			Home About us Contact

Resting Heart Rate (resting + heart_rate)

Distribution by Scientific Domains

Medical Sciences	50%
Life Sciences	50%

Selected Abstracts

Adrenergic Receptor Polymorphisms Associated with Resting Heart Rate: The HyperGEN Study

ANNALS OF HUMAN GENETICS, Issue 5 2006
J. B. Wilk
Summary The association between polymorphisms in the ,1, ,2 and ,2B adrenergic receptor (ADR) genes (ADRB1, ADRB2 and ADRA2B) and resting heart rate was examined in white and African-American participants of the HyperGEN Study. All analyses were adjusted for age, sex, body mass index, alcohol use, smoking status and daily exercise within strata of race, hypertension status and beta-blocker use. The Ser49Gly polymorphism of the ,1 ADR was associated with resting heart rate in hypertensive African-Americans and hypertensive whites taking beta-blockers, with carriers of the Gly allele having a higher mean resting heart rate by 2.7 and 4.4 beats per minute (bpm), respectively. The Arg389Gly polymorphism of the ,1 ADR was associated with lower heart rate in the normotensive African-American sample. A ,1 haplotype (Ser49Gly-Arg389Gly) was modestly associated with resting heart rate in the hypertensive African-Americans. The ,2B C/A polymorphism was associated with heart rate in hypertensive whites, and both whites and African-Americans taking beta-blockers, with carriers of the A allele having a higher mean resting heart rate. In summary, each of the ADR gene polymorphisms was associated with heart rate in at least one stratum studied, but there was no consistent association from which one would infer a large genetic contribution to heart rate. [source]

Cerebral oxygenation decreases during exercise in humans with beta-adrenergic blockade

ACTA PHYSIOLOGICA, Issue 3 2009
T. Seifert
Abstract Aim:, Beta-blockers reduce exercise capacity by attenuated increase in cardiac output, but it remains unknown whether performance also relates to attenuated cerebral oxygenation. Methods:, Acting as their own controls, eight healthy subjects performed a continuous incremental cycle test to exhaustion with or without administration of the non-selective beta-blocker propranolol. Changes in cerebral blood flow velocity were measured with transcranial Doppler ultrasound and those in cerebral oxygenation were evaluated using near-infrared spectroscopy and the calculated cerebral mitochondrial oxygen tension derived from arterial to internal jugular venous concentration differences. Results:, Arterial lactate and cardiac output increased to 15.3 ± 4.2 mm and 20.8 ± 1.5 L min,1 respectively (mean ± SD). Frontal lobe oxygenation remained unaffected but the calculated cerebral mitochondrial oxygen tension decreased by 29 ± 7 mmHg (P < 0.05). Propranolol reduced resting heart rate (58 ± 6 vs. 69 ± 8 beats min,1) and at exercise exhaustion, cardiac output (16.6 ± 3.6 L min,1) and arterial lactate (9.4 ± 3.7 mm) were attenuated with a reduction in exercise capacity from 239 ± 42 to 209 ± 31 W (all P < 0.05). Propranolol also attenuated the increase in cerebral blood flow velocity and frontal lobe oxygenation (P < 0.05) whereas the cerebral mitochondrial oxygen tension decreased to a similar degree as during control exercise (delta 28 ± 10 mmHg; P < 0.05). Conclusion:, Propranolol attenuated the increase in cardiac output of consequence for cerebral perfusion and oxygenation. We suggest that a decrease in cerebral oxygenation limits exercise capacity. [source]

Stress-Induced Wall Motion Abnormalities with Low-Dose Dobutamine Infusion Indicate the Presence of Severe Disease and Vulnerable Myocardium

ECHOCARDIOGRAPHY, Issue 7 2007
Stephen G. Sawada M.D.
Background: Patients with left ventricular (LV) systolic dysfunction due to coronary artery disease (CAD) may develop stress-induced wall motion abnormalities (SWMA) with low-dose (10 ,g/kg/min) dobutamine infusion. The clinical significance of low-dose SWMA is unknown. Objective: We investigated the clinical, hemodynamic and angiographic correlates of low-dose SWMA in patients with chronic ischemic LV systolic dysfunction. Methods: Seventy patients with chronic ischemic LV systolic dysfunction who had dobutamine stress echocardiography were studied. Clinical, hemodynamic, and angiographic parameters at rest and low-dose were compared between 38 patients (mean ejection fraction (EF) of 30 ± 8%) with low-dose SWMA and 32 patients (EF 30 ± 11%) without low-dose SWMA. Results: Multivariate analysis showed that the number of coronary territories with severe disease (stenosis ,70%)(P = 0.001, RR = 6.3) was an independent predictor of low-dose SWMA. An increasing number of collateral vessels protected patients from low-dose SWMA (P = 0.011, RR = 0.25). A higher resting heart rate was a negative predictor of low-dose SWMA (P = 0.015, RR = 0.92) but no other hemodynamic variables were predictors. In the patients with low-dose SMA, regions with low-dose SWMA were more likely to be supplied by vessels with severe disease than regions without low-dose SWMA (92% vs 58%, P < 0.001). Conclusion: In patients with ischemic LV systolic dysfunction, the extent of severe disease and a lower numbers of collaterals predict the occurrence of low-dose SWMA. Low-dose SWMA is a highly specific marker for severe disease. [source]

Continuous positive airway pressure treatment for obstructive sleep apnoea reduces resting heart rate but does not affect dysrhythmias: a randomised controlled trial

JOURNAL OF SLEEP RESEARCH, Issue 3 2009
SONYA CRAIG
Summary Obstructive sleep apnoea (OSA) is associated with cardiovascular morbidity and may precipitate cardiac dysrhythmias. Uncontrolled reports suggest that continuous positive airway pressure (CPAP) may reduce dysrhythmia frequency and resting heart rate. We undertook a randomised controlled trial of therapeutic CPAP and compared with a subtherapeutic control which included an exploration of changes in dysrhythmia frequency and heart rate. Values are expressed as mean (SD). Eighty-three men [49.5 (9.6) years] with moderate,severe OSA [Oxygen Desaturation Index, 41.2 (24.3) dips per hour] underwent 3-channel 24-h electrocardiograms during normal daily activities, before and after 1 month of therapeutic (n = 43) or subtherapeutic (n = 40) CPAP. Recordings were manually analysed for mean heart rate, pauses, bradycardias, supraventricular and ventricular dysrhythmias. The two groups were well matched for age, body mass index, OSA severity, cardiovascular risk factors and history. Supraventricular ectopics and ventricular ectopics were frequently found in 95.2% and 85.5% of patients, respectively. Less common were sinus pauses (42.2%), episodes of bradycardia (12%) and ventricular tachycardias (4.8%). Compared with subtherapeutic control, CPAP reduced mean 24-h heart rate from 83.0 (11.5) to 79.7 (9.8) (P < 0.002) in the CPAP group compared with a non-significant rise (P = 0.18) from 79.0 (10.4) to 79.9 (10.4) in the subtherapeutic group; this was also the case for the day period analysed separately. There was no significant change in the frequencies of dysrhythmias after CPAP. Four weeks of CPAP therapy reduces mean 24-h heart rate possibly due to reduced sympathetic activation but did not result in a significant decrease in dysrhythmia frequency. [source]

Adrenergic Receptor Polymorphisms Associated with Resting Heart Rate: The HyperGEN Study

Effects of Hormone Replacement Therapy on Heart Rate Variability in Postmenopausal Women

ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2001
Aylin Yildirir M.D.
Background: Hormone replacement therapy (HRT) is associated with reduced cardiovascular risk, but the underlying mechanism(s) are not fully understood. This study investigated the effects of a 6-month course of HRT on cardiac autonomic function parameters assessed by heart rate variability (HRV) in postmenopausal women. Methods: Forty-six healthy postmenopausal women (age 48 ± 5, range 40,60) with normal baseline electrocardiogram and negative exercise testing were enrolled. HRT, which was either 0.625 mg/day conjugated equine estrogen (CEE) plus 2.5 mg/day medroxyprogesterone acetate or 0.625 mg/day CEE alone were administered depending on hysterectomy status. Power spectral analysis of HRV was performed to calculate the low frequency component in absolute (LF) and normalized units (LF nu), high frequency component in absolute (HF), and normalized units (HF nu), and the LF/HF ratio. The standard deviation of RR intervals (SDNN) was calculated from the time series of RR intervals. Results: A 6-month course of HRT did not significantly alter resting heart rate (P > 0.05). The LF/HF ratio and LF nu significantly decreased after HRT (P = 0.022 and P = 0.032), whereas a significant increase was noted in the HF component of HRV (P = 0.043), indicating an improvement in cardiac autonomic function. The SDNN value, which was 28.8 ± 11.8 ms before HRT significantly increased to 35.4 ± 16.7 ms after 6 months (P = 0.011). Conclusion: Our results indicate that a 6-month course of HRT may significantly improve cardiac autonomic function parameters, a finding that could at least partly explain the potential cardiopro-tective effect(s) of HRT. A.N.E. 2001;6(4):280,284 [source]