Mechanisms of Ventricular Tachycardia in STEMI Patients
Ventricular tachycardia (VT) in STEMI patients occurs through multiple mechanisms including ongoing ischemia, hemodynamic and electrolyte abnormalities, reentry, and enhanced automaticity, with up to 20% of STEMI patients experiencing VF or sustained VT. 1
Primary Mechanisms of VT in STEMI
Ongoing myocardial ischemia is a major trigger for ventricular arrhythmias, with VT/VF often being the first manifestation of ischemia requiring immediate correction 1
Hemodynamic compromise including pump failure and cardiogenic shock creates an arrhythmogenic substrate that can trigger VT 1
Electrolyte disturbances, particularly hypomagnesemia and hypokalemia, significantly contribute to the development of VF and should be promptly corrected 1
Autonomic imbalance during acute ischemia alters cardiac electrical properties and can precipitate ventricular arrhythmias 1
Reentry circuits form in damaged myocardium, particularly at the border zones between infarcted and healthy tissue, creating a substrate for VT 1
Enhanced automaticity in surviving myocytes within and surrounding the infarct zone can trigger ventricular arrhythmias 1
Acid-base disturbances associated with acute ischemia can destabilize myocardial cell membranes and promote arrhythmogenesis 1
Timing and Incidence of VT in STEMI
Early VT/VF (within 48 hours of STEMI onset) occurs in approximately 5-6% of patients undergoing primary PCI, with 60-64% occurring within the first 24 hours 1, 2
Late VT/VF (after 48 hours) is less common but associated with higher mortality (33.3% vs. 17.2% for early VT/VF) 2
Reperfusion timing significantly impacts VT risk, with delayed reperfusion (>5 hours) conferring a sixfold increase in the odds of inducible VT compared to early reperfusion (≤3 hours) 3
Risk Factors for VT in STEMI
Pre-PCI TIMI flow grade 0 (complete occlusion) increases risk of early VT/VF nearly threefold 2
Inferior infarction is associated with more than double the risk of early VT/VF 2
Greater total baseline ST deviation correlates with increased VT/VF risk 2
Reduced creatinine clearance is an independent predictor of early VT/VF 2
Higher Killip class (>I) indicates nearly double the risk of early VT/VF 2
Lower baseline systolic blood pressure is associated with increased risk of both early and late VT/VF 2
Incomplete ST resolution (<70%) after reperfusion increases risk of late VT/VF more than threefold 2
Post-PCI TIMI flow less than grade 3 doubles the risk of late VT/VF 2
Structural Factors Contributing to VT
Left ventricular aneurysm formation (<5% of STEMI patients) creates a substrate for reentrant VT circuits, particularly in anterior infarctions 1
Papillary muscle dysfunction or rupture can lead to hemodynamic deterioration and trigger arrhythmias 1
Ventricular free wall rupture, while often fatal, can present with VT/VF as part of the clinical deterioration 1
Prevention and Management Considerations
Beta-blockers reduce VT/VF incidence in STEMI and should be administered early unless contraindicated 1
Prompt reperfusion therapy significantly reduces the risk of VT/VF, with early reperfusion associated with faster VT (shorter cycle length) but fewer spontaneous arrhythmias 3, 4
Arrhythmia monitoring should be initiated immediately on presentation with STEMI and continued for at least 12-24 hours after reperfusion 1
ICD implantation is indicated before discharge in patients who develop sustained VT/VF more than 48 hours after STEMI, provided the arrhythmia is not due to transient or reversible causes 1
Clinical Implications
VT/VF in STEMI is associated with significantly higher mortality (23.2% vs. 3.6% at 90 days) 2
Patients with early VT/VF have a higher risk of stent thrombosis (13.7% vs. 5.7% at 3 years) 5
The mechanisms of arrhythmias during acute ischemia differ from those in chronic stable ischemic heart disease, requiring different management approaches 1
Prophylactic lidocaine may reduce VF incidence but has been abandoned due to increased mortality from bradycardia and asystole 1