4 Along with the other diagnostic exams, in true drug- resistant hypertension, a 24-hour ambulatory BP monitoring should be considered valuable as it conﬁrms the oﬃce evaluation of BP levels and possibly helps the clinician assess the hemodynamic responsiveness to CPAP treatment better [33]. Furthermore, evaluating the dipping pattern and night- time BP levels in resistant hypertension is vital for a more comprehensive approach of the circadian BP variability, its response to therapy, and the potential implementation of chronotherapy issues [4]. Lifestyle modiﬁcations should always stand at the ﬁrst line of the therapeutic procedure in resistant hypertension associated with OSA. The importance of appropriate weight control must be underlined, and bariatric surgery should be encouraged if morbid obesity coexists. Additionally, the underlying pathophysiological mechanisms activated in the duo of resistant hypertension and OSA prompt to rigorous sodium intake restriction [4]. In resistant hypertension complicated by OSA, CPAP is imperative as it proved an eﬃcacious “add-on” to the conventional pharmacological treatment and succeeded to reverse nondipping proﬁle in most of the patients [31, 33]. In these lines, patients should be encouraged to wear their mask every night and possibly for the whole night. The antihypertensive eﬀect of CPAP seems to be more prominent in those with more severe OSA or hyper- tension, though there is limited evidence whether sleepy and nonsleepy patients with drug resistant hypertension beneﬁt the same in terms of BP reduction when compliant to CPAP treatment. Although, there is limited clinical evidence for the potential beneﬁt of mineralocorticoid antagonists in resistant hypertension and OSA [37], their use should be considered as an additional promising therapeutic strategy with a plausible pathophysiological background [6, 21]. Since resistant hypertension and OSA are accompanied either separately or in combination with highly increased prevalence of target organ damage and adverse cardiovas- cular outcome, combined treatment seems to be of the highest clinical priority. Targeting on both the maximum individual doses of antihypertensive drugs and the eﬀective implementation of CPAP should remain the main awareness of the physician dealing with this compound diﬃcult-to- treat hypertensive disorder. References [1] P. Lavie, P. Herer, and V. Hoﬀstein, “Obstructive sleep apnoea syndrome as a risk factor for hypertension: population study,” British Medical Journal, vol. 320, no. 7233, pp. 479–482, 2000. [2] F. Javier Nieto, T. B. Young, B. K. Lind et al., “Association of sleep-disordered breathing sleep apnea, and hypertension in a large community-based study,” Journal of the American Medical Association, vol. 283, no. 14, pp. 1829–1836, 2000. [3] O. Friedman and A. G. Logan, “The price of obstructive sleep apnea-hypopnea: hypertension and other ill eﬀects,” American Journal of Hypertension, vol. 22, no. 5, pp. 474–483, 2009. [4] C. Tsiouﬁs, A. Kasiakogias, C. Thomopoulos, A. Manolis, and C. Stefanadis, “Managing hypertension in obstructive sleep apnea: the interplay of continuous positive airway pressure, International Journal of Hypertension medication and chronotherapy,” Journal of Hypertension, vol. 28, no. 5, pp. 875–882, 2010. [5] C. Tsiouﬁs, C. Thomopoulos, and C. Stefanadis, “Obstructive sleep apnoea and hypertension: a growing clinical challenge,” Hellenic Journal of Cardiology, vol. 49, no. 5, pp. 299–302, 2008. [6] T. L. Goodfriend, “Obesity, sleep apnea, aldosterone, and hypertension,” Current Hypertension Reports, vol. 10, no. 3, pp. 222–226, 2008. [7] R. J. Garrison, W. B. Kannel, J. Stokes, and W. P. Castelli, “Incidence and precursors of hypertension in young adults: the Framingham oﬀspring study,” Preventive Medicine, vol. 16, no. 2, pp. 235–251, 1987. [8] A. V. Chobanian, G. L. Bakris, H. R. Black et al., “The seventh report of the Joint National Committee on prevention, detection, evaluation, and treatment of high blood pressure: the JNC 7 report,” Journal of the American Medical Association, vol. 289, no. 19, pp. 2560–2572, 2003. [9] G. Mancia, G. De Backer, A. Dominiczak et al., “2007 ESH-ESC practice guidelines for the management of arterial hypertension: ESH-ESC task force on the management of arterial hypertension,” Journal of Hypertension, vol. 25, no. 9, pp. 1751–1762, 2007. [10] O. Marrone, C. Lombardi, and G. Parati, “Eﬀects of continu- ous positive airway pressure therapy on hypertension control in patients with sleep-related breathing disorders: available evidence and unresolved issues,” Journal of Hypertension, vol. 28, no. 10, pp. 2012–2015, 2010. [11] K. M. Rexrode, J. E. Manson, and C. H. Hennekens, “Obesity and cardiovascular disease,” Current Opinion in Cardiology, vol. 11, no. 5, pp. 490–495, 1996. [12] P. Bramlage, D. Pittrow, H. U. Wittchen et al., “Hypertension in overweight and obese primary care patients is highly preva- lent and poorly controlled,” American Journal of Hypertension, vol. 17, no. 10, pp. 904–910, 2004. [13] W. C. Cushman, C. E. Ford, J. A. Cutler et al., “Success and predictors of blood pressure control in diverse North American settings: te antihypertensive and lipid-lowering treatment to prevent heart attact trial (ALLHAT),” Journal of Clinical Hypertension, vol. 4, no. 6, pp. 393–404, 2002. [14] W. G. Haynes, “Role of leptin in obesity-related hypertension,” Experimental Physiology, vol. 90, no. 5, pp. 683–688, 2005. [15] N. Tu¨mer, B. Erdo¨s, M. Matheny, I. Cudykier, and P. J. Scarpace, “Leptin antagonist reverses hypertension caused by leptin overexpression, but fails to normalize obesity-related hypertension,” Journal of Hypertension, vol. 25, no. 12, pp. 2471–2478, 2007. [16] C. Thomopoulos, D. P. Papadopoulos, O. Papazachou et al., “Free leptin is associated with masked hypertension in nonobese subjects a cross-sectional study,” Hypertension, vol. 53, no. 6, pp. 965–972, 2009. [17] H. Scha¨fer, D. Pauleit, T. Sudhop, I. Gouni-Berthold, S. Ewig, and H. K. Berthold, “Body fat distribution, serum leptin, and cardiovascular risk factors in men with obstructive sleep apnea,” Chest, vol. 122, no. 3, pp. 829–839, 2002. [18] J. E. Hall, “The kidney, hypertension, and obesity,” Hyperten- sion, vol. 41, no. 3, pp. 625–633, 2003. [19] C. Tsiouﬁs, C. Thomopoulos, K. Dimitriadis et al., “Associa- tion of obstructive sleep apnea with urinary albumin excretion in essential hypertension: a cross-sectional study,” American Journal of Kidney Diseases, vol. 52, no. 2, pp. 285–293, 2008. [20] K. Damman, V. M. van Deursen, G. Navis, A. A. Voors, D. J. van Veldhuisen, and H. L. Hillege, “Increased central venous pressure is associated with impaired renal function and