scholarly journals Childhood Bradycardia Associates With Atrioventricular Conduction Defects in Older Age: A Longitudinal Birth Cohort Study

2021 ◽  
Vol 10 (19) ◽  
Author(s):  
Constantin‐Cristian Topriceanu ◽  
James C. Moon ◽  
Rebecca Hardy ◽  
Alun D. Hughes ◽  
Gabriella Captur

Background This study explored the association between childhood bradycardia and later‐life cardiac phenotype using longitudinal data from the 1946 National Survey of Health and Development (NSHD) birth cohort. Methods and Results Resting heart rate was recorded at 6 and 7 years of age to provide the bradycardia exposure defined as a childhood resting heart rate <75 bpm. Three outcomes were studied: (1) echocardiographic data at 60 to 64 years of age, consisting of ejection fraction, left ventricular mass index, myocardial contraction fraction index, and E/e′; (2) electrocardiographic evidence of atrioventricular or ventricular conduction defects by 60 to 64 years of age; and (3) all‐cause and cardiovascular mortality. Generalized linear models or Cox regression models were used, and adjustment was made for relevant demographic and health‐related covariates, and for multiple testing. Mixed generalized linear models and fractional polynomials were used as sensitivity analyses. One in 3 older adults with atrioventricular conduction defects had been bradycardic in childhood, with defects being serious (Mobitz type II second‐degree atrioventricular block or higher) in 12%. In fully adjusted models, childhood bradycardia was associated with 2.91 higher odds of atrioventricular conduction defects (95% CI, 1.59–5.31; P =0.0005). Associations persisted in random coefficients mixed generalized linear models (odds ratio, 2.50; 95% CI, 1.01–4.31). Fractional polynomials confirmed a linear association between the log odds of atrioventricular conduction defects at 60 to 64 years of age and resting heart rate at 7 years of age. There was no association between bradycardia in childhood and mortality outcomes or with echocardiographic parameters and ventricular conduction defects in older age. Conclusions Longitudinal birth cohort data indicate that childhood bradycardia trebles the odds of having atrioventricular conduction defects in older age, 88% of which are benign. In addition, it does not influence mortality or heart size and function. Future research should concentrate on identifying children at risk.

2021 ◽  
Vol 35 ◽  
pp. 100830
Author(s):  
Julius C. Heemelaar ◽  
Augustinus D.G. Krol ◽  
Marloes Louwerens ◽  
Saskia L.M.A. Beeres ◽  
Eduard R. Holman ◽  
...  

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Yuksel Cavusoglu ◽  
Omer Kozan ◽  
Ahmet Temizhan ◽  
Serdar Kucukoglu

Purpose: Resting heart rate (HR), health related quality of life (HQoL) and NYHA functional capacity are referred as important determinants of prognosis and targets of therapy in heart failure (HF). REALITY HF (Resting Heart Rate and Real Life Treatment Modality in Outpatients with Left Ventricular Systolic Dysfunction) study data were analyzed for the evaluation of any relationship of resting HR with HQoL assessed by Kansas City Cardiomyopathy Questionnaire (KCCQ) and NYHA functional class. Methods: REALITY HF was a multicenter, prospective registry designed to evaluate HF patients’ characteristics and effects of treatment modalities on resting HR and enrolled 1057 patients (age 61±12 years) with LVEF <40%. 781 (74%) patients in sinus rhythm were included in this analysis. Patients were classified into 4 groups according to the quartiles of HR: Q1:<68 bpm (n=234), Q2:69-75 bpm (n=189), Q3:76-87 bpm (n=194) and Q4:>87 bpm (n=164). KCCQ was completed in a random sample of 320 (Q1:n=27, Q2:n=99, Q3:n=125, Q4:n=69) patients, in which higher scores show better patient’s health status. Results: During enrollment, 82% of patients were receiving ≥2 drugs including ACE[[Unable to Display Character: &#304;]]/ARB, beta blocker, aldosterone blocker, diuretic or digoxin. Resting HR was 76±14 bpm and 68% of patients had a resting HR ≥70 bpm. KCCQ overall summary score (OSC) was found to be 75.7±13.2 in those in Q1, 65.5±20.8 in Q2, 64.4±20.6 in Q3 and 58.3±21.2 in Q4 (p=0.004) and KCCQ clinical summary score (CSS) was 80.4±15.7 in those in Q1, 70.0±22.4 in Q2, 69.9±21.9 in Q3 and 63.8±23.3 in Q4 (p=0.016). Also, there was a significant negative correlation between resting HR and OSC (p=0.008) or CSS (p=0.031). The distribution of NYHA-I patients for Q1, Q2, Q3 and Q4 were 40.7%, 22.8%, 23.8% and 12.7%, NYHA-II patients-30.8%, 23.1%, 27.2% and 18.9%, NYHA-III patients-21.2%, 23.9%, 24.3% and 30.6% and NYHA-IV patients-22.7%, 34.1%, 22.7% and 20.5%, respectively (p<0.001). Also, resting HR were found to gradually and significantly increase across NYHA categories (72.8±12 bpm in NYHA-I, 76.1±13 bpm in NYHA-II, 80.2±15 bpm in NYHA-III and 78.9±16 bpm in NYHA-IV, p<0.001). Conclusions: These results suggest that elevated resting HR in HF patients is associated with impaired HQoL and worse NYHA functional capacity.


Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Ramtin Anousheh ◽  
David E Krummen ◽  
Navinder S Sawhney ◽  
Wei Chung Chen ◽  
Linda Tone ◽  
...  

To investigate the association between resting heart rate (HR) and defibrillation threshold (DFT) in patients (pts) undergoing ICD implantation. DFT testing is usually considered standard of care during ICD implantation. However, the risk factors for high DFTs remain ill defined and the extent of testing required at implant has not been well defined. Baseline HR has been associated with higher DFTs in prior studies. We studied 128 pts undergoing ICD implantation. Baseline HR and DFTs were determined. HR was determined using ECGs obtained in the resting position on the day of ICD implantation. DFT testing was done during ICD implantation. We excluded 13 pts who were on amiodarone. The baseline characteristics of pts in the study are shown below in the table below (values in parenthesis represents standard error of the mean): First, a multivariate analysis of the association between baseline HR and DFT was performed, adjusting for left ventricular ejection fraction (LVEF), gender, body surface area (BSA) and beta blocker therapy. For every 10 beat increase in heart rate, DFT increased by 1 joule (p=0.02). Gender and beta blocker therapy did not effect this association. Second, pts were dichotomized based on DFTs to low (<15 joules) and high (≥15 joules). Mean resting HR was significantly higher among pts with high DFT (79 bpm) compared to those with low DFT (70 bpm) after adjusting for LVEF and BSA (p=0.01). Baseline resting HR is a risk factor for high DFT and may help define a higher risk pt population undergoing DFT testing.


1987 ◽  
Vol 65 (2) ◽  
pp. 179-184 ◽  
Author(s):  
Leonard B. Bell ◽  
D. Fred Peterson

Factors known to influence left ventricular contractility include preload, afterload, circulating catecholamine concentration, efferent sympathethic discharge, and heart rate. Heart rate influences have been primarily determined in the dog, whereas the influence of heart rate in smaller mammals has not been determined. Eight pentobarbital-anesthetized rabbits were instrumented to measure electrocardiogram, heart rate, left ventricular pressure, end-diastolic pressure, dP/dt, and mean and pulsatile aortic pressures. Systematic bradycardia was induced by stimulating the peripheral end of the sectioned right vagus nerve. Between 293 and 235 beats/min, there was no change in (dP/dt)max as heart rate was decreased. Below this range there was a direct relationship between (dP/dt)max and heart rate. Preload remained unchanged down to 132 beats/min. There was a small but significant decrease in afterload (0.09 mmHg∙beat−1∙min−1; 1 mmHg = 133.32 Pa) throughout the decrease in heart rate. Infusion of propranolol (2.0 mg/kg) produced no marked change in the heart rate – (dP/dt)max relationship, although both resting heart rate and (dP/dt)max were reduced. This study demonstrates that (dP/dt)max is not influenced by changes in heart rate above 235 beats/min in the pentobarbital-anesthetized rabbit. These results differ from findings in other animals, and demonstrate that species and heart rate ranges must be considered when drawing conclusions regarding (dP/dt)max as a reliable index of contractility.


2014 ◽  
Vol 63 (12) ◽  
pp. 1182-1189 ◽  
Author(s):  
Anders Opdahl ◽  
Bharath Ambale Venkatesh ◽  
Veronica R.S. Fernandes ◽  
Colin O. Wu ◽  
Khurram Nasir ◽  
...  

2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Sarah L Sturgill ◽  
Lorien G Salyer ◽  
Vikram Shettigar ◽  
Elizabeth Brundage ◽  
Brandon J Biesiadecki ◽  
...  

In response to increase in metabolic demand (e.g., exercise), the heart must increase its pumping performance to meet this demand. To achieve this increase, the heart relies on its cardiac reserve, which is the ability to increase in its contractile and diastolic function. The mechanism responsible for cardiac reserve is poorly understood. The myofilament is the mechanism responsible for contraction and relaxation. Troponin I (the inhibitory subunit of troponin, TnI) is a key regulatory protein. Studies have shown TnI serine 23/24 (S23/S24) phosphorylation, the most abundant and important TnI phosphorylation, is a key mechanism for accelerating relaxation by decreasing Ca 2+ senstivity. The role of TnI in cardiac reserve is unknown. For this study, we thoroughly characterized the systolic and diastolic reserve in TnI S23/S24 phosphorylation-null transgenic mice (S23/S24 mutated to alanine, AA mice). Even with increased Ca 2+ sensitivity, the AA mice exhibited normal function at resting heart rate and no difference in cardiac structure compared to wildtype. To increase in vivo heart performance, the most important system is the Bowditch effect (i.e., an increase in contractile function with increasing heart rate). To examine the role TnI S23/S24 phosphorylation in systolic and diastolic reserve, we assessed hemodynamics via left ventricular catheterization on the Bowditch effect by increasing heart rate from 240 to 420 beats per minute. Our data exhibited a clear loss of diastolic and systolic reserve in the AA mice. Since we observed a clear inability to increase systolic and diastolic function in AA mice, we performed speckle tracking echocardiography to more quantitatively investigate AA mice function. We observed that AA mice demonstrated normal systolic function (radial strain rate) and impaired directional diastolic function (reverse radial strain rate) at resting heart rate. We conclude that TnI S23/S24 phosphorylation is essential for cardiac reserve by enhancing systolic and diastolic function. A blunted cardiac reserve leads to heart disease making TnI S23/S24 phosphorylation a potential therapeutic strategy.


Diabetes Care ◽  
2007 ◽  
Vol 31 (2) ◽  
pp. 335-339 ◽  
Author(s):  
M. R. Carnethon ◽  
L. Yan ◽  
P. Greenland ◽  
D. B. Garside ◽  
A. R. Dyer ◽  
...  

2016 ◽  
Vol 45 (2) ◽  
pp. 491-500 ◽  
Author(s):  
Joseph Murray ◽  
Pedro C Hallal ◽  
Gregore I Mielke ◽  
Adrian Raine ◽  
Fernando C Wehrmeister ◽  
...  

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