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Micardis(R) - MicardisPlus(R) - Hypertonie (38 Abbildungen)

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Abbildung 0

Micardis - Micardis Plus
Abbildung 1

Abbildung 2

Hypertonie - Ursachen
Abbildung 3: There is no single identifiable cause for most cases of hypertension.1 Hypertension is known to be a product of genetic predisposition with environmental and lifestyle factors.1 Beevers G, et al. The pathophysiology of hypertension. BMJ 2001;322:912–916.

Keywords: HypertonieUrsache
Hypertonie - Pathophysiologie
Abbildung 4: Numerous physiological systems contribute to determine an individual’s blood pressure.1 The environmental and genetic factors described in the previous slide cause hypertension by interacting with this physiological systems. Antihypertensives modulate one or more of these to reduce blood pressure.

Keywords: HypertoniePathophysiologie
Hypertonie - Klassifikation
Abbildung 5: Recent US and European guidelines have extended the range of blood pressure that is considered to be greater than optimal. JNC 7 introduced the concept of ‘pre-hypertension’, which indicates those patients who are at increased risk of progression to true hypertension.1 The European Society of Hypertension (ESH) guidelines introduced the concept of ‘high-normal’, to reinforce the idea that the real threshold for a ‘safe’ level of blood pressure depends on the total cardiovascular risk profile of each individual.2 Total cardiovascular risk is a product of the level of blood pressure and the presence of other risk factors, such as obesity, diabetes and albuminuria, as well as the presence of target-organ damage. Chobanian AV, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003;289:2560–2572. 2003 European Society of Hypertension – European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003;21:1011–1053.

Keywords: ESHHypertonieJNC 7Klassifikation
Hypertonie - Prävalenz
Abbildung 6: These data are from a meta-analysis of cross-sectional studies on the prevalence of hypertension around the world.1 Overall, 26% of adults have hypertension, with similar proportions for men and women.1 The prevalence of hypertension increases strongly with age, especially for women.1 Worldwide, the number of adults with hypertension is predicted to increase from 972 million in 2002 to 1,560 million in 2025, as the proportion of elderly people increases.1 Kearney PM et al. Global burden of hypertension: analysis of worldwide data. Lancet 2005;365:217–223.

Keywords: AlterDiagrammHypertoniePrävalenz
Abbildung 7: The most accurate method to measure blood pressure in the office is to listen for Korotkoff sounds in the brachial artery as cuff pressure is reduced. A mercury sphygmomanometer is very reliable, although aneroid devices, if regularly maintained, can also provide accurate pressure readings.1 White-coat hypertension is common, and occurs when a patient’s blood pressure increases in the presence of a physician.1 Blood pressure can also be assessed by the patient at home. This avoids the potential for white-coat hypertension, and makes the measure of early morning blood pressure more feasible. HBPM typically uses aneroid or oscillometric devices and may be semi-automated.1 The best technique for measuring blood pressure is to use an ambulatory monitor, which is typically a small, fully automatic device which can be worn on a belt around the waist.1 ABPM allows blood pressure to be measured several times an hour over a 24-h period, and provides an assessment of the patient’s circadian rhythm. 24-h mean blood pressure is typically lower than office blood pressure, partly due to white-coat hypertension in the office but mostly because blood pressure drops at night in most people.1 Pickering TG, et al. Recommendations for blood pressure measurement in humans and experimental animals. Part 1: blood pressure measurement in humans. Hypertension. 2005;45:142–161.

Keywords: BlutdruckmessungBluthochdruckMethoden
Abbildung 8: The Office versus Ambulatory (OvA) study looked at cardiovascular risk over 5 years in 1,963 patients subdivided at baseline according to their 24-h mean ambulatory blood pressure and their office blood pressure.1 Overall, the risk of a cardiovascular event was 3.2-fold higher in patients with a 24-h mean SBP ≥135 mmHg compared with a 24-hour ambulatory SBP <135 mmHg.1 Even after adjusting for office blood pressure, a 24-h mean SBP ≥135 mmHg indicated a 1.3-fold higher risk.1 The 24-h mean blood pressure is therefore an important independent indicator of cardiovascular risk.1 Clement DL, et al. Prognostic value of ambulatory blood-pressure recordings in patients with treated hypertension. N Engl J Med 2003;348:2407–2415.

Keywords: BlutdruckDiagrammMessungSBD
Morgendlicher Blutdruckanstieg
Abbildung 9: This slide shows the circadian rhythm of blood pressure in a normal individual.1,2 Blood pressure falls during sleep and rises rapidly just before the time of awakening. The maximum is reached as people arise and begin their routine daytime activities. 1. Millar-Craig M, et al. Circadian variation of blood pressure. Lancet 1978;1:795–797. 2. Mancia G, et al. Blood pressure and heart rate variabilities in normotensive and hypertensive human beings. Circ Res 1983;53:96–104.

Keywords: BlutdruckanstiegBlutdruckprofilDiagrammTageszeit
Morgendlicher Blutdruckanstieg
Abbildung 10: This figure shows the range of blood pressure over 24 hours in normotensives and patients with hypertension.1 In both groups, blood pressure shows a circadian rhythm, with a rapid increase in the early morning. 1. Millar-Craig MW, et al. Circadian variation of blood-pressure. Lancet 1978;1:795–797.

Keywords: BlutdruckanstiegDiagrammHypertonikerNormotonikerTageszeit
Morgendlicher Blutdruckanstieg
Abbildung 11: The early morning blood pressure surge has been shown to coincide with the peak incidence of a multitude of cardiovascular events. One study revealed that most (68 %) ischaemic episodes occurred between 07:30 and 19:30, with a peak in the morning and a lesser peak in the evening, a rhythm that resembles the occurrence of myocardial infarction and sudden death.1 The circadian rhythm of angina likewise follows a similar pattern to that of myocardial infarction.2 The incidence of stroke rises by around 60% in the early morning period.3 The circadian rhythm of variant angina peaks in the morning, coupled with a peak in plasma levels of fibrinopeptide A.4 The morning rise in blood pressure is also accompanied by a rise in platelet aggregability.5 1. Mulcahy D, et al. Circadian variation of total ischaemic burden and its alteration with anti-anginal agents. Lancet 1988;2:755–759. 2. Taylor CR, et al. Circadian rhythm of angina: similarity to circadian rhythms of myocardial infarction, ischemic ST segment depression, and sudden cardiac death. Am Heart J 1989;118:1098–1099. 3. Marler JR, et al. Morning increase in onset of ischemic stroke. Stroke 1989;20:473–476. 4. Ogawa H, et al. Circadian variation of plasma fibrinopeptide A level in patients with variant angina. Circulation 1989;80:1617–1626. 5. Oshchepkova EV, et al. [Morning rise of systolic blood pressure (by 24-hour ambulatory monitoring) and platelet aggregability in essential hypertension patients]. Ter Arkh 2000;72:47–51.

Keywords: Blutdruckanstiegkardiovaskuläre Komplikation
Morgendlicher Blutdruckanstieg
Abbildung 12: These data are from 2 studies that have analysed the circadian variation in the onset of acute myocardial infarction (n=2,999) or stroke (n=1,167).1,2 Both studies found a notable increase in the number of events in the early morning period, the time that corresponds to the early morning blood pressure surge (EMBPS). 1. Muller JE, et al. Circadian variation in the frequency of onset of acute myocardial infarction. N Engl J Med 1985;313:1315–1322. 2. Marler JR, et al. Morning increase in onset of ischemic stroke. Stroke 1989;20:473–476.

Keywords: BlutdruckanstiegDiagrammkardiovaskuläres Risiko
Morgendlicher Blutdruckanstieg
Abbildung 13: A significant (p<0.05) circadian pattern of cardiac death was apparent in a retrospective analysis of 94 cases of sudden cardiac death.1 The incidence of cardiac death peaked in the morning between 09:00 and 12:00 h and was lowest in the evening (18:00 to 21:00 h).1 There was an even stronger relationship with the time of waking, with a 2.6-fold increase in risk in the first 3 hours after waking compared with other times of the day.1 The peak incidence of cardiovascular events also occurs at the time of the EMBPS.2 1. Willich SN, et al. Increased onset of sudden cardiac death in the first three hours after awakening. Am J Cardiol 1992;70:65-68. 2. Rocco MB, et al. Circadian variation of transient myocardial ischaemia in patients with coronary artery disease. Circulation 1987;75:395–400.

Keywords: BlutdruckDiagrammIschämieplötzlicher HerztodTageszeit
Morgendlicher Blutdruckanstieg
Abbildung 14: These data are from a meta-analysis of 31 publications reporting the circadian timing of 11,816 strokes.1 There was a 79% increase in the incidence of stroke in the period 06:00–12:00 compared with other hours of the day. This increase in the morning period was found in all three stroke subtypes. 1. Elliott WJ. Circadian variation in the timing of stroke onset. Stroke 1998;29:992–996.

Keywords: BlutdruckDiagrammHämorrhagischer InsultIschämie
Tagesrhythmische Schwankungen
Abbildung 15: The EMBPS is accompanied by a surge in many other important physiological factors. This slide shows the percent change in key haemodynamic, electrolyte excretion and hormonal factors in the early morning period.1 A sharp increase in RAS activity contributes to the EMBPS. 1. White WB. Relevance of blood pressure variation in the circadian onset of cardiovascular events. J Hypertens 2003;21 (Suppl 6):S9–S15.

Keywords: BlutdruckDiagrammRAASTageszeit
Hypertonie - Risikofaktoren - Klinische Ereignisse
Abbildung 16: The concept of a cardiovascular continuum was first published in 1991.1 Factors such as hypertension can left ventricular hypertrophy (LVH), which increase the risk of cardio- and cerebrovascular events.1 Ventricular wall remodelling, if untreated, may ultimately result in congestive heart failure, end-stage heart disease and death. These can be accompanied by cognitive dysfunction and, as the disease progresses, dementia.2 Vascular remodelling, atherosclerosis and cardiac embolism can result in stroke. Hypertension and diabetes are also among the risk factors that lead to endothelial dysfunction. This can result in damage to the glomeruli, microalbuminuria and macroproteinuria, leading to progressive nephrosis and the development of renal failure.3–5 1. Dzau V, Braunwald E. Resolved and unresolved issues in the prevention and treatment of coronary artery disease: a workshop consensus statement. Am Heart J 1991; 121: 1244–1263. 2. Hofman A, et al. Atherosclerosis, apolipoprotein E, and prevalence of dementia and Alzheimer’s disease in the Rotterdam study. Lancet 1997; 349: 151–154. 3. Cooper ME. Pathogenesis, prevention and treatment of diabetic nephropathy. Lancet 1998; 352: 213–219. 4. Taylor AA. Pathophysiology of hypertension and endothelial dysfunction in patients with diabetes mellitus. Endocrinol Metabol Clin North Am 2001; 30: 983–997. 5. Erhardt LR. Endothelial dysfunction and cardiovascular disease: the promise of blocking the renin-angiotensin system. Int J Clin Pract 2003; 57: 211–218.

Keywords: BlutdruckKlinisches EreignisRisikofaktorSchema
Morgendlicher Bluthochdruck
Abbildung 17: The EMBPS causes stress to the cardiovascular system, leading to target-organ damage and pathological responses. For example, in a study of 507 untreated hypertensives, the magnitude of the EMBPS was found to be positively correlated with left ventricular mass, as well as with the risk of future cardiovascular complications.1 In 113 hypertensives with chronic renal insufficiency, followed for 3 years, the decline in GFR was most strongly correlated with morning SBP measured using HBPM (r=0.64, compared with r=0.43 for office SBP).2 A study in 170 type 2 diabetics found that hypertension in the morning (measured using HBPM) was linked to a significantly greater incidence of proteinuria. Office blood pressure was not found to be linked to proteinuria.3 Similar results were also found in patients with type 1 diabetes.4 1. Gosse P, et al. Blood pressure surge on rising. J Hypertens 2004; 22: 1113–1118. 2. Suzuki H, et al. Self-measured systolic blood pressure in the morning is a strong indicator of decline of renal function in hypertensive patients with non-diabetic chronic renal insufficiency. Clin Exp Hypertens 2002; 24: 249–260. 3. Kamoi K, et al. Usefulness of home blood pressure measurement in the morning in type 2 diabetic patients. Diabetes Care 2002; 25: 2218–2223. 4. Kamoi K, et al. Usefulness of home blood pressure measurement in the morning in type 1 diabetic patients. Diabetes Care 2003; 26: 2473–2475.

Keywords: BlutdruckKlinisches Ereignis
Endothel - Kardiovaskuläres Risiko
Abbildung 18: The endothelium responds to endogenous vasodilators and vasoconstrictors, and can play an important role in maintaining blood pressure and peripheral circulation. Endothelial dysfunction is an early marker of vascular disease in a range of different diseases, including diabetes, hypertension, hypercholesterolaemia and coronary heart disease.1 It contributes to cardiovascular disorders, such as atherosclerosis,2 hypertension and heart failure.3 In the kidney, endothelial dysfunction can result in intraglomerular hypertension and inflammation.4 1. Annuk M, et al. Endothelium-dependent vasodilation and oxidative stress in chronic renal failure: impact on cardiovascular disease. Kidney Int Suppl 2003; 84: 50–53. 2. Erhardt LR. Endothelial dysfunction and cardiovascular disease: the promise of blocking the renin-angiotensin system. Int J Clin Pract 2003; 57: 211–218. 3. Vapaatalo H, Mervaala E. Clinically important factors influencing endothelial function. Med Sci Monit 2001; 7: 1075–1085. 4. Klahr S, Morrissey JJ. The role of vasoactive compounds, growth factors and cytokines in the progression of renal disease. Kidney Int Suppl 2000; 75: S7–S14.

Keywords: BlutdruckEndothelkardiovaskuläres Risiko
Linksventrikuläre Hypertrophie - Kardiovaskuläres Risiko
Abbildung 19: Patients with hypertension have an elevated risk of cardiovascular events compared with normotensive individuals. However, if hypertension is associated with LVH, the overall risk of cardiovascular morbidity and mortality increases even more. Data from the 32-year Framingham Heart Study follow-up of men aged 32–64 years show that the presence of LVH in patients with established hypertension nearly triples the incidence of coronary heart disease and stroke, and increases the incidence of heart failure by about 7-fold.1 1. Kannel WB. Left ventricular hypertrophy as a risk factor in arterial hypertension. Eur Heart J 1992; 13 (Suppl D): 82–88.

Keywords: BlutdruckDiagrammHypertrophiekardiovaskuläres Risiko
Albuminurie - Kardiovaskuläres Risiko
Abbildung 20: 463 patients with type 2 diabetes and normoalbuminuria (n=330), microalbuminuria (n=106) or macroproteinuria (n=27) were followed for an average of 4.64 years.1 The overall cardiovascular morbidity and mortality rate was 3.7%/year.1 After multiple adjustment for co-existing risk factors, microalbuminuria was associated with a 1.9-fold increase in relative risk, and macroproteinuria with a 4.1-fold increase.1 1. Gimeno Orna JA, et al. [Microalbuminuria and clinical proteinuria as the main predictive factors of cardiovascular morbidity and mortality in patients with type 2 diabetes]. Rev Clin Esp 2003; 203: 526–531.

Keywords: AlbuminurieBlutdruckDiagrammkardiovaskuläres Risiko
Kardiovaskuläres Risiko - Blutdrucksenkung
Abbildung 21: A meta-analysis of 61 prospective, observational studies has shown that a 10 mmHg lower S BP is associated over the long term with a 40% lower risk of stroke death and a 30% lower risk of death from ischaemic heart disease (IHD) or other vascular causes.1 Even a small, 2 mmHg fall in mean S BP was associated with large reductions in premature deaths and disabling strokes.1 There was no evidence of a J-curve (i.e. a threshold of reduction beyond which risk begins to increase).1 The reduction in risk associated with a given reduction in mean blood pressure is approximately constant down to at least an SBP of 115 mmHg and a DBP of 75 mmHg – well beyond what is normally achieved.1 The reduction in risk holds for all age groups assessed from 40 up to 89 years old.1 1. Lewington S, et al. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet 2002; 360: 1903–1913.

Keywords: Blutdrucksenkungkardiovaskuläres RisikoSchema
Blutdrucksenkung - Zielorganschäden
Abbildung 22: This meta-analysis of clinical trials in diabetic and non-diabetic renal disease shows the direct and continuous relationship between the achieved blood pressure and the decline in GFR.1 In patients with proteinuria >1 g/day and renal insufficiency (GFR 13–55 mL/min/1.73 m2), optimal blood pressure is <125/75 mmHg.2 1. Bakris GL, et al. Preserving renal function in adults with hypertension and diabetes: a consensus approach. Am J Kidney Dis 2000; 36: 646–661. 2. Lazarus JM, et al. Achievement and safety of a low blood pressure goal in chronic renal disease. The Modification of Diet in Renal Disease Study Group. Hypertension 1997; 29: 641–650.

Keywords: BlutdrucksenkungDiagrammGFR
Blutdrucksenkung - Vorteile
Abbildung 23: Intensive antihypertensive treatment (i.e. with a target DBP ≤85 mmHg) can significantly reduce the risk of a major cardiovascular event compared with less intensive treatment (target DBP ≤90 mmHg). The data shown in this slide are from the Hypertension Optimal Treatment (HOT) study of 18,790 hypertensives treated for an average 3.8 years.1 Benefits were greatest in diabetics (relative risk = 0.53 for cardiovascular events).1 In non-smokers, there was reduced risk in many important patient groups, including those with a global risk considered to be high or very high.1 In smokers, more intensive DBP lowering was associated with increased risk of all types of cardiovascular event.1 1. Zanchetti A, et al. Benefits and risks of more intensive blood pressure lowering in hypertensive patients of the HOT study with different risk profiles: does a J-shaped curve exist in smokers? J Hypertens 2003; 21: 797–804.

Keywords: BlutdrucksenkungDiagramm
Antihypertensive Behandlungsziele
Abbildung 24: The treatment of patients with hypertension requires the identification of all reversible risk factors (for example, smoking and diabetes), as well as antihypertensive therapy.1 The target should be to reduce SBP and DBP to at least 140/90 mmHg. However, there is convincing evidence that further reductions, if they can be achieved without causing side effects, are beneficial in most patients. Diabetics are at increased risk of cardiovascular events, and so blood pressure should be reduced to at least 130/80 mmHg.1 1. 2003 European Society of Hypertension – European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003; 21: 1011–1053.

Keywords: BehandlungszielBlutdrucksenkung
Behandlungsschema - JNC 7
Abbildung 25: This is a section of the full treatment algorithm, focussing on the choice of antihypertensive class.1 The JNC 7 guidelines recommend lifestyle modifications as an intervention in all patients.1 Patients with Stage 2 hypertension (SBP/DBP ≥160/≥100 mmHg) should receive initial therapy with combination treatment.1 Although diuretics are the drugs of choice for uncomplicated hypertension, the presence of ‘compelling indications’ (see next slide) can dictate the initial use of other drug classes.1 1. Chobanian AV, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003; 289: 2560–2572.

Keywords: BehandlungJNC 7Schema
Behandlungsschema - ESH-ESC
Abbildung 26: ESH–ESCguidelines also emphasize the need to consider ancillary risk factors when setting treatment goals.1 Shown in this table is the blood pressure at diagnosis. Risk factors include diabetes, smoking, abdominal obesity and target-organ damage (such as LVH, microalbuminuria or increased serum creatinine), as well as associated clinical conditions such as cardiovascular or renal disease. Patients at high risk or very high risk should have their blood pressure treated if it is above 130/85 mmHg. Patients with blood pressure that is consistently >140/90 mmHg should usually have it treated, regardless of the presence of other risk factors. 1. 2003 European Society of Hypertension – European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003; 21: 1011–1053.

Keywords: BehandlungBlutdruckESCESH
Hypertonie - Bewußtsein
Abbildung 27: Hypertension is poorly controlled, even in western industrialized societies, as revealed in a survey of studies on hypertension treatment and control.1 Many patients, especially in Europe, are not even aware that they have hypertension. Many patients are not treated even when they have been diagnosed. Fewer than 30% of patients have their blood pressure reduced to recommended levels (i.e. <140/90 mmHg). 1. Wolf-Maier K et al. Hypertension Treatment and Control in Five European Countries, Canada, and the United States. Hypertension 2004; 43: 10–17.

Keywords: BehandlungBewusstseinBlutdruckDiagramm
Morgendlicher Blutdruck
Abbildung 28: Even when patients have controlled office blood pressure, their blood pressure in the early morning hours often is not controlled. Shown here are data from two studies: Analysis of the control of blood pressure using ambulatory blood pressure monitoring (ACAMPA) study in Spain in 290 treated hypertensives.1 Jichi Morning-Hypertension Research (J-MORE) study in 1027 treated hypertensives.2 Both studies found that 60% of treated and apparently well-controlled hypertensive patients still show high blood pressure levels in the morning hours. 1. Redón J, et al. Uncontrolled early morning blood pressure in medicated patients: the ACAMPA study. Blood Press Monit 2002; 7: 111–116. 2. Kario K et al. Morning Surge in Blood Pressure as a Predictor of Silent and Clinical Cerebrovascular Disease in Elderly Hypertensives. Circulation 2003; 108: 72e–73e.

Keywords: BlutdruckDiagrammTageszeit
Blutdrucksenkung - Through/Peak-Ratio
Abbildung 29: Poor control in the morning hours in patients with controlled office blood pressure may be a consequence of antihypertensives that do not maintain full efficacy throughout the dosing period. Blood pressure may be normal when the patient visits the office several hours after taking their morning dose, but may not be controlled in the early morning period. Antihypertensive agents which have short elimination half-lives and wide fluctuations in plasma concentrations during a dosage interval (i.e. a greater trough-to-peak ratio) will produce greater variability in blood pressure compared with antihypertensive agents with lower trough:peak ratios.1 1. Elliott HL, Meredith PA. Trough:peak ratio: clinically useful or practically irrelevant? J Hypertens 1995; 13: 279–283.

Keywords: BlutdrucksenkungDiagrammTageszeit
Hypertonie - Behandlung
Abbildung 30: Failure to achieve target blood pressure can also result when patients do not adhere to their treatment regimen. One reason for non-adherence is multiple daily dosing. This meta-analysis of 8 studies shows that adherence to a once-daily dosing regimen is significantly greater than that to a twice-daily or multiple-daily dosing regimen.1 1. Iskedjian M, et al. Relationship between daily dose frequency and adherence to antihypertensive pharmacotherapy: evidence from a meta-analysis. Clin Ther 2002; 24: 302–316.

Keywords: BehandlungDiagrammHypertonie
Hypertonie - Behandlung
Abbildung 31: The RAAS, in particular angiotensin II, contributes to cardiovascular disease by increasing blood pressure and also by causing inflammation, leading to sclerosis and tissue hypertrophy. ARBs and angiotensin-converting enzyme (ACE) inhibitors block the RAAS by different mechanisms. ACE inhibitors block the conversion of angiotensin I to angiotensin II. However, angiotensin II can be formed by other pathways. This can lead to a gradual return of angiotensin levels to baseline, a phenomenon termed ‘angiotensin II escape’.1 ACE inhibitors also have other physiological effects, some beneficial,2 but which can also result in cough. Two principal receptors mediate the effects of angiotensin II in humans. The AT1 receptor is responsible for most of the pathological effects associated with angiotensin II, whereas the AT2 receptor counteracts these effects.3 ARBs specifically block the AT1 receptor. Because ARBs specifically block the AT1 receptor but allow continued activation of the AT2 receptor, they can provide tissue-protective effects beyond their effects on blood pressure. 1. Hanon S, et al. Persistent formation of angiotensin II despite treatment with maximally recommended doses of angiotensin converting enzyme inhibitors in patients with chronic heart failure. J Renin Angiotensin Aldosterone Syst 2000; 1: 147–150. 2. Chen R, et al. Important role of nitric oxide in the effect of angiotensin-converting enzyme inhibitor imidapril on vascular injury. Hypertension 2003; 42: 542–547. 3. Hurairah H, Ferro A. The role of the endothelium in the control of vascular function. Int J Clin Pract 2004; 58: 173–183.

Keywords: Angiotensin IBehandlungDiagrammHypertonie
Antihypertensiva - Nebenwirkung
Abbildung 32: Another common reason for poor patient adherence is side effects. Because hypertension is largely asymptomatic, and because treatment can often last years or decades, good tolerability is essential. This slide lists some of the side effects commonly associated with widely used antihypertensive classes.1 1. National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: evaluation, classification, and stratification. Am J Kidney Dis 2002; 39 (2 Suppl 1): S1–S266.

Keywords: Angiotensin-I-RezeptorhemmerAntihypertensivum
Hypertonie - Behandlung
Abbildung 33: Patients prescribed ARBs as their initial medication are more likely to persist with treatment than patients prescribed other classes of antihypertensive medication. This study followed 14,062 newly-diagnosed hypertensives for 273 days.1 The slide shows the percentage of patients who received initial monotherapy and did not discontinue (i.e. did not stop medication or switch to another class) within the 9-month follow-up. Patients who continued their monotherapy but added an agent from another class were considered to be persistent. Since drugs were provided free by the Italian Health Service, the cost of medication is unlikely to have contributed to the discontinuation rates. 1. Esposti LD et al. Pharmacoeconomics of antihypertensive drug treatment: an analysis of how long patients remain on various antihypertensive therapies. J Clin Hypertens 2004; 6: 76–84.

Keywords: Angiotensin-I-RezeptorblockerDiagrammHypertonie
Antihypertensiva- Eigenschaften
Abbildung 34: Blockade of the renin–angiotensin–aldosterone system (RAAS) is a potent way to reduce hypertension, and the RAAS forms a target for modern antihypertensive therapy.1 Patient compliance with antihypertensive medication is significantly improved if it requires only once-daily administration.2 Increased compliance, coupled with a 24-h efficacy, may be expected to improve patient outcomes. The ideal antihypertensive should also provide round-the-clock activity, especially in the early morning hours when blood pressure increases and cardiovascular events are at their most frequent.3 As with any drug, the therapeutic objectives should be achieved with a minimum of side effects. 1. Weinen W, et al. A review on telmisartan: a novel, long-acting angiotensin II-receptor antagonist. Cardivasc Drug Rev 2000; 18: 127–156. 2. Iskedjian M, et al. Relationship between daily dose frequency and adherence to antihypertensive pharmacotherapy: evidence from a meta-analysis. Clin Ther 2002; 23: 302–316. 3. Mulcahy D. Circadian variation in cardiovascular events. Blood Press Monit 1998; 3: 29–34.

Keywords: AntihypertensivumRenin-Angiotensin-Aldosteron-System
Hypertonie - Behandlung - Richtlinien
Abbildung 35: The benefits of long-acting drugs were listed in the JNC 6 guidelines, as quoted on this slide.1 1. Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. The sixth report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. Arch Intern Med 1997; 157: 2413–2446.

Keywords: BehandlungHypertonieJNC-VI
Hypertonie - Behandlung - Zwingende Indikationen
Abbildung 36: Clinical trials have shown that some classes of antihypertensives can reduce the cardiovascular morbidity in patients with specific indications. The JNC 7 guidelines recommend the use of specific antihypertensive classes in such patient groups, based on such evidence.1 ARBs are recommended for patients with heart failure, diabetes and chronic kidney disease. Note that a lack of recommendation for a specific indication does not mean that the class has been shown to be non-beneficial. It may simply mean that large-scale trials have not yet been conducted. 1. Chobanian AV, et al. The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: The JNC 7 Report. JAMA 2003; 289: 2560–2572.

Keywords: BehandlungHypertonieIndikationJNC 7
Angiotensin-I-Rezeptorblocker - Einsatzbereich
Abbildung 37: This slide gives a list of the conditions that favour the use of ARBs, according to the ESH guidelines.1 1. 2003 European Society of Hypertension – European Society of Cardiology guidelines for the management of arterial hypertension. J Hypertens 2003; 21: 1011–1053.

Keywords: Angiotensin-I-RezeptorblockerESCESH
Hypertonie - Zusammenfassung
Abbildung 38

Keywords: Hypertonie
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