Disorders of Cardiac Function: Ischemic Heart Disease and Acute Coronary Syndromes

Disorders of Cardiac Function

Introduction

This study guide covers the pathophysiology, clinical presentation, and management of ischemic heart disease (IHD) and acute coronary syndromes (ACS), focusing on the balance between myocardial oxygen supply and demand, the role of atherosclerosis, and the clinical differentiation of various cardiac syndromes.

Coronary Artery Disease

Overview

• Coronary artery disease (CAD) is a condition characterized by impaired blood flow in the coronary arteries, most commonly due to atherosclerosis.

• CAD can manifest as ischemic heart disease (IHD) or as acute coronary syndromes (ACS).

Classification of Ischemic Heart Disease and Acute Coronary Syndromes

• Stable IHD (Angina): Predictable chest pain with exertion, relieved by rest or nitroglycerin.

• Variant Angina (Vasospastic, Prinzmetal’s): Chest pain at rest due to coronary artery spasm.

• Unstable IHD (Angina): New or worsening chest pain, not relieved by rest, may progress to myocardial infarction.

• Non-ST Elevated Myocardial Infarction (NSTEMI): Myocardial infarction without ST elevation on EKG.

• ST Elevated Myocardial Infarction (STEMI): Myocardial infarction with ST elevation, indicating full-thickness (transmural) infarction.

Ischemic Heart Disease

Pathophysiology

• IHD results from an imbalance between myocardial oxygen supply and oxygen demand.

• Most commonly related to atherosclerosis of the coronary arteries, which restricts blood flow.

• Reduced oxygen supply leads to ischemia and, if prolonged, infarction of myocardial tissue.

Oxygen Supply & Demand

Determinants

Oxygen Supply	Oxygen Demand
O2 saturation (%)	Contractility
Hemoglobin concentration	Heart rate
Cardiac output	Preload/Afterload
Heart rate
Patent (open) coronary artery

• Myocardial tissue extracts approximately 75% of the oxygen supplied to it under normal conditions.

Regulation of Coronary Blood Flow

Mechanisms

• Coronary blood flow primarily occurs during diastole (when the heart muscle is relaxed).

• Vasoconstriction is mediated by the sympathetic nervous system (SNS) and endothelin.

• Vasodilation (increasing blood flow 4-5 times) is mediated by adenosine, nitric oxide (NO), and hypoxia.

• Increased heart rate (HR) reduces diastolic filling time, potentially decreasing coronary perfusion.

• During systole, compression of coronary arteries reduces blood flow; most perfusion occurs in diastole.

Additional info: The left ventricle is especially dependent on diastolic perfusion due to higher wall pressures during systole.

Atherosclerosis and Coronary Blood Flow

Pathogenesis

• Atherosclerosis is the buildup of plaques within the coronary arteries, leading to narrowing and reduced blood flow.

• Plaques can be stable (less likely to rupture) or unstable (prone to rupture, leading to thrombosis).

• Commonly affected arteries include the left anterior descending, left circumflex, and right coronary arteries.

Clinical Presentation of Ischemic Heart Disease

Stable Angina

• Chest pain described as squeezing or suffocating, typically substernal or precordial, may radiate to neck, jaw, shoulder, or arm.

• Often triggered by exertion or emotional stress and relieved by rest or nitroglycerin.

• Duration is usually less than 10 minutes.

• May be confused with gastroesophageal reflux (heartburn).

Unstable Angina

• Chest pain occurs at rest or with minimal exertion, is more severe, prolonged, or frequent than stable angina.

• Not relieved by rest or nitroglycerin within 5-10 minutes.

• Represents a medical emergency and may progress to myocardial infarction.

Myocardial Infarction (MI)

Types

• ST-Elevated Myocardial Infarction (STEMI): Caused by complete thrombosis of a coronary artery, resulting in transmural (full-thickness) infarction.

• Non-ST Elevated Myocardial Infarction (NSTEMI): Caused by partial or intermittent occlusion, resulting in subendocardial (partial-thickness) infarction.

Clinical Presentation of STEMI

• Severe, crushing, or constricting chest pain not relieved by nitroglycerin.

• Associated symptoms: nausea, vomiting, indigestion, fatigue, anxiety, tachycardia, diaphoresis (sweating), and a sense of impending doom.

• Sudden cardiac death may occur within the first hour of MI onset.

Diagnosis of IHD/ACS

Laboratory Testing

• Troponins (I and T): Cardiac-specific proteins released from infarcted myocardial cells; highly sensitive and specific for myocardial injury.

• Troponin levels rise within hours of infarction and remain elevated for 7-10 days.

• Serial measurements are taken at ER arrival, 3 hours, and 6 hours.

• Troponin < 0.4 ng/mL is considered normal; > 0.4 ng/mL is consistent with MI.

Electrocardiogram (EKG) Findings

• ST segment elevation indicates transmural (full-thickness) infarction (STEMI).

• ST segment depression or T wave inversion suggests subendocardial ischemia or infarction (NSTEMI).

Sequelae of NSTEMI/STEMI

Ventricular Remodeling

• Infarcted tissue thins and dilates, while non-infarcted tissue undergoes hypertrophy to preserve stroke volume.

• Overall cardiac function is impaired, especially after STEMI.

Treatment of IHD/ACS

General Principles

• Treat underlying risk factors: hypertension, hyperlipidemia, and lifestyle modifications.

• Improve oxygen supply: supplemental oxygen, RBC transfusion if anemic, nitrates (e.g., nitroglycerin), and coronary vasodilation.

• Surgical interventions: stent placement, coronary artery bypass graft (CABG), balloon angioplasty.

• Pharmacologic interventions: antiplatelet agents (aspirin, clopidogrel, ticagrelor), anticoagulants (heparin, low-molecular-weight heparin), tissue plasminogen activator (for STEMI only).

• Decrease oxygen demand: beta-blockers (reduce heart rate and contractility), non-dihydropyridine calcium channel blockers (verapamil, diltiazem).

Summary Table: Key Features of IHD and ACS

Condition	Pathophysiology	Clinical Features	EKG Findings	Troponin
Stable Angina	Fixed atherosclerotic plaque	Predictable chest pain with exertion, relieved by rest	Usually normal	Normal
Unstable Angina	Plaque rupture, partial thrombosis	New/worsening chest pain, not relieved by rest	ST depression/T wave inversion	Normal
NSTEMI	Partial/intermittent occlusion	Prolonged chest pain, not relieved by rest	ST depression/T wave inversion	Elevated
STEMI	Complete occlusion, transmural infarction	Severe, persistent chest pain, not relieved by rest	ST elevation	Elevated

Key Equations

• Myocardial Oxygen Demand (MVO2):

$MVO_2 \propto \text{Heart Rate} \times \text{Systolic Blood Pressure}$

• Oxygen Delivery (DO2):

$DO_2 = \text{Cardiac Output} \times (1.34 \times \text{Hemoglobin} \times \text{SaO}_2 + 0.0031 \times \text{PaO}_2)$

Additional info: SaO2 is arterial oxygen saturation; PaO2 is arterial oxygen partial pressure.