Are there any myocardial (MI) occlusions that are more likely to present with supraventricular tachycardia (SVT)?

Myocardial Infarction Locations Associated with SVT Presentation

No specific MI occlusion locations are more likely to present with supraventricular tachycardia, but proximal right coronary artery occlusions causing inferior MI can trigger SVT through involvement of the sinoatrial nodal artery, which supplies the atria. 1

Mechanism of SVT in Acute MI

Inferior MI with proximal RCA occlusion is the primary anatomic pattern associated with SVT development because:

• The sinoatrial nodal artery, which provides major blood supply to the atria, typically arises from the proximal right coronary artery 1
• Occlusion at this location causes atrial ischemia in addition to ventricular infarction 1
• This atrial involvement creates the substrate for supraventricular arrhythmias including atrial fibrillation, atrial flutter, and supraventricular tachycardia 1

Incidence and Clinical Context

SVT occurs in 10-16% of acute MI patients overall, with higher rates in specific populations 1:

• Incidence increases with age: 4.2% in patients ≤59 years versus 16% in patients ≥70 years 1
• More common with anterior MI location 1
• Associated with larger infarct size 1
• Occurs more frequently when complicated by congestive heart failure, complex ventricular arrhythmias, advanced AV block, or pericarditis 1

Timing and Presentation

Most SVT episodes occur within the first 24-48 hours of MI 1, 2:

• 93% of supraventricular tachyarrhythmias begin within the first 48 hours 2
• Generally preceded by frequent or repetitive atrial premature beats 2
• Systemic embolization risk is highest on the first day, with >90% occurring by day 4 1

Critical Diagnostic Pitfall

ST segment depression during SVT does not necessarily indicate acute coronary occlusion or ongoing MI 3, 4:

• ST depression of 1-8 mm in multiple leads commonly occurs during SVT even without coronary disease 3
• This represents rate-related subendocardial ischemia from oxygen supply-demand mismatch, not epicardial coronary occlusion 3
• Myocardial lactate studies show no net lactate production during SVT in patients without coronary disease, despite marked ST depression 3
• ST depressions may persist even after SVT terminates, reflecting small vessel ischemia not visible on angiography 4
• Do not assume new coronary occlusion based solely on ST changes during tachycardia—the rapid rate itself causes these changes 3, 4

Hemodynamic Consequences

SVT causes severe hemodynamic compromise in approximately 20% of MI patients 2:

• Associated with older age and overt left ventricular dysfunction 2
• However, SVT is not an independent predictor of cardiac death during hospitalization or 2-year follow-up 2
• Medical therapy effectively suppresses these arrhythmias in most cases 2