Coronary Artery Disease Prevention

Etiology

CAD develops due to a mix of genetics, cardiometabolic risk factors, environmental influences, and ongoing inflammation. These factors lead to the buildup of atherosclerotic plaque.[2][3] Risk factors are grouped into nonmodifiable, modifiable, and risk-enhancing categories. Today, experts focus on a person’s lifetime exposure and overall risk, rather than just single cutoff values.[2]

Nonmodifiable Risk Factors

• Increasing age
• Male sex
• Race and ethnicity
• Family history of premature atherosclerotic cardiovascular disease (ASCVD) [2]

Modifiable Risk Factors

• Type 2 diabetes mellitus
• Hypertension
• Dyslipidemia (elevated high- and low-level lipoproteins-C, elevated triglycerides)
• Cigarette smoking and other tobacco exposure
• Obesity and metabolic syndrome
• Physical inactivity
• Chronic kidney disease [2][4][5]

Risk-Enhancing Factors

• Chronic systemic inflammatory disorders (eg, rheumatoid arthritis, systemic lupus erythematosus, HIV infection, psoriasis) [6]
• Adverse pregnancy-related conditions (preeclampsia, gestational diabetes, premature menopause) [2]
• Persistently elevated triglycerides and lipoprotein(a) [7]
• Psychosocial stressors and adverse social determinants of health [2]

Recent research shows that inflammation, insulin resistance, problems with the lining, and abnormal lipid metabolism accelerate atherosclerosis, especially in people with ongoing cardiometabolic risks.[3][6] As a result, prevention now focuses on early action, personalized risk assessment, and lowering overall ASCVD risk over a person’s life.[2]

Epidemiology

CAD is still the leading cause of death around the world, even with better prevention and treatment. Each year, ischemic heart disease causes more than 9 million deaths, with low- and middle-income countries affected the most.[8] In the United States, the American Heart Association reports that more than 18 million adults have coronary artery disease.[4]

The condition is more common in men and older adults than in women and younger individuals. While death rates have dropped in many wealthy countries because of better prevention, the total number of cases is still high. This is mostly because people are living longer, and rates of obesity and diabetes are rising.[4][8]  

There are still big differences in how often people acquire CAD and how they recover, depending on their race, ethnicity, and income. People from marginalized groups often get the disease earlier, face more complications, and have worse outcomes.[4][2] These gaps are mostly caused by more risk factors, less access to healthcare, and other social issues. In many developing areas, more people are dying from coronary artery disease because they cannot get preventive care, are diagnosed late, and do not get enough help managing risk factors.[8] These patterns show that we need both broad prevention efforts and personalized care to reduce the worldwide impact of coronary artery disease.[2]

Pathophysiology

CAD develops when long-term arterial inflammation begins with endothelial damage.[3][6] This damage occurs after prolonged exposure to risk factors such as high cholesterol, high blood pressure, smoking, high blood sugar, and overall body inflammation.[3] When the endothelium is damaged, it allows more low-density lipoproteins (LDL) particles to enter the arterial wall, where they are oxidized and modified by enzymes. These altered LDL particles attract monocytes from the blood and activate the body's immune response.

Monocytes differentiate into macrophages, take up oxidized LDL, and become foam cells. These foam cells constitute the first visible sign of atherosclerosis, known as a fatty streak.[9] Ongoing inflammation causes smooth muscle cells to migrate and proliferate, leading to the accumulation of material outside the cells. This forms a fibrous cap over a core of dead, fatty material.

At first, the artery may adapt to these changes and keep its opening size. But as the plaque grows and hardens and the cap becomes thinner, blood flow through the artery is reduced.[9] Plaque destabilization, rather than gradual arterial narrowing, is the main cause of acute coronary syndromes.[9][10] High-risk plaques often have the following features:

• Large cores filled with fatty, dead tissue
• Thin layers of fibrous tissue cover the plaque
• A high number of active immune cells (macrophages) within the plaque
• Bleeding inside the plaque
• Damage to the surface layer of the artery lining [9][10]

When a plaque ruptures or its surface is damaged, it exposes material that can trigger blood clots. This can quickly block the artery, leading to reduced blood flow to the heart or a heart attack.[9] Recent research also highlights how overall inflammation, changes in blood cell production, immune system dysfunction, and metabolic issues can increase the likelihood that plaques will lead to serious events.[11][12]

History and Physical

History-taking is an extremely valuable technique for distinguishing among different causes of chest discomfort. A thorough history and physical exam are the hallmarks of diagnosing coronary artery disease. For example, a history of typical anginal symptoms, decreased exercise tolerance, syncope, presyncope, orthopnea, or paroxysmal nocturnal dyspnea should prompt the clinician to obtain a detailed cardiovascular workup, including appropriate diagnostic tests (eg, electrocardiogram and cardiac enzymes for patients presenting with chest pain).[13] Physical exam should focus on the heart, identifying any murmurs, abnormal heart sounds, heart rate and rhythm, decreased or increased heart sounds, and evidence of reproducible or non-reproducible chest pain or atypical equivalents.

Symptoms of coronary artery disease presentations can vary from chest pain with exertion, also known as stable angina or angina pectoris, to acute coronary syndrome (unstable angina, non-ST-elevation myocardial infarction [NSTEMI], and STEMI), to sudden cardiac death. Chest pain seen with stable angina is often mid-sternal, with a squeezing quality, associated with a feeling of constriction or anxiety, and may radiate to the arms, neck, jaw, back, or upper abdomen.[14] In patients with stable angina, chest pain worsens with exertion (physical or emotional) due to increased oxygen demand and improves with rest. The level of physical activity at which symptoms begin is called the "angina threshold."[15]

Unstable angina is defined by similar chest pain to stable angina that additionally occurs at rest and is considered to be the first type of pathology associated with acute coronary syndrome. Patients with unstable angina have a normal (or stable) electrocardiogram (ECG) without new electrical changes and cardiac enzymes within normal limits, thus ruling out myocardial infarction.[16] NSTEMI presents with chest pain at rest and elevated cardiac enzymes, without ST-segment elevation on ECG.

Patients with NSTEMI may present with various ECG changes, including ST-segment depressions and T-wave inversions. Similarly, STEMI presents with crushing or sharp substernal chest pain, often excruciating, with nausea/vomiting, diaphoresis, and most notably ST-segment elevations on ECG with elevated cardiac enzymes.[17] Typically, STEMI presentations require immediate intervention and are therefore considered emergencies due to the high likelihood of mortality associated with them if left untreated.

Patients may present with absolutely no symptoms of chest pain or angina, and the initial presentation could be an abnormal electrocardiogram or echocardiogram ordered for other reasons. Properly evaluating the history of present illness in these patients, including past medical and social histories and risk factors for coronary artery disease, is necessary.[1][18] In the outpatient setting, a thorough review of a patient's risk factors, in conjunction with their history and physical, guides preventive measures to mitigate the effects of coronary artery disease.

Evaluation

ECG is a tool for assessing patients who are either stable or in emergent situations in both the inpatient and outpatient settings. The presence of specific ECG findings, such as ST-segment elevations, in a patient with elevated cardiac enzymes and chest pain should prompt immediate emergency department referral, when necessary, for thrombolysis or intervention. However, an ECG is not absolute, as ST-segment elevations are present in only 50% of myocardial infarctions confirmed by cardiac enzymes.[19][20][21]

Echocardiogram, stress testing, cardiac computed tomography, and cardiac MRI are invaluable tools for stratification and further workup of suspected coronary artery disease. Patient’s age, risk factors, and symptomatology may prompt additional testing. For example, the presence of wall motion abnormalities on a transthoracic echocardiogram may prompt ischemic workup for coronary artery disease in an asymptomatic patient without evidence of acute coronary syndrome.[22] Additionally, stress testing may be utilized to further differentiate/workup a patient for unstable angina vs stable angina. Cardiac computed tomography, cardiac MRI, and other imaging modalities may demonstrate calcification of various arteries surrounding the heart, prompting further workup in an otherwise asymptomatic patient or in a patient with stable disease.[23]

Treatment / Management

CAD management depends on the clinical presentation, such as acute coronary syndrome or chronic coronary disease, as well as ischemic risk, bleeding risk, and other health conditions.[24] The main goals are to quickly stabilize or restore blood flow as needed and to reduce long-term risks through intensive guideline-directed medical therapy.[25][24] If it is suspected that a patient may have acute coronary syndrome, quickly assess their risk, order an ECG and troponin, and start anti-ischemic and antithrombotic treatment. Use an early invasive approach if it fits the situation. The following are the main steps in the current guidelines:(A1)

• For STEMI, aim for rapid reperfusion with primary percutaneous coronary intervention (PCI) if possible. If PCI is not available soon, give fibrinolysis and then transfer the patient for angiography if needed.[25]
• In the acute phase, administer dual antiplatelet therapy (DAPT) and parenteral anticoagulation, adjusting based on each patient’s risk of ischemia and bleeding. High-risk NSTEMI patients often do better with early invasive evaluation.[25]
• Treat symptoms with anti-ischemic drugs like nitrates, unless the patient is hypotensive, has a right ventricular infarct, or is taking phosphodiesterase type 5 inhibitors. Use beta-blockers when appropriate. Give morphine only for severe pain or anxiety, and use it carefully, as it is not routine.[25]
• Begin early and intensive secondary prevention in the hospital. This means using high-intensity lipid-lowering, managing blood pressure, supporting smoking cessation, referring to cardiac rehab, and optimizing cardiometabolic treatments.[25][24]
(A1)

Chronic coronary disease (stable angina/chronic ischemic syndromes)

For patients with chronic coronary disease seen in outpatient settings, the main goals are to control symptoms, prevent heart attacks, strokes, and death, and reduce atherosclerotic risk. Current guidelines highlight the following points:  

• Adjust antianginal treatment based on the patient’s heart rate, blood pressure, and other health conditions. Start with beta-blockers or calcium channel blockers. If symptoms continue, add long-acting nitrates or ranolazine. If symptoms or ischemia are still present, consider lifestyle changes or revascularization [24][26]
• For many patients with established CAD, single antiplatelet therapy is the standard approach. After ACS or PCI, the duration and intensity of DAPT should be tailored to each patient’s ischemic and bleeding risks.[24][25]
• Renin–angiotensin system inhibitors, such as angiotensin-converting enzyme inhibitors or angiotensin II receptor blockers, are recommended for patients with coronary artery disease who also have high blood pressure, diabetes, chronic kidney disease, or left ventricular dysfunction. Beta-blockers with proven benefits are used for those with a recent heart attack, reduced ejection fraction, or ongoing angina.[24]
• Lowering cholesterol is a key part of treatment. High-intensity statins are the first choice. If LDL-C remains above target, ezetimibe should be added. Proprotein convertase subtilisin kexin type 9 (PCSK9) inhibitors or bempedoic acid can be considered next, depending on the patient’s risk, tolerance, cost, and the amount of LDL-C to be lowered.[24][27][28]
(A1)

Primary Prevention

Primary prevention involves assessing ASCVD risk in a structured way, making major lifestyle changes, and treating key risk factors such as cholesterol, blood pressure, diabetes, and smoking early. Treatment intensity should match the patient’s overall risk.[2][24](A1)

• Use validated tools to assess risk. Take into account risk enhancers and lifetime risk, and include patients in shared decisions about how intensive statin and blood pressure treatment should be.[24]
• Current prevention guidelines recommend focusing on all aspects of lifestyle, including diet, exercise, weight, sleep, nicotine use, blood pressure, lipids, and glucose. These areas should be regularly reassessed.[2]
• For patients with higher ASCVD risk, statins are the first choice. If LDL-C is not sufficiently lowered or statins are not tolerated, nonstatin options such as ezetimibe, PCSK9 inhibitors, or bempedoic acid can be added based on risk.[27][28]
• Routine aspirin use is generally not advised for primary prevention. If you are considering it, limit its use to adults with higher ASCVD risk and low bleeding risk, and decide together with the patient.[29]
• For people with type 2 diabetes who have a high risk of ASCVD, medications with proven heart benefits, such as sodium-glucose co-transporter 2 inhibitors or glucagon-like peptide-1 receptor agonists, should be considered along with metformin and lifestyle changes when suitable.[30]
(A1)

In 2020, the American Heart Association (AHA) developed a health prescription called "Life's Simple 7" designed to improve overall cardiovascular health and reduce the risk of cardiovascular disease. These recommendations are outlined below. 

Diet

Diet is a significant contributing factor to reducing the risk of coronary artery disease. According to the American College of Cardiology (ACC)/AHA 2019 guidelines, the plant-based Mediterranean diet (high in vegetables, fruits, legumes, nuts, whole grains, and fish) is highly recommended. Replacing saturated fats with dietary monounsaturated and polyunsaturated fats has been found to reduce cardiovascular risk.

Besides, dietary sodium reduction has been shown to lower blood pressure and reduce the risk of cardiovascular events, according to the Dietary Approaches to Stop Hypertension (DASH) trial. On the other side, sugar-sweetened and artificial sweeteners have been shown to increase the risk of diabetes, leading to an increased 10-year ASCVD risk. Moreover, increased trans fat intake also correlates with increased ASCVD risk.

Exercise, physical activity, and weight loss

Physical activity is also beneficial for reducing CAD risk. At least 150 minutes per week of moderate-intensity physical activity and more than 75 minutes per week of vigorous-intensity physical activity are helpful. Moderate activities include brisk walking (2.4 to 4 mph), biking (5 to 9 mph), active yoga, and recreational swimming, whereas vigorous activities include jogging/running, biking (10+ mph), playing tennis, or swimming.

Individuals are diagnosed as overweight when their body mass index (BMI) is between 25 and 29.8 kg/m^2 and obese when their BMI is greater than or equal to 30 kg/m^2. Conditions of both overweight and obesity increase the ASCVD risk compared to those of a normal weight. Recommendations include annual BMI calculation and lifestyle modifications, such as calorie restriction and weight loss, based on BMI values. Weight loss has consistently been shown to improve the ASCVD risk profile. Strong recommendations include high levels of physical activity (200 to 300 minutes per week), a low-calorie diet (800 to 1500 kcal/day), and, if possible, weight-loss maintenance programs.

Tobacco Use

Using tobacco is among the leading causes of preventable deaths in the United States and is also a significant risk factor for CAD. Tobacco use should be assessed in all adults at every primary care visit. A 3- to 10-minute status assessment, with counseling to quit, should take place at each clinical encounter.

For anyone who uses tobacco, healthcare providers should provide assistance on readiness to quit, with behavioral and pharmacological interventions. Nicotine replacement therapy is available in patches, gums, lozenges, nasal sprays, and oral inhalers. Other medications, such as bupropion and varenicline, are also used to assist tobacco cessation.

Hypertension management

The current definition of hypertension is systolic blood pressure greater than or equal to 130 mm Hg and diastolic blood pressure greater than or equal to 80 mm Hg. Stage 1 hypertension is defined as systolic BP between 130 and 139 and diastolic blood pressure between 80 and 89. Similarly, stage 2 hypertension is defined as systolic blood pressure greater than or equal to 140 and diastolic blood pressure greater than or equal to 90.

A 10-year ASCVD risk score for blood pressure is used to guide therapy for hypertension management. Initially, nonpharmacological measures with diet and exercise are recommended in the adult with stage 1 hypertension (130 to 139/80 to 89) with a 10-year ASCVD risk under 10%. However, if the 10-year ASCVD risk is over 10% with stage-1 hypertension, pharmacological management along with non-pharmacological measures is the recommended approach. For stage 2 hypertension, the clinician should initiate pharmacological therapy, along with nonpharmacological interventions.

Nonpharmacological interventions include lifestyle modifications such as diet and exercise. A heart-healthy diet, such as the DASH diet pattern, rich in fruits, vegetables, whole grains, and low-fat dairy products with reduced saturated fat, would lower systolic blood pressure by approximately 11 mm Hg. Similarly, reducing dietary sodium by 1000 to 1500 mg/day and increasing dietary potassium to 3500 to 5000 mg/dl by consuming potassium-rich foods can lower systolic blood pressure by approximately 5 points.

Weight loss also lowers blood pressure. A 1 kg reduction in body weight for overweight adults can lower systolic blood pressure by 1 mm Hg. Furthermore, physical activities such as aerobic exercise for 90 to 150 minutes per week and increasing heart rate reserve to 65% to 75% would lower systolic BP by 5 to 8 mmHg.

For those who prefer dynamic resistance training, a weekly total of 90 to 150 minutes of training, consisting of 6 exercises, 3 sets, and 10 repetitions per exercise, would lower systolic blood pressure by approximately 5 to 8 mm Hg. Other forms of exercise, such as isometric resistance (eg, 4 repetitions of 2-minute handgrip with 1-minute rest in between), 30% to 40% of maximum voluntary contraction, and 3 sessions per week for 8 to 10 weeks, would lower systolic blood pressure by approximately 4 mm Hg.

Reducing alcohol consumption also has blood-pressure-lowering effects. Current recommendations are for men to drink no more than two drinks per day and for women to drink no more than one drink per day. This would help lower the systolic BP by approximately 4 mm Hg.

Type 2 Diabetes mellitus 

Type 2 diabetes mellitus is diagnosed when hemoglobin A1c is greater than 6.5%. Type 2 diabetes mellitus is strongly associated with sedentary lifestyle, dietary habits, physical activity, and body weight. Among 12 % of the adults in the United States having diabetes, 90 to 95 % have type 2 diabetes mellitus; this condition is one of the major cardiovascular risk factors.

Initially, dietary modifications to a heart-healthy diet (such as the Mediterranean and DASH diets mentioned above) and physical activity (at least 150 minutes/week of moderate-to-vigorous activity) are encouraged. Additionally, weight loss is recommended for individuals who are overweight or obese. Metformin can also be considered first-line therapy for type 2 diabetes to improve glycemic control and reduce cardiovascular risk. If the HbA1c remains over 7% despite lifestyle modification and metformin, then the addition of sodium-glucose co-transporter 2 inhibitors or glucagon-like peptide-1 agonists can be considered, as they have been shown to reduce ASCVD risk.

Statin use

A moderate-intensity statin is recommended for any patient aged between 40 and 75 years with type 2 diabetes, regardless of cholesterol levels and ASCVD risk. In this age group, for patients with LDL exceeding 190, a high- or maximum-tolerable-intensity statin is recommended. In addition to diabetes and LDL levels, the 10-year ASCVD risk should guide statin use. If the 10-year ASCVD risk is high (>20%), the maximum-tolerated statin should be used to reduce LDL by less than 50%. For intermediate-risk (7.5% to 20%), a moderate-intensity statin is recommended to reduce LDL by 30% or more. Discussion about initiating statin should begin with patients who are at borderline risk (5% to 7.5%), and there are risk-enhancing factors.

Coronary artery calcium (CAC) scoring should be used to further guide decision-making when a 10-year ASCVD risk assessment cannot reach a decision, especially for patients at borderline or intermediate risk. If the CAC score is less than 0 and there are no risk factors, then holding statin therapy is reasonable; if the CAC score is above 100, then starting statin therapy is reasonable. A CAC score of 1 to 99 favors statin use, especially if the patient is aged 55 or older.

For patients aged 20 to 39, the ACC/AHA recommends calculating the lifetime risk of CAD to encourage lifestyle modification. Treatment with a statin should be a consideration if there is a significant family history of premature ASCVD and LDL is greater than or equal to 160. For patients older than 75, discussions between the patient and physician, assessment of risk factors, and consideration of side effects should all be taken into account when initiating or continuing statin therapy.

Aspirin

Aspirin is anti-thrombotic and reduces the risk of cardiovascular disease by irreversibly inhibiting platelet aggregation. However, the use of low-dose aspirin (75 to 100 mg orally) for primary prevention has become more controversial recently. Previous United States guidelines recommended aspirin for primary prevention in the settings of significant ASCVD risk factors.

However, according to the recent ACC/AHA 2019 guidelines, the use of aspirin may be considered in patients 40 to 70 years of age with significant risk factors for cardiovascular disease and no risk of bleeding. The strength of the recommendation is relatively weak, and a thorough evaluation, including a risk-versus-benefit assessment, is necessary. These guidelines for primary prevention should be evaluated on an individual basis, and risk-versus-benefit analyses should always be based on the physician’s best clinical judgment.[5](A1)

Secondary Prevention  

After myocardial infarction, PCI, coronary artery bypass grafting, or a diagnosis of CAD, secondary prevention is a lifelong and intensive process. The main goals are to lower LDL-C, control blood pressure, stop smoking, participate in cardiac rehab, and use proven medications to prevent future events.[25]

The key parts of secondary prevention are:

• Antiplatelet therapy, and dual antiplatelet therapy when needed after acute coronary syndrome or PCI, should be tailored to each patient’s risk of ischemia and bleeding.[24][25]
• Start with high-intensity lipid-lowering therapy and add nonstatin medications as needed to reach LDL-C targets and reduce the risk of future events.[24][27][28]
• Optimize blood pressure and use inhibitors or angiotensin II receptor blockers in patients with conditions such as diabetes, chronic kidney disease, or left ventricular dysfunction.[24]
• Encourage cardiac rehabilitation and structured lifestyle changes to help patients improve function, adhere to treatment, and achieve better long-term outcomes.[24][26]
• Focus on optimizing cardiometabolic health and, when appropriate, use diabetes treatments that also benefit the heart.[30]
(A1)

A large part of secondary prevention also includes pharmacological therapy. In contrast to primary prevention, anti-thrombotic therapy (low-dose aspirin) is strongly recommended unless contraindicated. The daily strength of 75 mg of clopidogrel is recommended for people who are intolerant or allergic to aspirin.

Blood pressure should be lowered in all patients with coronary artery disease and stage 1 hypertension using both nonpharmacological and pharmacological therapies. Metformin remains the first-line therapy in diabetic patients for secondary prevention. A high-intensity or maximally tolerated statin is part of secondary prevention, independent of lipid levels, as long as the patient can tolerate it; the goal is to achieve an LDL of less than 70.[31](A1)

Differential Diagnosis

When evaluating chest pain, consider the patient’s symptoms, related features, and cardiovascular risk factors. Although CAD is a major concern, other cardiac and noncardiac conditions can mimic myocardial ischemia and should be evaluated early.[32]

Cardiac Causes

• Acute coronary syndromes, including myocardial infarction and ischemia with non-obstructive coronary arteries 
• Coronary vasospasm and microvascular dysfunction
• Spontaneous coronary artery dissection, particularly in younger patients and women
• Myocarditis or pericarditis
• Acute aortic syndromes and arrhythmias 

Noncardiac Causes

• Pulmonary embolism, pneumonia, pleuritis, or pneumothorax
• Gastroesophageal reflux disease, esophageal spasm, or biliary disease
• Musculoskeletal chest wall pain, cervical radiculopathy, or intercostal neuralgia
• Anxiety and panic disorders 

A thorough history and physical exam help distinguish these conditions. Details like pain type, triggers, other symptoms, and risk factors help guide the right tests. Rapidly considering serious cardiac and non-cardiac causes is key to prompt treatment.

Prognosis

The outlook for CAD can vary widely from person to person and depends on the extent of atherosclerosis, other health conditions, the stage of the disease, and adherence to treatment plans. Thanks to advances in medicine, improved procedures to restore blood flow, and better prevention, age-adjusted death rates have decreased in wealthier countries. Still, CAD often leads to long-term health problems and can be fatal, especially due to repeated heart attacks, heart failure, and irregular heartbeats.

The risk is even higher for people with diabetes, chronic kidney disease, or blockages in several blood vessels. Even with the best cholesterol-lowering and recommended treatments, many patients still face ongoing risks for heart problems. Ongoing inflammation, metabolic problems, and unstable plaques in the arteries are common causes. Social factors matter too. People with less access to healthcare, late diagnoses, or trouble managing risk factors often have worse outcomes. Identifying high-risk individuals early, carefully managing risk factors, and following prevention strategies are all important for improving long-term health and reducing the risk of future heart problems.[2][4]

Complications

CAD can cause ongoing problems with blood flow to the heart, sudden plaque changes, and changes in the heart’s structure or electrical system. The most serious problems are acute coronary syndromes, such as ST-elevation and non-ST-elevation myocardial infarction. These can lead to high rates of illness and death, both soon after and long after they happen.

People with diabetes, chronic kidney disease, or poorly managed risk factors often have repeated episodes of reduced blood flow. Heart failure is a long-term result of CAD; this happens when the heart is repeatedly insulted over time, changes shape, and slowly loses its ability to pump effectively. CAD is still the main cause of heart failure with reduced ejection fraction, which leads to many hospital stays and deaths.

Arrhythmias, such as atrial fibrillation and ventricular tachyarrhythmias, can also occur due to poor blood flow or heart scarring. These raise the risk of sudden cardiac death. After a heart attack, other issues can develop, such as damage to the heart’s muscles or valves, holes in the heart wall, or bulges in the left ventricle. In severe cases, these problems can cause cardiogenic shock. CAD is also linked to atherosclerosis in other parts of the body, which increases the risk of stroke, peripheral artery disease, and repeated blood clots. Finding CAD early, preventing more problems, and following treatment guidelines over time are important for lowering these risks.[4][33]