Introduction to Ischemic Heart Disease

Ischemic heart disease (IHD), also known as coronary artery disease (CAD) or coronary heart disease (CHD), is a condition characterized by reduced blood flow to the myocardium due to obstruction of coronary arteries. It is a major cause of morbidity and mortality worldwide, responsible for a significant portion of cardiovascular deaths. Understanding the definition, epidemiology, risk factors, pathophysiology, and clinical implications of IHD is crucial for early detection, prevention, and effective management.

1. Definition of Ischemic Heart Disease

Ischemic heart disease (IHD) is defined as a group of syndromes resulting from imbalance between myocardial oxygen supply and demand, typically due to atherosclerotic narrowing of coronary arteries. The reduced oxygen supply can lead to myocardial ischemia, which manifests clinically as angina pectoris, myocardial infarction, heart failure, or sudden cardiac death.

Key Points:

The term “ischemia” refers to inadequate blood flow relative to tissue metabolic needs.
IHD encompasses both acute coronary syndromes (ACS) and chronic stable angina.
Other causes of IHD include coronary artery spasm, embolism, or microvascular dysfunction, although atherosclerosis remains the predominant etiology.

2. Epidemiology of Ischemic Heart Disease

2.1 Global Burden

IHD is the leading cause of death worldwide, accounting for approximately 9 million deaths annually.
Global prevalence is estimated at ~126 million cases.
Although traditionally more common in high-income countries, the incidence is rising in low- and middle-income countries due to lifestyle changes and urbanization.

2.2 Regional Variations

High-income countries: Incidence declining due to improved prevention, early diagnosis, and advanced therapies.
Low- and middle-income countries: Rapid increase due to urbanization, westernized diets, obesity, and limited access to healthcare.
Age and sex: IHD prevalence increases with age; men are affected earlier than women, but post-menopausal women show comparable risk.

2.3 Trends and Projections

Despite advances in therapy, cardiovascular disease, including IHD, remains a major contributor to disability-adjusted life years (DALYs).
Predicted increase in IHD prevalence globally due to population aging and lifestyle risk factors.

3. Risk Factors for Ischemic Heart Disease

Risk factors for IHD are classified into modifiable and non-modifiable categories. Understanding these factors is critical for primary and secondary prevention.

3.1 Non-Modifiable Risk Factors

Age: Risk increases significantly after 45 years in men and 55 years in women.
Sex: Men are at higher risk earlier in life; estrogen appears protective in premenopausal women.
Genetic predisposition: Family history of premature coronary artery disease increases risk.
Ethnicity: Certain populations (South Asians, African Americans) have higher susceptibility due to genetic and environmental factors.

3.2 Modifiable Risk Factors

Hypertension:
- Chronic high blood pressure increases arterial wall stress, accelerating atherosclerosis.
- Both systolic and diastolic hypertension contribute to risk.
Dyslipidemia:
- Elevated LDL cholesterol and reduced HDL cholesterol are major contributors to plaque formation.
- Triglycerides and lipoprotein(a) also play roles.
Diabetes Mellitus:
- Type 2 diabetes accelerates atherosclerosis.
- Hyperglycemia, insulin resistance, and dyslipidemia collectively increase IHD risk.
Smoking:
- Tobacco use promotes endothelial dysfunction, thrombosis, and atherosclerosis.
- Risk decreases significantly with cessation.
Obesity and Metabolic Syndrome:
- Central obesity correlates with insulin resistance, dyslipidemia, and inflammation.
- Metabolic syndrome markedly increases IHD risk.
Sedentary Lifestyle:
- Lack of physical activity contributes to obesity, hypertension, and insulin resistance.
Dietary Factors:
- High saturated fat, trans fats, and low fiber intake contribute to atherogenic lipid profiles.
- Diet rich in fruits, vegetables, and omega-3 fatty acids is protective.
Alcohol Consumption:
- Excessive alcohol increases blood pressure and triglycerides.
- Moderate intake may have protective effects in some populations.
Psychosocial Factors:
- Chronic stress, depression, and low socioeconomic status are associated with increased IHD risk.

4. Pathophysiology of Ischemic Heart Disease

4.1 Coronary Atherosclerosis

The primary mechanism of IHD is atherosclerosis, a progressive disease of coronary arteries.

Endothelial Dysfunction:
- Early step in atherosclerosis.
- Loss of nitric oxide-mediated vasodilation.
- Increased permeability to lipids and inflammatory cells.
Lipid Accumulation:
- LDL cholesterol infiltrates the intima, undergoes oxidation, triggering inflammation.
Inflammation and Plaque Formation:
- Macrophages engulf oxidized LDL → foam cell formation → fatty streaks.
- Smooth muscle proliferation and fibrous cap formation create stable plaques.
Plaque Rupture and Thrombosis:
- Plaque rupture exposes subendothelial collagen → platelet aggregation → thrombus formation.
- Leads to acute coronary syndromes (unstable angina, NSTEMI, STEMI).

4.2 Imbalance of Oxygen Supply and Demand

IHD arises when myocardial oxygen demand exceeds supply.

Increased demand: Tachycardia, hypertension, left ventricular hypertrophy, physical exertion.
Decreased supply: Coronary stenosis, spasm, anemia, hypotension, hypoxia.

4.3 Types of Ischemia

Stable Ischemia: Fixed stenosis → predictable angina on exertion.
Unstable Ischemia: Plaque rupture or thrombus → unpredictable angina, may progress to MI.
Silent Ischemia: No anginal symptoms, often in diabetics or elderly.

4.4 Cellular Consequences

Hypoxia: Impaired ATP production → altered ionic gradients.
Contractile dysfunction: Reduced myocardial contractility (myocardial stunning).
Cell injury and death: Prolonged ischemia leads to necrosis → myocardial infarction.
Electrical instability: Ischemia predisposes to arrhythmias.

5. Clinical Relevance of Ischemic Heart Disease

5.1 Symptomatology

Angina Pectoris:
- Chest pain/pressure, radiation to left arm, jaw, or neck.
- Precipitated by exertion, relieved by rest or nitrates.
Acute Coronary Syndromes:
- Unstable angina, NSTEMI, STEMI.
- May present with severe chest pain, diaphoresis, dyspnea, nausea.
Silent Ischemia:
- No pain; detected by ECG changes, stress testing, or imaging.
Heart Failure:
- Chronic ischemia leads to ventricular dysfunction.
Arrhythmias and Sudden Cardiac Death:
- Ischemic myocardium predisposes to ventricular tachyarrhythmias.

5.2 Impact on Healthcare Systems

IHD leads to frequent hospitalizations, interventions (PCI, CABG), and long-term therapy.
Major economic burden globally due to direct costs (hospitalization, procedures) and indirect costs (lost productivity).

5.3 Risk Stratification

Risk scores (e.g., TIMI, GRACE) help predict mortality and guide management.
Non-invasive testing and imaging assist in identifying high-risk patients.

6. Mortality and Prognosis

6.1 Global Mortality

IHD accounts for ~16% of all deaths worldwide, making it the leading single cause of mortality.
Mortality varies by region, socioeconomic status, and access to care.

6.2 Acute vs Chronic Mortality

Acute Coronary Events:
- STEMI mortality is highest in the first 24 hours.
- Early reperfusion therapy significantly reduces death.
Chronic Stable IHD:
- Mortality is lower but long-term risk of MI and heart failure persists.
- Aggressive risk factor management improves survival.

6.3 Prognostic Factors

Extent of coronary artery disease (single vs multi-vessel).
Left ventricular function and ejection fraction.
Comorbid conditions: Diabetes, renal dysfunction, heart failure.
Lifestyle and adherence to therapy.