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Pulse pressure, wide [keywords]
- A Computational Physiology Approach to Personalized Treatment Models: The Beneficial Effects of Slow Breathing on the Human Cardiovascular System. [JOURNAL ARTICLE]
- Am J Physiol Heart Circ Physiol 2014 Jul 25.
Heart rate variability biofeedback intervention involves slow breathing at a rate of ~6 breaths per min (resonance breathing) to maximize respiratory and baroreflex effects on heart period oscillations. This intervention has wide-ranging clinical benefits and is gaining empirical support as an adjunct therapy for biobehavioral disorders, including asthma and depression. Yet, little is known about the system-level cardiovascular changes that occur during resonance breathing or the extent to which individuals differ in cardiovascular benefit. This study used a computational physiology approach to dynamically model the human cardiovascular system at rest and during resonance breathing. Noninvasive measurements of heart period, beat-to-beat systolic and diastolic blood pressure, and respiration period were obtained from 24 healthy young men and women. A model with respiration as input was parameterized to better understand how the cardiovascular processes that control variability in heart period and blood pressure change from rest to resonance breathing. The cost function used in model calibration corresponded to the difference between the experimental data and model outputs. A good match was observed between the data and model outputs (heart period, blood pressure, and corresponding power spectral densities). Significant improvements in several modeled cardiovascular functions (e.g., blood flow to internal organs, sensitivity of the sympathetic component of the baroreflex, ventricular elastance) were observed during resonance breathing. Individual differences in the magnitude and nature of these dynamic responses suggest that computational physiology may be clinically useful for tailoring heart rate variability biofeedback interventions for the needs of individual patients.
- Single Nucleotide Polymorphism-Single Nucleotide Polymorphism Interactions Among Inflammation Genes in the Genetic Architecture of Blood Pressure in the Framingham Heart Study. [JOURNAL ARTICLE]
- Am J Hypertens 2014 Jul 25.
Hypertension is a major global health burden, but, although systolic and diastolic blood pressure (BP) each have estimated heritability of at least 30%, <3% of their variance has been attributed to particular genetic variants. Few studies have shown interactions between pairs of single nucleotide polymorphisms (SNPs) to be associated with BP. Although many studies use a Bonferroni correction for multiple testing to control type I error, thereby potentially reducing power, false discovery rate (FDR) approaches are also used in genome-wide studies. Renal ion balance genes have been associated with BP regulation, but, although inflammation has been studied in connection with BP, few studies have reported associations between inflammation genes and BP.We analyzed SNP-SNP interactions among 31 SNPs from genes involved in renal ion balance and 30 SNPs from genes involved in inflammation using data from the Framingham Heart Study.No evidence of association was found for interactions among renal ion balance SNPs for either systolic or diastolic BP. A group of 3 interactions involving 6 inflammation genes (IKBKB-NFKBIA, IKBKE-CHUK, and ADIPOR2-RETN) showed evidence of association with diastolic BP with an FDR of 4.2%; no single interaction reached experiment-wide significance.This study identified promising and biologically plausible candidates for interactions between inflammation genes that may be associated with DBP. Analysis using the FDR may allow detection of signals in the presence of modest noise (false positives) that a stringent approach based on Bonferroni-corrected P value thresholds may miss.
- Nutritional and health benefits of pulses. [JOURNAL ARTICLE]
- Appl Physiol Nutr Metab 2014 Jun 13.:1-8.
Pulses (beans, peas, and lentils) have been consumed for at least 10 000 years and are among the most extensively used foods in the world. A wide variety of pulses can be grown globally, making them important both economically as well as nutritionally. Pulses provide protein and fibre, as well as a significant source of vitamins and minerals, such as iron, zinc, folate, and magnesium, and consuming half a cup of beans or peas per day can enhance diet quality by increasing intakes of these nutrients. In addition, the phytochemicals, saponins, and tannins found in pulses possess antioxidant and anti-carcinogenic effects, indicating that pulses may have significant anti-cancer effects. Pulse consumption also improves serum lipid profiles and positively affects several other cardiovascular disease risk factors, such as blood pressure, platelet activity, and inflammation. Pulses are high in fibre and have a low glycemic index, making them particularly beneficial to people with diabetes by assisting in maintaining healthy blood glucose and insulin levels. Emerging research examining the effect of pulse components on HIV and consumption patterns with aging populations indicates that pulses may have further effects on health. In conclusion, including pulses in the diet is a healthy way to meet dietary recommendations and is associated with reduced risk of several chronic diseases. Long-term randomized controlled trials are needed to demonstrate the direct effects of pulses on these diseases.
- Dietary salt intake and hypertension. [Journal Article, Review]
- Electrolyte Blood Press 2014 Jun; 12(1):7-18.
Over the past century, salt has been the subject of intense scientific research related to blood pressure elevation and cardiovascular mortalities. Moderate reduction of dietary salt intake is generally an effective measure to reduce blood pressure. However, recently some in the academic society and lay media dispute the benefits of salt restriction, pointing to inconsistent outcomes noted in some observational studies. A reduction in dietary salt from the current intake of 9-12 g/day to the recommended level of less than 5-6 g/day will have major beneficial effects on cardiovascular health along with major healthcare cost savings around the world. The World Health Organization (WHO) strongly recommended to reduce dietary salt intake as one of the top priority actions to tackle the global non-communicable disease crisis and has urged member nations to take action to reduce population wide dietary salt intake to decrease the number of deaths from hypertension, cardiovascular disease and stroke. However, some scientists still advocate the possibility of increased risk of CVD morbidity and mortality at extremes of low salt intake. Future research may inform the optimal sodium reduction strategies and intake targets for general populations. Until then, we have to continue to build consensus around the greatest benefits of salt reduction for CVD prevention, and dietary salt intake reduction strategies must remain at the top of the public health agenda.
- Performance of the CHARGE-AF risk model for incident atrial fibrillation in the EPIC Norfolk cohort. [JOURNAL ARTICLE]
- Eur J Prev Cardiol 2014 Jul 24.
Identification of individuals at risk for developing atrial fibrillation (AF) will help to target screening and preventive interventions. We aimed to validate the CHARGE-AF model (including variables age, race, height, weight, blood pressure, smoking, antihypertensive medication, diabetes, myocardial infarction and heart failure) for prediction of five-year incident AF in a representative European population with a wide age range.The CHARGE-AF model was calculated in 24,020 participants of the population-based EPIC Norfolk study with 236 cases of hospitalization with diagnosis of AF within five years. The model showed good discrimination (c-statistic 0.81, 95% confidence interval (CI) 0.75-0.85), but weak calibration (Chi(2)-statistic 142) with an almost two-fold overestimation of AF incidence. A recalibration to characteristics of the European Prospective Investigation into Cancer and Nutrition (EPIC) Norfolk cohort improved calibration considerably (Chi(2)-statistic 13.3), with acceptable discrimination in participants both >65 and ≤65 years of age (c-statistics 0.70, 95% CI 0.61-0.77 and 0.83, 95% CI 0.74-0.88). The recalibrated model also showed good discrimination in participants free of cardiovascular disease (c-statistics 0.80, 95% CI 0.75-0.84). Categories of predicted risk (<2.5%, 2.5-5% or >5%) showed good concordance with observed five-year AF incidence of 0.62%, 3.49% and 8.74% (log rank test p < 0.001), respectively.A recalibration of the CHARGE-AF model is necessary for accurate predictions of five-year risk of AF in the EPIC Norfolk population. The recalibrated model showed good discrimination across a wide age range and in individuals free of cardiovascular disease, and hence is broadly applicable in primary care to identify people at risk for development of AF.
- Connecting Resident Education to Patient Outcomes: The Evolution of a Quality Improvement Curriculum in an Internal Medicine Residency. [JOURNAL ARTICLE]
- Acad Med 2014 Jul 22.
As part of the Accreditation Council for Graduate Medical Education's Next Accreditation System, residency programs must connect resident-physician education to improved patient care outcomes. Residency training programs, however, face multiple obstacles in doing so. Results from residency quality improvement (QI) curricula tend to show improvement in simple process-based measures but not in more complex outcomes of care such as diabetes or blood pressure control. In this article, the authors describe the evolution of their QI educational program for internal medicine residents at the University of Cincinnati Medical Center within the structure of a novel training model called the Ambulatory Long Block. They discuss a resident-run project that led to reduced rates of patients with uncontrolled diabetes as an example of improvement in outcome measures. Despite favorable results from that particular resident group, the successful intervention did not spread practice-wide. Using this example, they detail the phases of evolution and lessons learned from their curriculum from 2006 to 2014 within a framework of previously published general principles for successful QI education, including those of exemplary care and learning sites. Successful programs require leadership, faculty expertise and mentorship, data management, learner buy-in, and patient engagement. Their experience will hopefully be of help to others as they attempt to simultaneously improve care and education. Further research and innovation are needed in this area, including optimizing strategies for strengthening resident-driven projects through partnership with nursing, allied health, and longitudinally engaged faculty members.
- Adrenomedullin and Arterial Stiffness: An Integrative Approach Combining Monocyte ADM Expression, Plasma MR-proADM and Genome-Wide Association Study. [JOURNAL ARTICLE]
- Circ Cardiovasc Genet 2014 Jul 22.
-Adrenomedullin (ADM) is a circulating vasoactive peptide involved in vascular homeostasis and endothelial function. Single nucleotide polymorphisms (SNPs) of the ADM gene are associated with blood pressure variability, and elevated levels of plasma midregional proadrenomedullin (MR-proADM) are associated with cardiovascular diseases.-We investigated the sources of variability of ADM gene expression and plasma MR-proADM concentrations in the general population, and their relationship to markers of atherosclerosis. MR-proADM levels were assessed in 4155 individuals who underwent evaluation of carotid intima-media thickness (IMT) and arterial rigidity (reflection index [RI] and stiffness index [SI]). In a sub-sample of 1372 individuals, ADM gene expression was assessed as part of a transcriptomic study of circulating monocytes. Non-genetic factors explained 45.8% and 7.5% of MR-proADM and ADM expression variability, respectively. ADM expression correlated to plasma C-reactive protein, interleukin-receptor 1A and myeloperoxidase, while MR-proADM levels correlated to C-terminal pro-endothelin-1, creatinine and N-terminal pro-B-type natriuretic peptide. Genome-wide association study of ADM expression and MR-proADM levels both identified a single locus encompassing the ADM gene. ADM expression was associated to a single SNP rs11042717 (p=2.36 10(-12)) while MR-proADM was associated to 2 SNPs with additive effects, rs2957692 (p=1.54 10(-13)) and rs2957717 (p=4.24 10(-8)). RI was independently associated to rs11042717 (p<10(-4)) and ADM expression (p=0.0002) but not to MR-proADM. Weaker associations were observed for SI. IMT was not related to ADM SNPs or expression.-These results support an involvement of the ADM gene in the modulation of peripheral vascular tone.
- Brachial Pulse Pressure and Cardiovascular or All-Cause Mortality in the General Population: A Meta-Analysis of Prospective Observational Studies. [JOURNAL ARTICLE]
- J Clin Hypertens (Greenwich) 2014 Jul 23.
This study aimed to quantitatively evaluate the predictive value of brachial pulse pressure and cardiovascular or all-cause mortality in the general population based on prospective observational studies by conducting a meta-analysis. Only prospective observational studies investigating baseline brachial pulse pressure and cardiovascular or all-cause mortality risk were selected from PubMed and Embase databases until July 2013. Fourteen studies involving 510,456 participants were analyzed. Pooled risk ratio (RR) of cardiovascular and all-cause mortality for the highest vs lowest brachial pulse pressure category was 1.80 (95% confidence interval [CI], 1.49-2.17) and 1.32 (95% CI, 1.23-1.41), respectively. Pooled RR of cardiovascular and all-cause mortality per 10 mm Hg pulse pressure increment was 1.13 (95% CI, 1.10-1.17) and 1.09 (95% CI, 1.07-1.11), respectively. Wide brachial pulse pressure is associated with greater risk of cardiovascular and all-cause mortality. However, more well-designed studies specifically on age and sex are needed to further confirm these findings.
- Genetic evidence for a normal-weight "metabolically obese" phenotype linking insulin resistance, hypertension, coronary artery disease and type 2 diabetes. [JOURNAL ARTICLE]
- Diabetes 2014 Jul 21.
The mechanisms that predispose to hypertension, coronary artery disease (CAD) and type 2 diabetes (T2D) in individuals of normal weight are poorly understood. In contrast, in monogenic primary lipodystrophy - a reduction in subcutaneous adipose tissue - it is clear that it is adipose dysfunction that causes severe insulin resistance (IR), hypertension, coronary artery disease and type 2 diabetes. We aimed to test the hypothesis that common alleles associated with insulin resistance also influence the wider clinical and biochemical profile of monogenic insulin resistance. We selected 19 common genetic variants associated with fasting insulin based measures of insulin resistance. We used hierarchical clustering and results from genome wide association studies of 8 non-disease outcomes of monogenic insulin resistance, to group these variants. We analysed genetic risk scores against disease outcomes including 12,171 T2D cases, 40,365 CAD cases and 69,828 individuals with blood pressure measurements. Hierarchical clustering identified 11 variants associated with a metabolic profile consistent with a common, subtle, form of lipodystrophy. A genetic risk score consisting of these 11 IR risk alleles was associated with higher triglycerides (ß=0.018; p=4x10(-29)), lower HDL cholesterol (ß=-0.020; p=7x10(-37)), greater hepatic steatosis (ß=0.021; p=3x10(-4)) higher alanine transaminase (ß=0.002; p=3x10(-5)), lower SHBG (ß=-0.010; p=9x10(-13)) and lower adiponectin (ß=-0.015; p=2x10(-26)). The same risk alleles were associated with lower BMI (per-allele ß=-0.008; p=7x10(-8)), and increased visceral-to-subcutaneous adipose tissue ratio (ß=-0.015; p=6x10(-7)). Individuals carrying >= 17 fasting insulin raising alleles (5.5% population) were slimmer (0.30 kgm(-2)) but at increased risk of T2D (odds ratio [OR] 1.46, per-allele p=5x10(-13)), CAD (OR 1.12, per-allele p=1x10(-5)), and increased blood pressure (systolic and diastolic blood pressure of 1.21 mmHg (per-allele p=2x10(-5)), and 0.67 mmHg (per-allele p=2x10(-4)), respectively, compared to individuals carrying <=9 risk alleles (5.5% population). Our results provide genetic evidence for a link between the three diseases of the "metabolic syndrome" and point to reduced subcutaneous adiposity as a central mechanism.
- Cross sectional associations of Acylation Stimulating Protein (ASP) and adipose tissue gene expression with estradiol and progesterone in pre and postmenopausal women. [JOURNAL ARTICLE]
- Clin Endocrinol (Oxf) 2014 Jul 5.
Sex steroid hormones play an important regulatory role in fat metabolism and obesity. Objective: We hypothesized involvement of interactions between ovarian hormones with Acylation Stimulating Protein (ASP). Design: Patients and measurements: In 392 women with wide age (18 to 69 years) and body size (BMI: 17 to 90 kg/m(2) ) ranges, fasting plasma levels of ASP, ovarian hormones, glucose, adiponectin and lipids/apolipoproteins were assessed, along with determination of metabolic syndrome (MS) features. Gene expression of C3 (ASP precursor) and related receptors C5L2, C3aR and C5aR in subcutaneous and omental adipose tissues were measured in a subset. Results: ASP correlated negatively with concentrations of estradiol (p<0.0001), adiponectin (p<0.001) and apolipoprotein A1 (p<0.001) and positively with apolipoprotein B levels (P<0.001), systolic blood pressure (p< 0.001), waist circumference (p<0.001), and triglyceride concentrations (p<0.01). In aged-matched groups of lean, overweight, metabolically healthy obese (MHO) and obese with metabolic syndrome (MSO), there was a stepwise increase in ASP levels (p<0.001) while concentrations of adiponectin (p<0.0001) and estradiol (p<0.001) but not those of progesterone decreased. Progesterone but not estradiol levels correlated positively with C3 gene expression in omental adipose tissue (p<0.05) and negatively with C5L2 expression in both omental (p<0.01) and subcutaneous (p<0.05) adipose tissues. Conclusion: Our results are consistent with the concept that sex hormones differentially influence circulating ASP and adipose tissue gene expression of its related proteins in a depot-specific manner. ASP may play a role in the regulation of regional fat metabolism through interactions with sex hormones in women. This article is protected by copyright. All rights reserved.