Artificial pacemaker for treatment of Adams-Stokes syndrome and slow heart rate

1963 ◽  
Vol 65 (6) ◽  
pp. 731-748 ◽  
Author(s):  
Rune Elmgvist ◽  
Johan Landegren ◽  
Sven Olov Pettersson ◽  
Åke Senning ◽  
Göran William-Olsson
2011 ◽  
Vol 57 (3) ◽  
pp. 395-400 ◽  
Author(s):  
Anton Popov ◽  
Yevgeniy Karplyuk ◽  
Volodymyr Fesechko

Estimation of Heart Rate Variability Fluctuations by Wavelet TransformTechnique for separate estimation of fast and slow fluctuations in the heart rate signal is developed. The orthogonal dyadic wavelet transform is used to separate the slow heart rate changes in approximation part of decomposition and fast changes in detail parts. Experimental results using the recordings from persons practicing Chi meditation demonstrated the applicability of estimation heart rate fluctuations with the proposed approach.


1993 ◽  
Vol 264 (1) ◽  
pp. C209-C216 ◽  
Author(s):  
W. Rouslin ◽  
C. W. Broge

In the present study we compared the quantitatively most important, Pi-activated mechanisms for conserving ATP during ischemia in dog and rat cardiac muscle. Earlier studies by ourselves showed that dog heart, like all slow heart rate mammalian hearts examined, possesses the ability to inhibit its mitochondrial ATPase by binding IF1, the ATPase inhibitor protein, during ischemia. Rat heart, like other fast heart rate mammalian hearts studied, does not. The present study demonstrated that this IF1-mediated ATPase inhibition in ischemic dog heart, as in other slow heart rate hearts, appears to depend on matrix space acidification mediated largely by Pi-H+ symport via the mitochondrial Pi carrier. The present study further confirmed that maximal glycolytic flux rates are five- to sixfold greater in ischemic rat than in ischemic dog heart. Both of these systems are activated by increasing Pi concentration ([Pi]) during ischemia, and both appear to be regulated somewhat differently in dog than in rat heart. Thus intact dog heart mitochondria exhibited a [Pi]-dependent ATPase inhibition at low external pH, whereas rat heart mitochondria did not. The [Pi] required for maximal ATPase inhibition in dog heart mitochondria was approximately 6 mM. Although both dog and rat heart phosphofructokinase were stimulated by Pi, the enzyme in dog heart was maximally activated by approximately 6 mM Pi, whereas the rat heart enzyme required only approximately 3 mM Pi for its maximal stimulation under otherwise identical conditions. The most active nonmitochondrial ATPase in ischemic dog and rat cardiac muscle, the Ca(2+)-activated actomyosin ATPase, accounted for approximately one-half of the total nonmitochondrial ATPase activity in each species.(ABSTRACT TRUNCATED AT 250 WORDS)


2020 ◽  
Vol 26 (5) ◽  
pp. 449-453
Author(s):  
Michelle Teles Morlin ◽  
Carlos Janssen Gomes da Cruz ◽  
Paula Beatriz Silvestre Melo ◽  
Guilherme Henrique Ramos Lopes ◽  
Edgar de Melo Keene Von Koening Soares ◽  
...  

ABSTRACT Bradycardia in athletes can range from moderate to severe, and the factors that contribute to slow heart rate are complex. Studies investigating the mechanisms associated with this condition are controversial, and may be linked to the form of exercise practiced. A systematic literature review was conducted to discuss bradycardia mechanisms in athletes who practice different forms of sport. The databases consulted were Pubmed (MEDLINE), Clinical Trials, Cochrane, Scopus, Web of Science, SciELO, Sport Discus and PEDro. The search included English language articles published up to January 2019, that evaluated athletes who practiced different forms of sport. One hundred and ninety-three articles were found, ten of which met the inclusion criteria, with 1549 male and female athletes who practiced diverse forms of sport. Resting heart rate and cardiac structure were studied in association with the form of sport practiced, through heart rate variability, electrocardiogram, echocardiogram and pharmacological blockade. The studies suggest that a slow resting heart rate cannot be explained by increased vagal modulation alone, but also includes changes in cardiac structure. According to the studies, different sports seem to produce different cardiac responses, and the bradycardia found in athletes can be explained by non-autonomic and autonomic mechanisms, depending on the type of effort or the form of sport practiced. However, the mechanism underlying the slow heart rate in each form of sport is still unclear. Level of evidence II; Prognostic studies - Investigating the effect of a patient characteristic on the outcome of disease.


2017 ◽  
Vol 25 (7-8) ◽  
pp. 465-466 ◽  
Author(s):  
R. Joustra ◽  
M. Boulaksil ◽  
H. W. Meijburg ◽  
J. L. Smeets
Keyword(s):  

1994 ◽  
Vol 77 (4) ◽  
pp. 1935-1940 ◽  
Author(s):  
D. H. Paterson ◽  
D. A. Cunningham ◽  
J. G. Pickering ◽  
M. A. Babcock ◽  
D. R. Boughner

Our purpose was to examine the gas exchange response to exercise in heart transplant (HT) patients and to characterize the O2 uptake kinetics (tau VO2) during successive square-wave on-transients from loadless cycling to moderate exercise. We hypothesized that with a slow heart rate response (and O2 transport limitation) O2 kinetics would be slowed but that with a repeated exercise initiated while the heart rate remained elevated the tau VO2 would be faster. Six male HT patients performed two ramp-function tests to determine peak O2 uptake (1.32 +/- 0.23 l/min) and ventilation threshold (1.02 +/- 0.16 l/min). Patients subsequently completed two repeats of a square-wave forcing function and repeated this on 2 days. Alveolar gas exchange was measured breath by breath. A monoexponential fit of signal-averaged data of the first exercise on-transient (between days) yielded a significantly slower tau VO2 in HT subjects than in healthy men (mean age 47 yr; n = 8) (77 +/- 26 vs. 45 +/- 4 s). With successive exercise (2nd transition) initiated while HR remained elevated the tau VO2 of HT patients was 46 +/- 17 s. The faster O2 kinetics of the second transition suggests that O2 delivery was enhanced and therefore that the tau VO2 may reflect bioenergetic processes controlling the rate of oxidative metabolism.


2013 ◽  
Vol 21 (9) ◽  
pp. 423-423
Author(s):  
M. Boulaksil ◽  
D. Robbers-Visser ◽  
S. Westra ◽  
J. L. Smeets
Keyword(s):  

2017 ◽  
Vol 25 (7-8) ◽  
pp. 461-462 ◽  
Author(s):  
R. Joustra ◽  
M. Boulaksil ◽  
H. W. Meijburg ◽  
J. L. Smeets
Keyword(s):  

1988 ◽  
Vol 22 (11) ◽  
pp. 818-825 ◽  
Author(s):  
A. TOSAKI ◽  
S. BALINT ◽  
L. SZEKERES
Keyword(s):  

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