Conventional 24-h SD of BP is markedly influenced by nocturnal BP fall. The weighted 24-h SD of BP removes the mathematical interference from night-time BP fall and correlates better with end-organ damage, therefore it may be considered as a simple index of 24-h BP variability superior to conventional 24-h SD.

Abstract-Although the differences between central and peripheral blood pressure (BP) values have been known for decades, the consequences of decision making based on peripheral rather than central BP have only recently been recognized. There are only a few studies assessing the relationship between intraaortic BP and cardiovascular risk. In addition, the relationship between central BP and the risk of cardiovascular events in a large group of coronary patients has not yet been evaluated. Therefore, the aim of the study was to determine the prognostic significance of central BP-derived indices in patients undergoing coronary angiography. Invasive central BPs were taken at baseline, and study end points were ascertained during over a 4. Key Words: blood pressure Ⅲ central pulse pressure Ⅲ pulsatility Ⅲ cardiovascular risk Ⅲ atherosclerosis Ⅲ coronary artery disease D iastolic blood pressure (DBP) was previously believed to be the only meaningful predictor of cardiovascular events; however, systolic blood pressure (SBP) is now being considered an even more important cardiovascular risk factor. 1 Recently, the prospective and retrospective epidemiological studies have demonstrated that elevated pulse pressure (PP, the difference between systolic and diastolic pressure) is independently related to the risk of cardiovascular events, especially in the elderly. 1,2 Furthermore, new parameters (pulsatility and pulsatility index) of the pulsatile component of blood pressure (BP) have been developed. 3,4 Pulsatility is calculated as PP divided by mean blood pressure (MBP). 3 Unlike SBP, DBP, and PP, this new parameter is not correlated with MBP, and thus it may be very useful in research on atherosclerosis pathogenesis and its complications development. 5,6 Pulsatility may be seen as indicator of the relative changes of blood pressure in opposition to pulse pressure which is an index of absolute blood pressure changes.Although the differences between central and peripheral BP values have been known for decades, the consequences of decision making based on peripheral rather than central BP have only recently been recognized. 6 -9 As central BP directly affects heart and coronary as well as carotid arteries and is directly related to the incidence of major cardiovascular complications, more and more attention is being given to the ascending aortic BP measurements. 6,7 There are only a few studies assessing the relationship between central BP and cardiovascular risk. The relationship between pulsatility (as measured invasively in the ascending aorta) and the risk of cardiovascular events has not yet been evaluated. Therefore, the present study was designed for the assessment of the relationship between prognosis and the steady and pulsatile components of central BP. Methods Study PopulationConsecutive patients suspected of having coronary artery disease (CAD) who were undergoing nonemergency coronary angiography from

Ambulatory blood pressure increases progressively with increasing altitude, remaining elevated after 3 weeks. An angiotensin receptor blockade maintains blood pressure-lowering efficacy at 3400 m but not at 5400 m.

Both carvedilol and nebivolol partly counteract the increase in BP at altitude in healthy normotensive individuals but are associated with a lower SpO2. Carvedilol seems more potent in this regard, whereas nebivolol more effectively prevents the shift to a nondipping BP profile and is better tolerated.

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Slow deep breathing improves blood oxygenation (SpO2) and affects hemodynamics in hypoxic patients. We investigated the ventilatory and hemodynamic effects of slow deep breathing in normal subjects at high altitude. We collected data in healthy lowlanders staying either at 4559 m for 2–3 days (Study A; N = 39) or at 5400 m for 12–16 days (Study B; N = 28). Study variables, including SpO2 and systemic and pulmonary arterial pressure, were assessed before, during and after 15 minutes of breathing at 6 breaths/min. At the end of slow breathing, an increase in SpO2 (Study A: from 80.2±7.7% to 89.5±8.2%; Study B: from 81.0±4.2% to 88.6±4.5; both p<0.001) and significant reductions in systemic and pulmonary arterial pressure occurred. This was associated with increased tidal volume and no changes in minute ventilation or pulmonary CO diffusion. Slow deep breathing improves ventilation efficiency for oxygen as shown by blood oxygenation increase, and it reduces systemic and pulmonary blood pressure at high altitude but does not change pulmonary gas diffusion.

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SUMMARYAims: Exposure to high altitude (HA) hypoxia decreases exercise performance in healthy subjects. Although β-blockers are known to affect exercise capacity in normoxia, no data are available comparing selective and nonselective β-adrenergic blockade on exercise performance in healthy subjects acutely exposed to HA hypoxia. We compared the impact of nebivolol and carvedilol on exercise capacity in healthy subjects acutely exposed to HA hypobaric hypoxia. Methods: In this double-blind, placebo-controlled trial, 27 healthy untrained sea-level (SL) residents (15 males, age 38.3 ± 12.8 years) were randomized to placebo (n = 9), carvedilol 25 mg b.i.d. (n = 9), or nebivolol 5 mg o.d. (n = 9). Primary endpoints were measures of exercise performance evaluated by cardiopulmonary exercise testing at sea level without treatment, and after at least 3 weeks of treatment, both at SL and shortly after arrival at HA (4559 m). Results: HA hypoxia significantly decreased resting and peak oxygen saturation, peak workload, VO 2 , and heart rate (HR) (P < 0.01). Changes from SL (no treatment) differed among treatments: (1) peak VO 2 was better preserved with nebivolol (-22.5%) than with carvedilol (-37.6%) (P < 0.01); (2) peak HR decreased with carvedilol (-43.9 ± 11.9 beats/min) more than with nebivolol (-24.8 ± 13.6 beats/min) (P < 0.05); (3) peak minute ventilation (VE) decreased with carvedilol (-9.3%) and increased with nebivolol (+15.2%) (P = 0.053). Only peak VE changes independently predicted changes in peak VO 2 at multivariate analysis (R = 0.62, P < 0.01). Conclusions: Exercise performance is better preserved with nebivolol than with carvedilol under acute exposure to HA hypoxia in healthy subjects.