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  • 1. Bjorkander, Inge
    et al.
    Forslund, Lennart
    Kahan, Thomas
    Ericson, Mats
    KTH, School of Technology and Health (STH), Ergonomics (Closed 20130701).
    Held, Claes
    Rehnqvist, Nina
    Hjemdahl, Paul
    Differential index: a simple time domain heart rate variability analysis with prognostic implications in stable angina pectoris2008In: Cardiology, ISSN 0008-6312, E-ISSN 1421-9751, Vol. 111, no 2, p. 126-133Article in journal (Refereed)
    Abstract [en]

    OBJECTIVES: To examine the usefulness of time domain heart rate variability (HRV) measurements by a simple graphical method, the differential index (DI), in prognostic assessments of patients with chronic stable angina pectoris.

    METHODS: HRV measurements in the time domain by DI were compared to conventional measurements of standard deviation of all normal-to-normal intervals (SDNN), percent of differences between adjacent normal RR intervals >50 ms (PNN50) and square root of the mean of the sum of squares of differences between adjacent normal RR intervals (RMSSD) from 24-hour ambulatory electrocardiographic recordings in 678 patients in the Angina Prognosis Study in Stockholm. The patients received double-blind treatment with metoprolol or verapamil. Main outcome measures were cardiovascular death or non-fatal myocardial infarction during follow-up (median 40 months).

    RESULTS: Patients suffering cardiovascular death (n = 30) had lower DI, SDNN and PNN50 (all p < 0.001). In a multivariate Cox model, DI below median independently predicted cardiovascular death (p = 0.002), as did SDNN (p = 0.016) and PNN50 (p = 0.030), but not RMSSD (p = 0.10). The separation of survival curves was most pronounced and specificity was slightly better with DI. DI and PNN50 increased with metoprolol but not verapamil treatment. Short-term treatment effects were not related to prognosis.

    CONCLUSIONS: Low time domain HRV carries independent prognostic information regarding cardiovascular death in stable angina pectoris. The simple DI method provided equally good or better prognostic information than conventional, more laborious HRV methods.

  • 2.
    Govind, Satish C.
    et al.
    BMJ Heart Center, Bangalore, India.
    Brodin, Lars-Åke
    Department of Clinical Physiology, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Nowak, J.
    Department of Clinical Physiology, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Quintana, M.
    Department of Clinical Physiology, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Raumina, S.
    Department of Clinical Physiology, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Ramesh, S.S.
    BMJ Heart Center, Bangalore, India.
    Keshava, R.
    BMJ Heart Center, Bangalore, India.
    Saha, S.
    Department of Clinical Physiology, Karolinska University Hospital at Huddinge, Stockholm, Sweden.
    Isolated Type 2 Diabetes mellitus Causes Myocardial Dysfunction That Becomes Worse in the Presence of Cardiovascular Diseases: Results of the Myocardial Doppler in Diabetes (MYDID): Study 12005In: Cardiology, ISSN 0008-6312, E-ISSN 1421-9751, Vol. 103, no 4, p. 189-195Article in journal (Refereed)
    Abstract [en]

    Aims: Patients with type 2 diabetes mellitus (DM) often suffer disproportionately and have a worse outcome when burdened with cardiovascular complications compared with those without DM. A specific heart muscle disease reportedly caused by DM per se may explain this. We sought to investigate whether an echo Doppler diagnosis of such a myocardial disease is clinically relevant in DM with or without coexistent coronary artery disease (CAD) and/or hypertension ( HTN). Subjects and Methods: Two hundred subjects (127 males, 73 females, 56 +/- 10 years) including controls (n=23), patients with HTN (n=20), CAD (n=35), uncomplicated DM (n=59), DM+HTN (n=27), DM+ CAD (n=16) and DM+CAD+HTN (n=20) underwent tissue Doppler-enhanced dobutamine stress echocardiography. Myocardial function was assessed by measuring left ventricular myocardial peak systolic velocity (PSV) and early diastolic velocity at rest and during peak stress, besides measurements of standard Doppler variables. Results: Average left ventricular PSV at rest was significantly lower in CAD (4.7 +/- 1.5) compared with controls (5.7 center dot +/- 1.2) and in DM+CAD+HTN (4.6 +/- 1.4) compared with DM (5.6 +/- 1.3; all p < 0.05). During peak stress, lower PSV persisted in CAD (9.5 +/- 3.1) and DM+CAD+HTN (8.1 +/- 2.7), while appearing de novo in DM (11.3 +/- 2.6) and HTN (11.0 +/- 2.3) unlike in the controls (12.5 +/- 2.5; all p < 0.001). When pooled together, DM subjects with CAD and/or HTN or both had significantly lower PSV (9.1 +/- 2.7) than those without (10.0 +/- 2.8; p < 0.001). Early diastolic velocity response was equally lower in both groups compared with the controls. Conclusion: The results suggest that dobutamine stress unmasks myocardial functional disturbances caused by uncomplicated DM. The discrete disturbances become quantitatively more pronounced in the presence of coexistent cardiovascular diseases.

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