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How to reduce systolic blood pressure without lowering the diastolic ?
Diastolic blood pressure in coronary artery disease
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Hean T Ong, FACC, FESC HT Ong Heart Clinic, Penang, MALAYSIA
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htyl{at}streamyx.com Hean T Ong
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Messerli and colleagues suggest that there is a nadir for diastolic blood pressure below which coronary perfusion is impaired and cardiovascular events increased (1). Yet, numerous trials including VALUE and ASCOT clearly show that the arm treated to the lower blood pressure produce less cardiovascular events (2,3). How can we seek to "lower blood pressure" and yet try to "not lower diastolic blood pressure excessively" since all present anti-hypertensive agents lower both diastolic and systolic pressures?? References: 1. Messerli FH, Mancia G, Conti R, et al. Dogma disputed: Can aggressively lowering blood pressure in hypertensive patients with coronary artery disease be dangerous? Ann Intern Med 2006; 144:884-893. 2.Julius S,Kjeldsen SE, Weber M, et al. Outcomes in hypertensive patients at high cardiovascular risk treated with regimens based on valsartan or amlodipine: the VALUE randomised trial.Lancet 2004; 363: 2022 -31. 3. Dahlof B,Sever PS,Poulter NR, et al. Prevention of cardiovascular events with an antihypertensive regimen 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 2005; 366:895-906. Conflict of Interest:None declared |
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Thomas Weber, MD Cardiology Dept, Klinikum Wels, Austria, St Vincent´s Clinic, Sydney, Australia, Thomas Weber, Johann Auer, Bernd Eber, Michael F O´Rourke
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thomas.weber{at}klinikum-wels.at Thomas Weber, et al.
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In a recent issue of the Annals, Messerli et al provide new insights into the J-curve discussion in patients with hypertension and coronary artery disease (CAD) [1]. Briefly, they observed an increase in all-cause mortality and myocardial infarctions with lower diastolic blood pressure in the INVEST population, hypertensive patients with CAD, treated with a verapamil sustained release or atenolol-based strategy [2]. In the discussion, the authors mention impaired coronary perfusion, increased pulse pressure and arterial stiffness, and underlying chronic illness as possible pathophysiologic mechanisms. Clearly, we cannot speculate on the latter, but would like to support the two other explanations due to the following reasons: First, mean patient age in INVEST was 66 years. Generally, in this age group, isolated systolic hypertension (ISH) is by far the most common phenotype of hypertension [3], a condition characterized by widened pulse pressure, increased arterial stiffness, increased/premature arterial wave reflections, therefore decreased diastolic blood pressure and impaired coronary perfusion [4,5]. In the original publication, more than 50% of patients had “controlled” diastolic blood pressure at baseline, raising the possibility of ISH in many of them. It would be very interesting to perform complementary analysis in ISH patients, if they had been identified at baseline. Second, Chirinos et al [6] as well as our group [7] recently observed that increased arterial wave reflections, one of the main pathophysiologic principles contributing to an increased pulse pressure in these patients, are accompanied by an increase in major adverse cardiovascular events including myocardial infarction and death in CAD patients. In the Chirinos paper [6] as well as in a prior study showing a relationship between increased arterial wave reflections and the presence and extent of CAD [8], a lower diastolic blood pressure was a predictor of the unfavourable endpoint. Moreover, in the latter study, systolic blood pressure was identical in CAD and non-CAD patients, and the significant difference in pulse pressure was mediated mainly by a lower diastolic blood pressure in the CAD group. In other words, the only clue to the altered arterial characteristics in CAD patients was a lower diastolic pressure. Of note, most of the CAD patients in that study were treated hypertensives with a mean age of 63.8 years and, therefore, quite comparable to the INVEST population. In conclusion, although arterial properties were not reported in the INVEST study [1,2], the increased risk accompanying a lower diastolic blood pressure in treated hypertensive patients with CAD might be explained by increased arterial wave reflections and arterial stiffness. Thomas Weber Johann Auer Michael F. O`Rourke Bernd Eber 1 ... Messerli FH, Mancia G, Conti R, et al. Dogma disputed: can aggressively lowering blood pressure in hypertensive patients with coronary artery disease be dangerous? Ann Intern Med 2006; 144:884-93 2 ... Pepine CJ, Handberg EM, Cooper-DeHoff RM, et al. A calcium antagonist vs a non-calcium antagonist hypertension treatment strategy for patients with coronary artery disease. J Am Med Ass 2003; 290:2805-16 3 ... Franklin SS, Jacobs MJ, Wong ND, et al. Predominance of isolated systolic hypertension among middle-aged and elderly US hypertensives - analysis based on NHANES III. Hypertension 2001; 37:869-74 4 ... Nichols WW, O´Rourke MF. McDonald´s Blood Flow in Arteries. 5th ed. London, England:Hodder-Arnold, 2005 5 ... Franklin SS. Hypertension in older people: Part 1. J Clin Hypertens 2006; 8:444-9 6 ... Chirinos JA, Zambrano JP, Chakko S, et al. Aortic pressure augmentation predicts adverse cardiovascular events in patients with established coronary artery disease. Hypertension 2005;45:980–985 7 ... Weber T, Auer J, O´Rourke MF, et a. Increased arterial wave reflections predict severe cardiovascular events in patients undergoing percutaneous coronary interventions. Eur Heart J 2005; 26:2657-63 8 ... Weber T, Auer J, O´Rourke MF, et al. Arterial stiffness, wave reflections and the risk of coronary artery disease. Circulation 2004; 109:184-198 Conflict of Interest:None declared |
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