De Winter syndrome

Overview

De Winter syndrome is a specific electrocardiographic (ECG) pattern indicating acute blockage or severe narrowing of the proximal left anterior descending (LAD) coronary artery. Initially described by cardiologist Robbert J. de Winter in 2008, it represents a distinct variant of acute myocardial infarction (heart attack). Unlike classical ST-elevation myocardial infarction (STEMI), De Winter syndrome manifests as characteristic ECG changes without typical ST-segment elevations, potentially leading to delayed recognition and treatment if not promptly identified.

Causes

The underlying cause of De Winter syndrome is usually acute coronary artery occlusion or severe stenosis, most commonly involving the proximal portion of the LAD artery. This blockage is typically due to:

• Atherosclerosis: Progressive plaque buildup leading to narrowing and acute thrombotic blockage of the coronary artery.

• Blood clot (thrombosis): Sudden formation of a blood clot obstructing blood flow.

• Coronary artery spasm: Less common, sudden tightening of the arterial wall causing temporary blockage.

Risk factors include smoking, hypertension, diabetes, high cholesterol, obesity, and family history of heart disease.

Symptoms

Symptoms of De Winter syndrome closely mimic those of acute myocardial infarction (heart attack) and typically include:

• Chest pain or discomfort: Severe, pressing, squeezing sensation, often radiating to the arm, jaw, or neck.

• Shortness of breath: Sudden difficulty breathing.

• Nausea and vomiting: Frequently occurring alongside chest discomfort.

• Sweating (diaphoresis): Profuse sweating accompanying acute chest pain.

• Dizziness or weakness: Caused by reduced blood flow to the brain.

• Anxiety and restlessness: Common psychological response to acute cardiac ischemia.

Diagnosis

Prompt and accurate diagnosis of De Winter syndrome is essential for effective treatment. Diagnosis is primarily based on characteristic ECG changes, which include:

• Upsloping ST-segment depression: Usually seen prominently in leads V1–V4.

• Tall, symmetrical T-waves: Typically occurring in precordial leads.

• Absence of typical ST-segment elevation: Distinguishing it from a classic STEMI.

Additional diagnostic measures include:

• Coronary angiography: Definitive procedure revealing coronary artery blockage or severe narrowing.

• Cardiac biomarkers: Elevated levels of troponins confirming myocardial injury.

Treatment

Treatment for De Winter syndrome focuses on immediate restoration of blood flow to the affected coronary artery, similarly to treatment strategies used for STEMI. Essential interventions include:

• Emergency coronary angiography and percutaneous coronary intervention (PCI): Urgent catheterization to remove blockage and restore blood flow, typically with stent placement.

• Medication: Administration of antiplatelet agents (aspirin, clopidogrel), anticoagulants, beta-blockers, and nitroglycerin to manage pain and prevent further clotting.

• Supportive care: Supplemental oxygen, intravenous fluids, and pain management.

• Lifestyle modifications: Post-treatment recommendations including smoking cessation, dietary changes, exercise, and cardiac rehabilitation.

Prognosis

With prompt diagnosis and timely treatment, particularly early coronary intervention, the prognosis for patients experiencing De Winter syndrome is generally favorable. Delay in diagnosis and intervention, however, significantly increases the risk of extensive myocardial damage, heart failure, arrhythmias, and increased mortality. Long-term outcomes depend largely on the degree of heart muscle affected, adherence to post-treatment guidelines, and management of cardiovascular risk factors. Early recognition of the ECG pattern characteristic of De Winter syndrome is crucial to improving patient outcomes.