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Carolyn S.P. Lam, Amil M. Shah, Barry A. Borlaug, Susan Cheng, Anil Verma, Joseph Izzo, Suzanne Oparil, Gerard P. Aurigemma, James D. Thomas, Bertram Pitt, Michael R. Zile, Scott D. Solomon, Effect of antihypertensive therapy on ventricular–arterial mechanics, coupling, and efficiency, European Heart Journal, Volume 34, Issue 9, 1 March 2013, Pages 676–683, https://doi.org/10.1093/eurheartj/ehs299
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Abstract
To investigate the effect of antihypertensive therapy on ventricular–arterial mechanics, coupling, and efficiency in early-stage hypertension.
We studied 527 participants from two clinical trials assessing the effect of blood pressure lowering on diastolic function. Participants were aged ≥45 years with early-stage hypertension, no heart failure, ejection fraction (EF) ≥50%, and diastolic dysfunction using Doppler echocardiography. Effective arterial afterload and its components were assessed along with measures of left ventricular (LV) structure and function prior to and after 24–38 weeks of antihypertensive therapy. Systolic blood pressure decreased from 154 ± 18 to 137 ± 15 mmHg at follow-up. Blood pressure reduction was associated with decreases in ventricular and arterial stiffness, improvements in systemic arterial compliance and resistance, enhanced LV ejection, and reduction in cardiac work (all P < 0.001). Changes in Ea/Ees ratio were inversely correlated with those in EF (r = −0.25; P < 0.001), stroke work index (r = −0.13; P = 0.007), and LV efficiency (r = −0.98; P < 0.001); and directly related to changes in mitral E/e′ (r = 0.12; P = 0.01). Adjusting for age and blood pressure change, women and obese individuals had less enhancement in ventricular–arterial coupling and efficiency compared with men and non-obese individuals (P = 0.04 and 0.007, respectively).
Antihypertensive therapy reduces arterial and ventricular stiffness, enhances ventricular–arterial coupling, reduces cardiac work, and improves LV efficiency, systolic, and diastolic function. Attenuated responses in women and among obese subjects suggest that structure–function changes may be less reversible in these groups, possibly explaining their greater susceptibility to ultimately develop heart failure.
- obesity
- hypertension
- heart failure, diastolic
- systolic blood pressure
- cerebrovascular accident
- ischemic stroke
- heart failure
- left ventricle
- blood pressure
- diastole
- follow-up
- heart ventricle
- systole
- heart
- arterial stiffness
- ejection fraction
- antihypertensive therapy
- extraperitoneal approach
- attenuation
Comments
We agree that further research is needed to clarify the goal blood pressure to target in order prevent cardiac and non-cardiac end organ damage. Since the EXCEED trial evaluated an intensive vs. standard blood pressure lowering strategy (with target systolic blood pressures of <130 vs. <140 mmHg respectively),(1) we were able to assess the cardiovascular effects of blood pressure lowering below the traditional target of 140 mmHg. Our results showed a graded relationship between the extent of blood pressure lowering and reduction in arterial-ventricular stiffness, regression of left ventricular hypertrophy, and improvement in left ventricular diastolic function.(2) While we did not assess the relationship between blood pressure lowering and non-cardiac organ function in this study, we previously reported an association between renal dysfunction (albuminuria) and worsening of these arterial- ventricular properties in the same cohort.(3) These data therefore support a consideration of blood pressure targets in relation to cardiac and non- cardiac end organ function. More intriguingly, the differential cardiovascular responses to blood pressure lowering in women and obese individuals(2) raise the question of whether treatment targets should be sex-specific or scaled to body size.
References
1. Solomon SD, Verma A, Desai A, Hassanein A, Izzo J, Oparil S, Lacourciere Y, Lee J, Seifu Y, Hilkert RJ, Rocha R, Pitt B. Effect of intensive versus standard blood pressure lowering on diastolic function in patients with uncontrolled hypertension and diastolic dysfunction. Hypertension2010 Feb;55(2):241-8.
2. Lam CS, Shah AM, Borlaug BA, Cheng S, Verma A, Izzo J, Oparil S, Aurigemma GP, Thomas JD, Pitt B, Zile MR, Solomon SD. Effect of antihypertensive therapy on ventricular-arterial mechanics, coupling, and efficiency. Eur Heart J2013 Mar;34(9):676-83.
3. Shah AM, Lam CS, Cheng S, Verma A, Desai AS, Rocha RA, Hilkert R, Izzo J, Oparil S, Pitt B, Thomas JD, Zile MR, Aurigemma GP, Solomon SD. The relationship between renal impairment and left ventricular structure, function, and ventricular-arterial interaction in hypertension. J Hypertens. 2011 Sep;29(9):1829-36.
Conflict of Interest:
None declared
Although there is a view that the scientific basis for a "goal" blood pressure(BP) of < 140/90 mm Hg has never been formally evaluated(1), a reduction in blood pressure to levels of that order appears to achieve regression of target organ damage, as was the case in the study which showed a beneficial effect on ventricular-arterial mechanics as a consequence of a reduction in mean systolic BP from 154 mm Hg to 137 mm Hg(2). A goal more demanding than mere attainment of a BP < 140/90 mm Hg should be a further reduction in BP in order to achieve regression of residual parameters of target organ damage, as was the case in a study where a reduction of blood pressure already within the normal range generated further, and significant(p=0.014), regression in left ventricular mass(3). Where no residual, potentially reversible, target organ damage can be identified after achievement of a goal blood pressure of <140/90 mm Hg, the next aim should be to mitigate the risk of atrial fibrillation by further lowering the systolic BP to < 130 mm Hg, given the fact that, in one study, new-onset atrial fibrillation was significantly(p=0.044) less prevalent in previously hypertensive patients who had been managed on the basis of a "goal" BP of < 130 mm Hg than in counterparts with less "tight" control of systolic BP(4). Accordingly, the dilemna of whether antihypertensive treatment should be titrated to blood pressure reduction or to target organ damage regression(5) can best be resolved by the recognition that "tight" blood pressure control, as defined in one study(4) should complement the strategy of regression of target organ damage(3). The two strategies are not mutually exclusive
References
(1)Time to lower treatment BP targets for hypertension? Lancet 2009;374:503-504
(2)Lam CSP., Shah AM., Borlaug BA et al Effect of antihypertensive therapy on ventricular-arterial mechanics, coupling, and efficiency Eur Heart J 2013;34:676-683
(3) Simpson HJ., Gandy SJ., Houston JG et al Left ventricular hypertrophy: reduction of blood pressure already within the normal range further regresses left ventricular mass Heart 2010;96:148-152
(4) Verdecchia P., Staessen JA., Angeli F et al Usual versus tight control of systolic blood pressure in non-diabetic patients with hypertension(Cardio-Sis) an open-label randomised trial Lancet 2009;374:525-533
(5) Redon J Antihypertensive treatment: should it be titrated to blood pressure reduction or to target organ damage regression? Curr Opin Nephrol Hypertens 2005;14:448-452
Conflict of Interest:
None declared