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Search: WFRF:(Kahan T) > Royal Institute of Technology

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1.
  • Björkander, I., et al. (author)
  • Differential index, a novel graphical method for measurements of heart rate variability
  • 2005
  • In: International Journal of Cardiology. - : Elsevier BV. - 0167-5273 .- 1874-1754. ; 98:3, s. 493-499
  • Journal article (peer-reviewed)abstract
    • Background: Commonly used methods to evaluate heart rate variability require extensive filtering of the registrations in order to exclude artefacts and ectopic beats. We developed and validated a novel graphical method for time-domain measurements of heart rate variability, the differential index, which does not require filtering and is simple to use. Methods: The 24-h ambulatory long-term electrocardiogram recordings from 120 patients with angina pectoris and 49 control subjects were computerised without any filtering process. Sample density histograms of differences in the RR interval for successive beats were constructed and the widths of the histograms were used to obtain the differential index. For comparison, the same registrations were analysed by conventional methods. Results: The differential index was most closely related (P < 0.001) to conventional short-term time domain (e.g. percent of differences between adjacent normal RR intervals > 50 ms, pNN50, r = 0.81) and frequency-domain (e.g. high frequency power, r = 0.84) components, but also to long-term time domain (e.g. standard deviation of all normal-to-normal RR intervals for all 5-min segments of the entire registration, SDNNIDX, r = 0.72) and frequency-domain (e.g. low frequency power, r = 0.64) components. Conclusion: The differential index method shows good agreement with established indices of heart rate variability. The insensitivity to recording artefacts and short-lasting disturbances of sinus rhythm make the differential index method particularly suited when data quality is imperfect. The simplicity of the method is valuable when large numbers of registrations are to be evaluated.
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2.
  • Forslund, L, et al. (author)
  • Prognostic implications of autonomic function assessed by analyses of catecholamines and heart rate variability in stable angina pectoris.
  • 2002
  • In: Heart. - : BMJ. - 1355-6037 .- 1468-201X .- 0007-0769. ; 87:5, s. 415-22
  • Journal article (peer-reviewed)abstract
    • OBJECTIVE: To assess the prognostic impact of autonomic activity, as reflected by catecholamines and heart rate variability (HRV), in patients with stable angina pectoris. DESIGN: Double blind, randomised treatment with metoprolol or verapamil. 24 hour ambulatory ECG, used for frequency domain analyses of HRV, and symptom limited exercise tests at baseline and after one month of treatment. Catecholamine concentrations were measured in plasma (rest and exercise) and urine. SETTING: Single centre at a university hospital. PATIENTS: 641 patients (449 men) with stable angina pectoris. MAIN OUTCOME MEASURES: Cardiovascular (CV) death, non-fatal myocardial infarction (MI). RESULTS: During follow up (median 40 months) there were 27 CV deaths and 26 MIs. Patients who died of CV causes had lower total power and high (HF), low (LF), and very low (VLF) frequency components of HRV. HRV was not altered in patients who suffered non-fatal MI. Catecholamines did not differ between patients with and those without events. Metoprolol increased HRV. Verapamil decreased noradrenaline (norepinephrine) excretion. Multivariate Cox analyses showed that total power, HF, LF, and VLF independently predicted CV death (also non-sudden death) but not MI. LF:HF ratios and catecholamines were not related to prognosis. Treatment effects on HRV did not influence prognosis. CONCLUSIONS: Low HRV predicted CV death but not non-fatal MI. Neither the LF:HF ratio nor catecholamines carried any prognostic information. Metoprolol and verapamil influenced LF, HF, and catecholamines differently but treatment effects were not related to prognosis.
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4.
  • Quintana, M, et al. (author)
  • Left ventricular function and cardiovascular events following adjuvant therapy with adenosine in acute myocardial infarction treated with thrombolysis - Results of the ATTenuation by Adenosine of Cardiac Complications (ATTACC) study
  • 2003
  • In: European Journal of Clinical Pharmacology. - : Springer Science and Business Media LLC. - 0031-6970 .- 1432-1041. ; 59:1, s. 1-9
  • Journal article (peer-reviewed)abstract
    • Background: Reperfusion therapy for acute myocardial infarction (AMI) reduces mortality but is also associated with reperfusion injury. The present study tested the hypothesis that adjuvant therapy with a low anti-inflammatory dose of adenosine might prevent reperfusion injury and preserve left ventricular function. Methods: Six hundred and eight patients with ST-elevation AMI were randomised to receive infusions of adenosine (10 mug.kg(-1)min(-1)) or placebo (saline) to be started with thrombolysis and maintained for 6 h. The primary endpoint was global and regional left ventricular systolic and diastolic function, as assessed by two-dimensional and Doppler echocardiography before hospital discharge. The secondary end-point was all cause and cardiovascular mortality, and non-fatal myocardial infarction during 12 months of follow-up. Results: No beneficial effect of adenosine was found regarding echocardiographic indices of left ventricular systolic or diastolic function. Recruitment was stopped due to this apparent lack of effect after an interim analysis. However, after 12 months of follow-up, cardiovascular mortality was 8.9% with adenosine and 12.1% with placebo treatment [odds ratio (OR) 0.71, 95% confidence interval (C.I.) 0.4-1.2, P=0.2] among all patients and 8.4% vs 14.6% (OR 0.53, 95% C.I. 0.23-1.24, P=0.09) among patients with anterior AMI. All cause mortality differed similarly. Non-fatal AMI was not reduced similarly by adenosine treatment. Survival curves indicate that possible survival benefits are maintained after the first year of follow-up. Conclusions: Adenosine, given as adjunctive treatment with thrombolysis, did not provide detectable improvement of echocardiographic indices of left ventricular function when assessed before hospital discharge. Cardiovascular and all cause mortality appear to have been reduced by low-dose adenosine treatment, and the size of the effect appears to be clinically relevant (absolute risk reductions of approximate to4%). The power of the study regarding morbidity and mortality was, however, limited. The results are compatible with a beneficial anti-inflammatory effect of adenosine treatment on reperfusion injury after thrombolysis, which may be mediated by inhibition of leukocytes in peripheral blood. A larger trial is warranted to possibly establish beneficial effects of low-dose adenosine on survival after thrombolysis.
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