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Published on: August 17, 2022
Electrocardiographic changes in coronary endothelial dysfunction
Gautam Kumar1, Kyle W Klarich, Nicole D Collett
1Division of Cardiovascular Diseases, Mayo Clinic, Rochester, Minnesota 55905, USA.
Insights
Electrocardiogram (ECG) changes during acetylcholine testing can indicate coronary endothelial dysfunction, even without chest pain. Invasive studies are crucial for diagnosing this early stage of coronary artery disease.
Area of Science:
- Cardiology
- Vascular Biology
- Diagnostic Imaging
Background:
- Coronary endothelial dysfunction is a precursor to coronary artery disease.
- Electrocardiographic (ECG) changes can manifest during provocative testing.
Purpose of the Study:
- To document the incidence and types of ECG changes during acetylcholine-induced coronary endothelial dysfunction.
- To correlate ECG findings with coronary artery diameter and blood flow changes.
Main Methods:
- Intracoronary acetylcholine injections (10^-6 to 10^-4 mmol/l) were administered to 69 patients.
- Twelve-lead ECGs were recorded at baseline and after each injection.
- Exclusion criteria included prior nitroglycerin use, significant coronary artery disease, and age < 18.
Main Results:
- Five patients (7.2%) exhibited ECG changes, including ST-segment elevation and T-wave inversions.
- Acetylcholine administration prolonged QT and corrected QT intervals (P<0.05).
- Increased corrected QT interval correlated with greater coronary blood flow and less coronary artery diameter reduction (P<0.05).
Conclusions:
- ECG abnormalities can occur during acetylcholine testing for endothelial dysfunction.
- Invasive assessment is recommended for diagnosing coronary endothelial dysfunction, even with negative chest pain ECGs.
Objective:
Coronary endothelial dysfunction is the early stage of coronary artery disease. We documented the incidence and type of electrocardiographic changes during acetylcholine-induced coronary endothelial dysfunction.
Methods:
Endothelial function studies were performed with intracoronary injections of 10(-6), 10(-5), and 10(-4) mmol/l acetylcholine. Twelve-lead electrocardiograms were obtained at baseline, after each acetylcholine injection, and at the end of the procedure. Exclusion criteria included use of nitroglycerin within the previous 24 h, coronary artery disease with stenosis of more than 30% of the luminal diameter, intolerance to acetylcholine injection, and patient age younger than 18 years. Of the 75 patients enrolled, six were excluded, and 69 were analyzed (69.6% female, 30.4% male; mean age, 47.8 years).
Results:
Among the 69 patients, 11.6% had right bundle branch block and 4.3% had left anterior fascicular block; one had left ventricular hypertrophy by voltage criteria, and five had electrocardiographic changes during acetylcholine injection: one had inferior ST-segment elevations, three had T-wave inversions, and one had resolution of baseline T-wave inversions. Only one of these five patients had periprocedural chest pain; it was associated with a decrease in coronary artery diameter (P<0.05). QT and corrected QT intervals were prolonged after acetylcholine administration (P<0.05). An increase of 10 ms or more in the corrected QT interval was associated with a greater increase in coronary artery blood flow (P<0.05) and a smaller decrease in coronary artery diameter (P<0.05).
Conclusion:
For the diagnosis of coronary endothelial dysfunction, invasive studies should be conducted even if electrocardiograms during chest pain were negative.
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