Genetic insights into resting heart rate and its role in cardiovascular disease

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development.</p

Genetic insights into resting heart rate and its role in cardiovascular disease

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development

Upper instrumented vertebrae selection criteria for degenerative lumbar scoliosis based on the hounsfield unit asymmetry of the first coronal reverse vertebrae: an observational study

Abstract Background Selection of the upper instrumented vertebra (UIV) is crucial for surgical treatment of degenerative lumbar scoliosis (DLS), given the relevance of UIV in postoperative proximal adjacent segment degeneration (pASD). Our previous research found that selection of UIV not lower than (≤) the first coronal reverse vertebra (FCRV), which marks the turning point of Hounsfield unit (HU) asymmetry, could significantly reduce pASD. However, the degree of HU asymmetry can vary among patients, suggesting a demand for more individualized UIV selection criteria, which we aimed to develop using quantitative HU measurement in the current study. Methods We included 153 consecutive patients with DLS. Quantitative measurement of HU of both sides of the vertebrae of these patients was performed on three planes of CT reconstruction for average values and determination of FCRV. Pre- and postoperative X-ray plain films were examined for radiological measurements and determination of pASD. Further, 35 patients with lumbar disc herniation and without significant scoliosis were also included as the reference group, and their bilateral HU was measured. Results In all 153 patients, those with UIV ≤ FCRV had a significantly lower rate of pASD (9.4% vs. 24.6%, P = 0.011). The difference between HU of the left and right sides of the FCRV (dF) could range from close to 0–59.4. The difference between HU of the left and right sides of the vertebrae in the reference group had an average value of 5.21. In 101 dF ≥ 5 DLS patients, those with UIV ≤ FCRV had a significantly lower rate of pASD (7.6% vs. 28.6%, P = 0.005), while this rate was insignificant in the other 52 dF < 5 patients (13.3% vs. 18.2%, P = 0.708). No other general, radiological, or operative parameter was found to have significant influence on the occurrence of pASD. Conclusions Selection of UIV ≤ FCRV can significantly reduce the risk of pASD for patients with DLS with dF ≥ 5. Trial Registration Not applicable, since this is an observational study

Microwave catalytic pyrolysis of biomass: a review focusing on absorbents and catalysts

Abstract The quest for low-carbon alternatives to fossil fuels and the carbon emissions associated with the natural degradation of biomass have accelerated the development of biomass processing technologies. Microwave catalytic pyrolysis is emerging as a technology for efficient conversion of biomass into energy, fuels and chemicals. However, due to the inherent poor dielectric properties and complex composition of biomass, two main technical challenges faced by microwave catalytic pyrolysis of biomass are efficient heating of biomass and improving the selectivity of target products. Potential solutions involve the use of microwave absorbents and catalysts, respectively. This review begins by addressing the difficulty in balancing energy efficiency and conversion efficiency by introducing microwave absorbents that play a positive role in improving heating efficiency. The principle of microwave absorbents in assisting biomass heating is revealed, and the impacts of the microwave absorbent type (related to microwave properties and physical properties) and the additive amount on the heating effect and biomass pyrolysis product distribution are discussed. Subsequently, the search for catalysts applied in biomass microwave pyrolysis for modulation of product distribution is explored. Special attention has been paid to the catalysts with microwave absorption properties, including activated carbon, zeolites, some metal oxides and metal salts. In addition, the energy efficiency, economic feasibility, and environmental impacts of this processing technology utilizing microwave absorbents and catalysts are examined based on energy analysis, techno-economic assessment, and life cycle assessment. The current scale-up challenges of microwave catalytic pyrolysis of biomass and some potential solutions to enhance the commercial feasibility of this technology are also discussed. Finally, the review provides some future development directions of this technology

Genetic insights into resting heart rate and its role in cardiovascular disease.

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development

Genetic insights into resting heart rate and its role in cardiovascular disease.

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development

Genetic insights into resting heart rate and its role in cardiovascular disease

Funder: Not applicableFunder: NWO VENI grant 016.186.125Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development