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Wall motion abnormalities and late ventricular arrhythmia during the predischarge phase of acute myocardial
A L Bordalo-Sá1, M E Sá, M J Correia
1UTIC-Arsénio Cordeiro (CCU), Hospital Santa Maria, Faculdade de Medicina de Lisboa, Portugal.
Insights
Left ventricular aneurysm did not increase ventricular arrhythmia risk after myocardial infarction. Severe wall motion abnormalities, like dyskinesia, were linked to higher arrhythmia occurrence, suggesting functional, not anatomical, causes.
Area of Science:
- Cardiology
- Cardiac Electrophysiology
- Myocardial Infarction Research
Background:
- Left ventricular aneurysm is a known complication of acute myocardial infarction (MI).
- Aneurysms have been implicated as potential triggers for cardiac failure and ventricular arrhythmias.
- The relationship between severe left ventricular wall motion abnormalities and ventricular arrhythmia requires further investigation.
Purpose of the Study:
- To evaluate the association between severe left ventricular wall motion abnormalities and the occurrence of ventricular arrhythmia following acute myocardial infarction.
- To differentiate the arrhythmic potential of left ventricular aneurysm versus other forms of severe wall motion dysfunction.
Main Methods:
- 146 patients with acute MI were studied over two years.
- Radionuclide angiography assessed left ventricular wall motion and phase changes.
- Patients were categorized into: localized hypokinesia/akinesia (n=102), aneurysm (n=19), and dyskinesia/extensive akinesia (n=25).
- Ventricular arrhythmia was monitored via Holter ECG during the second week post-MI.
Main Results:
- Left ventricular aneurysm was not significantly associated with increased premature ventricular contractions (PVCs).
- Patients with dyskinesia/extensive akinesia showed significantly higher rates of frequent PVCs (>3/h) (48%) and repetitive PVCs (32%) compared to other groups.
- Hypokinesia/localized akinesia patients had the lowest incidence of PVCs across all categories.
Conclusions:
- Left ventricular aneurysm does not appear to be a significant predictor of ventricular arrhythmia post-MI.
- Functionally severe left ventricular wall motion abnormalities, specifically dyskinesia, are strongly associated with increased ventricular arrhythmia.
- These findings suggest that the electrophysiological mechanisms underlying ventricular arrhythmia are more closely related to the functional severity of wall motion impairment than to specific anatomical definitions like aneurysm.
Background:
Left ventricular wall aneurysm is a complication of acute myocardial infarction which has been considered a precipitating factor of cardiac failure and ventricular arrhythmia. We have evaluated the relation between severe left ventricular wall motion abnormalities and ventricular arrhythmia.
Methods:
During a two-year period 146 patients admitted to a coronary care unit with acute myocardial infarction were studied. Radionuclide angiography performed within the second and the fourth weeks was used to analyse phase and wall motility changes, and patients were divided into three groups: 1) Hypokinesia and/or akinesia localized to one segment: with no or slight changes in phase image--102 patients; 2) Aneurysm: left ventricular deformity with well-defined chromatic changes in phase image--19 patients; and 3) Dyskinesia and/or extensive akinesia of two or more segments: phase image with diffuse heterogeneous changes--25 patients. Ventricular arrhythmia was studied using Holter electrocardiography taken during the second week of acute myocardial infarction. Three rhythmic profiles were considered: no premature ventricular contractions--41 patients; with three or more than three premature ventricular contractions per hour--38 patients; repetitive premature ventricular contractions--20 patients.
Results:
Premature ventricular contractions were absent in 31 (30%) of the patients with hypokinesia/localized akinesia vs 8 (42%) of the patients with aneurysm, and vs 2 (8%) of the patients with dyskinesia/extensive akinesia. Premature ventricular contractions were frequent (> or = 3/h) in 22 (22%) of the patients with hypokinesia/localized akinesia vs 4 (21%) of the patients with aneurysm (p = 0.35; NS), and vs 12 (48%) of the patients with dyskinesia/extensive akinesia (p=0.003). Repetitive premature ventricular contractions were present in 10 (10%) of the patients with hypokinesia/localized akinesia vs 2 (11%) of the patients with aneurysm, and vs 8 (32%) of the patients with dyskinesia/extensive akinesia (p=0.008).
Conclusions:
We conclude that the presence of aneurysm was not associated with a higher occurrence of ventricular arrhythmia, but patients with dyskinesia/extensive akinesia had a higher occurrence of ventricular arrhythmia, > or = 3 premature ventricular contractions per hour and repetitive premature ventricular contractions. Our results suggest that ventricular arrhythmia is related to functionally severe wall motion abnormalities, and not to anatomical discriminants. This finding leads us to suggest different electrophysiological mechanisms behind these two entities.