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Our mission: To promote excellence in research, practice, education and policy in cardiovascular health, primary and secondary prevention.
Our goal is to reduce the burden in cardiovascular disease in Europe through percutaneous cardiovascular interventions.
Our Mission is "to improve the quality of life of the population by reducing the impact of cardiac rhythm disturbances and reduce sudden cardiac death"
To improve quality of life and logevity, through better prevention, diagnosis and treatment of heart failure, including the establishment of networks for its management, education and research.
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OUR MISSION: TO REDUCE THE BURDEN OF CARDIOVASCULAR DISEASE
Prof. Guido Grassi
The Strong Heart study, collected data in a general population of American Indians, and shows the predictive power of central pulse pressure in people apparently free from cardiovascular disease. The Anglo-Scandinavian Cardiac Outcomes Trial Conduit Artery Function Evaluation (ASCOT-CAFE´) study, 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. This data begs for studies to compare the predictive power of central blood pressure in regards to traditional blood pressure. With it, the appraisal of how central haemodynamics may provide a guidance in the choice of antihypertensive drugs may ensue.
There is a great deal of interest in central blood pressure due to current evidence that :
Preliminary evidence shows that central blood pressure’s predictive value is maintained after adjustment for peripheral blood pressure.
The 2007 European Guidelines for the diagnosis and treatment of hypertension acknowledge the fact that the determination of sphygmomanometric systolic and diastolic blood pressure values are a crucial step in the diagnosis of hypertension and contribute to defining hypertensive cardiovascular risk (1).
However the guidelines also emphasise that a number of limitations are inherant to clinical blood pressure measuring and that clinical blood pressure may interfere 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 further measurements, i.e. ‘central’ blood pressure, which is 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 from an assessment of pulse wave velocity and a calculation of the augmentation index (3).
Both pulse wave velocity and the augmentation index - serving to calculate central blood pressure - are impaired in established hypertensive states. These two parameters hold clinical value for predicting and stratifying cardiovascular risk in selected populations - end-stage renal disease, and patients with coronary artery disease undergoing percutaneous coronary intervention, as you will read below. There is also evidence that pulse wave velocity and the augmentation index :
Central blood pressure is determined by a variety of factors (Figure 1), which directly or indirectly modulate pressure within the aorta.
Pharmacological removal of such influences, elicited for example by brachial plexus anaesthesia, has been shown to increase arterial distensibility and thus reduce arterial stiffness. Despite these data, however, no conclusive information are available in man on the relationship between central blood pressure values and direct or indirect indices of adrenergic function and on their modifications induced by cardiovascular disease.
A number of studies carried out in recent years have convincingly shown that central systolic blood pressure, and more so central pulse pressure, holds a prognostic value for cardiovascular fatal and non fatal events.
Three considerations related to the above mentioned studies results deserve to be made.
Recent reports by a well known group of investigators provides further evidence of central blood pressure abnormalities in hypertension, by showing that
Taken together, these two series of data allow for an interesting hypothesis to be advanced, namely that important differences in the central haemodynamic profile characterise untreated normotensive subjects and hypertensive patients who achieve the ‘normotensive state’ in response to antihypertensive drug treatment.
The clinical evidence in favor of this hypothesis arises from the results of the Anglo-Scandinavian Cardiac Outcomes Trial Conduit Artery Function Evaluation (ASCOT-CAFE´) study (11), 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.
The importance handed to the possible effects of cardiovascular drugs on central blood pressure has been recently further implemented with the data collected in the Conduit Artery Function Evaluation - Lipid – Lowering - Arm (CAFE-LLA) (11), aimed at assessing whether and to what extent the reduced risk of cardiovascular events documented in hypertensive patients under statin treatment could arise from favorable effects of these drugs on central haemodynamics. The results did not support the hypothesis however, as they showed that the favorable effects of statins on cardiovascular risk profile are not mediated by an improvement in central blood pressure. Fig 1 : Factors determining central blood pressure.
A number of ongoing studies and clinical trials will allow to address some unsolved questions related to central blood pressure, namely, the predictive value of central blood pressure as compared to predictive value based on traditional blood pressure assessment. These ongoing studies will also include the possibility that the estimation of central haemodynamics will provide a guidance in the choice of antihypertensive drugs. Finally, ongoing studies will also allow to clarify whether and to what extent assessment of central blood pressure in the near future will replace clinic blood pressure measurement.
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. 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. 5. London GM, Blacher J, Pannier B, Guérin AP, Marchais SJ, Safar ME. Arterial wave reflections and survival in end-stage renal failure. Hypertension 2001;38:434-438. 6. Safar ME, Blacher J, Pannier B, Guerin AP, Marchais SJ, Guyonvarc'h PM, et al. Central pulse pressure and mortality in end-stage renal disease. Hypertension 2002;39:735-738. 7. Weber T, Auer J, O'rourke MF, Kvas E, Lassnig E, Lamm G, et al. Increased arterial wave reflections predict severe cardiovascular events in patients undergoing percutaneous coronary interventions. Eur Heart J 2005;26:2657-2663. 8. Roman MJ, Devereux RB, Kizer JR, Lee ET, Galloway JM, Ali T, et al. Central pressure more strongly relates to vascular disease and outcome than does brachial pressure: the Strong Heart Study. Hypertension 2007;50:197-203. 9. 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. 10. 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. 11. 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. 12. Williams B, Lacy PS, Cruickshank JK, Collier D, Hughes AD, Stanton A, et al. Impact of statin therapy on central aortic pressures and hemodynamics: principal results of the Conduit Artery Function Evaluation-Lipid-Lowering Arm (CAFE-LLA) Study. Circulation 2009;119:53-61.
Prof. Guido Grassi Clinica Medica, Ospedale San Gerardo, Università Milano-Bicocca, Via Pergolesi 33, 20052 Monza (Milan), Italy Phone: +39 039 2333275 FAX: +39 039 e-mail: email@example.com