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Coronary Artery Disease (CAD)

16 min read

Background #

Coronary Artery Disease (CAD) refers to the narrowing or blockage of coronary arteries due to atherosclerosis, resulting in reduced blood flow to the myocardium. This ischemia may lead to angina, myocardial infarction, heart failure, or sudden cardiac death.

CAD is also known as ischemic heart disease (IHD) or atherosclerotic heart disease.

Classification/Types

Coronary Artery Disease (CAD) is categorized into:

Stable Angina (Angina Pectoris): Predictable chest pain with exertion, relieved by rest or nitroglycerin.

Acute Coronary Syndromes (ACS):

I) Unstable Angina (UA): New or worsening chest pain, not relieved by rest.

II) Non-ST-Elevation Myocardial Infarction (NSTEMI): Chest pain at rest with elevated cardiac enzymes and no ST elevation.

III) ST-Elevation Myocardial Infarction (STEMI): Chest pain at rest with elevated cardiac enzymes and ST elevation.

Epidemiology

  • Sex: CAD is more common in men until women reach menopause, then risk equalizes
  • Age: Typically >45 years in men, >55 years in women
  • Race/Region: Higher in South Asians, African Americans; more prevalent in developed countries
  • Socioeconomic status: Increased in low SES due to risk factor clustering

Despite advances in prevention and treatment, CAD remains the leading cause of death globally and in the United States. [1][2] In 2021, coronary heart disease was the leading cause of deaths (40.3%) attributable to cardiovascular disease in the United States, followed by stroke (17.5%), other CVD (17.1%), high blood pressure (13.4%), heart failure (9.1%), and diseases of the arteries (2.6%). CHD caused 375,476 deaths in 2021. [3] In 2023, 919,032 people died from cardiovascular disease in the United States, representing 1 in every 3 deaths. [4]

Pathophysiology

Coronary Artery Disease (CAD) is an inflammatory disease characterized by atherosclerotic plaque formation in the coronary arteries. [5][6] The pathophysiology involves a complex interaction of endothelial dysfunction, lipid accumulation, inflammation, and thrombosis. [7][8]

The process begins with endothelial dysfunction, characterized by impaired nitric oxide production and increased permeability to lipoproteins. [9][10] Endothelial dysfunction is an early marker of atherosclerosis and serves as an integrated index of all atherogenic and atheroprotective factors. [11] This leads to accumulation of LDL cholesterol in the arterial intima, triggering inflammation and recruitment of monocytes and T lymphocytes. [12] Monocytes differentiate into macrophages, which engulf oxidized LDL to become foam cells, forming fatty streaks that progress to atherosclerotic plaques. [13]

Mature plaques consist of a lipid-rich necrotic core covered by a fibrous cap. Vulnerable plaques prone to rupture have thin, highly inflamed, and collagen-poor fibrous caps. These plaques contain elevated levels of matrix metalloproteinases (MMPs) secreted by macrophages, which degrade extracellular matrix components and weaken the fibrous cap, predisposing it to rupture. [14][15][16]

Acute Coronary Syndromes occur primarily through plaque rupture (60-80% of cases), which exposes thrombogenic material and activates the coagulation cascade. [17] The resulting thrombus can cause unstable angina (transient ischemia), NSTEMI (partial occlusion), or STEMI (complete occlusion). Alternative mechanisms include plaque erosion, which accounts for approximately 25-40% of acute coronary syndromes and is more common in younger patients, particularly women. Plaque erosion involves endothelial denudation without fibrous cap rupture and is characterized by less inflammation and disturbed flow. [18][19][20]

Etiology #

Coronary Artery Disease is caused by atherosclerosis of the coronary arteries due to endothelial injury and lipid deposition leading to plaque formation and vascular narrowing.

Risk Factors

I) Modifiable:

  • Hypertension
  • Diabetes mellitus (DM)
  • Hyperlipidemia
  • Smoking
  • Obesity
  • Sedentary lifestyle, poor diet, stress

II) Non-modifiable:

  • Age (men above age 45, women above age 55)
  • Sex (males)
  • Family history of premature CAD (men less than 55 years, women more than 65 years of age)
  • Others: Chronic inflammatory states (e.g., lupus), chronic kidney disease

Clinical Presentation #

I) History (Symptoms)

Stable Angina (Angina Pectoris): Exertional chest pain (pressure-like), relieved by rest or nitroglycerin

Acute Coronary Syndrome (ACS):

  • Chest pain at rest or with minimal exertion
  • Radiation to left arm, jaw, or back
  • Associated symptoms: dyspnea, diaphoresis, nausea, dizziness, palpitations

Note: Women, older adults, and patients with diabetes are more likely to present with atypical symptoms, including dyspnea, fatigue, nausea, or epigastric pain rather than classic chest pain.

II) Physical Exam (Signs)

Coronary artery disease (CAD) may not always have specific physical exam findings, especially in stable or early stages. However, certain signs can suggest CAD itself, its risk factors, or complications such as heart failure or prior myocardial infarction.

General Appearance

  • Anxious, diaphoretic during angina
  • Pale or cool skin in acute ischemia

Vital Signs

  • Hypertension or hypotension (esp. in MI)
  • Tachycardia or bradycardia
  • Low-grade fever post-MI
  • Narrow pulse pressure (LV dysfunction)

Cardiac Exam

  • Inspection: Levine sign, JVD in heart failure
  • Palpation: Displaced point of maximal impulse (PMI), heaves/thrills
  • Auscultation:
    • S4: Stiff ventricle (e.g., in chronic HTN, HFpEF)
    • S3: Volume overload (e.g., in HFrEF)
    • New murmur (e.g., MR)
    • Pericardial rub (pericarditis)
    • Diminished heart sounds (pericardial effusion, severe LV failure)

Pulmonary

  • Crackles/rales (pulmonary congestion)
  • Wheezing (cardiac asthma)
  • Dullness/decreased breath sounds (effusion)

Peripheral Vascular

  • Diminished pulses, carotid/femoral bruits
  • Peripheral edema
  • Cool extremities

Skin & Extremities

  • Xanthelasma/xanthomas (hyperlipidemia)
  • Cyanosis, mottling (low cardiac output)

Differential Diagnosis #

Cardiac Causes

  • Acute pericarditis
  • Myocarditis
  • Aortic dissection
  • Aortic stenosis
  • Hypertrophic cardiomyopathy
  • Takotsubo cardiomyopathy (stress-induced cardiomyopathy)
  • Cardiac arrhythmias

Pulmonary Causes

  • Pulmonary embolism
  • Pneumothorax
  • Pneumonia
  • Pleuritis
  • Pulmonary hypertension

Gastrointestinal Causes

  • Gastroesophageal reflux disease (GERD)
  • Esophageal spasm
  • Peptic ulcer disease
  • Cholecystitis
  • Pancreatitis
  • Esophageal rupture (Boerhaave syndrome)

Musculoskeletal Causes

  • Costochondritis
  • Chest wall trauma/rib fracture
  • Muscle strain
  • Herpes zoster (shingles)

Psychiatric Causes

  • Panic disorder/anxiety attack
  • Somatization disorder

Diagnostic Testing #

Initial Tests

I) Electrocardiogram (ECG)

Best initial test for chest pain (look for ST changes, arrhythmias).

ECG in Different CAD Presentations:

A) Stable Angina

  • Normal at rest
  • May show:
    • Non-specific ST-T changes
    • LVH, prior MI evidence (Q waves)
  • Exercise Stress Testing is used to detect ischemia

B) Unstable Angina (UA) / NSTEMI

  • ST-segment depression
  • T-wave inversion
  • No ST elevation
  • Cardiac enzymes (CK-MB, troponins) help differentiate UA (normal troponins) from NSTEMI (elevated troponin)

C) ST-Elevation Myocardial Infarction (STEMI)

  • Persistent ST-segment elevation in two or more contiguous leads
  • Q waves (develop later) = transmural infarction
  • Indicates complete coronary artery occlusion → emergent reperfusion needed

Localizing MI with EKG

MI LocationEKG LeadsArtery Involved
AnteriorV1–V4Left Anterior Descending (LAD)
LateralI, aVL, V5, V6Left Circumflex (LCx) or diagonal
InferiorII, III, aVFRight Coronary Artery (RCA) or LCx
PosteriorV7–V9 (optional leads)RCA or LCx
Right VentricularV4R (right-sided lead)Proximal RCA

II) Cardiac Enzymes (High-Sensitivity Troponins, CK-MB)

Cardiac biomarkers are essential for diagnosing myocardial infarction when a patient presents with acute chest pain. High-sensitivity cardiac troponin (hs-cTn) assays are now the preferred biomarker. To be classified as a high-sensitivity troponin assay, it must meet two analytical criteria: (1) have a total imprecision (CV) of ≤10% at the sex-specific 99th-percentile levels, and (2) detect troponin concentrations above the assay’s limit of detection (LoD) in at least 50% of healthy individuals for both men and women. [21][22]

Key Cardiac Biomarkers

BiomarkerRise TimePeak TimeReturn to NormalSource
High-Sensitivity Troponin I/T1–3 hrs12–24 hrs7–14 daysCardiac myocytes (highly specific)
CK-MB3–6 hrs12–24 hrs2–3 daysCardiac + skeletal muscle
Myoglobin1–2 hrs6–9 hrs24 hrsNonspecific (muscle)

A) High-Sensitivity Troponins (I & T)

Gold standard for detecting myocardial injury with superior sensitivity and specificity for cardiac muscle necrosis. High-sensitivity cardiac troponin is recognized as the preferred biomarker in the 2021 AHA/ACC guidelines, with endorsement of 99th percentile upper reference limits to define myocardial injury and the use of clinical decision pathways. [23][24] Elevated in NSTEMI and STEMI, but not in unstable angina. Serial measurements (typically at 0, 1, and 3 hours using rapid algorithms) help confirm rising or falling levels, which is key to diagnosing acute MI.

B) CK-MB

Less specific than troponin; elevated in skeletal muscle injury. Preferred to detect reinfarction (second MI within days), as it returns to baseline quicker than troponin.

C) Myoglobin

Very early marker; rises before troponin. Not specific for cardiac tissue → mostly used to rule out MI early due to its rapid normalization.

III) Stress Testing

Stress testing, in stable patients, identifies who may benefit from further testing or revascularization. The types of stress testing are exercise stress testing (EST), stress echocardiography, and nuclear stress test.

A) Exercise Stress Test is best for patients with normal resting ECG, low to intermediate pretest probability, and ability to exercise.

B) Stress Echocardiography combines exercise or pharmacologic stress with echocardiography. It detects new wall motion abnormalities during stress (suggesting ischemia), using dobutamine (increases HR and contractility). Stress echo is useful for patients unable to exercise or those with abnormal baseline ECG.

C) Nuclear Stress Test (Myocardial Perfusion Imaging) uses radioactive tracers (e.g., technetium-99m, thallium-201) to assess blood flow at rest and stress. Perfusion defects suggest ischemia or infarction. Pharmacologic agents used are: adenosine, regadenoson, dipyridamole (vasodilators). It is useful in baseline ECG abnormalities (e.g., LBBB, LVH) or inability to exercise.

IV) Coronary Angiography

Provides definitive diagnostic evaluation for CAD. Also called cardiac catheterization, coronary angiography is an invasive diagnostic procedure used to visualize the coronary arteries, evaluate the degree of stenosis, and guide management of suspected or known CAD, when diagnosis is unclear after noninvasive testing (equivocal stress test) or when urgent revascularization is needed.

Therapeutically, it provides Percutaneous Coronary Intervention (PCI) (e.g., stenting), Balloon Angioplasty, and assessment for Coronary Artery Bypass Grafting (CABG). The 2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes recommends the radial artery approach over the femoral approach to reduce the risk of bleeding, vascular complications, and death. Intravascular imaging to guide the PCI procedure is now a Class 1, Level of Evidence A recommendation. [25][26]

Additional Testing

  • Complete blood count (CBC)
  • Comprehensive metabolic panel (CMP)
  • Lipid panel
  • Chest X-ray (to rule out alternative causes of chest pain)
  • ABG if hypoxic
  • BNP (if heart failure suspected)
  • Type and crossmatch (in case of cath/blood loss)
  • Coagulation panel (PT, INR) [before anticoagulation or surgery]
  • Urine drug screen (if young or unclear etiology)

Treatment #

I) Stabilize if Unstable (ACS):

  • ABC approach
  • Oxygen (if hypoxic, O₂ <90%), IV access
  • Telemetry and cardiac monitoring
  • Aspirin 162-325 mg PO chewed (loading dose) [25]
  • Nitroglycerin (unless hypotensive or inferior/right ventricular MI)
  • Morphine (if pain persists despite nitroglycerin)
  • Beta-blockers (if no contraindications)
  • Heparin/enoxaparin
  • P2Y12 inhibitors (ticagrelor or prasugrel preferred over clopidogrel) [26][27]
  • High-intensity statin
  • Move to ICU or cath lab
  • Radial artery approach preferred for PCI [25]
  • Intravascular imaging to guide PCI (Class 1 recommendation) [26]
  • Cardiology consult for possible complete revascularization [27]
  • Cardiac rehabilitation referral before discharge (Class 1 recommendation) [28][29]

II) If Stable:

  • Lifestyle modification
  • Aspirin (75-162 mg maintenance dose for secondary prevention) + statin + beta-blocker (if indicated) + ACEi/ARB (if hypertensive or diabetic) [30][31]
  • Antianginals: nitrates, calcium channel blockers (for vasospasm or refractory angina)
  • Risk factor control: glucose, lipids, smoking cessation
  • Consider stress testing and elective angiography
  • Cardiac rehabilitation enrollment (Class 1 recommendation) [28][29]

Consults #

  • Cardiologist: All ACS, refractory or high-risk stable angina
  • Nutritionist: Heart-healthy diet planning (e.g., DASH or Mediterranean diet)
  • Social Worker: For medication access, transportation, insurance, substance use support
  • Cardiac Rehabilitation Team: All post-ACS and post-revascularization patients [28][29]

Patient Education #

Counseling:

Smoking Cessation: Clinicians should ask all adults about tobacco use, advise them to stop using tobacco, and provide behavioral interventions and FDA-approved pharmacotherapy for cessation to nonpregnant adults who use tobacco (USPSTF Grade A recommendation). For pregnant persons, clinicians should ask about tobacco use, advise them to stop, and provide behavioral interventions for cessation (USPSTF Grade A recommendation). [32]

Diet: Behavioral counseling interventions for promoting a healthy diet have a small net benefit on CVD risk. The USPSTF recommends offering or referring adults with cardiovascular disease risk factors to behavioral counseling interventions to promote a healthy diet and physical activity (USPSTF Grade B recommendation). [33] Recommended dietary patterns include low saturated fats, DASH or Mediterranean diet.

Exercise: Behavioral counseling interventions for physical activity in adults without CVD risk factors increased physical activity by approximately 33 minutes per week (USPSTF). [33] Recommendation: 30 min/day, 5x/week (as tolerated and per cardiac rehab recommendations).

Cardiac Rehabilitation: The 2024 AHA Scientific Statement updated the core components of cardiac rehabilitation programs to include: patient assessment, nutritional counseling, weight management and body composition, cardiovascular disease and risk factor management, psychosocial management, aerobic exercise training, strength training, physical activity counseling, and program quality. Referral to outpatient cardiac rehabilitation prior to hospital discharge is a Class 1 recommendation to reduce death, myocardial infarction, and hospital readmissions and to improve functional status and quality of life. [29]

Medication Adherence: Emphasize the importance of adherence to prescribed medications for secondary prevention.

Screening:

Lipid Panel: Screen adults aged 40 to 75 years for lipid disorders and assess cardiovascular disease (CVD) risk. Offer statin therapy for primary prevention based on calculated 10-year CVD risk (USPSTF Grade B recommendation for risk ≥10%).

Blood Pressure: Screen all adults aged 18 years or older for high blood pressure with office blood pressure measurement. Confirm the diagnosis with ambulatory or home blood pressure monitoring (USPSTF Grade A recommendation).

HbA1c (Diabetes Screening): Screen for prediabetes and type 2 diabetes in adults aged 35 to 70 years who have overweight or obesity. Offer or refer patients with prediabetes to effective preventive interventions (USPSTF Grade B recommendation).

Aspirin for Primary Prevention: The USPSTF concludes that aspirin use for the primary prevention of CVD events in adults aged 40 to 59 years who have a 10% or greater 10-year CVD risk has a small net benefit. The decision to initiate low-dose aspirin should be an individual one (USPSTF Grade C recommendation). The USPSTF recommends against initiating low-dose aspirin use for the primary prevention of CVD in adults 60 years or older (USPSTF Grade D recommendation). [34] Important Note: This recommendation does NOT apply to patients with a prior history of heart attack, stroke, bypass surgery, or recent stent procedure. Low-dose aspirin continues to be recommended for secondary prevention in patients with established ASCVD.

Vaccinations:

The 2025 Adult Immunization Schedule provides updated recommendations: [35]

Influenza: Annual influenza vaccination is recommended for all persons aged ≥6 months. High-dose inactivated (HD-IIV3) and adjuvanted inactivated (aIIV3) influenza vaccines are preferentially recommended for persons aged ≥65 years.

Pneumococcal: Pneumococcal vaccination is recommended for all adults aged ≥65 years. Adults aged 19-64 years with certain medical conditions (including heart disease, diabetes, chronic lung disease, immunocompromising conditions) should also receive pneumococcal vaccination. Recommended vaccines include PCV15, PCV20, or PCV21 followed by PPSV23 (if PCV15 is used), or PCV20 or PCV21 alone.

Tdap: One-time dose of Tdap for all adults who have not previously received it, followed by Td or Tdap booster every 10 years.

COVID-19: Stay up to date with COVID-19 vaccination per current CDC recommendations.

Follow-Up #

  • Cardiology and primary care follow-up in 1 week (post-discharge)
  • Monitor BP, lipid panel, renal function, treatment adherence
  • Cardiac rehabilitation referral and enrollment (improves mortality, reduces MI and hospital readmissions) [28][29]
  • Long-term secondary prevention management per the 2023 AHA/ACC/ACCP/ASPC/NLA/PCNA Guideline for the Management of Patients With Chronic Coronary Disease [31]

References #

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Updated on December 10, 2025