Zusammenfassung
In epidemiologischen Studien konnte gezeigt werden, dass nur der systolische Blutdruck im Altersverlauf zunimmt, der diastolische dagegen zwischen dem 55. und 60. Lebensjahr sein Maximum erreicht und danach abfällt. Diese Entwicklung führt dazu, dass die isoliert systolische Hypertonie (ISH) im Alter die vorherrschende Hypertonieform ist. Dabei nimmt bei einem gegebenen systolischen Druck die kardiovaskuläre Komplikationsrate mit sinkendem diastolischem und damit steigendem Pulsdruck (SBD minus DBD) zu. Durch die zunehmende Gefäßsteifigkeit der Arterien kommt es zu einem Anstieg der Pulswellengeschwindigkeit (PWV), zu verstärkten und frühzeitigeren Pulswellenreflexionen sowie zum Anstieg des zentral-aortalen Blutdrucks. Dabei entwickelt sich die ISH entweder neu, bevorzugt aus der Gruppe mit primär hochnormalem Blutdruck oder durch Ausbrennen einer systolisch-diastolischen Hypertonie. Generell führt die Senkung erhöhter Blutdruckwerte nachweislich in jedem Alter zu einer Lebensverlängerung – mit Zielwerten systolisch <140 mmHg und bei über 80-Jährigen <150 mmHg. Da in allen Interventionsstudien die ISH die geringste Rate blutdrucknormalisierter Patienten aufweist, ist i. d. R. eine antihypertensive Kombinationstherapie notwendig – mit der bisher besten Studienevidenz für ACE-Hemmer plus Kalziumantagonisten (bzw. Diuretika).
Abstract
Hypertension can be classified based on certain criteria, such as severity, existence of specific end-organ damage, or the dominant blood pressure subphenotype so that isolated diastolic hypertension (IDH), mixed systolic-diastolic hypertension (SDH), and isolated systolic hypertensive (ISH) states can be defined. The FRAMINGHAM study was the first to demonstrate a continuous increase of systolic blood pressure with age and a peak of diastolic pressure between 55 and 65 years of age. This results not only in a high prevalence of hypertension of approximately 50–80% beyond the age of 60 but also in a disproportionately high increase in isolated systolic hypertension. ISH develops either as a new condition mostly from the group of primary high-normal blood pressure or secondly through burnout of existing systolic-diastolic hypertension with highly progressive vascular ageing.
The pathophysiological background lies in remodeling processes in the macrovascular and microvascular compartments with stiffening of conduit and peripheral arterial vessels. In clinical practice these processes are easy to measure by determining pulse wave velocity (PWV), the augmentation index, and pulse pressure. These parameters are closely related to cardiovascular and cerebrovascular morbidity and mortality
ISH is not only a hypertension subphenotype but often indicates significant organ damage or may even be considered to be a secondary form of hypertension characterized by remodeled and stiffened arterial vessel walls and this condition is difficult to treat. It appears therefore that ISH warrants special therapeutic strategies with a focus on antiproliferative, antistiffening, anti-atherosclerotic, and vasodilating actions. As a result of the available data from the results of treatment studies it appears that renin-angiotensin system (RAS) blockers and calcium channel blockers (CCBs) are the preferred drugs for treatment of this condition.
Literatur
JNC VII (2003) The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure. JAMA 289:2560–2571
ESH/ESC Hypertension Guidelines Committee (2007) 2007 Guidelines for the management of arterial hypertension. Eur Heart J 28:1462–1536
Fang J, Mafhavan S, Cohen H et al (1995) Isolated diastolic hypertension: a favourable finding among young and middle-aged hypertensive subjects. Hypertension 26:377–382
Pickering TG (2003) Isolated diastolic hypertension. J Clin Hypertens 5:411–413
Black HR, Elliott WJ, Grandits G et al (2003) CONVINCE Research Group: Principal results of the Controlled Onset Verapamil Investigation of Cardiovascular Endpoints (CONVINCE) Trial. JAMA 289:2073–2082
Franklin SS, Pio JR, Wong ND et al (2005) Predictors of new-onset diastolic and systolic hypertension: the Framingham Heart Study. Circulation 111:1121–1127
Lieb W, Larson MG, Benjamin EJ et al (2009) Multimarker approach to evaluate correlates of vascular stiffness: the Framingham Heart Study. Circulation 119(1):37–43. Epub 2008 Dec 22
Franklin SS, Gustin W, Wong ND et al (1997) Hemodynamic patterns of age-related changes in blood pressure. The Framingham Heart Study. Circulation 96:308–315
Scholze J (2004) Pulse Pressure in der Therapiesteuerung der Hypertonie? Herz 29:276–289
Assmann G, Cullen P, Evers T et al (2005) Importance of arterial pulse pressure as a predictor of coronary heart disease risk in PROCAM. Eur Heart J 20:2120–2126
Bullpitt CJ, Palmer AJ, Fletcher AE et al (1995) Proportion of patients with isolated systolic hypertension who have burned-out diastolic hypertension. J Hum Hypertens 9:675–678
Oliver JJ, Webb DJ (2003) Noninvasive assessment of arterial stiffness and risk of atherosclerotic events. Arterioscler Thromb Vasc Biol 23(4):554–566
Schiffrin EL (2004) Vascular stiffening and arterial compliance. AJH 17:39S–48S
Safar ME (2008) Pulse pressure, arterial stiffness and wave reflections (augmentation index) as cardiovascular risk factors in hypertension. Ther Adv Cardiovasc Dis 2(1):13–24
Park JB, Intengan HD, Schiffrin EL (2000) Reduction of resistance artery stiffness by treatment with the AT 1 receptor antagonist losartan in essential hypertension. J Renin Angiotens Syst 1:40–45
Intengan HD, Thibault G, Li JS et al (1999) Resistance artery mechanics, structure and extracellular components in spontaneously hypertensive rats effects of angiotension receptor antagonism and converting enzyme inhibition. Circulation 100:2267–2275
Bakker ENTP, Meulen ET van der, Berg BM van den et al (2002) Inward remodeling follows chronic vasoconstriction in isolated resistance arteries. J Vasc Res 39:12–20
Levy BI, Ambrosio G, Pries AR et al (2001) Microcirculation in hypertension: a new target for treatment? Circulation 104:735–740
Nichols WW, O’Rourke M (1998) McConalds blood flow in arteries: Theoretical, experimental and clinical principles, 4. Aufl. Arnold, London UK, S 54–401
Beckett NS, Peters R, Fletscher AE et al (2008) Treatment of hypertension in patients 80 years of age or older. N Engl J Med 358:1887–1898
Liu L, Wang JG, Gong L et al (1998) Comparison of active treatment and placebo in older Chinese patients with isolated systolic hypertension. Systolic Hypertension in China (Syst-China) Collaborative Group. J Hypertens 16:1823–1829
SHEP Cooperative Research Group (1991) Prevention of stroke by antihypertensive drug treatment in older persons with isolated systolic hypertension. Final results of the Systolic Hypertension in the Elderly Program (SHEP). J Am Med Assoc 265:3255–3264
Staessen JA, Fagard R, Thijs L et al (1997) Randomised double-blind comparison of placebo and active treatment for older patients with isolated systolic hypertension. The Systolic Hypertension in Europe (Syst-Eur) Trial Investigators. Lancet 350:757–764
Lainscak M, Anker ST (2009) Prognostic factors in chronic heart failure. Herz 34(2):141–147
Staessen JA, Sasowski J, Wang JG et al (2000) Risks of untreated and treated isolates systolic hypertension in the elderly: meta-analysis of outcome trials. Lancet 355:865–872
Zhou MS, Hernandez Schulmann I, Jaimes EA et al (o J) Thiazide diuretics, endothelial function, and vascular oxidative stress. J Hypertens 26:494–500
Schiffrin EL (2003) Effect of antihypertensive treatment on small artery remodeling in hypertension. Can J Physiol Pharmacol 81:168–176
Kjeldsen SE, Dahlöf B, Devereux RB et al (2002) Effects of losartan on cardiovascular morbidity and mortality in patients with isolated systolic hypertension and left ventricular hypertrophy. JAMA 288:1491–1498
Os I, Gudmundsdottir H, Kjeldsen S et al (2006) Treatment of isolated systolic hypertension in diabetes mellitus type 2. Diabetes Obes Metab 8:381–387
Taddei S, Virdis A, Ghiadoni L et al (1997) Lacidipine restores endothelium-dependent vasodilation in essential hypertensive patients. Hypertension 30:1606–1612
Chen CH, Ting CT, Lin SJ et al (1995) Different effects of fosinopril and atenolol on wave reflections in hypertensive patients. Hypertension 25:1034–1041
Van Bortel LM, Kool Boudier HAS (1995) Effects of antihypertensive agents on local arterial distensibility and compliance. Hypertension 26:531–534
Asmar RG, London GM, O’Rourke ME et al (2001) Improvement in blood pressure, arterial stiffness and wave reflection with a very-low-dose perindopril/indapamide combination in hypertensive patients: a comparison with atenolol. Hypertension 38:922–926
Dahlöf B, Sever PS, Poulter NR et al (2005) Prevention of cardiovascular events with an antihypertensive regime of amlodipine adding perindopril as required versus atenolol adding bendroflumethiazide as required, in the Anglo-Scandinavian Cardiac Outcomes Trial-Blood Pressure Lowering Arm (ASCOT-BPLA): a multicentre randomised controlled trial. Lancet 366(9489):895–906
Williams B, Lacy PS, Thom SM et al (2006) Differential impact of blood pressure-lowering drugs on central aortic pressure and clinical outcomes: principal results of the Conduit Artery Function Evaluation (CAFE) study. Circulation 113(9):1213–1225
Jamerson KA, Bakris GL, Chuan-Chuan W et al (2004) Rationale and design of the Avoiding Cardiovascular events through COMbination therapy in Patients Living with Systolic Hypertension (ACCOMPLISH) Trial. AJH 17:793–801
Neutel JM, Smith DH, Weber MA (2004) Effect of antihypertensive monotherapy and combination therapy on arterial distensibility and left ventricular mass. Am J Hypertens 17:37–42
Mancia G, Laurent ST, Agabiti-Rosei E et al (2009) Reappraisal of European guidelines on hypertension management: a European Society of Hypertension Task Force document. Blood Press 18:308–347
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Der korrespondierende Autor weist auf folgende Beziehungen hin: Der Autor hat Vorträge zur ISH gehalten, die von verschiedensten Pharmafirmen gesponsert wurden.
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Scholze, J. Isolierte systolische Hypertonie. Herz 35, 568–575 (2010). https://doi.org/10.1007/s00059-010-3390-7
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DOI: https://doi.org/10.1007/s00059-010-3390-7