Mikko P Tulppo

Prof. Mikko P Tulppo


Research Focus & Metrics

Academic Career Length

31Years (1996-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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14 May 2001 in Clinical Physiology and Functional Imaging
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JPJani Penttilä
Jani Penttilä
AHAntti Helminen
Antti Helminen
TJTuomas Jartti
Tuomas Jartti
TKTom Kuusela
Tom Kuusela
HHHeikki V. Huikuri
Heikki V. Huikuri
HSHarry Scheinin
Harry Scheinin

1 July 1996 in American Journal of Physiology-Heart and Circulatory Physiology
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MTMikko P Tulppo
Mikko P Tulppo
TMT. H. Makikallio
T. H. Makikallio
TTT. E. Takala
T. E. Takala
TST. Seppanen
T. Seppanen
HHH. V. Huikuri
H. V. Huikuri
Beat-to-beat heart rate (HR) dynamics were studied by plotting each R-R interval as a function of the previous R-R interval (Poincare plot) during incremental doses of atropine followed by exercise for 10 subjects and during exercise without autonomic blockade for 31 subjects. A quantitative two-dimensional vector analysis of a Poincare plot was used by measuring separately the standard deviation of instantaneous beat-to-beat R-R interval variability (SD1) and the standard deviation of continuous long-term R-R interval variability (SD2) as well as the SD1/SD2 ratio. Quantitative Poincare measures were compared with linear measures of HR variability (HRV) and with approximate entropy (ApEn) at rest and during exercise. A linear progressive reduction was observed in SD1 during atropine administration, and it remained almost at the zero level during exercise after a parasympathetic blockade. Atropine resulted in more variable changes in SD2 and the SD1/SD2 ratio, but during exercise after parasympathetic blockade, a progressive increase was observed in the SD1/SD2 ratio until the end of exercise. The SD1/SD2 ratio had no significant correlations with the frequency domain measures of HRV. However, the SD1/SD2 ratio had a modest correlation with ApEn at rest (r = -0.69, P < 0.001), but not during exercise (r = 0.27, P = NS). All measures of vagal modulation of HR decreased progressively until the ventilatory threshold level was reached, when sympathetic activation was reflected as changes in the SD1/SD2 ratio. These results show that quantitative two-dimensional vector analysis of a Poincare plot can provide useful information on vagal modulation of R-R interval dynamics during exercise that are not easily detected by linear summary measures of HRV or by ApEn.

12 September 2007 in European Journal of Applied Physiology
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AKAntti Kiviniemi
Antti Kiviniemi
AHArto J. Hautala
Arto J. Hautala
HKHannu Kinnunen
Hannu Kinnunen
MTMikko P Tulppo
Mikko P Tulppo

19 July 2005 in Circulation
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MTMikko P Tulppo
Mikko P Tulppo
AKAntti Kiviniemi
Antti Kiviniemi
AHArto J. Hautala
Arto J. Hautala
MKMika Kallio
Mika Kallio
TSTapio SeppänEn
Tapio SeppänEn
HHHeikki V. Huikuri
Heikki V. Huikuri
Background— Altered fractal heart rate (HR) dynamics occur during various disease states, but the physiological background of abnormal fractal HR behavior is not well known. We tested the hypothesis that the fractal organization of human HR dynamics is determined by the balance between sympathetic and vagal outflow. Methods and Results— A short-term fractal scaling exponent (α 1 ) of HR dynamics, analyzed by the detrended fluctuation analysis (DFA) method, and the high-frequency (HF) and low-frequency (LF) spectral components of R-R intervals (0.15 to 0.4 Hz; n=13), along with muscle sympathetic nervous activity (MSNA) from the peroneus nerve (n=11), were assessed at rest and during cold face and cold hand immersion in healthy subjects. During cold face immersion, HF power increased (from 6.9±1.3 to 7.6±1.2 ln ms 2 , P <0.01), as did MSNA (from 32±17 to 44±14 bursts/100 heartbeats, P <0.001), and LF/HF ratio decreased ( P <0.01). Cold hand immersion resulted in a similar increase in MSNA (from 34±17 to 52±19 bursts/100 heartbeats, P <0.001) but a decrease in HF spectral power (from 7.0±1.3 to 6.5±1.1 ln ms 2 , P <0.05) and an increase in the LF/HF ratio ( P <0.05). The fractal scaling index α 1 decreased in all subjects (from 0.85±0.27 to 0.67±0.30, P <0.0001) during cold face immersion but increased during cold hand immersion (from 0.77±0.22 to 0.97±0.20, P <0.01). Conclusions— The fractal organization of human HR dynamics is determined by a delicate interplay between sympathetic and vagal outflow, with the breakdown of fractal HR behavior toward more random dynamics occurring during coactivation of sympathetic and vagal outflow.

1 February 1998 in American Journal of Physiology-Heart and Circulatory Physiology
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MTMikko P Tulppo
Mikko P Tulppo
TMTimo H. Mäkikallio
Timo H. Mäkikallio
TSTapio Seppänen
Tapio Seppänen
RLRaija T. Laukkanen
Raija T. Laukkanen
HHHeikki V. Huikuri
Heikki V. Huikuri
This study was designed to assess the effects of age and physical fitness on vagal modulation of heart rate (HR) during exercise by analyzing the instantaneous R-R interval variability from Poincaré plots (SD1) at rest and at different phases of a bicycle exercise test in a population of healthy males. SD1 normalized for the average R-R interval (SD1n), a measure of vagal activity, was compared at rest and during exercise among subjects of ages 24–34 (young, n = 25), 35–46 (middle-aged, n = 30), and 47–64 yr (old, n = 25) matched for peak O2 consumption (V˙o 2 peak) and among subjects withV˙o 2 peak of 28–37 (poor, n = 25), 38–45 (average, n = 36), and 46–60 ml ⋅ kg−1 ⋅ min−1(good, n = 25) matched for age. SD1n was higher at rest in the young subjects than in the middle-aged or old subjects (39 ± 14, 27 ± 16, and 21 ± 8, respectively; P < 0.001), but the age-related differences in SD1n were smaller during exercise [e.g., 11 ± 5, 9 ± 5, and 8 ± 4 at the level of 100 W; P = not significant (NS)]. The age-matched subjects with good, average, and poor V˙o 2 peakshowed no difference in SD1n at rest (32 ± 17, 28 ± 13, and 26 ± 11, respectively; P = NS), but SD1n differed significantly among the groups from a low to a moderate exercise intensity level (e.g., 13 ± 6, 10 ± 5, and 6 ± 3 for good, average, and poor fitness groups, respectively; P < 0.001, 100 W). These data show that poor physical fitness is associated with an impairment of cardiac vagal function during exercise, whereas aging itself results in more evident impairment of vagal function at rest.

18 March 2005 in European Heart Journal
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TMTimo H. Mäkikallio
Timo H. Mäkikallio
PBPetra Barthel
Petra Barthel
RSRaphael Schneider
Raphael Schneider
ABAxel Bauer
Axel Bauer
JTJari M. Tapanainen
Jari M. Tapanainen
HHHeikki V. Huikuri
Heikki V. Huikuri
Aims Current treatment may have changed the risk profiles of survivors of acute myocardial infarction (AMI). We evaluated the utility of Holter-based risk variables in the prediction of sudden cardiac death (SCD) among survivors of AMI treated with modern therapy. Methods and results A total of 2130 AMI patients (mean age 59±10 years) were included. The patients were treated with modern therapeutic strategies, for example, 94% were on β-blocking therapy and 70% underwent coronary revascularization. Various risk parameters from Holter monitoring were analysed. During a median follow-up of 1012 days (interquartile range: 750–1416 days), cardiac mortality was 113/2130, including 52 SCDs. All Holter variables predicted the occurrence of SCD (P<0.01), but only reduced post-ectopic turbulence slope (TS) (P<0.001) and non-sustained ventricular tachycardia (P0.35, particularly TS (hazard ratio 5.9; 95% CI 2.9–11.7, P<0.001). Conclusion Among the post-AMI patients treated according to the current guidelines, the incidence of SCD is low. Various Holter variables still predict the occurrence of SCD, particularly among the patients with preserved left ventricular function.