scholarly journals The impact of resting heart rate measured on cardiovascular events in subject with hypertension

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
P Sobieraj ◽  
J Lewandowski ◽  
M Sinski

Abstract Background Available evidence does not indicate whether resting heart rate (RHR) is an independent risk factor or just marker of elevated risk. None of the studies assessed impact of RHR on cardiovascular events, when RHR was measured using automated blood pressure measurements (AOBPM). Purpose To assess the relationship between RHR (measured using AOBPM) and cardiovascular events risk in subjects with hypertension. Methods The data of SPRINT trial obtained via NHLBI were used to perform the analysis. SPRINT trial assessed intensive lowering of systolic BP to a target <120 mm Hg in comparison to standard goal (<140 mm Hg). RHR was measured using AOBPM device and calculated as an average of 3 measurements during the baseline visit of the study. Clinical composite endpoint (CE) of the study was defined as: myocardial infarction, acute coronary syndrome, decompensation of heart failure, stroke or cardiovascular death. The relationship between RHR and CE was assessed according to presence of cardiovascular disease (CVD) in past medical history. The statistical methods included t-test and chi-square test, Cox proportional risk models. The Cox models were adjusted for adjusted for age, sex, current smoking status and mean SBP during the trial. Restricted cubic splines were used to describe the relationship between RHR and hazard ratio. Results Data of 1877 participants with CVD and 7484 participants without CVD were analyzed. Subjects with cardiovascular disease were older (69.7±9.5 vs 67.5 years ± 9.4, p<0.001), more often were men (72.8% vs 62.3%, p<0.001) and had prior chronic kidney disease (34.3% vs 26.8%, p<0.001) than subjects without CVD. CE was more than twice often when CVD was present (10.9% vs 4.8%, p<0.001). RHR was lower in subjects with CVD disease than in subjects without CVD (63.6±11 vs 66.9±11.6 bpm, p=0<00.1). Elevated RHR was associated with increased risk both in subjects with and without CVD (Figure 1). The multivariable Cox proportional hazard risk model revealed that RHR>80 bpm is an independent risk factor for CE in subjects without CVD (hazard ratio 1.37, 95% CI 1.01–1.85, p=0.043) while not in subjects with CVD (hazard ratio 0.99, 95% CI 0.57–1.71, p=0.98). Conclusion Elevated RHR (>80 bpm) measured using AOBPM is an independent risk factor for cardiovascular events in subjects with hypertension and without CVD. Figure 1. Heart ratio vs hazard ratio. Funding Acknowledgement Type of funding source: None

2021 ◽  
Vol 10 (15) ◽  
pp. 3264
Author(s):  
Piotr Sobieraj ◽  
Maciej Siński ◽  
Jacek Lewandowski

The association between elevated resting heart rate (RHR) as a cardiovascular risk factor and lowering of systolic blood pressure (SBP) to currently recommended values remain unknown. Systolic Blood Pressure Intervention Trial (SPRINT) data obtained from the NHLBI were used to describe the relationship between RHR and SBP reduction to <120 mmHg compared to SBP reduction to <140 mmHg. The composite clinical endpoint (CE) was defined as myocardial infarction, acute coronary syndrome, decompensation of heart failure, stroke, or cardiovascular death. Increased RHR was associated with a higher CE risk compared with low RHR in both treatment arms. A more potent increase of risk for CE was observed in subjects who were allocated to the SBP < 120 mmHg treatment goal. A similar effect of intensive and standard blood pressure (BP) reduction (p for interaction, 0.826) was observed in subjects with RHR in the 5th quintile (hazard ratio, 0.78, with 95% confidence interval (CI), 0.55–1.11) and in other quintiles of baseline RHR (hazard ratio, 0.75, with 95% CI, 0.62–0.90). Lower in-trial than baseline RHR was associated with reduced CE risk (hazard ratio, 0.80, with 95% CI, 0.66–0.98). We concluded that elevated RHR remains an essential risk factor independent of SBP reduction.


2010 ◽  
Vol 159 (4) ◽  
pp. 612-619.e3 ◽  
Author(s):  
Marie Therese Cooney ◽  
Erkki Vartiainen ◽  
Tinna Laakitainen ◽  
Anne Juolevi ◽  
Alexandra Dudina ◽  
...  

Open Heart ◽  
2019 ◽  
Vol 6 (1) ◽  
pp. e000856 ◽  
Author(s):  
Xiao-jing Chen ◽  
Salim Bary Barywani ◽  
Per-Olof Hansson ◽  
Erik Östgärd Thunström ◽  
Annika Rosengren ◽  
...  

BackgroundResting heart rate (RHR), a known cardiovascular risk factor, changes with age. However, little is known about the association between changes in RHR and the risk of cardiovascular events. The purpose of this study was therefore to assess the impact of RHR at baseline, and the change in RHR over time, on the risk of all-cause death and cardiovascular events.DesignA random population sample of men born in 1943 who were living in Gothenburg, Sweden was prospectively followed for a 21-year period.MethodsParticipants were examined three times: first in 1993 and then re-examined in 2003 and 2014. At each visit, a clinical examination, an ECG and laboratory analyses were performed. Change in RHR between 1993 and 2003 was defined as a decrease if RHR decreased by 5 beats per minute (bpm), an increase if RHR increased by 5 bpm or stable if the RHR change was <4bpm).ResultsParticipants with a baseline RHR of >75 bpm in 1993 had about a twofold higher risk of all-cause death (HR 2.3, CI 1.2 to 4.7, p=0.018), cardiovascular disease (CVD) (HR 1.8, CI 1.1 to 3.0, p=0.014) and coronary heart disease (CHD) (HR 2.2, CI 1.1 to 4.5, p=0.025) compared with those with <55 bpm in 1993. Participants with a stable RHR between 1993 and 2003 had a 44% decreased risk of CVD (HR 0.56, CI 0.35 to 0.87, p=0.011) compared with participants with an increasing RHR. Furthermore, every beat increase in heart rate from 1993 was associated with a 3% higher risk for all-cause death, 1% higher risk for CVD and 2% higher risk for CHD.ConclusionHigh RHR was associated with an increased risk of death and cardiovascular events in men from the general population. Moreover, individuals with an increase in RHR between 50 and 60 years of age had worse outcome.


2019 ◽  
Vol 22 (1) ◽  
pp. 45-56 ◽  
Author(s):  
Su-Chen Fang ◽  
Yu-Lin Wu ◽  
Pei-Shan Tsai

Lower heart rate variability (HRV) is associated with a higher risk of cardiovascular events and mortality, although the extent of the association is uncertain. We performed a meta-analysis of cohort studies to elucidate the association between HRV and the risk of all-cause death or cardiovascular events in patients with cardiovascular disease (CVD) during a follow-up of at least 1 year. We searched four databases (PubMed, MEDLINE, Embase, and Cochrane Central Register of Controlled Trials) and extracted the adjusted hazard ratio (HR) from eligible studies. We included 28 cohort studies involving 3,094 participants in the meta-analysis. Results revealed that lower HRV was associated with a higher risk of all-cause death and cardiovascular events; the pooled HRs were 2.12 (95% confidence interval [CI] = [1.64, 2.75]) and 1.46 (95% CI [1.19, 1.77]), respectively. In subgroup analyses, the pooled HR of all-cause death was significant for patients with acute myocardial infarction (AMI) but not for those with heart failure. The pooled HR for cardiovascular events was significant for the subgroup of patients with AMI and acute coronary syndrome but not for those with coronary artery disease and heart failure. Additionally, both time and frequency domains of HRV were significantly associated with risk of all-cause death and cardiovascular events in patients with CVD.


2015 ◽  
Vol 128 (3) ◽  
pp. 219-228 ◽  
Author(s):  
Michael Böhm ◽  
Jan-Christian Reil ◽  
Prakash Deedwania ◽  
Jae B. Kim ◽  
Jeffrey S. Borer

Blood ◽  
2011 ◽  
Vol 118 (21) ◽  
pp. 3135-3135
Author(s):  
Marieka A. Helou ◽  
India Sisler ◽  
Yi Ning ◽  
Hongjie Liu

Abstract Abstract 3135 Introduction: Childhood obesity has been linked to continued obesity and cardiovascular disease in adulthood. Studies in adults have established the relationship between morbid obesity and an increase in inflammatory markers. However, data in children is limited, with few studies examining white blood cell counts, and no studies that address platelet count. The objective of this study is to examine the relationship of obesity with hemoglobin, leukocyte and platelet counts among generally healthy children. Methods: Using the 2007–08 NHANES dataset, we analyzed data for children 2 to 17 year of age, including demographic characteristics, body mass index (BMI) and complete blood count (CBC) results. We excluded children with chronic disease and those reported as being in “fair” or “poor” health. We also excluded children whose caregiver reported them having an acute illness in the previous 30 days. Our main exposure variable was weight status as defined by BMI percentile for age. Weighted multiple regression modeling was used to examine relationships between obesity and white blood cells (WBC), platelets, hemoglobin concentration and CRP, controlling for age, gender and race. Results: There were 1482 eligible children aged 2 – 17 years in the dataset, of which 18.6% (276) were found to be obese and 16.2 % (240) were overweight. Multiple linear regression modeling revealed that being obese or overweight was significantly associated with increased cell counts when controlling for age, gender and race, but not hemoglobin concentration (see Table 1). Specifically, obesity was positively associated with WBC, neutrophil, and platelet counts (all p-values < 0.01.) Discussion: The present study found that obesity is an independent risk factor for having higher cell counts in children, specifically total WBC, neutrophils and platelets. Excess adipose tissue is characterized by inflammation and progressive infiltration by macrophages as obesity develops. The association of increased BMI with inflammatory cells likely exists through multiple pathways. For example, it has been suggested that the increase in leptin produced by adipose tissue may be responsible for the increase in inflammatory cells, possibly through and interaction with multi-lineage CD34+ cells. It has also been shown that the increase in inflammatory markers can lead to endothelial damage and structural arterial changes in children, placing them at increased risk for cardiovascular disease in adulthood. It is unclear as to whether our finding of increased platelets contributes to this risk. However, chronic thrombocytosis has been associated with a higher risk for cardiovascular disease in adults with essential thrombocythemia. If obesity is an independent risk factor for having higher cell counts at baseline, then this should be taken into account during hematologic evaluation. It should also be considered when assessing the potential impact of the current childhood obesity epidemic, and the possible long-term consequences. Further study is needed to confirm our findings. Disclosures: No relevant conflicts of interest to declare.


2021 ◽  
Author(s):  
Kaihang Xu ◽  
Le Wang ◽  
Chuyi Han ◽  
Yingyi Zhang ◽  
Rui Zhang ◽  
...  

Abstract Backgroud: Elevated lipoprotein(a) [Lp(a)] and thyroid stimulating hormone (TSH) are both associated with coronary artery disease (CAD), but it was controversial in ACS patients. Moreover, patients with elevated plasma TSH tend to have higher levels of lipoprotein. We supposed that patients with elevated LP (a) and TSH may have a adverse prognosis after coronary angiography.Methods: We consecutively recruited 1756 patients who underwent coronary angiography, of which 1473 patients with ACS were eventually enrolled. Major adverse cardiovascular events (MACEs) contained a complex of non-fatal stroke, non-fatal myocardial infarction, ischemic cardiovascular events, and cardiovascular death. According to the occurrence of end events within 27.4 months, the patients were split into two groups: non-endpoint event group (n = 1288) and endpoint event group (n = 185). The date between the two groups were compared. Serum LP (a) was measured by latex agglutination immunoassay (Roche Diagnostics GmbH, Mannheim, Germany).Results: During a median follow-up of 27.4 months, 185 (12.56%) MACEs occurred. Compared with the non-endpoints group,patients in the end-points group had higher level of preoperative LP (a), LDL and TSH (all P<0.05). Multivariate Cox proportional hazard model showed that LP (a) was an independent risk factor for adverse prognosis after coronary angiography in ACS patients, LP (a) > 53.8nmol/L (highest tertile ) predicted 1.704-fold risk for adverse prognosis of ACS (95%CI 1.194~2.433;P<0.05); Interestingly, patients with elevated LP (a) and TSH concomitantly conferred the highest risk for adverse prognosis OR=3.090 95%CI 1.657~5.765;P<0.001).Conclusion: LP (a) was an independent risk factor for adverse prognosis after coronary angiography in ACS patients, and the predictive efficacy was enhanced by TSH.


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