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Journal of Hypertension:
doi: 10.1097/HJH.0b013e3282f465e3
Editorial commentaries

Central blood pressure as estimate of cardiovascular risk: potentials and limitations

Grassi, Guidoa; Borghi, Claudiob

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aClinica Medica, Università Milano-Bicocca, Ospedale San Gerardo, Monza (Milan), Centro Interuniversitario di Fisiologia Clinica e Ipertensione, and Istituto Auxologico Italiano, Milan, Italy

bDipartimento di Medicina Clinica e Biotecnologia Applicata D Campanacci, Università degli Studi di Bologna, Bologna, Italy

Correspondence to Professor Guido Grassi, Clinica Medica, Ospedale S. Gerardo, Via Pergolesi 33, 20052 Monza, Milano, Italy Tel: +39 039 2333357; fax: +39 039 322274; e-mail: guido.grassi@unimib.it

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Introduction

The 2007 European Guidelines for the diagnosis and treatment of hypertension acknowledge that the determination of sphygmomanometric systolic and diastolic blood pressure values is a crucial step for the diagnosis of hypertension and contributes to defining hypertensive cardiovascular risk [1]. They also emphasize, however, that a number of limitations characterize clinical blood pressure, thereby interfering with the diagnosis of high blood pressure and risk assessment [1]. This explains why other blood pressure measurements have been developed and implemented, such as home and ambulatory blood pressure, which may provide additional and perhaps more stringent information of clinical, prognostic and therapeutic relevance. Recent technical developments in the field have provided a further measurement: the so-called ‘central’ blood pressure, which represents the pressure in the aortic vascular district and thus can be regarded as an index of aortic stiffness [2]. This ‘new’ blood pressure ‘marker’, originally determined by complex and invasive aortic measurements, can be calculated by an assessment of pulse wave velocity, as well as by calculation of the augmentation index [3]. Both these parameters are impaired in established hypertensive states and retain a clinical value for prediction and stratification of cardiovascular risk in selected populations [4–6]. There is also evidence that pulse wave velocity and augmentation index: (i) correlate better than peripheral (brachial) blood pressure with different measures of end-organ damage, such as left ventricular mass and carotid intima–media thickness [7,8], and (ii) may become important targets of antihypertensive drug treatment, with the impact of therapeutic intervention not necessarily being the same at central and peripheral sites, even when blood pressure appears to be fully normalized [9].

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Central blood pressure, cardiovascular risk and blood pressure control

In this issue of the journal, Protogerou et al. [10] and Safar et al. [11] report on the potentials and limitations of the use of central blood pressure as a predictor of cardiovascular risk. Protogerou et al. [10] show that abnormalities in the central haemodynamic profile may characterize patients displaying optimal to borderline blood pressure values. This finding is strengthened by observations on the marked mismatch observed in treated hypertensive patients between brachial and central blood pressure in the second study by the same group [11]. Taken together, the two series of data allow an interesting hypothesis to be proposed, namely that important differences in central haemodynamic profile characterize untreated normotensive subjects and hypertensive patients who achieve the ‘normotensive state’ in response to antihypertensive drug treatment. The abnormalities in central haemodynamics display an increasing clinical severity, ranging from the earlier functional alterations to the later structural changes, and appear to be proportional to the achieved blood pressure levels. Higher values of the augmentation index and lower blood pressure amplification are clearly also evident in the subgroup of patients with ‘optimal’ blood pressure control, in which the impact of antihypertensive drug treatment has to be regarded as very successful. This opens up an interesting debate on the crucial role in central haemodynamics for the definition of cardiovascular risk profile as well as in the overall interpretation of the effects of drug treatment in patients with hypertension. In particular, the lack of any improvement in the central haemodynamic state might be responsible for the residual elevated cardiovascular risk reported in treated hypertensive patients, despite a significant blood pressure reduction in response to drug treatment [12,13]. Conversely, the decrease in brachial and central blood pressure values, as achieved by drugs interacting with the renin–angiotensin system and/or calcium-channel blockers, provides a greater cardiovascular protection compared to a treatment strategy based on drugs with a less favorable impact on the arterial properties, despite a comparable blood pressure control (i.e. β-blockers). The clinical evidence in favor of this hypothesis arises from the results of the Anglo-Scandinavian Cardiac Outcomes Trial Conduit Artery Function Evaluation (ASCOT-CAFÉ) study [14], which demonstrates a more favorable cardiovascular outcome in hypertensive patients treated with a combination of drugs (amlodipine plus perindopril) capable of improving both brachial and (calculated) central blood pressure. Irrespective of the specific effects of a given drug regimen, however, the results of the studies by Protogerou et al. [10] and Safar et al. [11], and in particular the continuous interaction between baseline or achieved blood pressure and arterial properties, support the additional hypothesis that the antihypertensive effect of the drugs can be limited by the extent of the intrinsic vascular abnormalities. This would be responsible for a sort of mismatch between the achieved blood pressure control and the ‘actual’ blood pressure control that should be obtained to effectively decrease the overall cardiovascular risk in the presence of clearcut vascular involvement. This may also provide an explanation for the residual cardiovascular risk observed in a considerable proportion of patients with well controlled blood pressure.

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Central blood pressure: answers and questions

Basically, whatever the mechanism(s) responsible for the interaction between central haemodynamic parameters (pulse wave velocity, augmentation index and pulse pressure amplification) and blood pressure control, the results of the studies by Protogerou et al. [10] and Safar et al. [11] support some intriguing perspectives and speculations. First, the evidence provided expands previous observations collected in untreated hypertensive patients showing that profound abnormalities in the central haemodynamic profile also occur in hypertensive patients in whom effective blood pressure control has been achieved by antihypertensive drug treatment. Second, the relationship between changes in central haemodynamics and brachial blood pressure control is confirmed to be largely affected by the type of pharmacological treatment. Third, the non-invasive measurement of the central haemodynamic profile would increase the probability of a more reliable estimate of the overall cardiovascular risk in patients with hypertension beyond blood pressure control. This is in line with the indications of the European Society of Hypertension/European Society of Cardiology 2007 Guidelines on Hypertension [1], which emphasize that the presence of either functional or structural alterations of the vascular system should be assessed, whenever possible, even in patients with effective blood pressure control. Finally, the estimate of central haemodynamics might contribute towards guiding the choice of drugs, as well as deciding the use of a more or less aggressive type of drug treatment, with the aim of effectively reducing the cardiovascular risk associated with hypertension in addition to and beyond blood pressure control.

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References

1 Mancia G, De Backer G, Dominiczak A, Cifkova R, Fagard R, Germano G, et al. 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). J Hypertens 2007; 25:1105–1187.

2 O'Rourke MF, Gallagher DE. Pulse wave analysis. J Hypertens 1996; 14(S5):147–157.

3 Franklin SS, Wilkinson IB, Cockcroft JR. Brachial and central pulse pressure and cardiovascular risk. In: Safar ME, O'Rourke MF, editors. Handbook of hypertension 23: arterial stiffness in hypertension. Amsterdam: Elsevier; 2006. pp. 225–240.

4 Safar ME, Blacher J, Pannier B, Guerin AP, Marchais SJ, Guyonvanch PM, et al. Central pulse pressure and mortality in end-stage renal disease. Hypertension 2002; 39:735–738.

5 Waddell TK, Dart AM, Medley TL, Cameron JD, Kingwell BA. Carotid pressure is a better predictor of coronary artery disease severity than brachial pressure. Hypertension 2001; 38:927–931.

6 Philippe F, Chemaly E, Blacher J, Mourad JJ, Dibie A, Larrazet F, et al. Aortic pulse pressure and extent of coronary artery disease in percutaneous transluminal coronary angioplasty candidates. Am J Hypertens 2002; 15:672–677.

7 Saba PS, Roman MJ, Pini R, Spitzer M, Ganau A, Devereux RB. Relation of arterial pressure waveform to left ventricular and carotid anatomy in normotensive subjects. J Am Coll Cardiol 1993; 22:1873–1880.

8 Boutouyrie P, Bussy C, Lacolley P, Girerd X, Laloux B, Laurent S. Association between local pulse pressure, mean blood pressure, and large-artery remodeling. Circulation 1999; 100:1387–1393.

9 Agabiti-Rosei E, Mancia G, O'Rourke MF, Roman MJ, Safar ME, Smulyan H, et al. Central blood pressure measurements and antihypertensive therapy: a consensus document. Hypertension 2007; 50:154–160.

10 Protogerou A, Vergnaud AC, Blacher J, Safar ME. From ‘optimal’ to ‘borderline’ blood pressure in subjects under chronic antihypertensive therapy. J Hypertens 2008; 26:130–137.

11 Safar ME, Blacher J, Achimastos A, Protogerou A. Arterial stiffness and central haemodynamics in treated hypertensive subjects according to the ESH 2003 brachial blood pressure classification. J Hypertens 2008; 26:138–144.

12 Isles CG, Walker LM, Beevers GD, Brown I, Cameron HL, Clarke J, et al. Mortality in patients of the Glasgow Blood Pressure Clinic. J Hypertens 1986; 4:141–156.

13 Andersson OK, Almgren T, Persson B, Samuelsson O, Hedner T, Wilhelmsen L. Survival in treated hypertension: follow up study after two decades. BMJ 1998; 317:167–171.

14 Williams B, Lacy PS, Thom SM, Cruickshank K, Stanton A, Collier D, et al. 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 2006; 113:1213–1225.

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