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

ABCD
: Appropriate Blood pressure Control in Diabetes
ABI
: ankle–brachial index
ABPM
: ambulatory blood pressure monitoring
ACCESS
: Acute Candesartan Cilexetil Therapy in Stroke Survival
ACCOMPLISH
: Avoiding Cardiovascular Events in Combination Therapy in Patients Living with Systolic Hypertension
ACCORD
: Action to Control Cardiovascular Risk in Diabetes
ACE
: angiotensin-converting enzyme
ACTIVE I
: Atrial Fibrillation Clopidogrel Trial with Irbesartan for Prevention of Vascular Events
ADVANCE
: Action in Diabetes and Vascular Disease: Preterax and Diamicron-MR Controlled Evaluation
AHEAD
: Action for HEAlth in Diabetes
ALLHAT
: Antihypertensive and Lipid-Lowering Treatment to Prevent Heart ATtack
ALTITUDE
: ALiskiren Trial In Type 2 Diabetes Using Cardio-renal Endpoints
ANTIPAF
: ANgioTensin II Antagonist In Paroxysmal Atrial Fibrillation
APOLLO
: A Randomized Controlled Trial of Aliskiren in the Prevention of Major Cardiovascular Events in Elderly People
ARB
: angiotensin receptor blocker
ARIC
: Atherosclerosis Risk In Communities
ARR
: aldosterone renin ratio
ASCOT
: Anglo-Scandinavian Cardiac Outcomes Trial
ASCOT-LLA
: Anglo-Scandinavian Cardiac Outcomes Trial—Lipid Lowering Arm
ASTRAL
: Angioplasty and STenting for Renal Artery Lesions
A-V
: atrioventricular
BB
: beta-blocker
BMI
: body mass index
BP
: blood pressure
BSA
: body surface area
CA
: calcium antagonist
CABG
: coronary artery bypass graft
CAPPP
: CAPtopril Prevention Project
CAPRAF
: CAndesartan in the Prevention of Relapsing Atrial Fibrillation
CHD
: coronary heart disease
CHHIPS
: Controlling Hypertension and Hypertension Immediately Post-Stroke
CKD
: chronic kidney disease
CKD-EPI
: Chronic Kidney Disease—EPIdemiology collaboration
CONVINCE
: Controlled ONset Verapamil INvestigation of CV Endpoints
CT
: computed tomography
CV
: cardiovascular
CVD
: cardiovascular disease
D
: diuretic
DASH
: Dietary Approaches to Stop Hypertension
DBP
: diastolic blood pressure
DCCT
: Diabetes Control and Complications Study
DIRECT
: DIabetic REtinopathy Candesartan Trials
DM
: diabetes mellitus
DPP-4
: dipeptidyl peptidase 4
EAS
: European Atherosclerosis Society
EASD
: European Association for the Study of Diabetes
ECG
: electrocardiogram
EF
: ejection fraction
eGFR
: estimated glomerular filtration rate
ELSA
: European Lacidipine Study on Atherosclerosis
ESC
: European Society of Cardiology
ESH
: European Society of Hypertension
ESRD
: end-stage renal disease
EXPLOR
: Amlodipine–Valsartan Combination Decreases Central Systolic Blood Pressure more Effectively than the Amlodipine–Atenolol Combination
FDA
: U.S. Food and Drug Administration
FEVER
: Felodipine EVent Reduction study
GISSI-AF
: Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation
HbA1c
: glycated haemoglobin
HBPM
: home blood pressure monitoring
HOPE
: Heart Outcomes Prevention Evaluation
HOT
: Hypertension Optimal Treatment
HRT
: hormone replacement therapy
HT
: hypertension
HYVET
: HYpertension in the Very Elderly Trial
IMT
: intima-media thickness
I-PRESERVE
: Irbesartan in Heart Failure with Preserved Systolic Function
INTERHEART
: Effect of Potentially Modifiable Risk Factors associated with Myocardial Infarction in 52 Countries
INVEST
: INternational VErapamil SR/T Trandolapril
ISH
: Isolated systolic hypertension
JNC
: Joint National Committee
JUPITER
: Justification for the Use of Statins in Primary Prevention: an Intervention Trial Evaluating Rosuvastatin
LAVi
: left atrial volume index
LIFE
: Losartan Intervention For Endpoint Reduction in Hypertensives
LV
: left ventricle/left ventricular
LVH
: left ventricular hypertrophy
LVM
: left ventricular mass
MDRD
: Modification of Diet in Renal Disease
MRFIT
: Multiple Risk Factor Intervention Trial
MRI
: magnetic resonance imaging
NORDIL
: The Nordic Diltiazem Intervention study
OC
: oral contraceptive
OD
: organ damage
ONTARGET
: ONgoing Telmisartan Alone and in Combination with Ramipril Global Endpoint Trial
PAD
: peripheral artery disease
PATHS
: Prevention And Treatment of Hypertension Study
PCI
: percutaneous coronary intervention
PPAR
: peroxisome proliferator-activated receptor
PREVEND
: Prevention of REnal and Vascular ENdstage Disease
PROFESS
: Prevention Regimen for Effectively Avoiding Secondary Strokes
PROGRESS
: Perindopril Protection Against Recurrent Stroke Study
PWV
: pulse wave velocity
QALY
: Quality adjusted life years
RAA
: renin-angiotensin-aldosterone
RAS
: renin-angiotensin system
RCT
: randomized controlled trials
RF
: risk factor
ROADMAP
: Randomized Olmesartan And Diabetes MicroAlbuminuria Prevention
SBP
: systolic blood pressure
SCAST
: Angiotensin-Receptor Blocker Candesartan for Treatment of Acute STroke
SCOPE
: Study on COgnition and Prognosis in the Elderly
SCORE
: Systematic COronary Risk Evaluation
SHEP
: Systolic Hypertension in the Elderly Program
STOP
: Swedish Trials in Old Patients with Hypertension
STOP-2
: The second Swedish Trial in Old Patients with Hypertension
SYSTCHINA
: SYSTolic Hypertension in the Elderly: Chinese trial
SYSTEUR
: SYSTolic Hypertension in Europe
TIA
: transient ischaemic attack
TOHP
: Trials Of Hypertension Prevention
TRANSCEND
: Telmisartan Randomised AssessmeNt Study in ACE iNtolerant subjects with cardiovascular Disease
UKPDS
: United Kingdom Prospective Diabetes Study
VADT
: Veterans' Affairs Diabetes Trial
VALUE
: Valsartan Antihypertensive Long-term Use Evaluation
WHO
: World Health Organization

### 1.1 Principles

The 2013 guidelines on hypertension of the European Society of Hypertension (ESH) and the European Society of Cardiology …

/pdf/2013-esh-esc-guidelines-for-the-management-of-arterial-4ydvs5ifsx.pdf

2013 ESH/ESC Guidelines for the management of arterial hypertension: The Task Force for the management of arterial hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).

The development and use of a new scale, the Epworth sleepiness scale (ESS), is described. This is a simple, self-administered questionnaire which is shown to provide a measurement of the subject's general level of daytime sleepiness. One hundred and eighty adults answered the ESS, including 30 normal men and women as controls and 150 patients with a range of sleep disorders. They rated the chances that they would doze off or fall asleep when in eight different situations commonly encountered in daily life. Total ESS scores significantly distinguished normal subjects from patients in various diagnostic groups including obstructive sleep apnea syndrome, narcolepsy and idiopathic hypersomnia. ESS scores were significantly correlated with sleep latency measured during the multiple sleep latency test and during overnight polysomnography. In patients with obstructive sleep apnea syndrome ESS scores were significantly correlated with the respiratory disturbance index and the minimum SaO2 recorded overnight. ESS scores of patients who simply snored did not differ from controls.

A new method for measuring daytime sleepiness: the Epworth sleepiness scale.

2007 Guidelines for the Management of Arterial Hypertension : The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).

Background Limited data have suggested that sleep-disordered breathing, a condition of repeated episodes of apnea and hypopnea during sleep, is prevalent among adults. Data from the Wisconsin Sleep Cohort Study, a longitudinal study of the natural history of cardiopulmonary disorders of sleep, were used to estimate the prevalence of undiagnosed sleep-disordered breathing among adults and address its importance to the public health. Methods A random sample of 602 employed men and women 30 to 60 years old were studied by overnight polysomnography to determine the frequency of episodes of apnea and hypopnea per hour of sleep (the apnea-hypopnea score). We measured the age- and sex-specific prevalence of sleep-disordered breathing in this group using three cutoff points for the apnea-hypopnea score (≥ 5, ≥ 10, and ≥ 15); we used logistic regression to investigate risk factors. Results The estimated prevalence of sleep-disordered breathing, defined as an apnea-hypopnea score of 5 or higher, was 9 percent for w...

The Occurrence of Sleep-Disordered Breathing among Middle-Aged Adults

[Insomnia in infancy and childhood--causes, significance, assessment and approach to treatment].

Urinary ultradian rhythms in dogs

We very much appreciate the interest and constructive comments of Lavie and Lavie regarding our recent article on measurements of plasma homocysteine in otherwise healthy individuals with obstructive sleep apnoea.1 We are also very grateful for the kind and encouraging comments made in the thoughtful review by Winnicki and Palatini,2 which focused on our article as well as on the initial work on plasma homocysteine …

/pdf/obstructive-sleep-apnoea-and-plasma-homocysteine-2v7arqz384.pdf

Obstructive sleep apnoea and plasma homocysteine.

O0068 Oxidative stress and platelet activation in obstructive sleep apnea syndrome (OSAS)

By arguing that only sympathetic activity is responsible for cardiovascular morbidities in OSAS, Kohler & Stradling (2012) conveniently ignore a vast literature linking SA with oxidative stress. A PubMed search using the terms ‘sympathetic’ and ‘oxidative stress’ in the title/abstract revealed 366 publications. The evidence that ROS initiate SA and regulate sympathetic outflow from autonomic ganglia is overwhelming. Although Kohler and Stradling cited Prabhakar et al. (2009) to support their argument that IH augments chemoreflex-stimulated sympathetic outflow by modulating oxygen sensing in the carotid body, they ignored the fact that the IH-mediated carotid body plasticity requires redox signalling, a fundamental finding indicated in the title.

The mechanisms by which IH elevates ROS include activation of various NADPH oxidases, mitochondrial dysfunction, down-regulation of antioxidant enzymes, and AngII-dependent ROS formation resulting in hypertension (Lee & Griendling, 2008). Accordingly, in a double-blind placebo-controlled, randomized, crossover design, subjecting healthy humans to experimental IH increased blood pressure (BP) through activation of type I AngII (AT1) receptors and oxidative stress, and decreased nitric oxide (NO) metabolites. Moreover, treatment with losartan, an AT1 receptor blocker, abolished oxidative stress, improved NO bioavailability and prevented the IH-dependent increase in BP (Foster et al. 2010; Pialoux et al. 2011). Earlier, Mohan et al. (2001) demonstrated that decreased NO bioavailability was responsible for the increased sympathetic activation after 21 days of IH. These findings unequivocally support the involvement of ROS in elevating BP and augmenting sympathetic outflow under IH conditions.

Although Kohler and Stradling accepted that ‘laboratory studies may support plausible hypothesis’ they doubted their ‘relevance to clinical medicine’. To support their position they cite failure of some studies to lessen cardiovascular risks by antioxidant treatments, while accepting the success of randomized controlled studies to treat hypertension in OSAS. We disagree with this position. First, although successful CPAP therapy attenuates BP and SA in OSAS, CPAP also attenuates ROS production and oxidative stress. Second, failure of clinical trials with antioxidants treatment to prevent cardiovascular events emphasizes the importance of laboratory studies to understand the complexity of various ROS sources, their intra/extracellular sites of action and their interactions with other ROS to promote cardiovascular diseases. Intakes of non-specific antioxidants, such as vitamin E, do not neutralize all ROS and cannot reverse oxidative stress in vivo. Furthermore, because of the heterogeneity of ROS sources and the polymorphism of the enzymes producing them, decreased concentrations in a particular ROS by an antioxidant do not imply that all other types of ROS will be abolished. Therefore, inhibiting the systems producing ROS, rather than scavenging ROS after being formed, is the appropriate approach to prevent cardiovascular sequelae. Targeting NADPH oxidases in vascular disease is an ongoing promising therapeutic methodology, which only laboratory research can provide (Drummond et al. 2011).

Thus, it should be recognized that although SA contributes to hypertension and cardiovascular sequelae in OSAS, the dominant role of oxidative stress in activating SA is essential (Lavie & Lavie).

https://physoc.onlinelibrary.wiley.com/doi/pdf/10.1113/jphysiol.2012.235275

Peretz Lavie

Papers

[Insomnia in infancy and childhood--causes, significance, assessment and approach to treatment].

Urinary ultradian rhythms in dogs

Obstructive sleep apnoea and plasma homocysteine.

O0068 Oxidative stress and platelet activation in obstructive sleep apnea syndrome (OSAS)

Rebuttal from Lena Lavie and Peretz Lavie