https://nova.newcastle.edu.au/vital/access/ /manager/Index ${session.getAttribute("locale")} 5 https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51281 Wed 30 Aug 2023 09:59:56 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52384 Wed 28 Feb 2024 15:35:45 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53520 28.4 ng/mL) was independently associated with older age, use of beta-blockers, and number of MACE events within a 1 year period. In this patient cohort, elevated sST2 levels are associated with unplanned hospital admission due to MACE within 1 year, independent of the nature of the index cardiovascular admission.]]> Wed 28 Feb 2024 15:31:59 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52044 Wed 27 Sep 2023 10:07:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45109 n = 230 patients (mean age 65, males n = 124 (53.9%)) were treated with bevacizumab during the study period. N = 28 patients were admitted to hospital for a major cardiovascular-related event. Higher total treatment dose (p < 0.05), concomitant hypertension (p = 0.005), diabetes (p = 0.04), atrial fibrillation (p = 0.03), and lack of use of statin therapy (p = 0.03) were key contributors to hospital admission. Conclusions: Results of our study highlight the fact that patients with concomitant baseline cardiovascular disease/risk factors are at an increased risk of cardiovascular hospitalization related to bevacizumab treatment. Careful baseline cardiovascular assessment may be an essential step to minimize cardiovascular complications.]]> Wed 26 Oct 2022 13:22:56 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:45068 Wed 26 Oct 2022 12:31:21 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52741 Wed 25 Oct 2023 08:41:19 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33017 ~ATP), c) the rate of ATP production and d) flux through the creatine kinase (CK) reaction. At the lowest workload, the diastolic pressure-volume relationship was shifted upward in HFHS hearts, indicative of diastolic dysfunction, whereas systolic function was preserved. At this workload, the rate of ATP synthesis was decreased in HFHS hearts, and was associated with decreases in both [PCr] and ΔG_~ATP. Higher work demands unmasked the inability of HFHS hearts to increase systolic function and led to a further decrease in ΔG_~ATP to a level that is not sufficient to maintain normal function of sarcoplasmic Ca²⁺-ATPase (SERCA). While [ATP] was preserved at all work demands in HFHS hearts, the progressive increase in [ADP] led to a decrease in ΔG_~ATP with increased work demands. Surprisingly, CK flux, CK activity and total creatine were normal in HFHS hearts. These findings differ from dilated cardiomyopathy, in which the energetic deficiency is associated with decreases in CK flux, CK activity and total creatine. Thus, in HFHS-fed mice with MHD there is a distinct metabolic phenotype of the heart characterized by a decrease in ATP production that leads to a functionally-important energetic deficiency and an elevation of [ADP], with preservation of CK flux.]]> Wed 24 Nov 2021 15:52:41 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55729 Wed 19 Jun 2024 09:47:51 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55721 Wed 19 Jun 2024 09:33:01 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:33411 Wed 19 Jan 2022 15:18:12 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48902 Wed 19 Apr 2023 16:30:23 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53423 Wed 17 Apr 2024 14:39:15 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51034 Wed 16 Aug 2023 10:16:36 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54028 Wed 13 Mar 2024 07:47:53 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55657 80% of participants as essential. Of those, for 22 items, <80% reported the care as received. Gaps were identified in relation to GP consultation (1 item), preparation (1 item) subsequent decision making for treatment (1 item), prognosis (6 items) and post-treatment follow-up (1 item). Conclusions: Areas were identified where actual care fell short of patients' perceptions of essential care.]]> Wed 12 Jun 2024 10:07:58 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52438 Wed 11 Oct 2023 14:53:58 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:49072 Wed 03 May 2023 16:08:08 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48120 Wed 01 Mar 2023 15:36:11 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42651 Wed 01 Mar 2023 15:00:54 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52575 Tue 17 Oct 2023 15:48:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:41950 20 mm Hg and pulmonary capillary wedge pressure >15 mm Hg during right heart catheterization. LHD may lead to elevated left atrial pressure alone, which in the absence of intrinsic pulmonary vascular disease will result in PH without changes in pulmonary vascular resistance. Persistent elevation in left atrial pressure may, however, also be associated with subsequent pulmonary vascular remodeling, vasoconstriction, and an increase in pulmonary vascular resistance. Hence, there are 2 subgroups of PH due to LHD, isolated postcapillary PH and combined post- and precapillary PH, with these groups have differing clinical implications. Differentiation of pulmonary arterial hypertension and PH due to LHD is critical to guide management planning; however, this may be challenging. Older patients, patients with metabolic syndrome, and patients with imaging and clinical features consistent with left ventricular dysfunction are suggestive of LHD etiology rather than pulmonary arterial hypertension. Hemodynamic measures such as diastolic pressure gradient, transpulmonary gradient, and pulmonary vascular resistance may assist to differentiate pre- from postcapillary PH and offer prognostic insights. However, these are influenced by fluid status and heart failure treatment. Pulmonary arterial hypertension therapies have been trialed in the treatment with concerning results reflecting disease heterogeneity, variation in inclusion criteria, and mixed end point criteria. The aim of this review is to provide an updated definition, discuss possible pathophysiology, clinical aspects, and the available treatment options for PH due to LHD.]]> Tue 16 Aug 2022 14:31:43 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48338 per se, is sufficient to cause contractile dysfunction in MHD.]]> Tue 14 Mar 2023 17:22:37 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44253 Tue 11 Oct 2022 12:28:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55631 Tue 11 Jun 2024 18:36:59 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:46897 Tue 06 Dec 2022 13:41:57 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:55437 Thu 30 May 2024 14:32:42 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:43342 Thu 15 Sep 2022 15:18:47 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:51481 Thu 07 Sep 2023 10:51:46 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:53262 Mon 20 Nov 2023 12:14:02 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:44599 Mon 17 Oct 2022 16:08:38 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:50968 Mon 14 Aug 2023 15:20:39 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:47964 70 mm Hg associated with worse outcomes]), right atrial volume index (pinteraction=0·012 [≥29·7 mL/m2, worse outcomes]), and sex (pinteraction=0·02 [men, worse outcomes]). There were no differences in the composite safety endpoint between the two groups (n=116 [38%] for shunt device vs n=97 [31%] for sham procedure; p=0·11). Interpretation: Placement of an atrial shunt device did not reduce the total rate of heart failure events or improve health status in the overall population of patients with heart failure and ejection fraction of greater than or equal to 40%. Funding: Corvia Medical.]]> Mon 13 Feb 2023 15:45:01 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:52280 Mon 09 Oct 2023 10:02:50 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:54596 Mon 04 Mar 2024 08:42:35 AEDT ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:42207 2) during planned bariatric surgery. Compared with subcutaneous adipose tissue, visceral adipose tissue exhibited decreased complex II activity, which was restored with the reducing agent dithiothreitol (5 mM) (P < 0.01). A biotin switch assay identified that cysteine oxidative posttranslational modifications (OPTM) in complex II subunit A (succinate dehydrogenase A) were increased in visceral vs. subcutaneous fat (P < 0.05). Insulin treatment (100 nM) stimulated complex II activity in subcutaneous fat (P < 0.05). In contrast, insulin treatment of visceral fat led to a decrease in complex II activity (P < 0.01), which was restored with addition of the mitochondria-specific oxidant scavenger mito-TEMPO (10 µM). In a cohort of 10 subjects with severe obesity, surgical weight loss decreased OPTM and restored complex II activity, exclusively in the visceral depot. Mitochondrial complex II may be an unrecognized and novel mediator of insulin resistance associated with visceral adiposity. The activity of complex II is improved by weight loss, which may contribute to metabolic improvements associated with bariatric surgery.]]> Fri 26 Aug 2022 09:16:37 AEST ]]> https://nova.newcastle.edu.au/vital/access/ /manager/Repository/uon:48913 Fri 14 Apr 2023 18:21:40 AEST ]]>