BACKGROUND: The loss of the viscoelastic properties of central arteries independently of blood pressure loads could stimulate the development of left ventricular hypertrophy and dysfunction, renal failure, or cerebral vascular injury. OBJECTIVE: The aim of the present study is to determine if an elevated systolic aortic pressure is a marker of more frequent target organ damage (TOD) in hypertensive low cardiovascular risk (CVR) patients. METHODS: Hypertensive non treated consecutive patients (p) assisted at first visit in a specialized center with a CVR according to WHO Americas B area score less than 10 % were included. Left ventricular mass index (LVMI) and tissue Doppler diastolic and systolic function were measured as Lang et al. (J Am Soc Echocardiogr 18:1440-1463, 2005) and Nagueh et al. (J Am Soc Echocardiogr 22:107-133, 2009). Cardiac TOD was considered according to 2013 European Society of Hypertension/European Society of Cardiology. Glomerular filtration rate (GFR) was calculated by MDRD formula, a value <60 ml/min/1.73 m(2) was considered TOD. Systolic aortic pressured (CAoP) was measured by radial tonometry and classified according to criteria proposed by Herbert et al. (Eur Heart J 35:3100-3132, 2014). Continue variables are reported as means with standard deviation and discrete variables as absolute values and percentages. Statistical analysis was performed with Students t test, significant differences were considered with a p value < 0.05 RESULTS: 155 p were included; 23 p (14.8 %) had elevated CAoP while 132 p (85.2 %) had normal CAoP. Sample mean age was 54.1 + 12.9 years; 85 p (54.8 %) were males. Dyslipidemia was detected in 44 p (28.4 %), and 18 p (11.6 %) were smokers. Mean blood pressure was 143.7 + 17.1 mmHg/86.4 + 12.3 mmHg in p with normal (n) CAoP and 140.3 + 12 mmHg/81.9 + 6.8 mmHg in p with CAoP elevated e (p = NS). Mean CAoP in p with normal values was 117.4 + 10.9 mmHg and 116.9 + 10.7 in p with elevated values (p = NS). The average s wave was 7.42 + 1 cm/sec in n CAoP p vs 6.6 + 1 cm/sec in e CAoP p (p < 0.05) while and E/e' ratio >13 was detected in 14.4 % n CAoP p vs 8.7 % e CAoP p (p = NS). Mean GFR was 105.4 + 40.5 ml/min/1.73 m(2) in n CAoP p vs 103.9 + 45.6 ml/min/1.73 m(2) in e CAoP p (p = NS) and GFR <60 ml/min/1.73 m(2) was present in 4.5 % n CAoP p vs 26.1 % e CAoP p (p < 0.0125). CONCLUSIONS: At the same level of CVR according to WHO Americas B score patients with elevated CAoP had lower longitudinal left ventricular systolic function and renal function was more deteriorated.
BACKGROUND: The loss of the viscoelastic properties of central arteries independently of blood pressure loads could stimulate the development of left ventricular hypertrophy and dysfunction, renal failure, or cerebral vascular injury. OBJECTIVE: The aim of the present study is to determine if an elevated systolic aortic pressure is a marker of more frequent target organ damage (TOD) in hypertensive low cardiovascular risk (CVR) patients. METHODS:Hypertensive non treated consecutive patients (p) assisted at first visit in a specialized center with a CVR according to WHO Americas B area score less than 10 % were included. Left ventricular mass index (LVMI) and tissue Doppler diastolic and systolic function were measured as Lang et al. (J Am Soc Echocardiogr 18:1440-1463, 2005) and Nagueh et al. (J Am Soc Echocardiogr 22:107-133, 2009). Cardiac TOD was considered according to 2013 European Society of Hypertension/European Society of Cardiology. Glomerular filtration rate (GFR) was calculated by MDRD formula, a value <60 ml/min/1.73 m(2) was considered TOD. Systolic aortic pressured (CAoP) was measured by radial tonometry and classified according to criteria proposed by Herbert et al. (Eur Heart J 35:3100-3132, 2014). Continue variables are reported as means with standard deviation and discrete variables as absolute values and percentages. Statistical analysis was performed with Students t test, significant differences were considered with a p value < 0.05 RESULTS: 155 p were included; 23 p (14.8 %) had elevated CAoP while 132 p (85.2 %) had normal CAoP. Sample mean age was 54.1 + 12.9 years; 85 p (54.8 %) were males. Dyslipidemia was detected in 44 p (28.4 %), and 18 p (11.6 %) were smokers. Mean blood pressure was 143.7 + 17.1 mmHg/86.4 + 12.3 mmHg in p with normal (n) CAoP and 140.3 + 12 mmHg/81.9 + 6.8 mmHg in p with CAoP elevated e (p = NS). Mean CAoP in p with normal values was 117.4 + 10.9 mmHg and 116.9 + 10.7 in p with elevated values (p = NS). The average s wave was 7.42 + 1 cm/sec in n CAoP p vs 6.6 + 1 cm/sec in e CAoP p (p < 0.05) while and E/e' ratio >13 was detected in 14.4 % n CAoP p vs 8.7 % e CAoP p (p = NS). Mean GFR was 105.4 + 40.5 ml/min/1.73 m(2) in n CAoP p vs 103.9 + 45.6 ml/min/1.73 m(2) in e CAoP p (p = NS) and GFR <60 ml/min/1.73 m(2) was present in 4.5 % n CAoP p vs 26.1 % e CAoP p (p < 0.0125). CONCLUSIONS: At the same level of CVR according to WHO Americas B score patients with elevated CAoP had lower longitudinal left ventricular systolic function and renal function was more deteriorated.
Authors: Stephane Laurent; John Cockcroft; Luc Van Bortel; Pierre Boutouyrie; Cristina Giannattasio; Daniel Hayoz; Bruno Pannier; Charalambos Vlachopoulos; Ian Wilkinson; Harry Struijker-Boudier Journal: Eur Heart J Date: 2006-09-25 Impact factor: 29.983
Authors: Sherif F Nagueh; Christopher P Appleton; Thierry C Gillebert; Paolo N Marino; Jae K Oh; Otto A Smiseth; Alan D Waggoner; Frank A Flachskampf; Patricia A Pellikka; Arturo Evangelista Journal: J Am Soc Echocardiogr Date: 2009-02 Impact factor: 5.251
Authors: Julio A Chirinos; Patrick Segers; Ernst R Rietzschel; Marc L De Buyzere; Muhammad W Raja; Tom Claessens; Dirk De Bacquer; Martin St John Sutton; Thierry C Gillebert Journal: Hypertension Date: 2013-01-02 Impact factor: 10.190
Authors: Hendrik L Booysen; Gavin R Norton; Muzi J Maseko; Carlos D Libhaber; Olebogeng H I Majane; Pinhas Sareli; Angela J Woodiwiss Journal: J Hypertens Date: 2013-06 Impact factor: 4.844
Authors: Paolo Palatini; Edoardo Casiglia; Jerzy Gąsowski; Jerzy Głuszek; Piotr Jankowski; Krzysztof Narkiewicz; Francesca Saladini; Katarzyna Stolarz-Skrzypek; Valérie Tikhonoff; Luc Van Bortel; Wiktoria Wojciechowska; Kalina Kawecka-Jaszcz Journal: Vasc Health Risk Manag Date: 2011-12-07