Coronary Artery Disease I: Introduction

Coronary artery disease (CAD) is a blood vessel disorder classified under atherosclerosis, which involves hardening and narrowing of arteries due to plaque buildup. This plaque comprises cholesterol, fatty substances, inflammatory cells, calcium, and fibrin. CAD reduces blood flow to the heart muscle, increasing the risk of myocardial infarction and other cardiovascular complications.

Non-modifiable risk factors include age, with men over 45 and women over 55 at higher risk. Gender differences show men generally face higher CAD risk earlier in life, whereas women's risk increases significantly after menopause due to reduced estrogen protection. Family history of CAD further elevates risk for both genders.

Modifiable risk factors include smoking, hypertension, high LDL cholesterol, and low HDL cholesterol. Physical inactivity, poor diet rich in saturated fats, excessive alcohol intake, and psychosocial factors such as chronic stress, depression, and anxiety also increase CAD risk. A BMI greater than 30 kg/m² and excessive waist circumference are additional contributors.

Both type 1 and type 2 diabetes are associated with hyperglycemia, which induces oxidative stress and inflammation, accelerating atherosclerotic progression. Diabetes also contributes to dyslipidemia and endothelial dysfunction. Combined with obesity (BMI greater than 30 kg/m²), diabetes significantly elevates CAD risk.

Endothelial dysfunction occurs when the inner lining of blood vessels is damaged by risk factors such as smoking, high blood pressure, or diabetes. This damage triggers lipid deposition, where low-density lipoprotein particles penetrate and oxidize. Oxidized LDL attracts macrophages, forming foam cells and fatty streaks that progress to plaque formation.

In advanced stages, atherosclerotic plaques may rupture, forming a thrombus or blood clot that can completely block blood flow to the heart. This rupture represents a critical transition from chronic CAD to acute coronary syndrome, potentially causing myocardial infarction. Understanding acute coronary syndrome pathophysiology and clinical manifestations is essential for recognizing these acute events.

Advancements in genomics enable identification of specific polymorphisms linked to CAD risk. Emerging biomarkers like C-reactive protein and lipoprotein(a) offer insights into inflammation and inherited lipid abnormalities. Precision medicine innovations, such as PCSK9 inhibitors, have significantly improved lipid control and reduced cardiovascular events in at-risk populations.