Temporal Changes in Resting Heart Rate and Deaths From Ischemic Heart Disease

Nauman, Javaid; Janszky, Imre; Vatten, Lars J.; Wisløff, Ulrik

doi:10.1001/jama.2011.1826

Cited by 159 publications

(128 citation statements)

References 31 publications

Supporting

Mentioning

113

Contrasting

Unclassified

Order By: Relevance

“…Increased resting HR has been shown to be related to cardiovascular mortality, non-cardiovascular mortality, sudden death and coronary artery disease in males and females (22). A study done by Framingham with a follow up of 30 years has shown that resting HR is a risk factor for all-cause mortality and that, additionally, it increases with age and is accompanied by a higher rate of mortality (23).…”

Section: Discussionmentioning

confidence: 99%

The effect of Gilbert’s syndrome on the dispersions of QT and P-wave dispersion: an observational study

Cüre¹,

Yüce²,

Çiçek³

et al. 2013

Anadolu Kardiyol Derg

View full text Add to dashboard Cite

Objective: Gilbert's syndrome (GS) decreases the incidence of atherosclerotic heart disease. The aim of the study was to evaluate whether the arrhythmia risk markers such as P-wave dispersion (Pd), QT dispersion (QTd) are reduced in patients with GS compared with healthy subjects. Methods: Sixty-one patients diagnosed with GS (31 females, 30 males) who had applied to the internal medicine outpatient clinic in the hospital were included in this cross-sectional, observational study. A control group of 61 healthy persons (31 females, 30 males), who were non-smokers and drinkers, were included. Both groups were between 16-45 years old. Results of anthropometric measurements, laboratory assays and electrocardiographic findings were recorded for each participant. Independent sample t-test and nested ANOVA were used for data analysis. Results: In the GS group were Pd value 36±16.7 msec, QTd 48.7±10.7 msec and heart rate (HR) 74±8 beat/min. In the control group were Pd 51±28 msec, QTd 53±12 msec and HR 78±10 beat/min. The Pd of patients group (p<0.001), QTd (p=0.038) and HR (p=0.021) were significantly lower than the control group. Conclusion: According to our study's results, in these patients, increased bilirubin levels are associated with decrease in HR, Pd and QTd, which consequently might decrease the incidence of cardiac arrhythmias and coronary artery disease. Further studies are needed to clarify the protective role of bilirubin in risk of arrhythmias in this category of patients. (

show abstract

Section: Discussionmentioning

confidence: 99%

The effect of Gilbert’s syndrome on the dispersions of QT and P-wave dispersion: an observational study

Cüre¹,

Yüce²,

Çiçek³

et al. 2013

Anadolu Kardiyol Derg

View full text Add to dashboard Cite

show abstract

“…More research is needed to disentangle autonomic-dependent and -independent mechanisms related to pulsatile stress and arterial stiffness. This may provide insight into the numerous epidemiological studies that note associations between elevated resting HR and CV mortality independent of traditional risk factors [30][31][32][33][34][35][36][37] and inflammation 38) . Other limitations to this study should be noted.…”

Section: Discussionmentioning

confidence: 99%

Pulsatile Stress, Inflammation and Change in Arterial Stiffness

Jae

Heffernan

Yoon

et al. 2012

JAT

View full text Add to dashboard Cite

Aim: Understanding factors that contribute to changes in arterial stiffness over time is important as this may lead to therapies that can abrogate cardiovascular risk. We compared the contribution of pulsatile stress and inflammation to changes in arterial stiffness in middle-aged men using a 1-year follow-up study design. Methods: Arterial stiffness was derived from brachial-ankle pulse wave velocity (baPWV) in 107 men (mean age 53±6 yrs) on two separate occasions. The changes in outcome variables were calculated as the difference between the first and second examinations (mean interval 403±122 days). Pulsatile stress was calculated as the product of heart rate and brachial pulse pressure. C-reactive protein (CRP), white blood cell count (WBC) and fibrinogen were measured as inflammatory markers. Pulse wave velocity (PWV), an index of arterial stiffness, is associated with coronary atherosclerosis 1) and increased risk of cardiovascular (CV) events and mortality [2][3][4] , and lowering PWV with therapeutic intervention reduces CV risk 5) . Despite the clinical significance of PWV as a measure of CV risk, the mechanisms that contribute to changes in PWV remain poorly understood. It is often suggested that arterial stiffness is the integration of CV risk factors on the vessel wall over time 6) . Yet while numerous cross-sectional studies have noted that age and blood pressure are strong predictors of PWV 7,8) , other traditional CVD risk factors do not seem to play an integral role in modulating arterial stiffness 9) ; that is, the association of factors such as lipids, diabetes, sex, smoking and BMI with PWV is weak or insignificant, suggesting the dissociation of traditional risk factors and PWW 9) . Individual risk factors can fluctuate over time and their values, recorded at the time of risk assessment, may not reflect their true impact on the arterial wall 10) . Non-traditional CV risk factors may offer insight

show abstract

“…Given that information on pulse and its time-related changes is easy to obtain and follow up, our findings may be useful in identifying asymptomatic people at risk who could benefit from primary prevention measures, for example by vagal stimulation, antiinflammatory or anticholinesterase medications, or by physical activity, that limits increases in cardiovascular mortality risk (28). Future studies may focus on stress-inducible epigenetics (29), microRNA-mediated (21), and genetics changes (30).…”

Section: Significancementioning

confidence: 93%

Fear and C-reactive protein cosynergize annual pulse increases in healthy adults

Shenhar‐Tsarfaty

Yayon

Waiskopf

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Recent international terror outbreaks notably involve long-term mental health risks to the exposed population, but whether physical health risks are also anticipated has remained unknown. Here, we report fear of terror-induced annual increases in resting heart rate (pulse), a notable risk factor of all-cause mortality. Partial least squares analysis based on 325 measured parameters successfully predicted annual pulse increases, inverse to the expected age-related pulse decline, in approximately 4.1% of a cohort of 17,380 apparently healthy active Israeli adults. Nonbiased hierarchical regression analysis among 27 of those parameters identified pertinent fear of terror combined with the inflammatory biomarker C-reactive protein as prominent coregulators of the observed annual pulse increases. In comparison, basal pulse primarily depended on general physiological parameters and reduced cholinergic control over anxiety and inflammation, together indicating that consistent exposure to terror threats ignites fear-induced exacerbation of preexisting neuro-immune risks of all-cause mortality.pulse | terror | C-reactive protein | acetylcholinesterase | cholinergic status R ecent international terror outbreaks involve mass psychological trauma, leading to long-term mental health risks in the exposed population (1, 2). Fear-induced reactions involve cortical and limbic brain regions that together enhance threatpredictive sensory stimuli (3) by interacting with cholinergic signaling pathways (4) in the hippocampus (5), the central amygdala (6), and the prefrontal cortex, especially in adults (7). Imminent fear may even cause immediate cardiac death [e.g., after an earthquake (8)]. However, whether fear exposure elevates cardiac risks of death to otherwise healthy civilians, and if so, what are the causes of such risks, remains unknown.Pulse is a promising modifiable predictor of cardiovascular and all-cause mortality. Elevated pulse associates with increased systemic inflammation and endothelial dysfunction in older adults (9) and predicts increased risk of death from ischemic heart disease (10). Changes in basal pulse and pulse variability are tightly associated with sudden cardiac death and all-cause mortality, also in asymptomatic men (11). Pulse reflects a complex trait, determined by multiple genetic, environmental, and other endogenous factors that play a substantial role in population variation (12). These include excessive inflammation, shown to associate with pulse increases (13), to be controlled by cholinergic imbalance (decreased vagal tone or increased sympathetic activity) (14), and to increase mortality (15). However, whether specific psychological factors determine the basal pulse and annual pulse changes in active adults is still unknown, perhaps because the intensity of psychological phenomena largely depends on external sources and is highly variable.Although fear of terror (FOT) is universal, Israel has been exposed to the repeated stress of multiple wars and terror attacks for more than 60 y, with a ma...

show abstract

Temporal Changes in Resting Heart Rate and Deaths From Ischemic Heart Disease

Abstract: Among men and women without known cardiovascular disease, an increase in RHR over a 10-year period was associated with increased risk of death from IHD and also for all-cause mortality.

Cited by 159 publications

References 31 publications

The effect of Gilbert’s syndrome on the dispersions of QT and P-wave dispersion: an observational study

The effect of Gilbert’s syndrome on the dispersions of QT and P-wave dispersion: an observational study

Pulsatile Stress, Inflammation and Change in Arterial Stiffness

Fear and C-reactive protein cosynergize annual pulse increases in healthy adults

Contact Info

Product

Resources

About