Essential Hypertension

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Essential hypertension

SeminarEssential hypertensionFranz H Messerli, Bryan Williams, Eberhard RitzEssential hypertension can be deﬁ ned as a rise in blood pressure of unknown cause that increases risk for cerebral, cardiac, and re nal e ve nts. In industrialise d countrie s, the risk of be coming hype rte nsive (blood pre ssure >140/90 mm Hg) during a lifetime exceeds 90%. Essential hypertension usually clusters with other cardiovascular risk factors such as ageing, being overweight, insulin resistance, diabetes, and hyperlipidaemia. Subtle target-organ damage such as left-ventricular hypertrophy, microalbuminuria, and cognitive dysfunction takes place early in the course of hypertensive cardiovascular disease, although catastrophic events such as stroke, heart attack, renal failure, and dementia usually happen after long periods of uncontrolled hypertension only. All antihypertensive drugs lower blood pressure (by deﬁ nition) and this decline is the best determinant of cardiovascular risk reduction. However, diﬀ erences between drugs exist with respect to reduction of target-organ disease and prevention of major cardiovascular e ve nts. Most hype rte nsive patie nts ne e d two or more drugs for blood-pre ssure control and concomitant statintreatment for risk factor reduction. Despite the availability of eﬀ ective and safe antihypertensive drugs, hypertension and its concomitant risk factors remain uncontrolled in most patients. Introduction“The treatment of the hypertension itself is a diﬃ cultand almost hopeless task in the present state of our knowledge and in fact, for ought we know the hypertension may be an important compensatory mechanism which should not be tampered with even if it were certain that we could control it.”1With these words in 1931, Paul Dudley White described what is nowadays regarded as a common misconception about the clinical signiﬁ cance of essential hypertension: namely, that the increase in blood pressure was essential (or compensatory) to guarantee adequate perfusion of the target organs. Regrettably, this misconception lingered in published work (and in many doctors’ minds) until a few years ago, despite the results of the Veterans’ Administration studies 2,3attesting to the beneﬁ ts of antihypertensive treatment. Since then, ﬁ ndings of many trials have shown unequivocally that lowering blood pressure reduces cardiovascular morbidity and mortality for hypertension of all degrees of severity and even in high-risk normotensive individuals. As of July 1, 2007, a Medline search with the term “essential hypertension” retrieved a total of 22 376 articles, of which 3430 were reviews. Rather than attempting to review this work, we will focus here on a few key and emerging issues that we think are of interest to clinicians dealing with hypertensive cardiovascular disease. Ambulatory versus casual blood-pressure measurementsDiagnosis and treatment of hypertension hinges on correct measurement of blood pressure (panel 1). However, this seemingly simple procedure poses manypitfalls and—apart from the introduction of 24-h ambulatory blood-pressure measurement and automated self measurement—has progressed littlebeyond the procedure that Korotkoﬀintroduced 100 years ago.4As Kaplan noted: “The measurement of [blood pressure] is likely the clinical procedure of greatest importance that is performed in the sloppiest manner.”5 Diagnosis of hypertension should be based ideally onseveral blood-pressure measurements taken on separate days, as stated in guidelines.6 For this purpose, the mercury sphygmomanometer has an unsurpassed accuracy,7 but it has been substituted by aneroid and auscultatory or oscillometric semiautomatic devices. Aneroid manometers must be serviced and recali-brated periodically. The reliability of wrist blood-pressure measurements with oscillatory devices is limited.8,9 Home blood-pressure measurement permits identi ﬁ cation of so-called white-coat hypertension (see next section) correlates better than blood-pressurevalues measured in the doctor’s oﬃ ce with target-organdamage,10and could enhance patients’ adherence todrugs.White-coat hypertension and masked hypertensionBecause the correlation between 24-h ambulatory blood-pressure measurements and those taken in the doctor’s oﬃ ce is moderate, the diagnosis of hypertension can be missed by oﬃ ce blood-pressure measurements in some patients who are truly hypertensive (masked hypertension). Conversely, blood pressure can be raisedSearch strategy and selection criteria We scanned the leading journals that publish basic and clinical research in the area of hypertensive cardiovascular disease and searched Medline. The main terms we used were: “essential hypertension”, “cardiovascular disease”, “lifestyle modiﬁ cation”, and “antihypertensive drug therapy”. Additionally, the thoughts and input of our collaborators and colleagues and the reviewers of this Seminar were also considered.Lancet 2007; 370: 591–603 See Editorial page 539St Luke’s-Roosevelt Hospital Center, New York, NY, USA (F H Messerli FACP); Universityof Leicester School of Medicine,Leicester, UK(Prof B Williams MD); and University of Heidelberg, Heidelberg, Germany(Prof E Ritz MD)Correspondence to:Dr Franz H Messerli, Division of Cardiology, St Luke’s-RooseveltHospital Center, ColumbiaUniversity, College of Physiciansand Surgeons, 1000 TenthAvenue, New York, NY 10019,USAfmesserli@Seminarin the doctor’s oﬃce but not on ambulatory blood-pressure monitoring or at home—a situation known as white-coat hypertension. Risk of patients having white-coat hypertension was noted to be somewhat higher than in normotensive individuals but distinctly lower than in people with sustained hypertension.11–15 By contrast, masked hypertension is a less well known (but not necessarily a less frequent) entity with a more serious prognosis than white-coat hypertension. It was noted in as many as a third of the hypertensive population.16,17 In participants of the PAMELA study,18 those with masked hypertension had a higher prevalence of echocardiographic left-ventricular hypertrophy than did normotensive individuals. Inappropriate target-organ disease (for oﬃ ce blood-pressure levels) should trigger suspicion of masked hypertension and motivate doctors to undertake 24-h ambulatory blood-pressure monitoring in a patient. Upper limits for optimum, normal, and hypertensive blood-pressure levels have been redeﬁ ned (table).19 Importantly, rises in blood pressure in the doctor’s oﬃ ce, at home, and while ambulatory seem to have an additive eﬀ ect on cardiovascular risk.20Compared with white-coat hypertension, masked hypertension needs to be looked for and there are few clinical hints to its presence. Because most patients take their medication for hypertension in the morning, blood-pressure values in the doctor’s oﬃ ce usually are normal but can be raised at the end of the dosing interval (ie, during early morning hours). Many patients are still prescribed once-a-day atenolol—a drug that does not reduce heart attack or strokes. Atenolol’s ineﬃ ciency might be related to inappropriate duration of action, its pseudo-antihypertensive eﬀect, or both (see next section). For many clinicians, masked hypertension has unfortunately become a blind spot in antihypertensive treatment.21With respect to the therapeutic approach, we should remember that white-coat hypertension can only be over-treated; therefore, a conservative approach to treatment is justiﬁ ed. Conversely, masked hypertension has a more serious prognosis than white-coat hypertension and can only be under-treated; it deserves, therefore, an aggressive diagnostic and therapeutic approach.Aortic versus brachial blood pressureSince the pulse wave is ampliﬁ ed in transit from the heart to the brachial artery, central aortic systolic pressure is usually lower than brachial pressure.22 The magnitude of ampliﬁ cation is greatest in people with healthy compliant arteries and diminishes with age. Systolic pressure within the aorta is a composite of two items: 1) the outgoing pressure wave, generated by ventricular contraction; and 2) pressure wave reﬂ ection from periphery. The reﬂ ected wave should ideally return towards the heart during diastole to augment diastolic ﬁ lling. If it returns earlier during the cardiac cycle it ampliﬁ es the outgoing pressure wave and leads to an increase in central aortic pressure. The timing and magnitude of pressure-wave reﬂection is aﬀ ected by several factors, including: the stiﬀ ness of the aorta; the distance of reﬂection sites from the heart; and heart rate.As a result, brachial pressure can be an imperfect surrogate for central aortic pressure, particularly when drug treatments diﬀ erentially aﬀ ect central aortic haemodynamics, wave reﬂection, heart rate, or a combination.23 Findings of the CAFE study, in which pulse-wave analysis was used to derive central aortic pressures, showed that β blocker-based treatment was signiﬁcantly less eﬀective than a calcium-channel blocker-based regimen at lowering aortic systolic pressure and pulse pressure, despite identical brachialPanel 1: Points to consider for blood-pressure measurement in the doctor’s oﬃ ce• The patient should sit for several minutes in a quiet room before blood-pressure measurements are taken. Pain,stress, full urinary bladder, a recent meal, and talking oractive listening during measurement aﬀ ect bloodpressure• Take at least two measurements spaced by 1–2 min and additional measurements if the ﬁ rst two are quitediﬀ erent• Using a bladder that is too narrow yields false high readings. Instead of the standard bladder (12–13 cm long,35 cm wide) use an appropriate bladder in patients withincreased midarm circumference• Use phase I (ﬁ rst tapping sound) and V (disappearance) Korotkoﬀ sounds to identify systolic and diastolicblood-pressure values, respectively• Do not deﬂ ate the cuﬀ too rapidly, otherwise individual Korotkoﬀ sounds are missed and too low a value ismeasured; start with a deﬂ ation rate of 2 mm/s• Measure the heart rate by palpation and watch out for arrhythmia, which mandates repeated blood-pressuremeasurements• At the ﬁ rst visit, measure blood pressure in both arms and take the higher value as the reference; measure bloodpressure at 1 and 5 min after standing upright if thepatient has a disorder that frequently causes orthostatic hypotensionSeminar pressures in both treatment arms.24pseudo-antihypertensive eﬀ ect could account for whyβ blocker-based strategies are less eﬀ ective thanalternative treatments at regressing end-organ damageand in prevention of stroke.24–27 Whether central aorticpressure is a better predictor of outcome thanconventional brachial blood pressure remains to beestablished.Hypertension as a gateway to cardiovascularrisk managementAlthough measurement of blood pressure is a simpleprocedure to identify a risk phenotype of cardiovasculardisease, treatment of raised blood pressure alone isinsuﬃcardiovascular disease risk, and formal cardiovasculardisease risk estimation has been recommended. Riskcalculations based on the Framingham cohort used inthe USA and the UK28,29 can overestimate risk in Europeanpopulations by about 7% and by a larger proportion inrecommended use of the SCORE risk calculator.30Pragmatism in risk assessment is important, andavailable risk calculators are based on conventional riskmarkers that can be recorded in a basic clinicalsetting—ie, systolic blood pressure, age, sex, cholesterolconcentration, presence of diabetes, smoking history,and presence or absence of structural damage. Findingsof the INTERH EART study suggested that more than90% of population-attributable risk for acute myocardialinfarction can be accounted for by these risk factors.31Use of more elaborate risk assessment by a series ofbiomarkers adds little to the aforementioned conventionalmethods of cardiovascular disease risk estimation.32One of the most relevant criticisms of cardiovasculardisease risk estimation is that it is based on limited time projections—eg, 10-year absolute risk estimations—that strongly favour treatment of the elderly population versus young people because age is a powerful determinant of short-term risk. Additional factors contributing to and amplifying risk are diabetes30,33 and renal malfunction, as indicated by a low estimated glomerular ﬁ ltration rate34,35 and microalbuminuria or proteinuria.36 For both microalbuminuria and proteinuria, the conventional cutoﬀ points are arbitrary, particularly for albuminuria.37 Equally random is that a serum creatinine concentration of 107–133 µmol/L is a sign of target-organ damage and an amount greater than 133 µmol/L indicates renal disease. Assessment of renal malfunction was enhanced by estimation of the glomerular ﬁltration rate, taking into account age, sex, and body-mass index.38 Cardiac abnormalities by electrocardiography39 or echocardiography40 are correlated to outcome. Figure 1 outlines progression of the natural history of hypertensive cardiovascular disease. In a study of the natural history of (untreated) hypertension in control groups, wide variability of the absolute risk of stroke and heart attack was noted (ﬁ gure 2), but the relation between number ofevents prevented and absolute risk was near-linear forboth coronary heart disease and stroke.41Cardiovascular disease risk thresholds for interventioncurrently deﬁne high-risk patients as having a 10-yearFramingham-derived cardiovascular disease risk of 20% ormore. The typical hypertensive man aged 55 years or olderwill have this level of risk. This threshold takes account ofcurrent evidence and economics, and lower thresholds forintervention would also be cost eﬀective with existingcriteria for cost-beneﬁ t analyses.32 Of note, formalcardiovascular disease risk estimation is not necessary forpatients with hypertension and cardiovascular disease,diabetes, or overt end-organ damage. These patients are atsuﬃcient risk of cardiovascular disease to beneﬁ t frommultifactorial risk-factor intervention.The prothrombotic paradoxHypertension by deﬁ nition is a haemodynamic disorderand, as such, exposes the arterial tree to increasedpulsatile stress. Paradoxically, however, most majorcomplications of longstanding hypertension (ie, heartPrehypertensionProteinuriaNephrosclerosisEstablished hypertensionChronicrenalfailureCoronaryVentricularFigure 1: Range of hypertensive cardiovascular disease from prehypertension to target-organ damage and end-stage diseaseSeminarattack and strokes) are thrombotic rather than haemorrhagic, referred to as the so-called thrombotic paradox of hypertension. Virchow suggested three components facilitating thrombus formation: 1) damage to the vessel wall; 2) hypercoagulability; and 3) abnormal blood ﬂ ow. For thromboembolic events to take place, all the components of Virchow’s triad must be fulﬁ lled.42 In hypertensive individuals, abnormalities in blood ﬂ ow have been well recognised. Hypertension has also been associated with endothelial damage or dysfunction43 and a hypercoagulable state.42 This prothrombotic state could be the result of chronic low-grade inﬂ ammation. Chronic shear stress can lead to remodelling of the vascular endothelium, turning it from an anticoagulant into a procoagulant surface.The mechanisms leading to endothelial dysfunction are multifactorial and include decreased activity of vasodilator agents44–46 and increased activity (or sensitivity) to vasoconstrictor agents.45–47 Overall, ﬁ brinolytic activity is ascertained by the balance between tissue plasminogen activator and plasminogen activator inhibitor type 1 (SERPINE1). With respect to endothelial function, enhanced activity of the renin-angiotensin system and kallikrein-kinin system has opposite eﬀ ects, resulting in vasoc onstriction and vasodilation, respectively.48 By con t rast, with respect to coagulation, increased activity of the renin-angiotensin system and the kallikrein-kinin sys t em has a negative eﬀ ect, resulting in a hypercoagulable state.48 Thus, hypertension not only confers a hyper c oag u lable state(vulnerable blood) but also gives rise to left-ventricular hypertrophy, ventricular and atrial arrhyth m ias, and impaired coronary reserves (vulnerable myo c ar d ium),thereby fulﬁ lling all criteria for a vulnerable patient.49In enhancing the coagulation-ﬁ brinolysis balance, anti-hypertensive treatment can decrease the frequency of throm b o tic events independent of blood pressure. Whetherdiﬀ erences in antihypertensive drug classes48,50,51 will trans-late into altered outcomes remains to be established. Prehypertension and lifestyle interventionsThe issue of prehypertension has stirred tempers to an extent that seems more suitable to medieval theologians than modern scientists.52 Epidemiological evidence suggests a continuous relation between risk of cardiovascular disease and usual blood-pressure values of at least 115/75 mm Hg.53 In the Framingham cohort,a stepwise increase in cardiovascular events was reported in individuals with high baseline blood pressure within the normotensive range.54 Thus, in people without hypertension (blood pressure <140/90 mm H g), blood-pressure levels parallel cardiovascular disease risk in the same way as hypertension.55 Therefore, normotensive individuals with a host of risk factors could show higher overall risk than mildly hypertensive patients without risk factors. Furthermore, the absolute beneﬁ ts of antihypertensive treatment for such normotensive people can be greater than for uncomplicated hypertensive patients.Since individuals without hypertension still outnumber those with the disorder, the blood-pressure-related disease burden remains larger in the normotensive than the hypertensive population.55 Irrespective of the level of hypertension, lowering of blood pressure is always preferable by non-pharmacological means, such as a low salt diet, weight loss, exercise, and alcohol restriction. Indeed, a small but signiﬁ cant fall in blood pressure was noted in meta-analyses of these interventions (ﬁ gure 3).56–59 However, patients’ adherence to lifestyle interventions is notoriously poor; therefore, antihypertensive treatment might have to be considered even in some normotensive individuals. Since the beneﬁts in this population are fairly small, such an approach needs documents of long-term safety. Thus, drugs with metabolic side-eﬀ ects, such as β blockers and diuretics, are not suitable to be used in prehypertensive patients. Also, angiotensin-converting-enzyme inhibitors should probably be avoidedFigure 2: Correlation between absolute risk of coronary heart disease or stroke event in selected clinical trials and number of events prevented per 1000 patient-years of treatmentRelation between absolute risk and event prevented is steeper for stroke than for coronary heart disease, possibly because stroke is more dependent on blood pressure. Unweighted correlation coeﬃ cients were: r=0·89, p<0·0001 for stroke (dashed line), and r=0·87, p<0·0001 for coronary heart disease (solid line). Only trials in which 100 or more events were reported are included. Symbols are drawn encompassing an area proportional to the number of events in every trial. DIABHYCAR=DIABetes and HYpertension Cardiovascular events with Ramipril. DutchTIA=Dutch Transient Ischemic Attack trial. EUROPA=EUropean Reduction Of cardiac events with Perindopril in stable coronary Artery disease. EWPHE=European Working Party on Hypertension in the Elderly. FEVER=Felodipine EVEnts Reduction trial. HDFP=Hypertension Detection and Follow-up Program. HOPE=Heart Outcomes Prevention Evaluation. IDNT=Irbesartan Diabetes Nephropathy Trial. MRC=Medical Research Council Trial (in mild hypertension). MRC-E=Medical Research Council Trial in Older Patients.PATS=Post-stroke Antihypertensive Treatment Study. PEACE=Prevention of Events with Angiotensin-Converting Enzyme inhibition. PROGRESS=Perindopril pROtection aGainst REcurrent Stroke Study. QUIET=QUinapril Ischemic Events Trial. RENAAL=Reduction of Endpoints in Non-Insulin Dependent Diabetes Mellitus with the Angiotensin II Antagonist Losartan trial. SCOPE=Study on COgnition and Prognosis in the Elderly. SHEP=Systolic Hypertension in the Elderly Program. Syst-China=Systolic hypertension in China trial. Syst-EUR=Systolic hypertension in Europe trial.41Seminarbecause of risk for angio-oedema. The only two drug classes that presently fulﬁ l safety requirements are angiotensin-receptor blockers and some calcium-channel blockers. Indeed, in two studies (TROPH Y and PH ARAO), treatment of prehypertensive patients with renin-angiotensin system blockers delayed the onset of stage I hypertension and prolonged the hypertension-free period.60,61We certainly are not advocating treatment of all prehypertensive patients, which could be up to 45 million in the USA alone. However, in those with high-normal blood pressure and diabetes, or a history of cerebrovascular or coronary disease, evidence suggests that antihypertensive drugs are beneﬁ cial. Clearly, the timehas come to abandon the hypertension/normotension dichotomy and to focus on global risk reduction, either by antihypertensive drugs, lipid-lowering treatment, or their combination. New-onset diabetes with antihypertensivetreatmentEver since the report of Colin Dollery’s team more than 20 years ago,62,63 diuretic treatment—particularly when combined with a β blocker—has been known to increase risk for new-onset diabetes. From 1980 to 2004, the prevalence of diabetes more than doubled in the USA,and almost 10% of people older than age 20 years have this disease.64 Patients with hypertension are known to be at higher risk of developing new-onset diabetes than normotensive individuals. In the ALLH AT study, about 10% of all patients developed the disorder throughout the duration of the study.65However, the relative risk was 18% and 40% higher in the chlorthalidone arm than in the amlodipine and lisinopril arms, respectively.66In a network meta-analysis, Elliott and Meyer reported the odds ratio of new-onset diabetes to be 0·62 with angiotensin-receptor blockers, 0·67 with angiotensin-converting-enzyme inhibitors, 0·75 with placebo, 0·79 with calcium-channel blockers, and 0·9 with β blockers; diuretics were the reference.67Admittedly, risk for new-onset diabetes associated with β blockers, diuretics, or both 68 seems to be small. Over a 4-year period, in ALLH AT , the absolute risk was 3·5% higher with chlorthalidone than with lisinopril,65 and in ASCOT , risk was 2·5% higher in the atenolol arm than in the amlodipine arm.69 However, since in the USA alone about 20 million patients are on thiazide diuretics and an almost equal number are on β blockers, this risk translates into 250 000 cases of new-onset diabetes associated withthese so-called traditional antihypertensive drugs everyyear. This ﬁgure would indicate that about 20–25% of the 1 million cases of new-onset diabetes arising yearly in the USA could possibly be related to antihypertensivetreatment—not an insigniﬁcant number. An anonymous statement was published in the BMJ in 2003: “It can’t get clearer. Diuretics—the leastexpensive and most eﬀective agents—should be the ﬁ rst line treatment for almost everyone with hypertension,including patients with diabetes.”70 We beg to diﬀ er and think that in uncomplicated hypertension, diuretics and β blockers should no longer be considered for ﬁ rst-line treatment. The trade-oﬀ of lowering blood pressure at the expense of increasing risk for diabetes by up to 10% yearly is not acceptable. Not unexpectedly, Thomas Sydenham’s dictum of primum non nocere also appliesto ﬁrst-line antihypertensive treatment. First-line antihypertensive treatment and concomitant risk factor reductionThe most important question to ask when selecting initial drug treatment is which class of drug will deliver the most eﬀ ective blood-pressure lowering for thispatient? This question is most relevant becauseblood-pressure lowering is the driver of beneﬁt and initial reductions seem to be a determinant of early cardiovascular disease risk reduction and long-term quality of blood-pressure control.71,72 The response to diﬀ erent classes of drugs is similar when compared head-to-head in heterogeneous populations. H owever, individual responses can diﬀ er strikingly. Somecharacteristics can help predict the initial response to drugs that lower blood pressure. Blood-pressure lowering in older patients (eg, those older than age55 years) or those of black ethnic origin at any age will generally be greatest with thiazide-type diuretics orcalcium-channel blockers.65,71,72 In young people, who generally have a more active renin-angiotensin system than older individuals, blood pressure is loweredeﬀ ectively with inhibitors of the renin-angiotensinsystem—eg, angiotensin-converting-enzyme inhibitors or angiotensin-receptor blockers.73,74 Such stratiﬁ cationfor selection of drug type has been adopted by some guidelines, emphasising that eﬃ ciency of blood-pressure control should drive initial drug selection.75 For patients whose blood pressure is already 20 mm H g or more above their goal, guidelines recommend initial treatmentwith a two-drug combination because monotherapy is likely to be insuﬃ cient.76,77 If ﬁ ndings of an ongoing study 78conﬁ rm safety and eﬃ cacy then initial treatmentFigure 3: Estimated decrease in blood pressure mediated bynon-pharmacological intervention in hypertension56–59Seminarwith a combination of two drugs is likely to become common practice.High-risk patients with hypertension should not only undergo optimum blood-pressure control (with two drugs) but also receive a statin and low-dose aspirin.29,30 This strategy would halve deaths from cardiovascular disease in high-risk patients at a cost of less than US$1000 per quality-adjusted life-year gained.32 Traditional thinking about cardiovascular disease risk factors as individual entities has, unfortunately, impeded this idea of combined risk factor intervention.The complicated and refractory hypertensive patientRefractory (or resistant) hypertension is deﬁ ned as blood pressure that is persistently higher than target—ie, 140/90 mm H g for most hypertensive patients and 130/80 mm H g for individuals with diabetes or renal disease—despite prescription of three diﬀ erent antihypertensive drug classes, including a diuretic. Refractory hypertension is seen freq u ent-ly. Even in most controlled trials the mean achieved blood pressure failed to reach targets.79 Poor blood-pressure control in primary care,80 particularly in elderly people,81 is not surprising but, nevertheless, disquiet-ing because of the high associated cardiovascular risk.82,83 Two categories of refractory hypertension can be distinguished: 1) true resistance; and 2) apparent resistance .84True resistancePanel 2 summarises factors that can lead to true resistant hypertension. Most patients in this category can be treated by omitting relevant drugs and altering the antihypertensive drug regimen. In a few individuals, secondary causes of hypertension can be noted.One major step forward in management of patients with true resistance has been recognition that inappropriate aldosterone concentrations (raised aldosterone/renin ratio) arise in up to 20% of people,85–87 including hypertensive emergencies.88Although patients are frequently normokalaemic,89 only a few have surgically correctable adenoma.90Irrespective of whether or not an adenoma is present, aldosterone antagonists provide relevant additional blood-pressure reduction 85,87,91,92independent of aldosterone concen t rations. H yper-kalaemia is rare,85 at least as long as renal function is not impaired.Apparent resistanceA typical cause of faulty blood-pressure measurement is use of a cuﬀ that is too small relative to the circumference of the arm, particularly in obese individuals. The blood-pressure value taken in the doctor’s oﬃ ce mightalso be raised if the patient smoked or had coﬀ ee before their appointment. A less frequent occurrence is malfunction of the measuring device used by the patient. A rare cause is so-called pseudohypertension as a result ofstiﬀor calciﬁ ed brachial arteries, which should be suspected if either measured blood-pressure values are inappropriate for target-organ damage or antihypertensivedrugs provoke symptoms of hypotension despite persistent raised blood pressure. Non-speciﬁc but helpful is Osler’s manoeuvre—ie, a palpable radial artery when the brachial artery is occluded.93 Another common cause of apparent refractoryhypertension is an inadequate drug regimen—ie,insuﬃcient dosing, selection of inadequate combi-nations of drugs, and choice of antihypertensive agentswith insuﬃcient duration of action. The solution is long-acting well-tolerated drugs or drug combinations, including a diuretic, taken once a day.94 Arguably the most frequent cause of apparent resistant hypertensionis non-adherence to treatment.Non-adherence to treatment“I’ve also been treating the high cholesterol and then Istopped the medicine because I got my cholesterol down low. And, I had in the past, a little [blood pressure]problem, which I treated and then I got it down…” (Former US President Clinton, awaiting coronary bypass surgery, calls into Larry King Live from his hospital bed; posted Friday, Sept 3, 2004, 23:31 h EST).Panel 2: True resistant hypertensionVolume overload• Excessive dietary sodium intake• Compensatory response to vasodilatory antihypertensive drugs • Insuﬃ cient diuretic treatment • Reduced renal function • HyperaldosteronismContraindicated drugs or exogenous substances • Non-steroidal anti-inﬂ ammatory drugs, COX2 inhibitors • Sympathicomimetics (nasal drops, appetite suppressants)• Cocaine • Oral contraceptives • Glucocorticoids • Mineralocorticoids • Liquorice • Herbal drugs (ginseng, yohimbin)• Drugs (eg, erythropoietin, cyclosporin, tacrolimus)• Diﬀ erent types of drugs can also aﬀ ect pharmacokinetics and cause rapid inactivation of antihypertensive drugs Associated condition • Smoking • Obesity (visceral obesity)• Metabolic syndrome or type 2 diabetes • Excess alcohol intake• Anxiety-induced hyperventilation or panic attacks • Pain。

高血压病

29
常用降压药物---①利尿剂（Diuretic）
– 噻嗪类、袢利尿剂、保钾利尿剂 – 降压机制：排钠，减少血容量，降低外周血管阻力 – 副作用: 低钾，影响血糖、血脂、血尿酸 – 保钾利尿剂可引起高血钾
30
常用降压药物---①利尿剂（Diuretic）
类别噻嗪类适应征心衰，老年高血压，单纯收缩期高血压肾功能不全，心衰痛风禁忌征强制性可能妊娠
11.88 7.73 5.11
1959
1979
1991
2002年
8
流行病学
• 我国高血压的“三低”：知晓率低、治疗率低、控制率低知晓率（%）治疗率（%）控制率（%)
中国
1991年 2002年
26.3 30.2 60 70
12.1 24.7 40 59
2.8 6.1 25 34
美国
1980年 2000年
90~99 100~109 ≥110 ＜90
注：以上为成人高血压标准，儿童则采用不同年龄组血压值 6 的95%位数。
血压水平与心血管发病危险之间的关系是连续的。血压从115/75mmHg开始，每升高20/10mmHg，心血管危险增加1倍!
7
流行病学
近50年来，我国高血压患病率快速上升
高血压患病率（ % ） 20 18 16 14 12 10 8 6 4 2 0 18.8
10
高血压的发病机制
1. 交感神经系统活性亢进
病因感N CNS功能异常儿茶酚胺神经递质，交阻力血管收缩
2. 肾性水钠潴留
交感N亢进/肾血管阻力增加、肾小球微小的结构病变、肾内/外排钠激素、潴钠激素。
11

减重手术治疗原发性高血压

减重手术治疗原发性高血压陆佳军(综述);朱江帆(审校)【摘要】[Summary] Obesity is the most important risk factor of essential hypertension.Obesity-related hypertention has become a worldwide problem.Many clinical studies show that bariatric surgery has significant therapeutic effect on essential hypertension, but the specific mechanism of the condition remains to be fully understood.This paper tried to explainthe mechanism of the treatment of bariatric surgery for essential hypertension from the following two aspects: the reversal of the sympathetic disorder and the decline of plasma leptin.%肥胖是原发性高血压第一危险因素，肥胖性高血压已成为一个不容忽视的全球性问题。

许多临床研究证实，减重手术对原发性高血压有明显的治疗效果，但机制尚未完全阐明。

本文着重从交感神经紊乱逆转和血浆瘦素的下降阐述减重手术治疗原发性高血压可能的机制。

【期刊名称】《中国微创外科杂志》【年(卷),期】2015(000)012【总页数】4页(P1125-1128)【关键词】减重手术;原发性高血压【作者】陆佳军(综述);朱江帆(审校)【作者单位】大连医科大学，大连 116044; 同济大学附属东方医院肥胖与代谢病外科，上海 200123;大连医科大学，大连 116044; 同济大学附属东方医院肥胖与代谢病外科，上海 200123【正文语种】中文【中图分类】R656.6+1;R544.1随着生活水平的提高及人们饮食习惯的改变，肥胖人群日益增多，肥胖是原发性高血压的危险因素之一。

临床实验报告英文

Title: Evaluation of the Efficacy and Safety of a New Antihypertensive Drug in Patients with Essential HypertensionIntroduction:Hypertension, also known as high blood pressure, is a common chronic condition affecting millions of people worldwide. It is a major risk factor for cardiovascular diseases, including stroke, myocardial infarction, and heart failure. The aim of this clinical trial was to evaluate the efficacy and safety of a new antihypertensive drug, Drug X, in patients with essential hypertension.Materials and Methods:Study Design:This was a randomized, double-blind, placebo-controlled, parallel-group clinical trial. The study duration was 12 weeks.Participants:A total of 200 patients with essential hypertension were enrolled in the study. The inclusion criteria were as follows:1. Age between 18 and 70 years2. Diagnosed with essential hypertension according to the American Heart Association guidelines3. Systolic blood pressure (SBP) ≥ 140 mmHg and/or diastolic blood pressure (DBP) ≥ 90 m mHg at baseline4. Willingness to comply with the study protocolExclusion Criteria:1. Patients with secondary hypertension or other cardiovascular diseases2. Patients with a history of allergic reactions to the study drug orits active ingredients3. Patients on concurrent antihypertensive medications4. Patients with severe liver or kidney dysfunction5. Pregnant or lactating womenRandomization and Blinding:Participants were randomly assigned to two groups: the Drug X group and the placebo group. The randomization process was performed using a computer-generated randomization list. Both the participants and the investigators were blinded to the treatment allocation.Interventions:The participants in the Drug X group received Drug X at a dose of 10 mg once daily, while the participants in the placebo group received a matching placebo. All participants continued their baseline antihypertensive therapy throughout the study.Outcome Measures:The primary outcome measure was the change in SBP and DBP from baseline to the end of the study. Secondary outcome measures included the proportion of participants achieving blood pressure control (SBP < 140 mmHg and DBP < 90 mmHg), the incidence of adverse events, and the changes in laboratory parameters.Data Analysis:The data were analyzed using descriptive statistics, including means, standard deviations, frequencies, and percentages. The primary and secondary outcome measures were compared between the two groups using the independent t-test or chi-square test, as appropriate. The safety analysis was performed using descriptive statistics, and adverse events were categorized based on the World Health Organization's Common Terminology Criteria for Adverse Events (CTCAE).Results:Of the 200 enrolled participants, 191 completed the study. Baseline characteristics were similar between the two groups. At the end of the study, the mean change in SBP from baseline was -15.2 mmHg in the Drug Xgroup and -8.5 mmHg in the placebo group (p < 0.001). The mean change in DBP from baseline was -9.8 mmHg in the Drug X group and -5.2 mmHg in the placebo group (p < 0.001). The proportion of participants achieving blood pressure control was 78% in the Drug X group and 38% in the placebo group (p < 0.001).The incidence of adverse events was similar between the two groups, with the most common being dizziness, headache, and nausea. All adverse events were mild to moderate in severity and resolved without any intervention.Conclusion:The results of this clinical trial demonstrate that Drug X is an effective and safe antihypertensive agent in patients with essential hypertension. The drug significantly reduced SBP and DBP, leading to a higher proportion of participants achieving blood pressure control. The adverse event profile was favorable, with no significant differences between the Drug X group and the placebo group.Recommendations:Based on the findings of this study, Drug X can be considered as a potential treatment option for patients with essential hypertension. Further research is needed to evaluate the long-term efficacy and safety of the drug in a larger population.Authors' Contributions:- Author 1: Conceived and designed the study, collected and analyzed the data, and wrote the manuscript.- Author 2: Contributed to the study design, analyzed the data, and reviewed the manuscript.- Author 3: Provided statistical analysis and reviewed the manuscript.Conflict of Interest:The authors declare no conflicts of interest.Funding:This study was funded by [Funding Source Name].Ethical Approval:The study was approved by the Institutional Review Board [IRB Name] and was conducted in accordance with the Declaration of Helsinki.Acknowledgments:We thank the participants for their contribution to this study.References:- [List of references]。

高血压名词解释基础护理学

高血压名词解释基础护理学高血压（Hypertension）是指人体动脉血压长期持续升高的一种疾病。

可以分为原发性高血压和继发性高血压。

原发性高血压也称为essential hypertension，是指血压升高的原因不明确，可能与遗传、环境、生活方式等因素有关。

继发性高血压是指高血压是由其他疾病或药物引起的，如肾脏疾病、心脏病、甲状腺问题等。

下面是一些与高血压相关的基础护理学名词的解释：1. 血压（Blood pressure）：指心脏收缩和舒张时血液对动脉壁产生的压力。

2. 收缩压（Systolic pressure）：指心脏收缩时动脉内的最高压力。

3. 舒张压（Diastolic pressure）：指心脏舒张时动脉内的最低压力。

4. 高血压病期（Stages of hypertension）：将高血压按血压水平分为不同的阶段。

常见的分期有高血压前期、一级高血压、二级高血压和三级高血压。

5. 高血压危险因素（Risk factors for hypertension）：指可能导致高血压发生的因素，包括年龄、遗传因素、体重超标、高盐摄入、饮酒和缺乏运动等。

6. 血压控制（Blood pressure control）：指通过生活方式改变、药物治疗等手段，使患者的血压保持在正常范围内，预防并控制高血压相关并发症的发生。

7. 血压计（Sphygmomanometer）：用于测量血压的仪器，主要包括袖带、压力计和听诊器等组成部分。

8. 抗高血压药物（Antihypertensive drugs）：用于治疗高血压的药物，包括钙通道阻滞剂、ACE抑制剂、β受体阻滞剂、利尿剂等。

这些药物可以通过不同的途径降低血压。

以上是一些高血压相关的基础护理学名词的解释，希望对您有帮助。

Antihypertensive Drugs-Cardiovascular Pharmacology抗高血压,心血管药理学

Cardiac Output X Peripheral Resistance = Arterial Pressure
Since the product of heart rate and stroke volume equals cardiac output, an increase
in heart rate will increase arterial blood pressure, all other factors remaining equal.
Adrenergic Neuron Blocker
Guanethidine Reserpine
Adrenoceptor Antagonists
Labetalol (alpha & beta) Prazosin (alpha) Terazosin (alpha)
Vasodilators
Diazoxide Hydralazine Minoxidil Nitroprusside sodium
Angiotensin Converting Enzyme Inhibitors (ACEI)
Benazepril Captopril Enalapril Fosinopril Quinapril Ramipril
Angiotensin Receptor Blocker
Saralasin Losartan Irbesartin
Peripheral resistance:
For a given cardiac output, blood pressure depends only on peripheral resistance. Some antihypertensive drugs act to reduce peripheral resistance.

医学英语翻译与写作MedicalEnglishTranslationandwriting

English Translation and the Chinese Attainment
To avoid a lack of subjects
1. In regard to the operation tomorrow, it is postponed. 2. Only with large numbers of patients can we be confident that a small difference between two forms of treatment will be detected. 3. As it is digested slowly, milk sugar remains in the intestinal tract for a longer period than do other sugars.
English Translation and the Chinese Attainment
To decrease English-style expressions
Illness prevented him from going there. 原译：疾病妨碍他去那里。（此译文不符合汉语的表达习惯，主要是因为这种译法硬按原文的语法结构来翻译。此句的关键是将原文中的宾语him译成汉语中的主语“他”）改译：他因病未去那里。
Translation and English Grammar
1. The patient is not so sick but he should be hospitalized. 2. When you exercise vigorously, waste products which act as mild poisons to the nervous system are formed. 3. From this you can find out the ratio of oxygen reacting to water formed.

高血压病患者生活方式的健康教育及护理干预

高血压病患者生活方式的健康教育及护理干预AbstractHypertension is a chronic non-communicable disease characterized by high blood pressure. It is a major risk factor for cardiovascular diseases, stroke, and kidney failure. Hypertension has an incredibly high prevalence worldwide, with an increasing trend in developing countries. The lifestyle of hypertensive patients plays a critical role in the prevention and management of hypertension. Health education and nursing interventions are essential strategies that can help hypertensive patients to improve theirlifestyle and achieve better blood pressure control. This paper discusses the health education and nursinginterventions that have been used to manage hypertension in various countries worldwide.IntroductionHypertension, also known as high blood pressure, is a chronic non-communicable disease affecting millions of people worldwide. According to the World Health Organization (WHO), hypertension is defined as a systolic blood pressure of 140 mmHg or higher, and/or a diastolic blood pressure of 90 mmHg or higher. Hypertension is a significant risk factor for cardiovascular diseases, stroke, chronic kidney disease, and other complications (1).Global prevalence of hypertension is rising rapidly, and it is estimated that approximately one billion peopleworldwide have hypertension. Moreover, hypertension is responsible for about 9.4 million deaths annually worldwide, making it one of the leading causes of death globally (2, 3).Lifestyle interventions constitute the first-line management of hypertension. Appropriate lifestyle changes can lower blood pressure (BP) and reduce the need for medication.Health education and nursing interventions play an essential role in the management and prevention of hypertension. Therefore, this paper aims to review health education and nursing interventions that are effective in managing hypertension and improving the quality of life of hypertensive patients.Health EducationHealth education is the process of educating people about health and disease prevention, to help them improve their health and well-being. The goal of health education in hypertension management is to raise awareness among patients about their condition and how to control it. Health education for hypertension includes information on the cause and risk factors for hypertension, its complications, lifestyle modifications, and the significance of adherence to medication (4).Effective health education strategies for hypertension may include the following:1. Stress management trainingStress is a significant risk factor for hypertension. Therefore, teaching patients methods of managing stress such as relaxation exercises can help lower blood pressure (5).2. Dietary modificationsHealth education on dietary modifications is essential in hypertension management. Hypertensive patients need to beeducated about dietary changes such as reducing salt intake, increasing potassium intake, and avoiding excess alcohol and caffeine (6).3. Physical activityRegular physical activity is essential in hypertension management. Hypertensive patients should be encouraged to engage in moderate-intensity physical activity such as brisk walking, cycling, or swimming for at least 30 minutes every day (6).4. Smoking cessationSmoking cessation is crucial in hypertension management. Hypertensive patients who smoke should be advised to quit smoking to prevent further damage to the blood vessels (7).5. Medication adherenceHealth education on medication adherence is essential in hypertension management. Patients should be advised to adhere to prescribed medication, the correct dosages, and frequencies to achieve better blood pressure control (8).Nursing InterventionsThe role of nurses in hypertension management is significant. Nurses have a crucial role in helping hypertensive patients to achieve better blood pressurecontrol and improve their quality of life. Nursing interventions that may help in hypertension management include the following:1. Blood pressure monitoringBlood pressure monitoring is an essential component of hypertension management. Nurses can monitor and record the patient's blood pressure regularly and provide feedback to the patient on blood pressure control (9).2. Lifestyle modificationsNurses can educate hypertensive patients about lifestyle modifications such as dietary changes and physical activity. Nurses can also provide guidance in making small but sustainable changes in lifestyle (10).3. Medication managementNurses can help in medication management by reminding patients to take their medication, ensuring the correct medication, dose, and frequency. Additionally, nurses can monitor the side effects or adverse effects of medication and report them to the physician (11).4. Patient education on self-careNurses can educate hypertensive patients on self-monitoring, self-care, and importance of adherence to medication to control blood pressure. Patient education onself-care also includes adherence to follow-up appointments with physicians and regular blood pressure monitoring at home (9).5. Collaborative careCollaborative care involves collaboration among nurses, physicians, and other healthcare professionals to manage hypertension effectively. Collaborative care is crucial in hypertension management, taking into consideration the significant comorbidities that hypertensive patients may have, such as diabetes and obesity (12).ConclusionHypertension is a significant global health problem that affects millions of people worldwide. The lifestyle of hypertensive patients plays a crucial role in hypertension management. Health education and nursing interventions are essential to help hypertensive patients achieve better blood pressure control and improve their quality of life. Healtheducation strategies include stress management training, dietary modifications, physical activity, smoking cessation, and medication adherence. Nursing interventions include blood pressure monitoring, lifestyle modifications, medication management, patient education on self-care, and collaborative care. Effective hypertension management requires a collaborative approach among nurses, physicians, and other healthcare professionals.。

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Estimates of the genetic contribution to BP variation range from 30% to 50%.
2. Environmental influences
(1) High diet salt intake There is positive association between dietary salt-overload and the prevalence of hypertension with salt-sensitive persons. Salt-sensitive means individual response of BP to variation in sodium intake widely.
2. Kidney
(1) nephrosclerosis is common (2) if without accelerated or malignant hypertension AKF is not common. (3) With hypertension for long time , patients have Nocturia : uria increase in night. Intermittent hematuria is less.
Essential Hypertension
Ⅰ. General Considerations
Essential Hypertension(EH) is a popular disease in the world.
The cardiovascular morbidity and mortality is much high. Cardiac, renal, cerebral complications are the main problems of hypertension. 95% patients with HBP are called essential or primary hypertension. 5% patients with specific cause are called secondary hypertension.
(2) High weight and obesity There is strong positive correlation between body mass index(BMI) and BP level. obesity is associated with insulin resistance and hyperinsulinemia
Smoking
Alcohol
Physical inactivity
Байду номын сангаас
Risk factors associated with EH
1. Family history
BP level is correlated among family members a fact attributable to common genetic background.
(4) Smoking
Cigarette smoking is
a powerful risk factor for cardiovascular disease.
(5) Alcohol
Excessive alcohol intake is an important risk factor for HBP. It can cause resistant to antihypertensive therapy. It is a risk factor for stroke.
Ⅴ.Laboratory Tests and
Other Findings
In the early EH just BP is high , lab test is normal .
When target-organ damage, we can find lab test changes as follows:
3. Kidney
Most hypertensive patients company with nephrosclerosis . patients have no signs in the early. If patients with HBP have very severe kidney damage , patient occur Edema .
1. Heart
SYMPTOMS
No symptoms in early. If untreated hypertension for long time , patients will progressively occur Dyspnea on exertion Paroxysmal nocturnal dyspnea Orthpnea This means from compensation to decompensation.
4. Brain (Central nervous system)
There may be a positive Babinski, Hoffman reflex, in the patients with stroke.
same side arm and leg can not move. some patients can not speak.
90-99 90-94 100-109 110 < 90 < 90
Ⅱ. Risk factors associated with EH
EH
Family History GENETIC
Environmental
High diet salt intake Obesity
Psychological stress
3. Central nervous systems
Hypertension resulting in cerebral damage is mainly stroke.( Acute interruption of the blood supply to localized area of the brain causes stroke.)
(6) Physical inactivity
It increase risk of CHD
It isn’t benefit to control HBP.
3. Others
Age, Dyslipidemia, Diabetes mellitus
Ⅳ. Clinical Manifestation
Signs
1. Heart LV enlargement. Precordial heave (forcible) . Third and fourth heart sounds (gallop rhythm) .
2. Blood vessels
Pulmonary rales is valuable in recognizing early left ventricular failure Pulses alternans is one of the sign of left ventricular failure Buits in the epigastrium may suggest renovascular hypertension
5. Retinas
We can find different retinopathy in the retinas by funduscopy, it indicated different group of hypertension from mild to very severe. Funduscopic examination for hypertension retinopathy Arterolar narrowing , focal arteriolar constriction Arterovenous crossing changes Hemorrhages and exudates Disc edema
There is no specific symptoms in early. If patients have hypertension for
long time . It result in important target-organs damaged: brain,
heart, kidney ,blood vessels and retina.
Ⅲ .Definition and classification
of Hypertension (WHO 1999)
Category SBP(mmHg) DBP(mmHg) < 80 < 85 85-89 Optimal < 120 Normal 130 High-Normal 130-139 Hypertension Grade (mild) 140-159 Subgroup: borderline 140-149 Grade (moderate) 160-179 Grade (severe) 180 Isolated Systolic Hypertension 140 Subgroup: borderline 140-149
The most common type is thrombotic cerebral infarction. It result from atherosclerosis . The second is cerebral hemorrhage. But it dangerous is higher than thrombotic cerebral infarction.
Laboratory Evaluation of Newly Diagnosed Hypertensive Patients