment.[3][10] (Level of Evidence: B)”

Class IIa

“1. In men 50 years of age or older or women 60 years of age or older with low-density lipoprotein cholesterol less than 130 mg/dL; not on lipid-lowering, hormone replacement, or immunosuppressant therapy; without clinical CHD, diabetes, chronic kidney disease, severe inflammatory conditions or contraindications to statins, measurement of CRP can be useful in the selection of patients for statin therapy.[11] (Level of Evidence: B)”

Class IIb

“1. In asymptomatic intermediate-risk men 50 years of age or younger or women 60 years of age or younger, measurement of CRP may be reasonable for cardiovascular risk assessment.[3][10] (Level of Evidence: B)”

Class IIb

“1. Measurement of hemoglobin A1C may be reasonable for cardiovascular risk assessment in asymptomatic adults without a diagnosis of diabetes.[12][13] (Level of Evidence: B)”

Class IIa

“1. In asymptomatic adults with hypertension or diabetes, urinalysis to detect microalbuminuria is reasonable for cardiovascular risk assessment.[14][15] (Level of Evidence: B)”

Class IIb

“1. In asymptomatic adults at intermediate risk without hypertension or diabetes, urinalysis to detect microalbuminuria might be reasonable for cardiovascular risk assessment.[16] (Level of Evidence: B)”

Class IIb

“1. Lipoprotein-associated phospholipase A2 might be reasonable for cardiovascular risk assessment in intermediate-risk asymptomatic adults.[17][18] (Level of Evidence: B)”

Class IIa

“1. A resting electrocardiogram (ECG) is reasonable for cardiovascular risk assessment in asymptomatic adults with hypertension or diabetes.[19][20] (Level of Evidence: C)”

Class IIb

“1. A resting ECG may be considered for cardiovascular risk assessment in asymptomatic adults without hypertension or diabetes.[21][22] (Level of Evidence: C)”

Class III: No Benefit

“1. Echocardiography is not recommended for cardiovascular risk assessment of CHD in asymptomatic adults without hypertension. (Level of Evidence: C)”

Class IIb

“1. Echocardiography to detect left ventricular hypertrophy may be considered for cardiovascular risk assessment in asymptomatic adults with hypertension.[23][24] (Level of Evidence: B)”

Class IIa

“1. Measurement of carotid artery intima-media thickness is reasonable for cardiovascular risk assessment in asymptomatic adults at intermediate risk.[25][26] Published recommendations on required equipment, technical approach, and operator training and experience for performance of the test must be carefully followed to achieve high-quality results.[26] (Level of Evidence: B)”

Class III: No Benefit

“1. Peripheral arterial flow-mediated dilation (FMD) studies are not recommended for cardiovascular risk assessment in asymptomatic adults.[27][28] (Level of Evidence: B)”

Class III: No Benefit

“1. Measures of arterial stiffness outside of research settings are not recommended for cardiovascular risk assessment in asymptomatic adults. (Level of Evidence: C)”

Class IIa

“1. Measurement of ankle-brachial index is reasonable for cardiovascular risk assessment in asymptomatic adults at intermediate risk.[29] (Level of Evidence: B)”

Class IIb

“1. An exercise ECG may be considered for cardiovascular risk assessment in intermediate-risk asymptomatic adults (including sedentary adults considering starting a vigorous exercise program), particularly when attention is paid to non-ECG markers such as exercise capacity.[30][31] (Level of Evidence: B)”

Class III: No Benefit

“1. Stress echocardiography is not indicated for cardiovascular risk assessment in low- or intermediate-risk asymptomatic adults. (Exercise or pharmacologic stress echocardiography is primarily used for its role in advanced cardiac evaluation of symptoms suspected of representing CHD and/or estimation of prognosis in patients with known coronary artery disease or the assessment of patients with known or suspected valvular heart disease.) (Level of Evidence: C)”

Class III: No Benefit

“1. Stress MPI is not indicated for cardiovascular risk assessment in low- or intermediate-risk asymptomatic adults. (Exercise or pharmacologic stress MPI is primarily used and studied for its role in advanced cardiac evaluation of symptoms suspected of representing CHD and/or estimation of prognosis in patients with known CAD.).[32] (Level of Evidence: C)”

Class IIb

“1. Stress myocardial perfusion imaging (MPI) may be considered for advanced cardiovascular risk assessment in asymptomatic adults with diabetes or asymptomatic adults with a strong family history of CHD or when previous risk assessment testing suggests a high risk of CHD, such as a coronary artery calcium (CAC) score of 400 or greater. (Level of Evidence: C)”

Class III: No Benefit

“1. Persons at low risk (<6% 10-year risk) should not undergo CAC measurement for cardiovascular risk assessment.[33][34][35] (Level of Evidence: B)”

Class IIa

“1. Measurement of CAC is reasonable for cardiovascular risk assessment in asymptomatic adults at intermediate risk (10% to 20% 10-year risk).[33][34] (Level of Evidence: B)”

Class IIb

“1. Measurement of CAC may be reasonable for cardiovascular risk assessment persons at low to intermediate risk (6% to 10% 10-year risk).[34][36] (Level of Evidence: B)”

Class III: No Benefit

“1. Coronary Computed Tomography Angiography is not recommended for cardiovascular risk assessment in asymptomatic adults.[37] (Level of Evidence: C)”

Class III: No Benefit

“1. MRI for detection of vascular plaque is not recommended for cardiovascular risk assessment in asymptomatic adults. (Level of Evidence: C)”

Class IIa

“1. In asymptomatic adults with diabetes, 40 years of age and older, measurement of CAC is reasonable for cardiovascular risk assessment.[38][39][40] (Level of Evidence: B)”

Class IIb

“1. Measurement of hemoglobin A1C may be considered for cardiovascular risk assessment in asymptomatic adults with diabetes.[41] (Level of Evidence: B)”

“1. Stress MPI may be considered for advanced cardiovascular risk assessment in asymptomatic adults with diabetes or when previous risk assessment testing suggests a high risk of CHD, such as a CAC score of 400 or greater. (Level of Evidence: C)”

Class I

“1. A global risk score should be obtained in all asymptomatic women.[3][42] (Level of Evidence: B)”

“2. Family history of CVD should be obtained for cardiovascular risk assessment in all asymptomatic women.[3][4] (Level of Evidence: B)”

Coronary artery calcium (CAC) scoring adds 4% the C-statistic for predicting ASCVD outcomes^[1].

The United States Preventive Service Task Force (USPSTF) does not recommend screening with the CAC^[2].