Non-invasive predictors of mortality after acute myocardial infarction
1University of Oulu, Faculty of Medicine, Department of Internal Medicine
|Online Access:||PDF Full Text (PDF, 1.4 MB)|
|Persistent link:|| http://urn.fi/urn:isbn:9514270118
|Publish Date:|| 2003-05-03
|Thesis type:||Doctoral Dissertation
|Defence Note:||Academic Dissertation to be presented with the assent of the Faculty of Medicine, University of Oulu, for public discussion in the Auditorium 10 of the University Hospital of Oulu, on May 3rd, 2003, at 12 noon.
Docent Juha Hartikainen
Docent Juhani Koistinen
There is a need to identify patients with an increased risk of dying after acute myocardial infarction (AMI), because sudden cardiac death (SCD) and potentially fatal ventricular tachyarrhythmias can be prevented by an implantable cardioverter-defibrillator, or in some cases, with aggressively optimized drug or revascularization therapy. The present study was designed to study the predictive power of non-invasive risk markers and all-cause, cardiac and arrhythmic mortality in 700 consecutive post-AMI patients discharged alive with optimal medication according to contemporary guidelines.
Detrended fluctuation analysis of heart rate variability (HRV) predicted all-cause mortality beyond clinical variables as well as left ventricular function in post-AMI patients. The predictive power of the short-term scaling exponent α₁ was higher than that of the traditional indexes of HRV (for α₁ < 0.65, the risk ratio (RR) in multivariate analysis was 5.1, with 95% confidence intervals (CI) 2.9–8.9; p < 0.001). HRV results from a conventional 24-hour electrocardiographic (ECG) recording system differed significantly when compared to a system with a higher sampling frequency. The difference was generally more pronounced in post-AMI patients than in healthy subjects.
The presence of sustained T-wave alternans during a predischarge exercise test after AMI was not a marker of mortality. However, the inability to perform an exercise test or to reach the heart rate of 105 beats/min predicted independently all-cause (RR 9.3, 95% CI 2.0–43.3, p < 0.01) and cardiac mortality (RR 11.1, 95% CI 2.4–50.8, p < 0.01). High levels of natriuretic peptides were associated with both sudden and non-sudden cardiac mortality. B-type natriuretic peptide provided more specific independent information on the risk for subsequent SCD (RR 3.9, 95% CI 1.2–12.3, p < 0.05) than non-SCD.
SCDs occurred mainly more than 18 months after AMI, and the proportion of SCD was less than 40% of all cardiac deaths. Common arrhythmia markers such as the presence of ventricular premature beats or episodes of nonsustained ventricular tachycardia during ambulatory recordings, the time domain parameters of HRV, baroreflex sensitivity, QT dispersion and QRS complex duration provided only limited predictive power on the risk of SCD or arrhythmic events in patients with optimized beta-blocking therapy. Many risk variables previously considered to predict SCD were better predictors of non-SCD than SCD.
Conclusions: 1. The epidemiological pattern of SCD was different from that reported previously. 2. Many arrhythmia risk markers provided only limited information on the risk of SCD. 3. Short-term fractal scaling exponent α₁ provided potentially useful information on the risk for all-cause mortality, and BNP was useful in predicting the risk of SCD in a post-AMI population with optimized therapy.
Acta Universitatis Ouluensis. D, Medica
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