Atherosclerosis / Coronary Artery Disease

Cardiovascular

Description

Atherosclerosis is a chronic, progressive disease in which lipid-rich plaques form within the intima of medium and large arteries; when it involves the epicardial coronary vessels the clinical entity is termed coronary artery disease. Progressive plaque enlargement or acute plaque rupture reduces myocardial perfusion, manifesting first as exertional angina and later as acute coronary syndromes—unstable angina, non-ST-elevation myocardial infarction and ST-elevation myocardial infarction—culminating in heart failure, lethal arrhythmia or sudden cardiac death.

Symptoms

Stable coronary artery disease presents with predictable substernal pressure or heaviness triggered by exertion, emotional stress or cold and relieved by rest or nitroglycerin; equivalent symptoms include dyspnoea, fatigue or epigastric discomfort, particularly in women, the elderly and diabetics. Progressive plaque instability or thrombosis causes prolonged or rest pain, diaphoresis, nausea and anxiety characteristic of acute coronary syndrome. Silent ischemia, detectable only by ECG or imaging, is frequent in diabetes and after cardiac transplantation.

Risk Factors

Non-modifiable risks include advancing age, male sex, premature family history of coronary events and inherited lipid disorders such as familial hypercholesterolaemia. Modifiable risks encompass hypertension, elevated LDL-C, low HDL-C, diabetes mellitus, insulin resistance and metabolic syndrome, cigarette smoking, central obesity, physical inactivity, diets high in saturated and trans fats, psychosocial stress, obstructive sleep apnoea and chronic kidney disease. Emerging factors—lipoprotein(a) excess, high-sensitivity C-reactive protein, clonal haematopoiesis, air pollution exposure and autoimmune disease activity—add incremental risk.

Diagnosis

Initial assessment combines history, physical examination, fasting lipid profile, glucose or HbA1c, renal function and resting 12-lead ECG. Pre-test probability guides selection of stress testing—exercise ECG, stress echocardiography, myocardial perfusion scintigraphy or pharmacologic cardiac MRI—to document inducible ischaemia. Coronary computed-tomographic angiography visualises non-obstructive and obstructive plaques and quantifies calcium score for risk stratification. Invasive coronary angiography remains the gold standard when non-invasive tests are high risk, symptoms refractory or revascularisation is contemplated; fractional flow reserve <0.80 identifies haemodynamically significant lesions. High-sensitivity cardiac troponin distinguishes chronic disease from acute coronary syndrome.

Treatment

Optimal medical therapy begins with lifestyle modification—Mediterranean diet rich in fruits, vegetables, whole grains and oily fish, regular aerobic exercise 150 min weekly, weight management and smoking cessation. High-intensity statin therapy (atorvastatin 40–80 mg or rosuvastatin 20–40 mg) lowers LDL-C ≥50 %; ezetimibe or PCSK9 monoclonal antibodies are added if LDL-C remains above goal (<55 mg/dL in very-high-risk patients). Low-dose aspirin 75–100 mg daily is recommended for secondary prevention; clopidogrel substitutes in aspirin-intolerant individuals. ACE inhibitors or ARBs improve endothelial function and survival in patients with hypertension, diabetes or left-ventricular dysfunction; β-blockers alleviate angina and reduce post-MI mortality; long-acting nitrates, calcium-channel blockers or ranolazine relieve residual angina. For refractory symptoms or prognostic benefit in left-main or multivessel disease with impaired ejection fraction, revascularisation is indicated: percutaneous coronary intervention with drug-eluting stents offers symptom relief, whereas coronary-artery bypass grafting confers survival advantage in diabetics and complex triple-vessel disease. Adjunctive therapies include influenza vaccination, high-dose omega-3 ethyl esters for hypertriglyceridaemia and sodium–glucose cotransporter-2 inhibitors or GLP-1 agonists in diabetics.

Outlook

With guideline-directed medical therapy, annual cardiovascular-event rates fall below two percent in contemporary cohorts; however, residual risk persists due to non-culprit plaque rupture and systemic inflammation. Long-term prognosis correlates with adherence to therapy, LDL-C reduction, blood-pressure control, glycaemic management and smoking abstinence. Post-procedure restenosis risk is below five percent with current drug-eluting stents, and five-year survival after CABG exceeds 90 % in stable patients.

Complications

Myocardial infarction, heart-failure with reduced ejection fraction, life-threatening ventricular tachyarrhythmias, sudden cardiac death, chronic stable angina limiting quality of life, repeat revascularisation, ischaemic cardiomyopathy, mitral regurgitation from papillary-muscle dysfunction and post-infarction mechanical complications—ventricular septal rupture, free-wall rupture, left-ventricular aneurysm—can ensue.

Prevention

Primordial prevention focuses on healthy diet, daily physical activity, avoidance of tobacco, maintenance of healthy body mass index and adequate sleep. Primary prevention employs periodic lipid and blood-pressure screening, aggressive treatment of hypertension and dyslipidaemia, statin use according to ASCVD risk score, glucose control in diabetes, low-dose aspirin in select high-risk adults without bleeding predisposition and air-quality improvements on a societal level.

Support

Patients should monitor blood pressure and lipid results, attend cardiac-rehabilitation programmes, take medications at the same time daily, carry nitroglycerin for acute symptoms, practise stress-reduction techniques such as mindfulness and ensure regular follow-up for therapy titration. Family members can learn cardiopulmonary resuscitation and recognise heart-attack signs.