Gavin W Lambert

Baker IDI Heart and Diabetes Institute, Melbourne, Victoria, Australia

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Publications (262)1356.72 Total impact

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    ABSTRACT: There is concern that intentional weight loss may generate excessive loss of fat free mass (FFM). Idealists target minimal loss of FFM while others accept up to 25% of weight lost.In a cross-sectional study of 275 weight stable overweight or obese adults, whole body dual-energy X-ray absorptiometry measured FFM. A range of models was used to estimate the expected ∆FFM/∆weight to attain body composition of a weight stable individual at a lower BMI. Higher body mass index (BMI) was associated linearly with higher FFM in men and women. Proportional ∆FFM/∆weight was influenced by sex, BMI and age. Direct scatter plot analysis, quadratic curve fit modelling and linear FFM-BMI modelling provide similar estimates of ∆FFM/∆weight, with 40% for men and 33% for women. These results confirm the 25% rule is inappropriate and our estimates are above those generally reported following intentional weight loss indicating favourable preservation of fat free mass.
    Diabetes Obesity and Metabolism 09/2014; · 5.18 Impact Factor
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    ABSTRACT: Context: Insulin resistance and sympathetic nervous system overactivity are closely associated and contribute to cardiovascular risk. Objective: To test the hypotheses that pharmacological improvement in insulin sensitivity would (1) attenuate sympathetic neural drive and (2) enhance neuronal norepinephrine uptake. Participants and Methods: A randomised double-blind trial was conducted in 42 obese, un-medicated individuals with metabolic syndrome (mean age 56 ± 1 years, body mass index 34 ± 0.6 kg/m(2)) who received 12-weeks pioglitazone (PIO)(15 mg for 6 weeks, then 30 mg daily) or matched placebo. Clinical measurements included whole-body norepinephrine kinetics (spillover rate, plasma clearance and the steady-state ratio of tritiated 3,4-dihydroxyphenylglycol to tritiated norepinephrine ([(3)H]-DHPG : [(3)H]-NE) as an index of neuronal uptake-1), muscle sympathetic nerve activity (MSNA), spontaneous baroreflex sensitivity, euglycemic hyperinsulinemic clamp, oral glucose tolerance test (OGTT), ambulatory blood pressure and Doppler echocardiography. Results: PIO treatment increased glucose utilisation by 35%, and was accompanied by significant reductions in diastolic blood pressure and improved left ventricular (LV) diastolic and endothelial function. Resting MSNA burst frequency decreased by -6 ± 3 burst/min compared to baseline (P=0.03), but the magnitude of change was not different from placebo (P=0.89). Norepinephrine spillover and clearance rates and baroreflex sensitivity were unchanged. Post hoc subgroup analyses revealed an 83% increase in [(3)H]-DHPG : [(3)H]-NE ratio in hyperinsulinemic (P=0.04) but not normoinsulinemic subjects (time x group interaction P=0.045). Change in [(3)H]-DHPG : [(3)H]-NE ratio correlated with improvements in diastolic blood pressure (r=-0.67, P=0.002), mitral E/A ratio (r=0.62, P=0.008), E wave deceleration time (r=-0.48, P=0.05) and Δ insulin AUC0-120 during OGTT (r=-0.42, P=0.08). Conclusions: Compared to placebo, PIO does not affect resting sympathetic drive or norepinephrine disposition in obese subjects with MetS. Treatment induced changes in [(3)H]-DHPG : [(3)H]-NE ratio related to reduction in hyperinsulinemia and improvements in diastolic function.
    The Journal of clinical endocrinology and metabolism. 06/2014;
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    ABSTRACT: The 'obesity paradox' refers to observations that run counter to the thesis that normal weight (BMI 18.5-24.9 kg/m(2)) provides the lowest mortality and higher weight is associated with greater mortality. We argue that the weight of lowest mortality is influenced by aging and chronic disease, with mortality advantage extending into the overweight and even class I obese ranges under some circumstances. A focus on quality nutrition, physical activity, fitness, and maintaining function in these weight ranges may be preferable to a focus on intentional weight loss, which has uncertain effects. The 'obesity paradox' is no 'paradox' if one defines and interprets 'ideal' weight appropriately.International Journal of Obesity accepted article peview online, 15 April 2014. doi:10.1038/ijo.2014.59.
    International journal of obesity (2005) 04/2014; · 5.22 Impact Factor
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    ABSTRACT: Renal denervation (RDN) reduces muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in resistant hypertension. Although a persistent BP-lowering effect has been demonstrated, the long-term effect on MSNA remains elusive. We investigated whether RDN influences MSNA over time. Office BP and MSNA were obtained at baseline, 3, 6, and 12 months after RDN in 35 patients with resistant hypertension. Office BP averaged 166±22/88±19 mm Hg, despite the use of an average of 4.8±2.1 antihypertensive drugs. Baseline MSNA was 51±11 bursts/min ≈2- to 3-fold higher than the level observed in healthy controls. Mean office systolic and diastolic BP significantly decreased by -12.6±18.3/-6.5±9.2, -16.1±25.6/-8.6±12.9, and -21.2±29.1/-11.1±12.9 mm Hg (P<0.001 for both systolic BP and diastolic BP) with RDN at 3-, 6-, and 12-month follow-up, respectively. MSNA was reduced by -8±12, -6±12, and -6±11 bursts/min (P<0.01) at 3-, 6-, and 12-month follow-up. The reduction in MSNA was maintained, despite a progressive fall in BP over time. No such changes were observed in 7 control subjects at 6-month follow-up. These findings confirm previous reports on the favorable effects of RDN on elevated BP and demonstrate sustained reduction of central sympathetic outflow ≤1-year follow-up in patients with resistant hypertension and high baseline MSNA. These observations are compatible with the hypothesis of a substantial contribution of afferent renal nerve signaling to increased BP in resistant hypertension and argue against a relevant reinnervation at 1 year after procedure.
    Hypertension 04/2014; · 6.87 Impact Factor
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    ABSTRACT: Obesity is associated with elevated cardiovascular mortality, which may be attributed, in part, to sympathetic nervous system (SNS) activation and an associated poor metabolic profile. We examined the effects of laparoscopic adjustable gastric band (LAGB) on SNS activity and cardiovascular profile when the initial weight loss of 10%, corresponding to the recommendation of clinical guidelines, was reached. Direct muscle sympathetic nerve activity (MSNA, microneurography), baroreflex function, and cardiovascular profile were examined before and after a predetermined weight loss of 10% in 23 severely obese nondiabetic individuals. The 10% weight loss was achieved at an average of 7.3±1.4 months (range = 1.3-23.3 months). This was associated with significant improvement in office systolic and diastolic blood pressure (BP) (-12mm Hg and -5mm Hg, respectively), a decrease in MSNA (33±3 to 22±3 bursts per minute), improvement in cardiac (16±3 to 31±4ms/mm Hg) and sympathetic (-2.23±0.39 to -4.30±0.96 bursts/100 heartbeats/mm Hg) baroreflex function, total cholesterol (5.33±0.13 to 4.97±0.16 mmol/L), fasting insulin (29.3±2.4 to 19.6±1.1 mmol/L), and creatinine clearance (172±11 to 142±8ml/min). None of the cardiovascular risk improvement related to the rate of weight loss. The change in systolic and diastolic BP correlated with change in waist circumference (r = 0.46, P = 0.04; r = 0.50, P = 0.02, respectively). The initial 10% weight loss induced by LAGB was associated with substantial hemodynamic, metabolic, SNS, and renal function improvements. Changes in waist circumference appear to be an important factor contributing to BP adaptation after LAGB surgery.
    American Journal of Hypertension 04/2014; · 3.67 Impact Factor
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    ABSTRACT: Metabolic syndrome is associated with adverse health outcomes and is a growing problem worldwide. Although efforts to harmonise the definition of metabolic syndrome have helped to better understand the prevalence and the adverse outcomes associated with the disorder on a global scale, the mechanisms underpinning the metabolic changes that define it are incompletely understood. Accumulating evidence from laboratory and human studies suggests that activation of the sympathetic nervous system has an important role in metabolic syndrome. Indeed, treatment strategies commonly recommended for patients with metabolic syndrome, such as diet and exercise to induce weight loss, are associated with sympathetic inhibition. Pharmacological and device-based approaches to target activation of the sympathetic nervous system directly are available and have provided evidence to support the important part played by sympathetic regulation, particularly for blood pressure and glucose control. Preliminary evidence is encouraging, but whether therapeutically targeting sympathetic overactivity could help to prevent metabolic syndrome and attenuate its adverse outcomes remains to be determined.
    The lancet. Diabetes & endocrinology. 04/2014;
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    ABSTRACT: An exaggerated morning surge in blood pressure (BP) closely relates to target organ damage and cardiovascular risk, but whether the causative mechanism involves greater reactivity of the sympathetic nervous system (SNS) is unknown. We determined whether the response of the SNS to a cold pressor test predicted the BP morning surge. Ambulatory BP recordings were obtained from 14 men and 19 women (age = 41±4 years), and the amplitude (day-night difference), rate of rise (RoR), rate by amplitude product (BPPower), and morning BP surge (MBPS; post-awake minus pre-awake) of morning mean arterial pressure (MAP) were determined. The reactivity of the SNS to CPT was assessed by recording of muscle sympathetic nerve activity (MSNA). CPT induced a marked increase in MAP and all parameters of MSNA, including burst amplitude. Log-normalized BPPower positively correlated with the overall average CPT-induced increases in total MSNA (r = 0.38; P = 0.04) and burst amplitude (r = 0.43; P = 0.02) but was not related to the increase in MSNA frequency. Furthermore, a strong positive linear trend in the CPT-induced changes in burst amplitude across tertiles of BPPower and RoR was observed. BPPower and RoR were not related to CPT-induced hemodynamic changes. The MBPS did not correlate with any of the CPT-induced changes in vascular or MSNA variables. These results suggest that the central nervous system mechanisms influencing the increase in MSNA burst amplitude during arousal may also be fundamental in determining the rate and power of BP rise during the morning period.
    American Journal of Hypertension 01/2014; · 3.67 Impact Factor
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    ABSTRACT: The exact pathophysiology of Tako-Tsubo cardiomyopathy (TTC) remains unknown but a role for sympathetic hyperactivity has been suggested. Up to now, no direct evidence of sympathetic nerve hyperactivity has been established nor involvement of sympathetic baroreflex identified. The aim of our study was to determine, by direct sympathetic nerve activity (SNS) recording if sympathetic nervous system activity is increased and spontaneous baroreflex control of sympathetic activity reduced in patients with TTC. We included 13 patients who presented with TTC and compared their SNS activity and spontaneous baroreflex control of sympathetic activity with that of 13 control patients with acutely decompensated chronic heart failure. SNS activity was evaluated by microneurography, a technique assessing muscle sympathetic nerve activity (MSNA). Spontaneous baroreflex control of sympathetic activity was evaluated as the absolute value of the slope of the regression line representing the relationship between spontaneous diastolic blood pressure values and concomitant SNS activity. Control patients were matched for age, sex, left ventricular ejection fraction and creatinine clearance. The mean age of the patients with TTC was 80 years, all patients were women. There were no significant differences between the two groups of patients for blood pressure, heart rate or oxygen saturation level. TTC patients presented a significant increase in sympathetic nerve activity (MSNA median 63.3 bursts/min [interquartile range 61.3 to 66.0] vs median 55.7 bursts/min [interquartile range 51.0 to 61.7]; p = 0.0089) and a decrease in spontaneous baroreflex control of sympathetic activity compared to matched control patients (spontaneous baroreflex control of sympathetic activity median 0.7%burst/mmHg [interquartile range 0.4 to 1.9] vs median 2.4%burst/mmHg [interquartile range 1.8 to 2.9]; p = 0.005). We report for the first time, through direct measurement of sympathetic nerve activity, that patients with TTC exhibit elevated SNS activity associated with a decrease in spontaneous baroreflex control of sympathetic activity. These data may explain the pathophysiology and clinical presentation of patient with TTC.
    PLoS ONE 01/2014; 9(3):e93278. · 3.53 Impact Factor
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    Elisabeth Lambert, Gavin W Lambert
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    ABSTRACT: Orthostatic intolerance is the inability to tolerate the upright posture and is relieved by recumbence. It most commonly affects young women and has a major impact on quality of life and psychosocial well-being. Several forms of orthostatic intolerance have been described. The most common one is the recurrent vasovagal syncope (VVS) phenotype which presents as a transient and abrupt loss of consciousness and postural tone that is followed by rapid recovery. Another common type of orthostatic intolerance is the postural orthostatic tachycardia syndrome (POTS) which is characterized by an excessive rise in heart rate upon standing and is associated with symptoms of presyncope such as light-headedness, fatigue, palpitations, and nausea. Maintenance of arterial pressure under condition of reduced central blood volume during the orthostasis is accomplished in large part through sympathetic efferent nerve traffic to the peripheral vasculature. Therefore sympathetic nervous system (SNS) dysfunction is high on the list of possible contributors to the pathophysiology of orthostatic intolerance. Investigations into the role of the SNS in orthostatic intolerance have yielded mixed results. This review outlines the current knowledge of the function of the SNS in both VVS and POTS.
    Frontiers in physiology. 01/2014; 5:280.
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    ABSTRACT: The Postural Orthostatic Tachycardia Syndrome (POTS) is a condition in which heart rate increases abnormally when the individual assumes an upright position. In addition to the marked tachycardia, presyncope, and syncope, patients with POTS often complain of light-headedness, fatigue, and difficulty in concentrating. The present study assessed individuals with POTS for psychiatric comorbidity, anxiety sensitivity and health related quality of life and examined general cognitive ability. Data was obtained from patients with POTS (n = 15, 12 female, aged 30 ± 3 years) and age matched healthy subjects (n = 30, 21 female, aged 32 ± 2 years). Patients with POTS commonly presented with symptoms of depression, elevated anxiety and increased anxiety sensitivity, particularly with regards to cardiac symptoms, and had a poorer health related quality of life in both the physical and mental health domains. While patients with POTS performed worse in tests of current intellectual functioning (verbal and non-verbal IQ) and in measures of focused attention (digits forward) and short term memory (digits back), test results were influenced largely by years of education and the underlying level of depression and anxiety. Acute changes in cognitive performance in response to head up tilt were evident in the POTS patients. From results obtained, it was concluded that participants with POTS have an increased prevalence of depression and higher levels of anxiety. These underlying symptoms impact on cognition in patients with POTS, particularly in the cognitive domains of attention and short-term memory. Our results indicate that psychological interventions may aid in recovery and facilitate uptake and adherence of other treatment modalities in patients with POTS.
    Frontiers in physiology. 01/2014; 5:230.
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    ABSTRACT: The underlying cause of predisposition to obesity is complex but one marker is cortisol responsiveness. Selection of sheep for high (HR) or low (LR) cortisol responses to adrenocorticotropin shows that HR are more likely to become obese. Increased propensity to obesity is associated with reduced skeletal muscle thermogenesis. We sought to determine whether metabolic or behavioral responses to stress also contribute to altered propensity to obesity in LR and HR. Animals (n = 5–10/group) were exposed to 3 stressors and we measured food intake and thermogenesis (recorded with dataloggers implanted into muscle). Stressors were hypoglycaemia (0.125 units/kg insulin, IV), a barking dog and immune challenge (200 ng/kg lipopolysaccharide – LPS, IV). LR animals showed a greater catabolic state in response to both immune and psychosocial stressors. LPS reduced (P < 0.01) food intake in both groups but LR showed a greater (P < 0.05) reduction in food intake and a more substantial (P < 0.05) rise in muscle temperature. Introduction of the barking dog reduced (P < 0.05) food intake in LR only. These metabolic differences coincided with differences in cortisol responsiveness, where HR animals had increased (P < 0.05) cortisol in response to both immune and psychosocial stressors. We also assessed behavior in the following paradigms: 1, isolation in the open field test; 2, response to a human intruder; and 3, food competition. LR had greater (P < 0.05) activity, reduced fearfulness and displayed a proactive coping style of behavior. Thus we demonstrate that high cortisol responsiveness identifies animals with stress-induced metabolic and behavioral traits that may contribute to susceptibility to obesity.
    Psychoneuroendocrinology 01/2014; 47:166–177. · 5.14 Impact Factor
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    ABSTRACT: It is known that low testosterone (T) and high cortisol levels are associated with hypertension as well as with chronic stress, linking stress with elevated blood pressure (BP). However, the association between acute stress-, chronic stress responses and BP is not clear in Africans. Therefore, we examined the association between cortisol, psychological distress and BP responses in low- and high-T male subgroups. Beat-to-beat and ambulatory blood pressure (ABPM) and electrocardiogram measures were obtained. Serum samples were collected and analyzed for sex hormones and cortisol. Chronic psychological distress was verified with the General Health Questionnaire and acute stress with the cold pressor test. More chronic psychological distress was observed in both low- and high-T Africans compared with the Caucasians. The low-T Africans tended to have more ischemic events (P=0.06) and ABPM values (P0.01) than any of the other groups. Both chronic distress (cortisol) and acute stress (total peripheral resistance cold pressor responses) were associated with ABPM in the low-T African group. Acute and chronic stress may contribute to increased BP in low-T African men. Their cortisol and vascular responses supported a tendency for ischemia, increasing their risk for coronary artery disease.Journal of Human Hypertension advance online publication, 28 November 2013; doi:10.1038/jhh.2013.124.
    Journal of human hypertension 11/2013; · 2.80 Impact Factor
  • Gavin W Lambert, Arup K Dhar, Markus P Schlaich
    EuroIntervention: journal of EuroPCR in collaboration with the Working Group on Interventional Cardiology of the European Society of Cardiology 10/2013; 9(6):665-7. · 3.17 Impact Factor
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    ABSTRACT: Objectives: This study was conducted to examine 1) the effects of dietary weight loss on indices of norepinephrine (NE) turnover and 2) whether baseline hyperinsulinemia modulates sympathetic neural adaptations. Design and Methods: Obese individuals aged 56 + 1 yr, BMI 32.5 + 0.4 kg/m(2) , with metabolic syndrome, underwent a 12-week hypocaloric diet (HCD, n=39) or no treatment (n=26). Neurochemical measurements comprised arterial dihydroxyphenylalanine (DOPA), 3,4-dihydroxyphenylglycol (DHPG) and NE concentrations, the steady-state ratio of [(3) H]-DHPG to [(3) H]-NE, as an index of neuronal uptake, and calculated whole-body plasma NE clearance and spillover rates. Results: Body weight decreased by -7.4 + 0.5% in HCD group (P<0.001) and was accompanied by reductions in DOPA, NE and DHPG averaging -14 + 5% (P=0.001), -23 + 4% (P<0.001) and -5 + 4% (P=0.03), respectively. NE spillover rate decreased by -88 + 39 ng/min (P=0.01), whereas neuronal uptake and NE plasma clearance were unchanged. Despite similar weight loss, hyperinsulinemic subjects exhibited greater reductions in NE and NE spillover rate, compared to normoinsulinemic subjects (group by time interaction P<0.05). Conclusions: Weight loss is associated with down regulation of sympathetic nervous activity but no overall alteration in disposition indices. Hyperinsulinemic subjects derive a greater sympathoinhibitory benefit during weight loss.
    Obesity 09/2013; · 3.92 Impact Factor
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    ABSTRACT: Objective This study investigated the impact of stress on effectors of the L-arginine/nitric oxide (NO) system including the endogenous inhibitor asymmetric dimethylarginine (ADMA).Methods Black (n = 168) and white (n = 206) South African teachers were exposed to a mental and a physical stressor for 1 minute, respectively. Serum samples for determination of L-arginine, NO metabolites, ADMA, and symmetric dimethylarginine (SDMA) were obtained at rest and during stress exposure. Perception of task stressfulness was assessed on a 7-point Likert scale, and psychological distress was estimated by the General Health Questionnaire.ResultsBlack South Africans exhibited higher resting levels of NO metabolites (adjusted mean [standard error of the mean] = 11.3 [1.3] versus 3.9 [1.1] μmol/l, p < .001) but lower circulating ADMA (0.62 [0.02] versus 0.70 [0.02] μmol/l, p = .004) and SDMA (0.41 [0.01] versus 0.53 [0.01] μmol/l, p < .001) than did white South Africans. Ethnicity-by-psychological distress interaction was observed for resting levels of ADMA (p = .002), SDMA (p = .038), and L-arginine (p = .048). Ethnic differences in responses to experimental stress were evident for NO metabolites (blacks versus whites: 5.94 [1.55] versus -0.74 [1.25] μmol/l, p = .004) and SDMA (blacks versus whites: -0.02 [0.01] versus 0.02 [0.01] μmol/l, p = .004). Ethnicity-by-psychological distress interaction for stress responses was found for L-arginine/ADMA ratio (p = .027).Conclusions The L-arginine/NO system is affected by psychosocial distress with higher susceptibility in black South Africans. This interaction may contribute to the higher cardiovascular disease risk in black South Africans.
    Psychosomatic Medicine 08/2013; · 4.08 Impact Factor
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    ABSTRACT: To examine the emotional well-being of severely obese Australians with type 2 diabetes, along with markers of social and economic disadvantage, using the Diabetes MILES - Australia dataset. Diabetes MILES - Australia was a national survey of 3338 adults with diabetes that focused on psychosocial issues; 1795 had type 2 diabetes and reported BMI. We extracted data regarding depression (PHQ-9), anxiety (GAD-7), obesity- and diabetes-related comorbidities, and demographics. The severely obese group (SOG) (BMI≥35; median BMI=41.6) constituted 530 (30%) of the type 2 diabetes respondents and was matched with 530 controls (CG) (BMI<35; median BMI=28.2). Within- and between-group trends were examined. The SOG had higher depression scores (median (IQR) 6.0 (3-12)) than CG (5.0 (2-10)); p<0.001, and were more likely to report moderate-severe depressive symptoms (37% versus 27%; p<0.001). The groups did not differ on anxiety. The SOG, compared with the CG, were more likely to live alone (21% versus 17%), receive a disability pension (21% versus 15%), earn ≤$40.000/year (51% versus 41%; all p<0.05), and were less likely to be employed (46% versus 53%), university or higher educated (17% versus 26%), or have health insurance (50% versus 60%; all p≤0.01). Moderate-severe depression was positively associated with cumulative stressors of severe obesity, socioeconomic disadvantage, and obesity- and diabetes-related comorbidity. Severely obese people living with type 2 diabetes have cumulative stressors related to health, disability, demographic and socioeconomic factors, and impaired emotional well-being.
    Diabetes research and clinical practice 06/2013; · 2.74 Impact Factor
  • Arup K Dhar, Gavin W Lambert
    Hypertension 05/2013; · 6.87 Impact Factor
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    ABSTRACT: OBJECTIVE:: Renal denervation (RDN) has been demonstrated to reduce muscle sympathetic nerve activity (MSNA) and blood pressure (BP) in patients with resistant hypertension. Whether alterations of arterial stiffness may contribute to BP-lowering effects of RDN is unknown. METHODS:: We measured office BP and arterial stiffness using fingertip tonometry-derived augmentation index (EndoPAT2000) at baseline and at 3-month follow-up in 50 consecutive patients with resistant hypertension. Forty patients received RDN and 10 patients served as controls. MSNA was obtained in 20 RDN and 10 non-RDN patients. RESULTS:: Baseline BP averaged 170/92 ± 19/15 mmHg (RDN) and 171/93 ± 14/8 mmHg (non-RDN) despite the use of 4.9 ± 1.9 and 4.4 ± 2.0 antihypertensive drugs, respectively. RDN significantly reduced SBP (170 ± 19 vs. 154 ± 25 mmHg; P < 0.001) and DBP (92 ± 15 vs. 84 ± 16 mmHg; P < 0.001), augmentation index (30.6 ± 23.8 vs. 22.7 ± 22.4%; P = 0.002), AI@75 corrected for heart rate (22.4 ± 21.6 vs. 14.4 ± 20.7; P = 0.002) and MSNA (80 ± 15 vs. 71 ± 18 bursts/100 heartbeats; P < 0.01). Changes in AI@75 with RDN were unrelated to SBP (r = 0.043; P = 0.79), and DBP (r = 0.092; P = 0.57) and MSNA changes (r = -0.17; P = 0.49). No changes in BP, augmentation index, AI@75 or MSNA were observed in the non-RDN group. CONCLUSION:: RDN results in a substantial and rapid reduction in augmentation index, which appears to be independent of BP and MSNA changes. These findings are indicative of a beneficial effect of RDN on arterial stiffness in patients with resistant hypertension and may contribute to the sustained BP-lowering effect of RDN.
    Journal of Hypertension 05/2013; · 4.22 Impact Factor
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    ABSTRACT: BACKGROUND: Oxytocin is known for its capacity to facilitate social bonding, reduce anxiety and for its actions on the stress hypothalamopituitary adrenal (HPA) axis. Since oxytocin can physiologically suppress activity of the HPA axis, clinical applications of this neuropeptide have been proposed in conditions where the function of the HPA axis is dysregulated. One such condition is major depressive disorder (MDD). Dysregulation of the HPA system is the most prominent endocrine change seen with MDD, and normalizing the HPA axis is one of the major targets of recent treatments. The potential clinical application of oxytocin in MDD requires improved understanding of its relationship to the symptoms and underlying pathophysiology of MDD. Previous research has investigated potential correlations between oxytocin and symptoms of MDD, including a link between oxytocin and treatment related symptom reduction. The outcomes of studies investigating whether antidepressive treatment (pharmacological and non-pharmacological) influences oxytocin concentrations in MDD, have produced conflicting outcomes. These outcomes suggest the need for an investigation of the influence of a single treatment class on oxytocin concentrations, to determine whether there is a relationship between oxytocin, the HPA axis (e.g., oxytocin and cortisol) and MDD. Our objective was to measure oxytocin and cortisol in patients with MDD before and following treatment with selective serotonin reuptake inhibitors, SSRI. METHOD: We sampled blood from arterial plasma. Patients with MDD were studied at the same time twice; pre- and post- 12 weeks treatment, in an unblinded sequential design (clinicaltrials.govNCT00168493). RESULTS: Results did not reveal differences in oxytocin or cortisol concentrations before relative to following SSRI treatment, and there were no significant relationships between oxytocin and cortisol, or these two physiological variables and psychological symptom scores, before or after treatment. CONCLUSIONS: These outcomes demonstrate that symptoms of MDD were reduced following effective treatment with an SSRI, and further, stress physiology was unlikely to be a key factor in this outcome. Further research is required to discriminate potential differences in underlying stress physiology for individuals with MDD who respond to antidepressant treatment, relative to those who experience treatment resistance.
    BMC Psychiatry 04/2013; 13(1):124. · 2.23 Impact Factor
  • Hypertension 04/2013; 61(4):e39. · 6.87 Impact Factor

Publication Stats

6k Citations
1,356.72 Total Impact Points

Institutions

  • 2002–2014
    • Baker IDI Heart and Diabetes Institute
      • Diabetic Complications Division
      Melbourne, Victoria, Australia
  • 2013
    • University of Gothenburg
      • Institute of Clinical Sciences
      Göteborg, Vaestra Goetaland, Sweden
  • 2012–2013
    • French Institute of Health and Medical Research
      • Institut des Maladies Métaboliques et Cardiovasculaires (I2MC) U1048
      Paris, Ile-de-France, France
  • 2006–2013
    • Monash University (Australia)
      • • Faculty of Medicine, Nursing and Health Sciences
      • • Department of Physiology
      • • Department of General Practice
      Melbourne, Victoria, Australia
  • 2011
    • Diabetes Australia, Victoria
      Melbourne, Victoria, Australia
    • Medical University of Gdansk
      • Department of Hypertension and Diabetes
      Gdańsk, Pomeranian Voivodeship, Poland
  • 2008–2011
    • University of Adelaide
      • • Discipline of Medicine
      • • School of Medicine
      • • Centre for Biomedical Engineering (CBME)
      Adelaide, South Australia, Australia
  • 2005–2008
    • Heart Research Institute
      Newtown, New South Wales, Australia
  • 2001–2008
    • Baker College, Australia
      Hornsby, New South Wales, Australia
  • 1988–2008
    • Alfred Hospital
      • Department of Nuclear Medicine
      Melbourne, Victoria, Australia
  • 1999–2006
    • Sahlgrenska University Hospital
      • Department of Cardiology
      Goeteborg, Västra Götaland, Sweden
  • 2004–2005
    • Friedrich-Alexander Universität Erlangen-Nürnberg
      Erlangen, Bavaria, Germany
  • 2003–2004
    • University of Melbourne
      • Department of Pharmacology
      Melbourne, Victoria, Australia
  • 1999–2001
    • French National Centre for Scientific Research
      Lutetia Parisorum, Île-de-France, France
  • 2000
    • Umeå University
      Umeå, Västerbotten, Sweden
  • 1994–1997
    • Deakin University
      • Department of Biological Sciences
      Geelong, Victoria, Australia
  • 1994–1996
    • National Institutes of Health
      • Branch of Behavioral Neuroscience
      Bethesda, MD, United States