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Segmental wall motion abnormalities alter vulnerability to ventricular ectopic beats associated with acute increases
K Siogas1, S Pappas, G Graekas
1Cardiology Department, University General Hospital, Leoforos Panepistimiou, Ioannina, Greece.
Insights
Patients with coronary artery disease and wall motion abnormalities are prone to ventricular arrhythmias when blood pressure increases. Segmental wall motion abnormalities are a key risk factor for these pressure-related arrhythmias.
Area of Science:
- Cardiology
- Electrophysiology
- Cardiac Imaging
Background:
- Coronary artery disease (CAD) can lead to impaired myocardial function.
- Ventricular arrhythmias are a significant concern in patients with CAD.
- The relationship between hemodynamic changes and arrhythmia susceptibility in CAD requires further investigation.
Purpose of the Study:
- To determine if patients with coronary artery disease (CAD) are susceptible to ventricular arrhythmias induced by increased aortic pressure.
- To identify potential risk factors for pressure-related ventricular arrhythmias in CAD patients.
Main Methods:
- An interventional study involving 43 patients with ischemic heart disease undergoing coronary arteriography.
- Metaraminol was administered to increase systolic aortic pressure in patients meeting specific criteria.
- Ventricular ectopic activity was monitored before and during metaraminol infusion.
Main Results:
- Systolic aortic pressure increased significantly during metaraminol infusion (131 to 199 mm Hg).
- Ventricular ectopy increased by over 100% in 13/43 patients.
- A strong association was found between ventricular arrhythmia appearance and segmental wall motion abnormalities (akinesia/dyskinesia), with 83.3% of patients with these abnormalities developing arrhythmias. Ejection fraction was also a significant risk factor.
Conclusions:
- Patients with CAD and segmental wall motion abnormalities are predisposed to ventricular arrhythmias during elevated systolic aortic pressure.
- Electrophysiological inhomogeneity, potentially linked to mechanical inhomogeneity (e.g., post-infarction akinesia/dyskinesia), may explain this predisposition.
- Mechanical inhomogeneity influences the aortic pressure threshold at which ventricular arrhythmias manifest.
Objective:
To evaluate whether patients with coronary artery disease are susceptible to pressure related ventricular arrhythmias, and if so to identify possible risk factors.
Design:
Interventional study.
Methods:
Metaraminol was given to 43 patients undergoing coronary arteriography for ischaemic heart disease to increase their aortic pressure, provided their systolic blood pressure was < 160 mm Hg and they were in sinus rhythm, without any ventricular ectopic activity (or with fewer than six ventricular ectopic beats a minute) during a five minute control period.
Results:
During the metaraminol infusion, systolic aortic pressure rose from 131 (15) to 199 (12) mm Hg (mean (SD)). Ventricular ectopy appeared (or ventricular ectopic beats increased by > 100%) in 13/43 patients. Ventricular ectopy was not related to age, sex, presence of hypertension, history of myocardial infarction, use of beta blockers, positive exercise test, number of vessels diseased, or heart rate change during metaraminol infusion. There was a strong relation between the appearance of ventricular arrhythmia and segmental wall motion abnormalities: 1/19 (5.3%, 95% confidence interval 0.1% to 26.0%) without abnormality; 2/12 (16.7%, 2.1% to 48.4%) with hypokinesia; and 10/12 (83.3%, 51.6% to 97.1%) with akinesia or dyskinesia, chi 2 = 22.7, p < 0.001). Ejection fraction was also a significant but not independent risk factor.
Conclusions:
Patients with segmental wall motion abnormalities are predisposed to ventricular ectopic beats during an increase in systolic aortic pressure. This could be explained by associated electrophysiological inhomogeneity. The presence of mechanical inhomogeneity, as may occur in postinfarction akinesia or dyskinesia, may affect the aortic pressure above which ventricular arrhythmias appear.