Acute coronary syndrome

Introduction

Acute coronary syndrome (ACS) refers to a spectrum of clinical conditions associated with sudden, reduced blood flow to the heart muscle. It represents a major cause of morbidity and mortality worldwide and requires prompt diagnosis and management. Understanding the underlying mechanisms and clinical presentation is critical for effective treatment and improved outcomes.

Anatomy and Physiology of the Coronary Arteries

Coronary Artery Anatomy

The coronary arteries are the blood vessels responsible for supplying oxygenated blood to the myocardium. The main coronary arteries include:

• Left Coronary Artery (LCA): Divides into the left anterior descending (LAD) artery and the left circumflex (LCX) artery, supplying the anterior and lateral walls of the heart.
• Right Coronary Artery (RCA): Supplies the right atrium, right ventricle, and inferior portion of the left ventricle.
• Major Branches: Include diagonal branches from the LAD and marginal branches from the LCX, each supplying specific myocardial territories.

Physiology

Coronary blood flow is regulated to match the oxygen demand of the myocardium. Factors influencing coronary perfusion include:

• Myocardial Oxygen Demand: Determined by heart rate, contractility, and wall stress.
• Coronary Blood Supply: Modulated by coronary artery diameter, vascular resistance, and autoregulatory mechanisms.
• Balance of Supply and Demand: ACS occurs when myocardial oxygen supply falls below demand, often due to obstruction or thrombosis within the coronary arteries.

Pathophysiology of Acute Coronary Syndrome

Atherosclerosis and Plaque Formation

The primary underlying cause of ACS is atherosclerosis, a condition characterized by the accumulation of lipids, inflammatory cells, and fibrous tissue within the coronary artery walls. Over time, this leads to plaque formation, which can narrow the vessel lumen and reduce blood flow. Plaques may remain stable or become vulnerable to rupture depending on their composition and inflammatory activity.

Plaque Rupture and Thrombosis

Acute events in ACS often result from the rupture or erosion of vulnerable plaques. When the plaque surface breaks, it exposes thrombogenic material to the bloodstream, triggering platelet aggregation and clot formation. This intracoronary thrombus can partially or completely obstruct blood flow, causing ischemia and myocardial injury.

Types of ACS

ACS encompasses a spectrum of conditions based on the severity and extent of myocardial ischemia:

• ST-Segment Elevation Myocardial Infarction (STEMI): Complete coronary artery occlusion leading to significant myocardial necrosis, visible as ST-segment elevation on ECG.
• Non-ST-Segment Elevation Myocardial Infarction (NSTEMI): Partial occlusion causing myocardial injury without ST-segment elevation, often associated with elevated cardiac biomarkers.
• Unstable Angina: Chest pain due to transient ischemia without detectable myocardial necrosis, characterized by ECG changes without biomarker elevation.

Risk Factors

Modifiable Risk Factors

Several lifestyle and medical conditions increase the risk of developing acute coronary syndrome, which can be managed or modified:

• Hypertension: Elevated blood pressure contributes to endothelial damage and plaque formation.
• Diabetes Mellitus: High blood glucose accelerates atherosclerosis and increases thrombotic risk.
• Smoking: Promotes vascular inflammation, platelet aggregation, and endothelial dysfunction.
• Dyslipidemia: Elevated LDL cholesterol and low HDL cholesterol favor plaque development.
• Obesity: Associated with metabolic syndrome, insulin resistance, and systemic inflammation.

Non-Modifiable Risk Factors

Certain risk factors cannot be changed but are important for risk stratification:

• Age: Risk increases significantly after 45 years in men and 55 years in women.
• Gender: Men generally have higher ACS incidence at an earlier age; postmenopausal women experience increased risk.
• Family History: Genetic predisposition to premature coronary artery disease increases susceptibility.
• Genetic Factors: Specific gene variants may influence lipid metabolism, inflammatory response, and thrombosis.

Clinical Presentation

Symptoms

The hallmark symptom of ACS is chest discomfort, but presentations may vary:

• Chest Pain: Typically retrosternal, pressure-like, radiating to the left arm, neck, jaw, or back.
• Dyspnea: Shortness of breath due to myocardial ischemia or heart failure.
• Diaphoresis: Excessive sweating caused by sympathetic activation.
• Nausea and Vomiting: Often associated with inferior wall myocardial infarction.
• Syncope or Dizziness: May indicate arrhythmias or severe ischemia.

Physical Examination

Physical findings can vary based on the severity and location of ischemia:

• Vital Signs: May reveal hypotension, tachycardia, or signs of shock.
• Cardiac Findings: S4 gallop, new murmurs indicating mitral regurgitation or ventricular septal defect.
• Systemic Findings: Pulmonary crackles in heart failure, peripheral cyanosis, or diaphoresis.

Diagnostic Evaluation

Electrocardiography (ECG)

ECG is the first-line diagnostic tool for ACS and helps differentiate between STEMI, NSTEMI, and unstable angina:

• STEMI: Persistent ST-segment elevation in contiguous leads indicates complete coronary occlusion.
• NSTEMI: ST-segment depression or T-wave inversion suggests subendocardial ischemia without complete occlusion.
• Serial ECGs: Repeated recordings are important for detecting dynamic changes and evolving infarction.

Cardiac Biomarkers

Measurement of cardiac-specific enzymes and proteins confirms myocardial injury:

• Troponins (I and T): Highly sensitive and specific markers for myocardial necrosis, rising within 3-6 hours and remaining elevated for 7-10 days.
• Creatine Kinase-MB (CK-MB): Useful for detecting reinfarction due to its shorter half-life.
• Interpretation: Serial measurements are essential to differentiate acute from chronic elevations.

Imaging Studies

Imaging complements ECG and biomarkers to assess cardiac structure and coronary anatomy:

• Echocardiography: Evaluates wall motion abnormalities, ventricular function, and complications such as pericardial effusion.
• Coronary Angiography: Gold standard for identifying the location and severity of coronary obstruction and guiding intervention.
• CT Coronary Angiography: Non-invasive alternative for evaluating coronary anatomy in selected patients.

Management

Initial Stabilization

Prompt stabilization of ACS patients is critical to limit myocardial damage and improve outcomes:

• Oxygen Therapy: Administered if oxygen saturation is below 90% or the patient is in respiratory distress.
• Analgesia: Morphine may be used to relieve severe chest pain and anxiety.
• Monitoring: Continuous ECG, blood pressure, and oxygen saturation monitoring to detect arrhythmias or hemodynamic instability.
• Antiplatelet Therapy: Aspirin and P2Y12 inhibitors reduce thrombus formation.
• Anticoagulation: Heparin or other anticoagulants prevent further clot propagation.

Reperfusion Strategies

Restoration of coronary blood flow is essential in ACS, particularly STEMI:

• Percutaneous Coronary Intervention (PCI): Preferred method for reperfusion, involving balloon angioplasty and stent placement.
• Thrombolytic Therapy: Used when PCI is not immediately available; drugs such as alteplase or tenecteplase dissolve the thrombus.
• Timing: Early reperfusion within the first 90-120 minutes of symptom onset is critical for optimal outcomes.

Medical Management

Adjunctive pharmacologic therapies help reduce myocardial workload, prevent complications, and improve prognosis:

• Beta-Blockers: Decrease heart rate and myocardial oxygen demand.
• ACE Inhibitors/ARBs: Reduce afterload, prevent ventricular remodeling, and improve survival.
• Statins: Lower LDL cholesterol and stabilize atherosclerotic plaques.
• Other Medications: Nitrates for ischemic pain, and antiarrhythmics if necessary.

Long-Term Management

Secondary prevention aims to reduce recurrence and improve long-term survival:

• Lifestyle Modifications: Smoking cessation, healthy diet, weight control, and regular exercise.
• Medication Adherence: Continued use of antiplatelets, statins, beta-blockers, and ACE inhibitors as indicated.
• Cardiac Rehabilitation: Structured programs to restore physical function, manage risk factors, and provide psychosocial support.

Complications

Acute coronary syndrome can lead to several serious complications, which may arise during the acute phase or later in the disease course:

• Arrhythmias: Ventricular tachycardia, ventricular fibrillation, or atrial fibrillation may occur due to ischemic myocardium.
• Heart Failure: Impaired ventricular function can result in pulmonary congestion, edema, and reduced cardiac output.
• Cardiogenic Shock: Severe myocardial damage can lead to hypotension, end-organ hypoperfusion, and high mortality risk.
• Mechanical Complications: Include ventricular septal rupture, papillary muscle rupture causing mitral regurgitation, and free wall rupture leading to cardiac tamponade.
• Pericarditis: Inflammation of the pericardium may develop post-infarction.

Prognosis

The prognosis of ACS depends on the extent of myocardial injury, timeliness of treatment, and underlying comorbidities:

• Short-Term Outcomes: Early reperfusion therapy significantly reduces mortality and limits infarct size.
• Long-Term Outcomes: Patients with preserved ventricular function and controlled risk factors have improved survival.
• Factors Influencing Prognosis: Age, comorbidities, infarct location and size, left ventricular ejection fraction, and timely initiation of reperfusion therapy all impact outcomes.

Prevention

Primary Prevention Strategies

Preventing the first occurrence of acute coronary syndrome involves addressing modifiable risk factors and promoting cardiovascular health:

• Lifestyle Modifications: Adopting a heart-healthy diet, engaging in regular physical activity, maintaining a healthy weight, and avoiding tobacco use.
• Management of Comorbidities: Effective control of hypertension, diabetes, and dyslipidemia through medication and lifestyle measures.
• Regular Screening: Periodic cardiovascular risk assessments to detect early signs of atherosclerosis.

Secondary Prevention Measures

For patients with a history of ACS, secondary prevention aims to reduce recurrence and improve long-term survival:

• Medication Adherence: Continued use of antiplatelets, statins, beta-blockers, and ACE inhibitors as prescribed.
• Cardiac Rehabilitation: Structured programs combining exercise, education, and psychosocial support to optimize recovery.
• Ongoing Risk Factor Management: Regular monitoring and lifestyle adjustments to control blood pressure, blood glucose, and cholesterol levels.
• Patient Education: Encouraging awareness of symptoms, prompt medical attention for recurrent angina, and adherence to healthy habits.

References

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