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.

Learning Objectives

• Differentiate between ischemic heart disease and acute coronary syndromes (stable IHD, unstable IHD, NSTEMI, STEMI) based on clinical presentation and pathophysiology.

• Identify determinants of myocardial oxygen supply and demand.

• Describe how blood is supplied to the myocardium, including mediators of vasoconstriction and vasodilation.

• Recognize clinical issues affecting cardiac oxygen supply and demand.

Coronary Artery Disease: Overview

• Ischemic Heart Disease (IHD): Includes stable angina and variant angina (vasospastic, Prinzmetal’s angina).

• Acute Coronary Syndromes (ACS): Includes unstable angina, non-ST elevated myocardial infarction (NSTEMI), and ST elevated myocardial infarction (STEMI).

Ischemic Heart Disease

Pathophysiology

• IHD results from an imbalance between oxygen (O2) supply and O2 demand in myocardial tissue.

• Most commonly related to atherosclerosis of the coronary arteries, which restricts O2 supply.

Oxygen Supply & Demand

Determinants

O2 Supply	O2 Demand
O2 percentage in blood	Myocardial contractility
Hemoglobin concentration	Heart rate
Cardiac output	Preload/Afterload
Heart rate
Patency of coronary arteries

• Myocardial tissue extracts approximately 75% of the O2 supplied to it.

Regulation of Coronary Blood Flow

Mechanisms

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

• 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, 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 in the coronary arteries, leading to reduced blood flow.

• Plaques can be stable (causing predictable angina) or unstable (prone to rupture, leading to ACS).

• Commonly affects 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, possibly radiating to the neck, jaw, shoulder, or arm.

• Pain is usually triggered by exertion or emotional stress and relieved by rest or nitroglycerin.

• Duration is typically less than 10 minutes.

• May be confused with gastroesophageal reflux (heartburn).

Unstable Angina

• Angina at rest, new onset, or increasing in severity, frequency, or duration.

• Pain is more severe, not relieved by nitroglycerin, and may last longer than 10 minutes.

• Represents a transition to acute coronary syndrome.

Acute Coronary Syndromes (ACS)

Types

• Unstable Angina: No myocardial necrosis; negative cardiac biomarkers.

• NSTEMI (Non-ST Elevated Myocardial Infarction): Subendocardial infarction; positive cardiac biomarkers; no ST elevation on EKG.

• STEMI (ST Elevated Myocardial Infarction): Transmural (full-thickness) infarction; positive cardiac biomarkers; ST elevation on EKG.

Pathophysiology

• ACS is usually caused by rupture of an atherosclerotic plaque and subsequent thrombosis, leading to partial or complete occlusion of a coronary artery.

Clinical Presentation of STEMI

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

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

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

Diagnosis of IHD and ACS

Laboratory Testing

• Cardiac troponins (I and T): Proteins released from infarcted myocardial cells; highly sensitive and specific for myocardial infarction.

• 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 depression: Indicates ischemia or subendocardial infarction (NSTEMI).

• ST segment elevation: Indicates transmural infarction (STEMI).

Sequelae of NSTEMI/STEMI

• Infarcted tissue undergoes ventricular remodeling: thinning and dilation of the affected wall.

• Non-infarcted tissue may hypertrophy to preserve stroke volume and overcome increased afterload.

• Overall, cardiac function is impaired, especially after STEMI.

Treatment of IHD and ACS

Address Underlying Risk Factors

• Control hypertension, hyperlipidemia, and encourage lifestyle modifications (diet, exercise, smoking cessation).

Improve Oxygen Supply

• Supplemental oxygen, RBC transfusion if anemic.

• Nitrates (e.g., nitroglycerin, isosorbide dinitrate) for coronary vasodilation.

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

• Tissue plasminogen activator (tPA) to lyse clots (STEMI only).

Prevent Clot Extension

• Antiplatelet agents: aspirin, clopidogrel, ticagrelor.

• Anticoagulants: heparin, low-molecular-weight heparin.

Decrease Oxygen Demand

• Reduce heart rate and contractility with beta-blockers.

• Calcium channel blockers (non-dihydropyridine, e.g., verapamil, diltiazem) may also be used.

Summary Table: Types of Ischemic Heart Disease and Acute Coronary Syndromes

Condition	Pathophysiology	EKG Findings	Biomarkers	Clinical Features
Stable Angina	Fixed atherosclerotic plaque; demand ischemia	Normal or transient ST depression during pain	Negative	Predictable chest pain with exertion, relieved by rest
Unstable Angina	Plaque rupture, partial thrombosis	ST depression or T wave inversion	Negative	New, worsening, or rest angina; not relieved by rest
NSTEMI	Subendocardial infarction	ST depression or T wave inversion	Positive	Prolonged chest pain, not relieved by rest
STEMI	Transmural infarction	ST elevation	Positive	Severe, persistent chest pain, systemic symptoms

Additional info: Early recognition and intervention in ACS can significantly reduce morbidity and mortality. Collateral vessel formation may develop in chronic ischemia, providing some protection against infarction.