Our data show that device-guided breathing exercises have an antihypertensive effect that can be seen in conditions closer to daily life than the setting of the physician's office.

Abstract-In rats, an increase in heart rate by pacing is accompanied by progressive large-artery stiffening. Whether this is also the case in humans is unknown. We enrolled 20 patients who were chronically implanted with a pacemaker because of atrioventricular block or sick sinus syndrome. Arterial distensibility was measured by an echo-tracking device. In 10 patients, the evaluation was performed on the radial artery by using continuous finger blood pressure measurements, whereas in the remaining 10 patients, the common carotid artery was studied with a semiautomatic measure of brachial artery blood pressure. Diastolic diameter, systodiastolic diameter change, and distensibility were obtained at baseline (heart rate 63Ϯ2 beats/min) and after atrial and ventricular sequential pacing at a heart rate of 90 and 110 beats/min. At baseline, the diameter was 7.8Ϯ0.3 mm in the carotid artery and 2.4Ϯ0.1 mm in the radial artery; the respective systodiastolic diameter change values were 375.4Ϯ31.0 and 55.9Ϯ9.0 (m) and the distensibility values were 1.4Ϯ0.1 and 0.7Ϯ0.1 (1/mm Hg 10 Ϫ3 ). Blood pressure and diameter were not significantly modified by increasing heart rate, which markedly modified systodiastolic diameter change and distensibility. In the radial artery, distensibility was reduced by 47% (PϽ0.05) at a heart rate of 90 beats/min with no further reduction at 110 beats/min. In the carotid artery, distensibility was reduced by 20% at a heart rate of 90 beats/min (PϽ0.05) with a further reduction at 110 beats/min (45%, PϽ0.05). These data provide the first evidence in humans that acute increases in heart rate markedly affect arterial distensibility and that this occurs in both large-and middle-size muscle arteries within the range of "normal" heart rate values. Key Words: arterial stiffness Ⅲ heart rate Ⅲ risk factors Ⅲ human S tudies performed in rats have shown that when heart rate (HR) is increased by pacing, carotid and femoral artery distensibilities (Dist) are reduced. 1 This suggests that HR might be one of the factors that modulates arterial mechanical properties and thus, potentially participates in their abnormality in several conditions and diseases.Little evidence exists, however, as to whether HR plays a similar role in humans. This is because although a weak, positive correlation has been reported to exist between HR and pulse wave velocity in a cross-sectional survey of normotensive and hypertensive individuals, 2 studies measuring arterial stiffness during HR changes have given conflicting results. [3][4][5][6] The purpose of the present study was to fill this gap by measuring arterial Dist in response to pacing-induced increases in HR. Dist was measured both in a carotid (CA) and a radial (RA) artery because previous studies had shown that large elastic and middle-size arteries behave differently in a number of circumstances, 7-10 including those elicited in animals by HR changes. 1,11 Care was taken to exclude subjects with uncontrolled blood pressure (BP) values, hypercholesterolemia, diabetes, a...

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Objective-Hypercholesterolemia markedly impairs endothelial function. Whether this is the case for hypertriglyceridemia is less clear, however, and limited evidence exists on the effect of an acute increase in triglyceridemia caused by a high-fat meal. Methods and Results-In 16 normotensive subjects with an untreated mild hypertriglyceridemia and dyslipidemia and in 7 normal controls, we measured radial artery diameter and blood flow by an echo-tracking device (NIUS02). Data were obtained at baseline, at the release of a 4-minute ischemia of the hand, which causes an increase in arterial diameter dependent on nitric oxide (NO) secretion, and at the release of a 12-minute exclusion of the arm by an arm cuff to obtain a larger increase in arterial diameter mainly of nonendothelial nature. Measurements were performed before and 6 hours after a high-fat meal (680 kcal/m 2 body surface; 82% lipids). In mild dyslipidemic hypertriglyceridemic subjects, the high-fat meal did not alter baseline blood pressure (beat-to-beat finger measurement), heart rate, radial artery diameter, and blood flow. It also did not alter the increase in blood flow induced by the 4-minute ischemia (ϩ42.7Ϯ10.4 and ϩ43.7Ϯ10.4 mL/min), whereas it markedly attenuated the concomitant increase in arterial diameter (ϩ0.31Ϯ0.06 versus 0.13Ϯ0.06 mm; PϽ0.05). The alteration of the diameter response did not correlate with changes in total cholesterol, but it showed a significant correlation with the increase in serum triglycerides induced by high-fat meal (rϭ0.49, PϽ0.05). This attenuation was not seen in control subjects and in subjects in whom measurements were repeated after a 6-hour observation period. It was also not paralleled by an alteration of the endothelially independent response to a 12-minute ischemia whose larger effects on arterial diameter and blood flow were similar before and after the high-fat meal. Key Words: blood flow Ⅲ vasodilation Ⅲ endothelium Ⅲ triglyceridemia Ⅲ acute triglyceridemia increase S everal studies have shown that an increased level of serum triglycerides can be an independent risk factor for coronary disease, when occurring alone and when occurring on the background of other alterations in lipid profile. [1][2][3][4] This has stimulated research on whether triglycerides cause endothelial dysfunction, which starts the cascade of events that lead to the atherosclerosis, ie, the anatomic lesion responsible for coronary heart disease. [5][6][7][8] Evidence that this is the case is not conclusive, however, because triglycerides were reported both to worsen and to have no measurable effect on endothelial function. 9 -18 Furthermore, little evidence has been obtained on whether triglycerides affect endothelial function in individuals with more complex, yet common, alterations in lipid profile, despite the evidence that under this circumstance the role of triglycerides as a cardiovascular risk factor may be enhanced. [1][2][3][4] Our study was aimed at providing further information on this issue by examining the effect of se...