G lobally, cardiovascular disease (CVD) is the leading cause of death accounting for 31% in 2008.1 Obesity is an independent predictor of CVD and weight loss has been shown to improve many obesity-related risk factors. 2 However, there are few studies investigating the effect of weight loss on cardiovascular end points. The Trial of Nonpharmacological Interventions in the Elderly enrolled subjects >60 years with hypertension to investigate the effect of weight loss on blood pressure and cardiovascular outcomes.3 After a median follow-up of 29 months, the hazard ratio (HR) for a cardiovascular end point or diagnosis of high blood pressure in the weight reduction group was 0.64 (95% confidence interval [CI], 0.49, 0.85; P=0.002). 4 More recently, the Look AHEAD trial (n=5145) failed to show a benefit of weight reduction on cardiovascular end points in subjects with type 2 diabetes mellitus after a median followup of 9.6 years. 5 In the Look AHEAD trial, the mean weight loss in the intervention group was 6%, compared with 3.5% in the control group.Carotid femoral pulse wave velocity (cfPWV) is considered the gold standard method for measuring arterial stiffness because it measures the propagation of the forward pressure at the level of the aorta.6 A meta-analysis of individual participant data from 17 studies (17 635 participants) showed that cfPWV was an independent predictor of coronary heart disease (HR, 1.23; 95% CI, 1.11 to 1.35), stroke (HR, 1.28; 95% CI, 1.16 to 1.42), CVD (HR, 1.30; 1.18 to 1.43), CVD mortality (HR, 1.28; 95% CI, 1.15 to 1.43), and all-cause mortality (HR, 1.17; 1.11 to 1.22), after adjustment for established risk factors. Furthermore, the addition of cfPWV to conventional Framingham risk factors improved 10-year CVD risk prediction by 13% in those at intermediate risk of CVD. 7 Many studies indicate that weight loss may improve pulse wave velocity (PWV), although in about half of the studies the change is not statistically significant. A meta-analysis has not been conducted to assess the overall effect of weight loss. The primary aim of this meta-analysis of intervention trials is © 2014 American Heart Association, Inc. Objective-To conduct a systematic review and meta-analysis of clinical trials involving adults, to determine the effect of weight loss induced by energy restriction with or without exercise, antiobesity drugs or bariatric surgery on pulse wave velocity (PWV) measured at all arterial segments. Approach and Results-A systematic search of Pubmed (1966Pubmed ( to 2014, EMBASE (1947EMBASE ( to 2014, MEDLINE (1946MEDLINE ( to 2014, and the Cochrane Library (1951 to 2014) was conducted and the reference lists of identified articles were searched to find intervention trials (randomized/nonrandomized) that aimed to achieve weight loss and included PWV as an outcome. The search was restricted to human studies. Two independent researchers extracted the data. Data were analyzed using Comprehensive Meta Analysis version 2 using random effects analysis. A total of 22 studies wer...

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Oxygen administration is thought to suppress periodic breathing (PB) by reducing carotid body activity, and yet earlier experiments in neonates have shown that PB incidence may be increased following the application of hyperoxia. To clarify this paradox, we studied the changes in the pattern of PB that occur following administration of oxygen in a lamb model of PB. PB was induced in eleven of seventeen anaesthetized lambs following passive hyper‐ventilation with air. When oxygen was administered during PB, the pattern was first enhanced, as evidenced by a sudden decrease in the ratio of the ventilatory duration to the apnoeic pause duration, and then suppressed, as evidenced by a progressive return to stable breathing which was associated with an increase in minute ventilation. Five of the six lambs that did not show PB following passive hyperventilation with air could be made to do so if oxygen was substituted for air as the inspired gas following passive hyperventilation. Five of the eleven lambs that showed PB following hyperventilation with air responded to the application of oxygen during PB by switching to a gross form of episodic breathing consisting of long apnoeic pauses followed by equally long periods of breathing during which minute ventilation fell progressively with time. We conclude that when applied against a background of arterial hypoxaemia, oxygen has a destabilizing influence on ventilation in that (a) it accentuates the unstable breathing that occurs during PB, (b) it induces PB in lambs that exhibited stable breathing in air, and (c) it may precipitate episodic breathing.

The progressive decrease in the periodic cycle duration (PCD) of periodic breathing with postnatal age in term infants has been previously reported by a number of authors and is thought to be associated with peripheral chemoreceptor maturation. We hypothesized that a similar decrease should be observed in preterm infants. Therefore, in this study we measured the changes in PCD with postnatal age in a small group of preterm ( n = 4) infants followed longitudinally (36 afternoon nap studies) over the first 6 mo postnatally. PCD declined in these infants from 17.1 ? 3.3 s (mean -t-2 SD) at 9 d to 9.8 +-3.2 s (mean I 2 SD) at 105 d. The regression slope was -0.072 s/d. Beyond 105 d there was no change in PCD up to 6 mo postnatally. We found no significant difference between active and quiet sleep. These results are similar to results previously published in term infants but apparently contradict recent data on a group of preterm infants. Possible reasons for this discrepancy are discussed. By examining long epochs of periodic breathing in these infants we also identified characteristic changes in PCD and VIA ratio, defined as the duration of the ventilatory period divided by the duration of the apneic interval. VIA ratio fell from the start of an epoch from 1.21 2 0.08 (mean + SEM) to a minimum of 0.62 2 0.03 and then increased again to 0.8 -C 0.05 at the end of the epoch. We conclude that important maturational changes occu~ in the neonatal respiratory control system during the first 6 mo postnatally and that these changes are reflected in a fall in PCD of periodic breathing over this period. We also conclude that the characteristic changes which occur in VIA ratio and PCD are consistent with a role for chemical stimuli in the genesis of periodic breathing. (Pediatr Res 38: 533-538, 1995) Abbreviations SIDS, sudden infant death syndrome VIA, ratio of the duration of ventilation to the duration of apnea in one cycle of periodic breathing To, start time of a long epoch of periodic breathing Tmi,, time from To at which VIA ratio reaches its minimum value T,,,, end time of a long epoch of periodic breathing PCD, periodic breathing cycle duration A PCD, change in PCD during long epochs PNA, postnatal age PNA,,, postnatal age at which PCD ceases to decrease Sao,, arterial oxygen saturation ASao,, deviation between the mean Sao, and the peak or trough of the oscillation in Sao, during periodic breathing Periodic breathing has been studied extensively in both preterm and term infants. These studies have been aimed primarily at elucidating the causes of this type of breathing pattern in neonates and establishing the incidence during the first months of life (1,2).Much of the incentive for these studies came from earlier clinical observations that long apneas were often preceded by periodic breathing in preterm infants (3), although this finding has been disputed more recently (4). Also, a high incidence of periodic breathing has been reported in apparent life-threatening events and SIDS sibling infants when compared with ag...

Background: It is known that increased potassium and reduced sodium intakes can improve postprandial endothelial function. However, the effect of increasing potassium in the presence of high sodium in the postprandial state is not known. Objective: We aimed to determine the effect of high potassium and high sodium on postprandial endothelial function as assessed by using flow-mediated dilatation (FMD) and arterial compliance as assessed by using pulse wave velocity (PWV) and central augmentation index (AIx). Design: Thirty-nine healthy, normotensive volunteers [21 women and 18 men; mean 6 SD age: 37 6 15 y; BMI (in kg/m 2 ): 23.0 6 2.8] received a meal with 3 mmol K and 65 mmol Na (low-potassium, high-sodium meal (LKHN)], a meal with 38 mmol K and 65 mmol Na [high-potassium, high-sodium meal (HKHN)], and a control meal with 3 mmol K and 6 mmol Na (low-potassium, low-sodium meal) on 3 separate occasions in a randomized crossover trial. Brachial artery FMD, carotid-femoral PWV, central AIx, and blood pressure (BP) were measured while participants were fasting and at 30, 60, 90, and 120 min after meals. Results: Compared with the LKHN, the addition of potassium (HKHN) significantly attenuated the postmeal decrease in FMD (P-meal by time interaction , 0.05). FMD was significantly lower after the LKHN than after the HKHN at 30 min (P , 0.01). AIx decreased after all meals (P , 0.05). There were no significant differences in AIx, PWV, or BP between treatments over time. Conclusion: The addition of potassium to a high-sodium meal attenuates the sodium-induced postmeal reduction in endothelial function as assessed by FMD. This trial was registered at

Improving dietary quality in people with well-controlled type 1 and type 2 diabetes may slow CCA IMT progression. This trial was registered at https://www.anzctr.org.au as ACTRN12613000251729.