Heart disease kills more people globally than any other cause — nearly 18 million deaths annually according to the World Health Organization. In the United States alone, someone has a heart attack every 40 seconds, and heart disease claims one in every five deaths. Yet here’s the remarkable fact that gets lost in these grim statistics: most heart disease is preventable.

Heart disease refers to several conditions affecting the heart itself, with coronary artery disease (CAD)—the buildup of atherosclerotic plaque in the arteries supplying the heart—being the most common and deadly type. When coronary arteries become severely narrowed or blocked, the result is angina (chest pain), and when a blockage is complete, a heart attack occurs, potentially causing permanent heart damage or death.

This article focuses on heart disease — conditions directly affecting your heart. While related cardiovascular conditions like stroke and peripheral artery disease share similar causes and risk factors (covered in our separate Cardiovascular Disease guide), we’ll concentrate here on understanding, detecting, and preventing the conditions that threaten your heart specifically.

What makes heart disease particularly insidious is its decades-long silent development. Arterial damage begins in early adulthood, progressing invisibly for 20, 30, even 40 years before symptoms appear. A routine blood test showing elevated cholesterol at age 35 isn’t just a number — it’s a window into a process that’s already underway and will, if left unaddressed, culminate in a heart attack at age 55. The liver enzymes, blood pressure readings, fasting glucose levels, and inflammatory markers your doctor measures aren’t abstract data points; they’re real-time indicators of whether your coronary arteries are aging normally or racing toward catastrophic failure.

Understanding heart disease — what actually happens in your coronary arteries, which risk factors matter most, how to detect problems before symptoms appear, and most importantly, how to prevent or reverse arterial damage through targeted interventions—provides the knowledge foundation for avoiding what remains, despite being largely preventable, the leading cause of premature death worldwide.

Quick Summary:

• Heart disease is the #1 cause of death in the United States killing 695,000 Americans annually
• Most heart disease is preventable through lifestyle changes and management of risk factors
• Primary type: Coronary artery disease (CAD)—plaque buildup in coronary arteries supplying the heart
• Major complications: Angina (chest pain), heart attack, heart failure, arrhythmias
• Underlying mechanism: Atherosclerosis developing over decades in coronary arteries
• Key risk factors: High LDL cholesterol, high blood pressure, diabetes, smoking, obesity, physical inactivity
• Often asymptomatic until serious event occurs (angina or heart attack)
• Early detection crucial: Blood tests reveal risk factors decades before symptoms
• Comprehensive testing includes: Lipid panel (LDL, HDL, triglycerides), blood pressure, glucose/HbA1c, CRP
• Prevention works: Mediterranean diet reduces cardiac events by 30%, statins by 25-35%, exercise by 30-40%
• Strong metabolic links: Insulin resistance, metabolic syndrome, obesity, and diabetes dramatically increase heart disease risk

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What Is Heart Disease?

Heart disease encompasses various conditions affecting the heart’s structure and function. While the broader term “cardiovascular disease” includes conditions affecting blood vessels throughout the body (such as stroke and peripheral artery disease), heart disease specifically refers to problems with the heart itself.

The most common and deadly form is coronary artery disease (CAD), but heart disease also includes heart rhythm problems, heart muscle disorders, and valve abnormalities. Understanding these different types helps clarify your specific risks and appropriate prevention strategies.

Note: This article focuses specifically on heart disease — conditions affecting your heart. For comprehensive information about cardiovascular diseases affecting blood vessels throughout your body, including stroke and peripheral artery disease, see our complete [Cardiovascular Disease Guide] (coming soon).

Types of Heart Disease

Coronary Artery Disease (CAD):

The most common form of heart disease, affecting the arteries supplying blood to the heart muscle. Atherosclerotic plaque narrows these coronary arteries, reducing blood flow to the heart. When severe, this causes chest pain (angina) during exertion. When a plaque ruptures and forms a blood clot, it completely blocks blood flow, causing a heart attack.

CAD develops silently over decades, with most people having no symptoms until a significant blockage develops or a heart attack occurs. This is why it’s often called a “silent killer.”

Heart Attack (Myocardial Infarction):

Occurs when blood flow to part of the heart muscle is blocked completely, typically by a blood clot forming at the site of a ruptured atherosclerotic plaque. Without oxygen, heart muscle cells begin dying within minutes. The extent of damage depends on how quickly blood flow is restored—every minute counts.

Symptoms include chest pressure or pain, shortness of breath, cold sweat, nausea, and pain radiating to the arm, jaw, or back. However, some heart attacks present with minimal symptoms, particularly in women and people with diabetes.

Heart Failure:

A condition where the heart cannot pump blood effectively to meet the body’s needs. This doesn’t mean the heart has “stopped”—rather, it’s weakened and functioning inefficiently. Heart failure typically develops gradually as a consequence of longstanding high blood pressure, coronary artery disease causing heart attacks that damage heart muscle, or heart valve problems.

Symptoms include shortness of breath, fatigue, leg swelling, and reduced exercise capacity. Heart failure is often the end stage of untreated heart disease.

Arrhythmias:

Abnormal heart rhythms, ranging from benign to life-threatening. Atrial fibrillation, the most common arrhythmia, increases stroke risk fivefold due to blood clot formation in the heart. While not all arrhythmias stem from coronary artery disease, cardiovascular risk factors and heart disease increase arrhythmia occurrence.

Heart Valve Disease:

Problems with one or more of the heart’s four valves that control blood flow through the heart chambers. Valves can become narrowed (stenosis), leak (regurgitation), or fail to close properly. Some valve problems are congenital, others develop from age-related degeneration, rheumatic fever, or endocarditis (infection).

Cardiomyopathy:

Disease of the heart muscle itself, causing the heart to become enlarged, thick, or rigid. This impairs the heart’s ability to pump blood effectively. Causes include genetic factors, long-term hypertension, heart attacks, viral infections, alcohol abuse, or certain medications.

Related Cardiovascular Conditions

While this article focuses on heart disease, it’s important to know that atherosclerosis—the same plaque-building process affecting coronary arteries—also causes other serious conditions:

Stroke: When atherosclerosis affects arteries supplying the brain, blockages cause strokes. The risk factors and prevention strategies are identical to heart disease.

Peripheral Artery Disease (PAD): Atherosclerosis affecting arteries in the legs causes pain with walking. PAD indicates widespread atherosclerosis and significantly elevated heart attack and stroke risk.

These conditions are covered in detail in our Cardiovascular Disease guide, as they share the same underlying causes and prevention strategies as heart disease.

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Atherosclerosis: The Underlying Process in Coronary Arteries

Understanding heart disease requires understanding atherosclerosis—the decades-long process of plaque buildup in the coronary arteries that supply your heart muscle. While atherosclerosis can affect arteries throughout the body, when it occurs in the coronary arteries, it causes coronary artery disease and leads to heart attacks.

How Atherosclerosis Develops

Stage 1: Endothelial Dysfunction (Early Adulthood)

The process begins with damage to the endothelium—the thin inner lining of arteries. Risk factors like high LDL cholesterol, high blood pressure, diabetes, smoking, and inflammation cause endothelial cells to become “activated” and dysfunctional. This damaged endothelium becomes permeable, allowing LDL cholesterol particles to enter the arterial wall.

Stage 2: LDL Accumulation and Oxidation (20s-30s)

Once inside the arterial wall, LDL particles become trapped and undergo oxidation—a chemical modification that makes them toxic. The immune system recognizes oxidized LDL as foreign and dangerous, triggering an inflammatory response. White blood cells called monocytes enter the arterial wall and transform into macrophages that engulf oxidized LDL, becoming foam cells.

Stage 3: Fatty Streak Formation (30s-40s)

Foam cells accumulate, forming fatty streaks—the earliest visible signs of atherosclerosis. These yellow deposits beneath the endothelium contain cholesterol, inflammatory cells, and cellular debris. Fatty streaks themselves don’t cause symptoms but represent the foundation for more advanced plaques.

Stage 4: Plaque Growth and Fibrous Cap Formation (40s-50s)

As inflammation continues, smooth muscle cells migrate into the developing plaque and produce collagen, forming a fibrous cap over the fatty core. The plaque grows outward (initially not narrowing the artery lumen due to arterial remodeling) and then inward, progressively narrowing the arterial opening.

At this stage, significant plaques may cause symptoms with exertion as blood flow can’t increase adequately to meet tissue oxygen demands.

Stage 5: Plaque Rupture and Thrombosis (50s-70s+)

The most dangerous development occurs when a plaque’s fibrous cap becomes thin and ruptures, exposing the thrombogenic core to flowing blood. This triggers rapid blood clot (thrombus) formation that can completely block the artery within minutes, causing a heart attack or stroke.

Paradoxically, the plaques most likely to rupture aren’t necessarily the largest or most severely narrowed—they’re plaques with thin fibrous caps and large lipid cores (vulnerable plaques). This is why someone with “only 40% blockage” can suffer a sudden fatal heart attack.

The Role of Inflammation

Atherosclerosis is fundamentally an inflammatory disease, not simply cholesterol accumulation. Inflammation drives every stage of plaque development, from initial endothelial dysfunction through plaque rupture. This is why C-reactive protein (CRP), a marker of systemic inflammation, powerfully predicts cardiovascular events independent of cholesterol levels.

Chronic inflammatory conditions (rheumatoid arthritis, lupus, psoriasis) significantly increase cardiovascular risk precisely because inflammation accelerates atherosclerosis. Conversely, anti-inflammatory interventions show cardiovascular benefits—another line of evidence supporting inflammation’s central role.

Why Prevention Must Start Early

Given that atherosclerosis develops over decades, prevention must begin long before symptoms appear. Waiting until age 50 to address high cholesterol means allowing 20-30 years of arterial damage to accumulate. The cumulative lifetime exposure to elevated LDL cholesterol (often quantified as LDL-years, similar to pack-years for smoking) determines plaque burden far more than cholesterol level at any single point.

This is why comprehensive blood testing in your 20s and 30s isn’t premature—it’s essential for identifying risk factors when intervention can prevent arterial damage rather than merely slow its progression.

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Risk Factors for Heart Disease

Heart disease risk results from the interaction of multiple factors over decades. Some risk factors are modifiable through lifestyle changes or medication, while others are fixed but important for risk assessment.

Non-Modifiable Risk Factors

Age:

Heart disease risk increases progressively with age. Men’s risk rises significantly after age 45, women’s after 55 (post-menopause). However, age reflects cumulative exposure to risk factors rather than being purely biological—a healthy 70-year-old can have cleaner coronary arteries than an unhealthy 50-year-old.

Sex:

Men develop heart disease 7-10 years earlier than women on average. Before menopause, women have some protection from estrogen’s beneficial effects on cholesterol and blood vessels. After menopause, women’s risk accelerates and eventually equals men’s.

Women more frequently experience atypical heart attack symptoms (fatigue, shortness of breath, nausea rather than classic chest pain), leading to delayed diagnosis and treatment.

Family History:

Premature heart disease in first-degree relatives—particularly parents or siblings with heart attacks before age 55 (men) or 65 (women)—substantially increases your risk. This reflects both shared genes affecting cholesterol metabolism, blood pressure, and inflammation, plus shared environmental factors.

Strong family history warrants earlier and more aggressive screening and prevention efforts.

Genetics:

Specific genetic variants affect heart disease risk through multiple mechanisms: cholesterol metabolism (familial hypercholesterolemia, ApoE variants), blood pressure regulation, inflammation, thrombosis tendency, and metabolism. Genetic testing is increasingly available but currently less important than measuring the actual manifestations of genetic risk (cholesterol levels, blood pressure, etc.).

Major Modifiable Risk Factors

High LDL Cholesterol:

Low-density lipoprotein (LDL) cholesterol is the primary driver of atherosclerosis. LDL particles carry cholesterol into the arterial wall where they become oxidized and trigger plaque formation. The relationship between LDL and cardiovascular risk is direct, continuous, and causal—confirmed by genetic studies, animal models, and randomized trials showing that lowering LDL reduces cardiovascular events proportionally.

Optimal LDL depends on overall risk:

• General population: Below 100 mg/dL
• Moderate risk: Below 70 mg/dL
• High risk (established disease, diabetes): Below 55 mg/dL

Lower is better—there’s no threshold below which LDL stops contributing to atherosclerosis.

High Blood Pressure (Hypertension):

Elevated blood pressure damages endothelium directly through mechanical stress and accelerates atherosclerosis development. Hypertension also causes direct organ damage to the heart (left ventricular hypertrophy, heart failure), brain (stroke), and kidneys.

Blood pressure above 130/80 mmHg increases cardiovascular risk progressively. Optimal is generally 110-120 systolic, though very low pressure can cause symptoms in some individuals.

Diabetes:

Type 2 diabetes doubles to quadruples cardiovascular risk through multiple mechanisms: elevated glucose damages blood vessels directly, diabetes typically coexists with other risk factors (obesity, high triglycerides, low HDL, high blood pressure), and diabetics develop more extensive and aggressive atherosclerosis.

Even prediabetes and insulin resistance increase cardiovascular risk before diabetes develops, emphasizing the importance of addressing metabolic dysfunction early.

Smoking:

Tobacco use promotes atherosclerosis through endothelial damage, increased inflammation, promotion of blood clotting, and adverse effects on cholesterol (lowers HDL, raises LDL). Smoking roughly doubles cardiovascular risk, but risk declines rapidly after quitting—within 1-2 years, excess risk is substantially reduced.

Obesity:

Excess body weight, particularly visceral (abdominal) fat, increases cardiovascular risk through multiple pathways: worsening insulin resistance, raising blood pressure, promoting dyslipidemia (high triglycerides, low HDL), increasing inflammation, and causing sleep-disordered breathing.

The relationship between BMI and cardiovascular risk is continuous, but central obesity (measured by waist circumference or waist-to-hip ratio) predicts risk better than BMI alone. Metabolically unhealthy obesity poses much higher risk than metabolically healthy obesity.

Physical Inactivity:

Sedentary lifestyle independently increases cardiovascular risk by 30-40%. Regular exercise protects through multiple mechanisms: improving insulin sensitivity, lowering blood pressure, raising HDL cholesterol, reducing triglycerides, promoting weight loss, decreasing inflammation, and directly improving endothelial function.

Target: 150+ minutes moderate-intensity aerobic activity weekly plus resistance training twice weekly.

Unhealthy Diet:

Dietary patterns high in saturated fat, trans fat, refined carbohydrates, and sodium while low in vegetables, fruits, whole grains, and fish promote atherosclerosis. The Mediterranean diet—rich in olive oil, fish, vegetables, legumes, and nuts—reduces cardiovascular events by approximately 30% compared to typical Western diets.

Specific dietary factors matter: trans fats should be eliminated completely, saturated fat should be limited, refined carbohydrates and added sugars minimized, and sodium intake kept moderate.

Metabolic Risk Factors

Insulin Resistance:

The underlying metabolic defect in type 2 diabetes, prediabetes, and metabolic syndrome. Insulin resistance promotes atherosclerosis even before diabetes develops through adverse effects on lipids (high triglycerides, low HDL, small dense LDL particles), blood pressure, inflammation, and endothelial function.

Insulin resistance is the common thread linking obesity, fatty liver disease, type 2 diabetes, and cardiovascular disease.

Metabolic Syndrome:

A clustering of risk factors—central obesity, elevated triglycerides, low HDL cholesterol, high blood pressure, and elevated fasting glucose—reflecting underlying insulin resistance. Meeting 3 of 5 criteria defines metabolic syndrome, which roughly doubles cardiovascular risk compared to having none.

Metabolic syndrome affects approximately 34% of US adults and represents a critical intervention point before diabetes or cardiovascular disease develops.

Non-Alcoholic Fatty Liver Disease (NAFLD):

Fatty liver disease not caused by alcohol consumption strongly associates with insulin resistance and cardiovascular disease. NAFLD increases cardiovascular risk independent of other risk factors, and cardiovascular disease is actually the leading cause of death in people with NAFLD—not liver disease.

The connection reflects shared underlying causes (insulin resistance, obesity, dyslipidemia) and potentially direct effects of liver-produced inflammatory and clotting factors.

Emerging and Additional Risk Factors

Chronic Inflammation:

Systemic inflammation, measured by C-reactive protein (CRP), predicts cardiovascular events independent of cholesterol. CRP >2 mg/L indicates elevated cardiovascular risk. Chronic inflammatory conditions (rheumatoid arthritis, psoriasis, inflammatory bowel disease) increase cardiovascular risk by 50-100%.

Lipoprotein(a) – Lp(a):

A genetic variant of LDL that’s particularly atherogenic and prothrombotic. Elevated Lp(a) (>50 mg/dL or >125 nmol/L) increases cardiovascular risk 2-4 fold. Lp(a) is genetically determined and largely unresponsive to lifestyle changes or most medications, though PCSK9 inhibitors lower it somewhat.

Testing Lp(a) once in life identifies those with this genetic risk factor who may benefit from more aggressive management of other risk factors.

ApoB (Apolipoprotein B):

A measurement of the number of atherogenic lipoprotein particles. ApoB may better predict cardiovascular risk than LDL cholesterol alone, particularly when triglycerides are elevated. Target ApoB <80-90 mg/dL for moderate risk, <65 mg/dL for high risk.

Sleep Apnea:

Obstructive sleep apnea increases cardiovascular risk through multiple mechanisms: intermittent hypoxia damages endothelium, sleep disruption promotes inflammation, and apnea often coexists with obesity and metabolic syndrome. CPAP treatment for moderate-severe apnea may reduce cardiovascular risk.

Chronic Kidney Disease:

Even mild kidney dysfunction (reduced eGFR) substantially increases cardiovascular risk. The kidney-cardiovascular connection is bidirectional—cardiovascular disease damages kidneys, and kidney disease accelerates cardiovascular disease progression through effects on blood pressure, anemia, mineral metabolism, and inflammation.

Psychosocial Factors:

Chronic stress, depression, social isolation, and low socioeconomic status each independently increase cardiovascular risk by 30-50%. Mechanisms include stress hormones promoting inflammation and clotting, behavioral factors (poor diet, smoking, inactivity), and healthcare access issues.

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Symptoms and Warning Signs

The dangerous reality of cardiovascular disease is that most people have no symptoms until a serious event occurs. Understanding both the silent nature of disease development and recognizing warning signs when they appear can be lifesaving.

The Silent Years

Atherosclerosis develops asymptomatically for decades. You don’t feel plaque accumulating in your arteries. High cholesterol causes no symptoms. Blood pressure of 150/95 produces no pain. Insulin resistance goes unnoticed. This is why cardiovascular disease is called a “silent killer”—by the time symptoms appear, disease is often advanced.

Early detection depends entirely on screening—measuring blood pressure, checking lipid panels, assessing glucose metabolism—not waiting for symptoms. Blood tests in your 30s and 40s revealing elevated cholesterol or glucose aren’t premature; they’re catching disease processes already underway that will cause problems in 10-20 years without intervention.

Stable Angina (Chronic Symptoms)

Chest Discomfort:

The classic symptom of significant coronary artery disease is angina—chest discomfort triggered by exertion or stress and relieved by rest. Described as pressure, tightness, squeezing, or heaviness rather than sharp pain. Location is typically substernal (behind the breastbone) but may radiate to shoulders, arms, neck, jaw, or back.

Stable angina occurs predictably with certain levels of exertion as narrowed coronary arteries can’t increase blood flow adequately to meet the heart’s increased oxygen demand during exercise.

Shortness of Breath:

May occur with or without chest discomfort, particularly during exertion. Results from the heart’s inability to pump effectively when oxygen supply is insufficient.

Fatigue:

Unusual tiredness, particularly with activities previously tolerated well, can indicate reduced cardiac output from coronary disease or heart failure.

Heart Attack Symptoms (Acute Emergency)

Classic Presentation:

Sudden severe chest pain or pressure, often described as “elephant sitting on chest.” Pain may radiate to left arm, right arm, both arms, jaw, neck, back, or upper abdomen. Associated symptoms include shortness of breath, cold sweats, nausea or vomiting, and sense of impending doom. Symptoms persist beyond 15-20 minutes and don’t respond to rest.

Atypical Presentations:

Women, elderly, and diabetics more frequently experience atypical symptoms: unusual fatigue, shortness of breath, nausea, indigestion, upper back pain, or dizziness without significant chest pain. This leads to delayed recognition and treatment, contributing to worse outcomes in these groups.

Silent Heart Attacks:

Approximately 20-45% of heart attacks produce minimal or no symptoms and are discovered only later on EKG or imaging. More common in diabetics due to neuropathy affecting pain perception.

Stroke Warning Signs

FAST Acronym:

• Face drooping (one side of face numb or drooping, uneven smile)
• Arm weakness (one arm weak or numb, drift downward when raised)
• Speech difficulty (slurred speech, unable to repeat simple phrase)
• Time to call 911 (time is brain—every minute counts)

Additional Signs:

Sudden severe headache, sudden vision loss or double vision, sudden difficulty walking or loss of balance, sudden confusion or difficulty understanding, sudden numbness on one side of body.

Heart Failure Symptoms

Progressive Breathlessness:

Shortness of breath initially with exertion, then with minimal activity, eventually occurring at rest or when lying flat (orthopnea). Many people sleep propped up on multiple pillows to breathe easier.

Fluid Retention:

Leg and ankle swelling, weight gain from fluid accumulation, abdominal swelling.

Reduced Exercise Capacity:

Fatigue, weakness, inability to perform previously tolerated activities.

Paroxysmal Nocturnal Dyspnea:

Waking suddenly at night gasping for breath due to fluid accumulation in lungs when lying flat.

Peripheral Artery Disease Symptoms

Claudication:

Leg pain, cramping, or fatigue with walking that’s relieved by rest. Indicates inadequate blood flow to leg muscles. Severity correlates with degree of arterial narrowing—some people develop pain after several blocks, others after just a few steps.

Advanced PAD:

Foot pain at rest (indicates severe blockage), non-healing wounds, cold feet, color changes, hair loss on legs.

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Diagnosis and Testing for Heart Disease

Early detection of heart disease and risk factors depends on comprehensive testing, starting with routine screening in young adulthood and intensifying based on risk factor presence.

Blood Tests for Heart Disease Risk Assessment

Lipid Panel (Lipoprotein Profile):

The foundation of cardiovascular risk assessment, measuring cholesterol and triglycerides.

Components:

• Total cholesterol
• LDL cholesterol (calculated or directly measured) – target depends on risk
• HDL cholesterol – higher is better, >40 mg/dL men, >50 mg/dL women
• Triglycerides – target <150 mg/dL, ideally <100 mg/dL

Requires 9-12 hour fast for accurate triglyceride measurement. Should be checked at least once in 20s to establish baseline, then every 4-6 years if normal, more frequently if elevated or other risk factors present.

Advanced Lipid Testing:

• ApoB (Apolipoprotein B): Measures number of atherogenic particles, may better assess risk than LDL alone, especially when triglycerides elevated. Target <80-90 mg/dL.
• Lp(a): Genetic risk factor, measure once in lifetime. Elevated if >50 mg/dL or >125 nmol/L.
• LDL particle number (LDL-P): Direct measurement of particle count via NMR or ion mobility. May identify discordance between LDL cholesterol and particle number.

Glucose Metabolism:

• Fasting glucose: Target <100 mg/dL; 100-125 mg/dL = prediabetes; ≥126 mg/dL = diabetes
• HbA1c: 3-month average glucose; <5.7% normal, 5.7-6.4% prediabetes, ≥6.5% diabetes
• Fasting insulin: Elevated insulin indicates insulin resistance even before glucose rises
• HOMA-IR: Calculated from fasting glucose and insulin, quantifies insulin resistance

Metabolic health profoundly affects cardiovascular risk, making glucose and insulin testing essential.

Inflammatory Markers:

• hsCRP (high-sensitivity C-reactive protein): Predicts cardiovascular events independent of cholesterol. <1 mg/L = low risk, 1-3 mg/L = moderate risk, >3 mg/L = high risk. CRP >10 mg/L suggests acute infection or inflammation.

Kidney Function:

• Creatinine and eGFR: Even mild kidney dysfunction increases cardiovascular risk
• Albumin-to-creatinine ratio (urine): Detects early kidney damage, marker of endothelial dysfunction

Other Markers:

• Homocysteine: Elevated levels may increase CVD risk, though causality uncertain
• TSH: Hypothyroidism affects cholesterol and cardiovascular risk
• Vitamin D: Deficiency associated with increased cardiovascular risk

Blood Pressure Measurement

Blood pressure should be checked at every healthcare visit, minimum yearly starting in young adulthood. Elevated readings require confirmation with repeated measurements or home monitoring before diagnosis.

Classification:

• Normal: <120/80 mmHg
• Elevated: 120-129/<80 mmHg
• Hypertension Stage 1: 130-139 or 80-89 mmHg
• Hypertension Stage 2: ≥140 or ≥90 mmHg

Home monitoring provides more accurate assessment than office readings, avoiding “white coat hypertension” and detecting “masked hypertension.”

Physical Examination

BMI and waist circumference assess obesity and central adiposity. Cardiovascular examination checks for heart murmurs, irregular rhythms, signs of heart failure. Peripheral pulse examination detects peripheral artery disease. Fundoscopic examination reveals hypertensive or diabetic retinal changes.

Electrocardiogram (EKG/ECG)

Records heart’s electrical activity, detects arrhythmias, prior heart attacks, left ventricular hypertrophy from hypertension, and ischemia patterns. Baseline EKG reasonable in adults over 40 or earlier if risk factors present or planning to start vigorous exercise.

Exercise Stress Testing

Used when symptoms suggest coronary disease or to assess exercise capacity and risk. Exercise stress test involves walking on treadmill while EKG monitors heart. Nuclear perfusion imaging or echocardiography adds sensitivity for detecting coronary blockages.

Limitations: Less sensitive for detecting moderate blockages, normal test doesn’t rule out atherosclerosis presence.

Coronary Calcium Score (CT)

Non-invasive CT scan quantifies calcium in coronary arteries, a marker of atherosclerotic plaque burden. Score of zero indicates very low risk (though doesn’t exclude non-calcified plaque). Scores >100-400 indicate significant plaque and elevated risk, >400 indicates very high risk.

Calcium scoring helps refine risk assessment in intermediate-risk individuals where treatment decisions are unclear. Generally performed once—plaque doesn’t disappear, and repeating adds radiation exposure without much additional information.

Coronary Angiography (Cardiac Catheterization)

The gold standard for directly visualizing coronary arteries, performed by threading a catheter through an artery (typically wrist or groin) into coronary arteries and injecting contrast dye while X-ray images are recorded. Identifies exact location and severity of blockages.

Angiography is invasive with small risks, so it’s reserved for people with symptoms suggesting coronary disease or very high risk, not for screening.

Advanced Imaging

• Coronary CT angiography: Non-invasive visualization of coronary arteries using IV contrast
• Carotid ultrasound: Assesses carotid artery narrowing and plaque, correlates with coronary disease
• Ankle-brachial index (ABI): Compares blood pressure in ankle vs arm, detects peripheral artery disease
• Echocardiography: Ultrasound of heart assesses function, valve problems, structural issues

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Prevention Strategies for Heart Disease

The overwhelming majority of heart disease is preventable through lifestyle interventions and management of risk factors. Prevention is far more effective than treatment after disease develops.

Diet for Heart Health

Mediterranean Diet – The Gold Standard:

The most extensively studied dietary pattern for heart disease prevention. The landmark PREDIMED trial demonstrated that Mediterranean diet supplemented with extra-virgin olive oil or nuts reduced major cardiac events (heart attacks, strokes, and cardiovascular deaths) by 30% compared to a low-fat diet.

Key components:

• Abundant vegetables, fruits, legumes, whole grains
• Olive oil as primary fat source
• Fatty fish 2-3 times weekly
• Nuts and seeds daily
• Moderate wine consumption (optional)
• Limited red meat, processed meats, sweets

The Mediterranean diet improves all heart disease risk factors: lowers LDL cholesterol, raises HDL, reduces triglycerides, lowers blood pressure, improves insulin sensitivity, and decreases inflammation.

DASH Diet:

Developed specifically to lower blood pressure. Emphasizes vegetables, fruits, whole grains, lean proteins, low-fat dairy while limiting sodium, saturated fat, and added sugars. The DASH diet lowers blood pressure comparable to medications in many people.

Portfolio Diet:

Combines four cholesterol-lowering food components: soluble fiber (oats, barley, psyllium), plant sterols (fortified foods), soy protein, and tree nuts. Can lower LDL cholesterol by 20-30%, approaching statin effectiveness through diet alone.

Key Dietary Principles:

• Minimize saturated fat (from meat, full-fat dairy, tropical oils)
• Eliminate trans fats completely
• Increase soluble fiber (10-25g daily lowers LDL ~10%)
• Include omega-3 fatty acids (fatty fish, walnuts, flaxseed)
• Limit refined carbohydrates and added sugars
• Moderate sodium intake (<2,300 mg daily, ideally <1,500 mg if hypertensive)
• Emphasize whole, minimally processed foods

Foods to Limit or Avoid:

Red meat and processed meats increase cardiovascular risk. Refined grains (white bread, white rice, pastries) promote obesity and worsen glycemic control. Added sugars, particularly sugar-sweetened beverages, contribute to obesity, diabetes, and dyslipidemia. Trans fats (partially hydrogenated oils) should be eliminated entirely. Excessive sodium raises blood pressure in salt-sensitive individuals.

Physical Activity and Exercise for Heart Health

Regular physical activity reduces heart attacks and cardiac deaths by 30-40% even independent of weight loss. Exercise benefits virtually every heart disease risk factor: lowers blood pressure, raises HDL cholesterol, lowers triglycerides, improves insulin sensitivity, promotes weight loss, reduces inflammation, improves endothelial function, and directly strengthens the heart.

Aerobic Exercise:

Target: 150-300 minutes moderate-intensity or 75-150 minutes vigorous-intensity aerobic activity weekly. Moderate intensity means working hard enough to raise heart rate and break a sweat but still able to talk. Examples: brisk walking, cycling, swimming, dancing, jogging.

More is better—300 minutes weekly provides greater benefits than 150 minutes. However, even moderate amounts provide substantial protection compared to being sedentary.

Resistance Training:

Strength training 2-3 days weekly targeting all major muscle groups. Builds muscle mass, improves insulin sensitivity, raises resting metabolic rate, and complements aerobic exercise benefits. Particularly important for preventing age-related muscle loss.

Reducing Sedentary Time:

Independent cardiovascular risk from prolonged sitting, separate from exercise amount. Break up sitting every 30 minutes with light activity. Standing desks, walking meetings, and active hobbies help reduce total sedentary time.

Weight Management

Even modest weight loss (5-10% of body weight) significantly improves all cardiovascular risk factors: lowers blood pressure, improves lipids, enhances insulin sensitivity, reduces inflammation. For people with obesity, greater weight loss provides proportionally greater benefits.

Weight loss is most effectively achieved through combination of reduced calorie intake and increased physical activity, rather than diet or exercise alone. Behavioral strategies supporting long-term adherence are crucial since maintaining weight loss is often more challenging than initial loss.

Smoking Cessation

Quitting smoking is among the most impactful interventions for cardiovascular disease prevention. Risk begins declining within months and after 1-2 years of abstinence, excess cardiovascular risk is substantially reduced, though not completely eliminated.

Combination of behavioral support and pharmacological aids (nicotine replacement, bupropion, varenicline) provides highest quit rates. Repeated quit attempts are common before achieving lasting abstinence—persistence is key.

Alcohol Consumption

The relationship between alcohol and cardiovascular disease is complex. Light to moderate consumption (1 drink daily for women, 1-2 for men) associates with slightly lower cardiovascular risk compared to abstinence in observational studies, possibly through effects on HDL cholesterol.

However, alcohol increases other health risks (cancer, liver disease, accidents), and any cardiovascular benefits don’t justify recommending alcohol to non-drinkers. For those who drink, moderation is key, and avoiding heavy drinking or binge drinking is crucial.

Stress Management

Chronic stress independently increases cardiovascular risk through multiple pathways: direct effects of stress hormones on blood pressure and metabolism, stress-induced behaviors (poor diet, smoking, inactivity), and inflammation. Depression and anxiety similarly increase cardiovascular risk.

Effective stress management techniques include regular exercise, meditation or mindfulness practices, adequate sleep, social connection, professional counseling or therapy when needed, and cognitive-behavioral strategies for managing stress responses.

Sleep

Both insufficient sleep (<6 hours nightly) and excessive sleep (>9 hours) associate with increased cardiovascular risk. Sleep apnea substantially increases risk through multiple mechanisms and should be diagnosed and treated. Target 7-9 hours of quality sleep nightly.

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Medications for Heart Disease Prevention and Treatment

When lifestyle interventions are insufficient to achieve risk factor targets, medications play crucial roles in preventing heart attacks and other cardiac events.

Statins (HMG-CoA Reductase Inhibitors)

The cornerstone of pharmacological heart disease prevention. Statins lower LDL cholesterol by inhibiting the liver enzyme responsible for cholesterol production. Extensive randomized trials demonstrate that statins reduce heart attacks, cardiac deaths, and need for cardiac procedures by 25-35%, with greater absolute benefit in higher-risk individuals.

Common statins: atorvastatin (Lipitor), rosuvastatin (Crestor), simvastatin, pravastatin. High-intensity statins (atorvastatin 40-80mg, rosuvastatin 20-40mg) lower LDL by 50% or more.

Side effects: Muscle aches occur in 5-10% of users but are usually mild. Severe myopathy is rare. Statins slightly increase diabetes risk in predisposed individuals, but cardiovascular benefits outweigh this risk. Liver enzyme elevation is uncommon and rarely clinically significant.

Indications: Established cardiovascular disease, LDL ≥190 mg/dL, diabetes age 40-75, or calculated 10-year cardiovascular risk ≥7.5-10%.

Ezetimibe

Blocks cholesterol absorption in the intestine, lowering LDL by ~20%. Added to statin when statin alone doesn’t achieve target LDL or when statin doses can’t be increased due to side effects. The IMPROVE-IT trial demonstrated that adding ezetimibe to statin reduced cardiovascular events by additional 6.4% over statin alone.

Well tolerated with minimal side effects. Often combined with statin in single-pill combinations.

PCSK9 Inhibitors

Powerful injectable medications (evolocumab, alirocumab) that lower LDL by 50-60% beyond statin effects. Reserved for very high-risk patients who can’t achieve LDL targets despite maximal statin and ezetimibe, or those with familial hypercholesterolemia.

Clinical trials demonstrate significant cardiovascular event reduction but medications are expensive. Administered as subcutaneous injections every 2-4 weeks.

Bempedoic Acid

Newer oral medication inhibiting cholesterol synthesis similar to statins but without muscle side effects. Lowers LDL by ~20%. Option for statin-intolerant patients or added to statin for additional LDL lowering.

Blood Pressure Medications

Multiple classes with different mechanisms, often used in combination:

ACE Inhibitors/ARBs: Block renin-angiotensin system, particularly beneficial in diabetes or kidney disease Calcium Channel Blockers: Relax blood vessels Diuretics: Reduce fluid volume Beta-Blockers: Slow heart rate, reduce cardiac workload Other agents: Various additional medication classes for resistant hypertension

Target blood pressure generally <130/80 mmHg, sometimes lower depending on individual circumstances.

Antiplatelet Therapy

Aspirin:

Low-dose aspirin (81-100mg daily) reduces cardiovascular events in people with established disease (secondary prevention) by preventing clot formation. Benefit in primary prevention (without prior cardiovascular disease) is more controversial—small cardiovascular benefit is offset by increased bleeding risk.

Current guidelines generally recommend aspirin for secondary prevention but only selective primary prevention in higher-risk individuals after considering bleeding risk.

P2Y12 Inhibitors:

Clopidogrel, prasugrel, ticagrelor—more potent antiplatelet medications used after heart attack or stent placement, often combined with aspirin for defined periods (dual antiplatelet therapy).

Diabetes Medications with Cardiovascular Benefits

Newer diabetes medications demonstrate cardiovascular benefits beyond glucose lowering:

SGLT2 Inhibitors: Reduce heart failure hospitalizations and kidney disease progression GLP-1 Receptor Agonists: Reduce cardiovascular events in people with established disease

These medications are increasingly used not only for diabetes treatment but for cardiovascular and kidney protection.

Omega-3 Fatty Acids (Prescription)

High-dose prescription omega-3 (icosapent ethyl, EPA) reduces cardiovascular events by 25% when added to statin in people with elevated triglycerides, as shown in the REDUCE-IT trial. Over-the-counter fish oil supplements haven’t shown consistent cardiovascular benefits in trials, likely due to lower omega-3 content and different formulations.

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Living With Cardiovascular Disease

For people diagnosed with established cardiovascular disease—whether recovering from heart attack, living with stable angina, or managing heart failure—ongoing management focuses on preventing disease progression and additional events.

Secondary Prevention

People with established cardiovascular disease face substantially elevated risk for additional events. Aggressive risk factor management becomes even more critical:

• LDL cholesterol target <55-70 mg/dL
• Blood pressure <130/80 mmHg
• HbA1c <7% if diabetic
• Complete smoking cessation
• Consistent medication adherence (statins, antiplatelet therapy, blood pressure medications)
• Regular exercise as tolerated
• Mediterranean diet pattern
• Achieving and maintaining healthy weight

Cardiac Rehabilitation

Structured program of supervised exercise, education, and behavioral interventions after heart attack or cardiac procedures. Cardiac rehabilitation reduces cardiovascular mortality by ~25% and improves quality of life, yet remains vastly underutilized—only 20-30% of eligible patients participate.

Components include progressive exercise training, nutritional counseling, medication management, psychosocial support, and education on cardiovascular disease and risk factors.

Monitoring and Follow-Up

Regular monitoring ensures treatment effectiveness and detects any disease progression:

• Blood pressure monitoring at home or frequent office checks
• Lipid panel every 3-6 months until stable, then annually
• Glucose/HbA1c monitoring if diabetic
• Medication adherence and side effect assessment
• Exercise tolerance and symptom assessment
• Echocardiography or stress testing as indicated to assess cardiac function

Recognizing Complications

Be alert for symptoms indicating disease progression or complications:

• New or worsening chest pain or shortness of breath
• Heart failure symptoms (leg swelling, breathlessness, fatigue)
• Arrhythmia symptoms (palpitations, dizziness)
• Signs of stroke or TIA
• Medication side effects

Prompt reporting of new symptoms allows timely adjustment of treatment.

Emotional and Psychological Impact

Diagnosis of cardiovascular disease understandably causes anxiety, fear, and depression. Cardiac events can be traumatic experiences triggering PTSD-like responses. Depression after heart attack is common (affecting 20-40% of patients) and associated with worse outcomes.

Mental health is integral to cardiovascular health. Don’t hesitate to seek support through counseling, support groups, stress management programs, or medication for anxiety/depression if needed.

Advance Care Planning

As cardiovascular disease progresses, particularly in advanced heart failure, discussing preferences for care becomes important. This includes decisions about procedures, device implantation (defibrillators, pacemakers), and ultimately end-of-life care preferences.

Having these conversations with family and documenting wishes ensures care aligns with personal values and preferences.

Understanding your cardiovascular risk begins with comprehensive blood testing. Lipid panels (LDL, HDL, triglycerides, ApoB), metabolic markers (fasting glucose, insulin, HbA1c), inflammatory markers (CRP), blood pressure, and kidney function (creatinine, eGFR) provide the foundation for early detection and prevention of heart disease.