The National High Blood Pressure Education Program presents the complete Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Like its predecessors, the purpose is to provide an evidence-based approach to the prevention and management of hypertension. The key messages of this report are these: in those older than age 50, systolic blood pressure (BP) of greater than 140 mm Hg is a more important cardiovascular disease (CVD) risk factor than diastolic BP; beginning at 115/75 mm Hg, CVD risk doubles for each increment of 20/10 mm Hg; those who are normotensive at 55 years of age will have a 90% lifetime risk of developing hypertension; prehypertensive individuals (systolic BP 120-139 mm Hg or diastolic BP 80-89 mm Hg) require health-promoting lifestyle modifications to prevent the progressive rise in blood pressure and CVD; for uncomplicated hypertension, thiazide diuretic should be used in drug treatment for most, either alone or combined with drugs from other classes; this report delineates specific high-risk conditions that are compelling indications for the use of other antihypertensive drug classes (angiotensin-converting enzyme inhibitors, angiotensin-receptor blockers, beta-blockers, calcium channel blockers); two or more antihypertensive medications will be required to achieve goal BP (<140/90 mm Hg, or <130/80 mm Hg) for patients with diabetes and chronic kidney disease; for patients whose BP is more than 20 mm Hg above the systolic BP goal or more than 10 mm Hg above the diastolic BP goal, initiation of therapy using two agents, one of which usually will be a thiazide diuretic, should be considered; regardless of therapy or care, hypertension will be controlled only if patients are motivated to stay on their treatment plan. Positive experiences, trust in the clinician, and empathy improve patient motivation and satisfaction. This report serves as a guide, and the committee continues to recognize that the responsible physician's judgment remains paramount.

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

The Japanese Society of Hypertension Guidelines for the Management of Hypertension (JSH 2009)

/pdf/the-japanese-society-of-hypertension-guidelines-for-the-ruw2o2jwbh.pdf

ContextObstructive sleep apnea (OSA) has been increasingly implicated in the
initiation and progression of cardiovascular diseases.ObjectiveTo systematically review the interactions of OSA with cardiovascular
pathophysiology and diseases.Data Sources and Study SelectionThe MEDLINE database from January 1966 to March 2003 was searched using
the Medical Subject Headings sleep, sleep apnea, obesity, hypertension, heart failure, cardiac
arrhythmia, coronary artery disease, stroke, sympathetic activity, endothelium, inflammation, and continuous positive airway pressure (CPAP) to identify peer-reviewed studies of OSA. Priority was given
to large prospective cohort studies and to randomized controlled trials.Data ExtractionWe identified 154 original investigations and reviews of sleep-related
breathing disorders. Data from these studies were examined for relevance and
extracted by one of the authors.Data SynthesisApproximately 1 in 5 adults has at least mild OSA (apnea-hypopnea index
[ie, the number of apneic and hypopneic events per hour], 5-15), and 1 in
15 adults has at least moderate OSA (apnea-hypopnea index, 15-30). Repetitive
apneic events disrupt the normal physiologic interactions between sleep and
the cardiovascular system. Such sleep fragmentation, as well as abnormalities
evident in patients with OSA (eg, increased sympathetic activation, vascular
endothelial dysfunction, increased oxidative stress, inflammation, increased
platelet aggregability, metabolic dysregulation), may be implicated in the
initiation and progression of cardiac and vascular disease. Persuasive data
implicate OSA in the development of hypertension, and OSA also may contribute
to cardiac ischemia, congestive heart failure, cardiac arrhythmias, and perhaps
also to cerebrovascular disease and stroke.ConclusionsObstructive sleep apnea is common, readily diagnosed, and usually treatable.
It frequently coexists undiagnosed in patients with cardiovascular disease,
activates disease mechanisms known to elicit cardiac and vascular damage,
and may be implicated in progression of cardiovascular disease and resistance
to conventional therapeutic strategies. In the absence of definitive evidence
from large-scale trials and a better understanding of potential cost-effectiveness,
the likely benefits of diagnosis and treatment of OSA are presently best appraised
on an individualized patient basis.

https://jamanetwork.com/journals/jama/articlepdf/197410/jcc30007.pdf

Obstructive sleep apnea: implications for cardiac and vascular disease.

Obstructive sleep apnea, obesity, and the risk of incident atrial fibrillation.

The importance of sleep to hormones and glucose metabolism was first documented more than four decades ago. Since then, sleep curtailment has become an endemic behavior in modern society. In addition, the prevalence of sleep disorders, particularly obstructive sleep apnea (OSA), has increased. OSA is very common in endocrine and metabolic disorders, but often remains undiagnosed. This Review summarizes the laboratory and epidemiologic evidence that suggests how sleep loss, either behavioral or disease-related, and poor quality of sleep might promote the development of obesity and diabetes mellitus, and exacerbate existing endocrine conditions. Treatment of sleep disorders has the potential to improve glucose metabolism and energy balance. Screening for habitual sleep patterns and OSA might be critically important for patients with endocrine and metabolic disorders.

/pdf/effects-of-poor-and-short-sleep-on-glucose-metabolism-and-37c2wdswus.pdf

Effects of poor and short sleep on glucose metabolism and obesity risk

Patients with obstructive sleep apnea (OSA) are frequently obese and are predisposed to weight gain. They also have heightened sympathetic drive. We reasoned that noradrenergic activation of β3-receptors on adipocytes would inhibit leptin production, predisposing to obesity in sleep apnea. We therefore tested the hypothesis that obesity and predisposition to weight gain in OSA are associated with low levels of plasma leptin. We prospectively studied 32 male patients (43 ± 2 yr) with OSA who were newly diagnosed and never treated and who were free of any other diseases. Control measurements were obtained from 32 similarly obese closely matched male subjects (38 ± 2 yr). Leptin levels were 13.7 ± 1.3 and 9.2 ± 1.2 ng/ml in patients with OSA and controls, respectively (P = 0.02). Weight gain over the year before diagnosis was 5.2 ± 1.7 and 0.5 ± 0.9 kg in sleep apnea patients and similarly obese control subjects, respectively (P = 0.04). Muscle sympathetic activity was 46 ± 4 and 30 ± 4 bursts/min in patient...

https://www.physiology.org/doi/pdf/10.1152/ajpheart.2000.279.1.H234

Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea

Objective Administration of leptin to animals increases sympathetic nerve activity and heart rate. We therefore tested the hypothesis that plasma leptin is linked independently to muscle sympathetic nerve activity (MSNA) and heart rate in healthy humans. Methods We measured plasma leptin, plasma insulin, body mass index (BMI), percent body fat, waist : hip ratio, MSNA, heart rate and blood pressure in 88 healthy individuals (50 men and 38 women). Results In men, plasma leptin concentration correlated significantly with BMI (r 0.75, P < 0.001), percent body fat (r 0.70, P < 0.001), waist : hip ratio (r 0.69, P < 0.001), insulin (r 0.37, P 0.009), and age (r 0.38, P 0.006). Only BMI and waist : hip ratio were linked independently to plasma leptin concentration (r 0.78, P < 0.001). Plasma leptin concentrations also correlated with heart rate (r 0.39, P 0.006) and mean arterial pressure (MAP; r 0.38, P 0.007), but not with MSNA (r 0.17, P 0.24). After adjustment for BMI and waist : hip ratio, plasma leptin concentration correlated significantly only with heart rate (r 0.29, P 0.04), and not with MAP (r 0.21, P 0.14). Individuals were divided into high-leptin and low-leptin subgroups on the basis of plasma leptin concentrations adjusted for BMI and waist : hip ratio. Those with high leptin concentrations had significantly faster heart rates than those with low leptin. MAP and MSNA were similar in both subgroups. No relationship between leptin and either heart rate or MSNA was evident in women. Conclusions In normal men, heart rate, but not MSNA, is linked to plasma leptin concentration. This sex-specific relationship between heart rate and plasma leptin is independent of plasma insulin, BMI, waist : hip ratio and percentage body fat. J Hypertens 19:1089‐1094 & 2001 Lippincott Williams & Wilkins.

Leptin interacts with heart rate but not sympathetic nerve traffic in healthy male subjects.

OBJECTIVE To examine the influence of genetic factors on plasma leptin levels. SUBJECTS AND METHODS We measured plasma leptin levels, body mass index and body fat distribution in healthy young female monozygotic (n = 19) and dizygotic (n = 14) twins. The twin zygosity was verified by determination of short tandem repeat and amplified fragment length polymorphism systems. The genetic analysis included analysis of variance-based and maximum likelihood-based methods. RESULTS Plasma leptin levels were correlated significantly with body mass index (r = 0.59, P < 0.001), waist circumference (r = 0.54, P < 0.001) and hip circumference (r = 0.63, P < 0.001), but not with age (r = -0.17) or the waist:hip ratio (r = 0.02). The heritability estimates derived from intraclass correlations were significant for body mass index (P = 0.001), waist circumference (P = 0.004), hip circumference (P = 0.01) and plasma leptin levels (P = 0.005), but not for the waist:hip ratio (P = 0.22). In the maximum likelihood-based path analysis, heritability was estimated at 79% for body mass index and at 73% for plasma leptin levels. After adjustment for body mass index, the heritability estimate for leptin levels from the model-fitting approach was 55%. CONCLUSIONS Genetic factors are major determinants of plasma leptin levels in humans and may account for as much as half of the variance in leptin levels.

Ian Choe

Papers

Increases in leptin levels, sympathetic drive, and weight gain in obstructive sleep apnea

Leptin interacts with heart rate but not sympathetic nerve traffic in healthy male subjects.

Heritability of plasma leptin levels: a twin study.