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"Reciprocal" depression of the ST segment in acute myocardial infarction
Insights
Reciprocal ST depression in acute myocardial infarction may indicate ischemia in new areas. This finding is linked to increased risks of arrhythmias and later health issues.
Area of Science:
- Cardiology
- Ischemic Heart Disease
Background:
- ST elevation myocardial infarction (STEMI) is often associated with reciprocal ST depression.
- Reciprocal ST depression is traditionally attributed to reciprocal changes, not local ischemia.
Purpose of the Study:
- To investigate if reciprocal ST depression in acute myocardial infarction (AMI) reflects local ischemia.
- To assess the association between reciprocal ST depression and patient outcomes.
Main Methods:
- 103 patients with AMI underwent exercise testing 12 days post-infarction.
- Reciprocal change defined as ≥1 mm ST depression in remote leads within 48 hours of infarction.
- Coronary arteriography or necropsy assessed coronary artery disease.
Main Results:
- 34% of patients showed reciprocal ST depression.
- 63% of those with reciprocal ST depression developed exercise-induced ST depression in the same leads.
- Patients with reciprocal ST depression had higher rates of reinfarction, pulmonary edema, death, and in-hospital ventricular fibrillation.
Conclusions:
- Reciprocal ST depression in AMI may signify ischemia in territories distant from the infarct site.
- This finding is an indicator of increased risk for fatal arrhythmias and long-term morbidity.
Abstract:
In acute myocardial infarction depression of the ST segment in leads distant from those showing ST elevation has been considered to be "reciprocal" but might reflect local ischaemia. To examine this possibility 103 consecutive patients who underwent exercise testing early after myocardial infarction were reviewed. Treadmill exercise testing was performed a mean of 12 (range 5-30) days after infarction using a limited Naughton protocol. Thirty five (34%) of the patients had had reciprocal change, defined as greater than or equal to 1 mm ST depression in leads remote from the site of the infarct, within 48 hours of infarction. Twenty two (63%) of the 35 patients developed exercise induced ST depression in the leads previously showing reciprocal change. Coronary artery disease was assessed in 10 of these patients by arteriography and in four at necropsy: all but one had stenosis of greater than or equal to 50% in a coronary artery supplying the reciprocal territory in addition to the disease in the vessel to the infarct site. Of patients with reciprocal ST depression, 23.5% experienced nonfatal reinfarction, pulmonary oedema after discharge, or death compared with only 9.5% of patients without reciprocal ST depression. Eight (23.5%) patients with reciprocal depression had ventricular fibrillation while in hospital compared with only two (3%) patients without. Reciprocal ST depression in acute myocardial infarction may reflect ischaemia in territory distant from the site of infarction and is associated with a high risk of fatal arrhythmias and late morbidity.