What Is Coronary Artery Disease and How Does It Develop?
Coronary artery disease develops when cholesterol-rich plaque accumulates inside coronary arteries over decades, progressively narrowing them and reducing blood flow to the heart muscle. This process, called atherosclerosis, begins in childhood and accelerates with age and risk factors like high cholesterol, smoking, and diabetes.
Your heart muscle requires constant oxygen delivery to function, supplied by the coronary arteries—small blood vessels on the heart's surface. Coronary artery disease develops through atherosclerosis, a chronic inflammatory process where cholesterol, fats, calcium, and other substances accumulate in artery walls, forming plaque. This process begins with damage to the inner arterial lining (endothelium) from high blood pressure, smoking, high cholesterol, diabetes, or inflammation. Once damaged, LDL cholesterol particles infiltrate the artery wall. White blood cells migrate to the area, engulf cholesterol, and become foam cells that die and release their contents, forming a growing plaque with a cholesterol-rich core covered by a fibrous cap.
As plaque grows, it narrows the artery opening (stenosis), reducing blood flow. When an artery is narrowed by 50-70%, blood flow is usually adequate at rest but cannot meet increased demands during exertion, causing angina. Severe narrowing (70-90% blockage) may cause symptoms with minimal activity or even at rest. The most dangerous scenario is acute plaque rupture—the fibrous cap cracks, exposing the cholesterol core to blood. This triggers rapid blood clot formation that can completely block the artery within minutes, cutting off all blood flow and causing a heart attack. Surprisingly, heart attacks often result from plaques causing only 40-50% narrowing (not visibly 'severe') that rupture unexpectedly. This is why stabilizing plaques and preventing rupture through medications like statins and aspirin is so important.
What Are the Symptoms of Coronary Artery Disease?
The main symptom is angina—chest discomfort or pressure typically triggered by exertion and relieved by rest. Other symptoms include shortness of breath, fatigue, and in severe cases, heart attack. However, many people have no symptoms ('silent ischemia') until a heart attack occurs.
Stable angina is the classic symptom of CAD—predictable chest discomfort triggered by physical exertion, emotional stress, cold weather, or heavy meals, improving with rest or nitroglycerin within 5-10 minutes. It typically feels like pressure, squeezing, heaviness, or tightness in the center or left chest, often radiating to the left arm, shoulders, neck, jaw, or back. The Canadian Cardiovascular Society grades angina severity: Class I (angina only with strenuous exertion), Class II (slight limitation—angina with normal activities like climbing stairs or walking uphill), Class III (marked limitation—angina with mild exertion like walking one to two blocks), and Class IV (inability to perform any activity without angina, or angina at rest).
Other symptoms of CAD include shortness of breath (dyspnea) with exertion or sometimes at rest, often accompanying or replacing angina; unusual fatigue, particularly in women; and palpitations or irregular heartbeat. Some people experience atypical symptoms, especially women, people with diabetes, and older adults. These may include upper abdominal discomfort, nausea, back pain, or jaw pain. Silent ischemia (reduced blood flow without symptoms) occurs in about 20-30% of people with CAD, particularly those with diabetes. These individuals may have their first symptom be a heart attack. Unstable angina—chest pain at rest, new-onset severe angina, or rapidly worsening angina—is a medical emergency signaling that a heart attack is imminent and requires immediate hospitalization.
What Are the Risk Factors and Causes of CAD?
Major risk factors include high LDL cholesterol, high blood pressure, smoking, diabetes, obesity, physical inactivity, unhealthy diet, and family history of premature heart disease. Most risk factors are modifiable through lifestyle changes and medications. Age, male sex, and genetics are non-modifiable.
Modifiable risk factors that accelerate atherosclerosis include: High LDL cholesterol deposits in artery walls, while low HDL cholesterol means less cholesterol is removed—optimal levels dramatically reduce CAD risk. High blood pressure damages artery linings and accelerates plaque formation. Cigarette smoking directly damages blood vessel walls, reduces oxygen delivery, promotes blood clotting, and lowers HDL—smokers have 2-4 times the CAD risk of non-smokers. Diabetes dramatically accelerates atherosclerosis through multiple mechanisms including glycation of proteins, oxidative stress, and inflammation. Obesity, especially abdominal obesity, promotes insulin resistance, inflammation, high blood pressure, and abnormal cholesterol. Physical inactivity increases all cardiovascular risk factors. Unhealthy diet high in saturated fats, trans fats, refined carbohydrates, and low in fruits, vegetables, and whole grains promotes CAD.
Non-modifiable risk factors include: Age—atherosclerosis is a progressive disease accumulating over decades; men develop CAD earlier than women (risk increases at age 45 for men, 55 for women), though women's risk accelerates after menopause; family history of premature CAD (heart attack before age 55 in father or brother, before age 65 in mother or sister) indicates genetic susceptibility. Additional risk factors include chronic inflammation (measured by high-sensitivity C-reactive protein), chronic kidney disease, sleep apnea, excessive alcohol consumption, and chronic stress. Certain autoimmune conditions like rheumatoid arthritis and lupus also increase CAD risk. Having metabolic syndrome (combination of abdominal obesity, high blood pressure, high blood sugar, high triglycerides, and low HDL) substantially increases risk. Understanding your personal risk profile helps guide prevention and treatment strategies.
How Is Coronary Artery Disease Diagnosed?
Diagnosis involves medical history, physical exam, and tests including electrocardiogram, stress testing, echocardiogram, coronary CT angiography, and coronary angiography (cardiac catheterization). These tests determine if CAD is present, how severe it is, and guide treatment decisions.
Initial evaluation includes detailed medical history about symptoms, risk factors, and family history, plus physical examination checking blood pressure, heart sounds for murmurs, peripheral pulses, and signs of atherosclerosis elsewhere. Baseline tests include: Electrocardiogram (ECG) detects rhythm abnormalities, evidence of prior heart attack, or heart muscle strain. Blood tests measure cholesterol levels, blood sugar (diabetes screening), kidney function, and sometimes inflammatory markers like hs-CRP or lipoprotein(a). Chest X-ray checks heart size and lung condition. These tests establish baseline cardiovascular health and guide further testing.
Stress testing evaluates how your heart responds to increased demand: Exercise stress test monitors ECG and symptoms while you walk on a treadmill or pedal a bike at increasing intensity—abnormal ECG changes or symptoms suggest CAD. Stress echocardiography uses ultrasound before and immediately after exercise to detect wall motion abnormalities indicating reduced blood flow. Nuclear stress testing (SPECT or PET scan) uses radioactive tracers to image blood flow to heart muscle during stress and rest—areas with reduced flow indicate blockages. For people who can't exercise, pharmacologic stress testing uses medications (dobutamine, adenosine, or regadenoson) to simulate exercise effects. Coronary CT angiography (CCTA) is a non-invasive test where IV contrast dye is injected and CT scanning creates detailed images of coronary arteries—it can detect blockages and assess plaque composition. Coronary calcium score CT measures calcium in coronary arteries, providing risk assessment. Coronary angiography (cardiac catheterization) is the gold standard where catheters are threaded through arteries to the heart, contrast dye is injected, and X-rays show exact blockage location and severity—it's both diagnostic and therapeutic (stents can be placed during the same procedure).
What Medications Treat Coronary Artery Disease?
Key medications include statins to lower cholesterol and stabilize plaque, aspirin or other antiplatelet agents to prevent blood clots, beta-blockers and ACE inhibitors to reduce heart workload, and nitrates to relieve angina. Most CAD patients need multiple medications for optimal protection.
Statins (atorvastatin, rosuvastatin, simvastatin) are cornerstone therapy that lower LDL cholesterol by 30-50%, stabilize atherosclerotic plaques, reduce inflammation, and decrease heart attack and death risk by 25-35%. Most people with CAD should take high-intensity statins to lower LDL below 70 mg/dL (or even below 55 mg/dL for very high-risk patients). Antiplatelet agents prevent blood clots from forming on plaques: Aspirin (75-325 mg daily) reduces heart attack risk by about 25% in people with CAD. Clopidogrel (Plavix), prasugrel, or ticagrelor are more potent alternatives, particularly after stent placement. Dual antiplatelet therapy (aspirin plus a second agent) is standard for 6-12 months after stent placement, then usually aspirin alone continues indefinitely.
Additional medications that improve outcomes include: Beta-blockers (metoprolol, carvedilol, atenolol) slow heart rate, reduce blood pressure, decrease the heart's oxygen demand, and improve survival after heart attack—they reduce death by 20-25% in CAD patients. ACE inhibitors (lisinopril, enalapril) or ARBs (losartan, valsartan) lower blood pressure, protect blood vessels, and reduce cardiovascular events, especially if you have heart failure, diabetes, or high blood pressure. Nitrates (nitroglycerin, isosorbide) dilate coronary arteries and relieve angina—short-acting nitroglycerin treats acute angina, while long-acting forms prevent angina. Ranolazine is an anti-anginal medication that works differently than nitrates and can be added if angina persists despite other treatments. Newer medications like PCSK9 inhibitors (evolocumab, alirocumab) dramatically lower LDL cholesterol and are used in very high-risk patients or those with familial hypercholesterolemia. Adherence to medications is crucial—studies show only about 50% of patients take all prescribed cardiovascular medications consistently, missing major opportunities to prevent heart attacks.
When Are Stents or Bypass Surgery Needed?
Percutaneous coronary intervention (PCI/stenting) or coronary artery bypass grafting (CABG) are recommended for severe symptoms limiting daily life, high-risk anatomy on angiography, or acute heart attack. For stable CAD, medications and lifestyle changes are often tried first unless anatomy is very high-risk.
Percutaneous coronary intervention (PCI), commonly called angioplasty or stenting, involves threading a catheter to the blocked artery, inflating a balloon to compress plaque, and placing a metal mesh tube (stent) to keep the artery open. Modern drug-eluting stents release medication to prevent re-narrowing (restenosis). PCI is performed during cardiac catheterization and requires only local anesthesia and small groin or wrist incisions. Hospital stay is typically 1-2 days. PCI is clearly beneficial for heart attacks (restores blood flow immediately) and relieves angina effectively in most people. However, for stable CAD, the COURAGE trial showed PCI plus medications is not superior to medications alone for preventing heart attack or death—it's primarily used when symptoms limit quality of life despite medications.
Coronary artery bypass grafting (CABG) is open-heart surgery where blocked arteries are bypassed using blood vessels taken from the chest (internal mammary artery), leg (saphenous vein), or arm (radial artery). These grafts create new pathways for blood to flow around blockages. CABG requires general anesthesia, sternotomy (chest opening), heart-lung machine support (usually), and 5-7 day hospital stay with 6-12 week recovery. CABG is generally preferred over PCI for: left main coronary artery disease, severe three-vessel disease (especially with diabetes), complex anatomy with multiple blockages, or reduced heart function. Studies show CABG provides better long-term outcomes than PCI for complex disease, particularly in diabetic patients. However, CABG has higher upfront risk (stroke, infection, bleeding) while PCI has higher re-intervention rates. The choice between PCI, CABG, or continued medical therapy depends on anatomy, symptoms, other medical conditions, and patient preferences—a heart team including interventional cardiologists and cardiac surgeons reviews complex cases to recommend the best approach.
