Impact of type 2 diabetes on cardiac autonomic responses to sympathetic stimuli in patients with coronary artery disease

Kiviniemi, Antti M.; Hautala, Arto J.; Karjalainen, Jaana; Piira, Olli-Pekka; Lepojärvi, Samuli; Tiinanen, Suvi; Seppänen, Tapio; Ukkola, Olavi; Huikuri, Heikki V.; Tulppo, Mikko P.

doi:10.1016/j.autneu.2013.08.068

Cited by 9 publications

(5 citation statements)

References 38 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Activation of the baroreceptors would augment the activity of the sympathetic nerves to the heart and reduce vagal activity. Spontaneous baroreflex sensitivity is comparable in db/db and db/+ mice [ 19 ], and it is not affected by the presence of diabetes in patients with coronary artery disease [ 38 ]. Notwithstanding, cardiac autonomic neuropathy and vagal remodeling is a serious complication of diabetes; however, animal studies have shown that cardiac cholinergic neurons and atrial sensitivity to acetylcholine are not lost [ 39 ].…”

Section: Discussionmentioning

confidence: 99%

Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

Soltysinska

Speerschneider

Winther

et al. 2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

BackgroundThe aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding of the mechanism behind this conundrum and the consequences thereof.MethodsCardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+ mice.ResultsWe found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+ controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region.ConclusionsEnhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients.

show abstract

Section: Discussionmentioning

confidence: 99%

Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

Soltysinska

Speerschneider

Winther

et al. 2014

Cardiovasc Diabetol

View full text Add to dashboard Cite

show abstract

“…Patients with angiographically documented CAD ( n = 146) and willing to participate exercise training intervention were recruited from the ARTEMIS database, observing the exclusion criteria described elsewhere in details (Kiviniemi et al, 2013 ). Patients with pre-diabetes, verified by fasting glucose and oral glucose tolerance test (Alberti and Zimmet, 1998 ), were excluded because of the main focus of the ARTEMIS project.…”

Section: Methodsmentioning

confidence: 99%

Acute post-exercise change in blood pressure and exercise training response in patients with coronary artery disease

Kiviniemi

Hautala²,

Karjalainen

et al. 2015

Front. Physiol.

Self Cite

View full text Add to dashboard Cite

We tested the hypothesis that acute post-exercise change in blood pressure (BP) may predict exercise training responses in BP in patients with coronary artery disease (CAD). Patients with CAD (n = 116, age 62 ± 5 years, 85 men) underwent BP assessments at rest and during 10-min recovery following a symptom-limited exercise test before and after the 6-month training intervention (one strength and 3-4 aerobic moderate-intensity exercises weekly). Post-exercise change in systolic BP (SBP) was calculated by subtracting resting SBP from lowest post-exercise SBP. The training-induced change in resting SBP was −2 ± 13 mmHg (p = 0.064), ranging from −42 to 35 mmHg. Larger post-exercise decrease in SBP and baseline resting SBP predicted a larger training-induced decrement in SBP (β = 0.46 and β = −0.44, respectively, p < 0.001 for both). Acute post-exercise decrease in SBP provided additive value to baseline resting SBP in the prediction of training-induced change in resting SBP (R2 from 0.20 to 0.26, p = 0.002). After further adjustments for other potential confounders (sex, age, baseline body mass index, realized training load), post-exercise decrease in SBP still predicted the training response in resting SBP (β = 0.26, p = 0.015). Acute post-exercise change in SBP was associated with training-induced change in resting SBP in patients with CAD, providing significant predictive information beyond baseline resting SBP.

show abstract

“…Mean HR, root mean square of successive differences in R-R intervals (rMSSD, ms), spectral power densities (fast Fourier transform, length 512 beats) at low (LF, 0.04-0.15 Hz, ms 2 ) and high frequency (HF, 0.15-0.40 Hz, ms 2 ) components of HRV, and their ratio (LF/HF) were analyzed (28). For the BRS analysis, a fast Fourier transform (Welch method, segments of 128 samples with 50% overlap, length 1024 samples) was performed to analyze the LF power of R-R interval and SBP oscillations (LF ms 2 , LFSBP mmHg 2 ) for subsequent analysis of BRS by the alpha method if sufficient coherence (≥0.5) between LF oscillations in R-Rinterval and SBP was verified(29,30). Out of 2 726 recordings, BRS was successfully calculated for 2 641 participants in the seated position and 2 617 while they were standing.…”

mentioning

confidence: 99%

Childhood growth patterns and cardiovascular autonomic modulation in midlife: Northern Finland 1966 Birth Cohort Study

et al. 2019

Self Cite

View full text Add to dashboard Cite

Objectives: To test the hypothesis that age and body mass index (BMI) at BMI peak during infancy and at BMI rebound in childhood are related to cardiovascular autonomic modulation in adulthood. Methods: At the age of 46, a sample (n=5 861) of the participants of the Northern Finland Birth Cohort 1966 took part in follow-up examinations. Heart rate variability (HRV), baroreflex sensitivity (BRS) and low-frequency oscillations of systolic blood pressure (LFSBP) were measured during sympathetic stimulus by standing. BMI at various ages was calculated from frequent anthropometric measurements collected from child welfare clinical records. BRS and LFSBP were available for 1243 participants with BMI peak data and 1524 participants with BMI rebound data, and HRV for 2137 participants with BMI peak data and 2688 participants with BMI rebound data. Results: Age at BMI rebound had a significant inverse association with LFSBP (Beta=-0.071, p=0.006) after all adjustments (p<0.001) and was also directly associated with BRS (Beta=0.082, p=0.001) independently of birth and maternal factors (p=0.023). BMI at BMI peak and at BMI rebound was inversely associated with high frequency component of HRV (HF) (Beta=-0.045, p=0.036 for BMI at peak; Beta=-0.043, p=0.024 for BMI at rebound) and directly associated with the ratio of low-and highfrequency components of HRV (LF/HF ratio) (Beta=0.084, p=<0.001 for BMI at peak; Beta=0.069, p<0.001 for BMI at rebound). These associations remained significant after all adjustments (p<0.05 for all). Conclusions: This novel study shows that younger age at BMI rebound and higher BMI at BMI peak and at BMI rebound are associated with higher levels in markers 4 suggestive of augmented sympathetic and reduced vagal cardiovascular modulation in 65 midlife. 66

show abstract

Impact of type 2 diabetes on cardiac autonomic responses to sympathetic stimuli in patients with coronary artery disease

Cited by 9 publications

References 38 publications

Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice

Acute post-exercise change in blood pressure and exercise training response in patients with coronary artery disease

Childhood growth patterns and cardiovascular autonomic modulation in midlife: Northern Finland 1966 Birth Cohort Study

Contact Info

Product

Resources

About