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- Barbato, E, et al.
(författare)
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Renal denervation in the management of hypertension in adults. A clinical consensus statement of the ESC Council on Hypertension and the European Association of Percutaneous Cardiovascular Interventions (EAPCI)
- 2023
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 44:15, s. 1313-1330
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Tidskriftsartikel (refereegranskat)abstract
- Since the publication of the 2018 European Society of Cardiology/European Society of Hypertension (ESC/ESH) Guidelines for the Management of Arterial Hypertension, several high-quality studies, including randomised, sham-controlled trials on catheter-based renal denervation (RDN) were published, confirming both the blood pressure (BP)-lowering efficacy and safety of radiofrequency and ultrasound RDN in a broad range of patients with hypertension, including resistant hypertension. A clinical consensus document by the ESC Council on Hypertension and the European Association of Percutaneous Cardiovascular Interventions (EAPCI) on RDN in the management of hypertension was considered necessary to inform clinical practice. This expert group proposes that RDN is an adjunct treatment option in uncontrolled resistant hypertension, confirmed by ambulatory BP measurements, despite best efforts at lifestyle and pharmacological interventions. RDN may also be used in patients who are unable to tolerate antihypertensive medications in the long term. A shared decision-making process is a key feature and preferably includes a patient who is well informed on the benefits and limitations of the procedure. The decision-making process should take (i) the patient’s global cardiovascular (CV) risk and/or (ii) the presence of hypertension-mediated organ damage or CV complications into account. Multidisciplinary hypertension teams involving hypertension experts and interventionalists evaluate the indication and facilitate the RDN procedure. Interventionalists require expertise in renal interventions and specific training in RDN procedures. Centres performing these procedures require the skills and resources to deal with potential complications. Future research is needed to address open questions and investigate the impact of BP-lowering with RDN on clinical outcomes and potential clinical indications beyond hypertension.
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- Costantino, S, et al.
(författare)
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Impact of Glycemic Variability on Chromatin Remodeling, Oxidative Stress, and Endothelial Dysfunction in Patients With Type 2 Diabetes and With Target HbA1c Levels
- 2017
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Ingår i: Diabetes. - : American Diabetes Association. - 1939-327X .- 0012-1797. ; 66:9, s. 2472-2482
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Tidskriftsartikel (refereegranskat)abstract
- Intensive glycemic control (IGC) targeting HbA1c fails to show an unequivocal reduction of macrovascular complications in type 2 diabetes (T2D); however, the underlying mechanisms remain elusive. Epigenetic changes are emerging as important mediators of cardiovascular damage and may play a role in this setting. This study investigated whether epigenetic regulation of the adaptor protein p66Shc, a key driver of mitochondrial oxidative stress, contributes to persistent vascular dysfunction in patients with T2D despite IGC. Thirty-nine patients with uncontrolled T2D (HbA1c >7.5%) and 24 age- and sex-matched healthy control subjects were consecutively enrolled. IGC was implemented for 6 months in patients with T2D to achieve a target HbA1c of ≤7.0%. Brachial artery flow-mediated dilation (FMD), urinary 8-isoprostaglandin F2α (8-isoPGF2α), and epigenetic regulation of p66Shc were assessed at baseline and follow-up. Continuous glucose monitoring was performed to determine the mean amplitude of glycemic excursion (MAGE) and postprandial incremental area under the curve (AUCpp). At baseline, patients with T2D showed impaired FMD, increased urinary 8-isoPGF2α, and p66Shc upregulation in circulating monocytes compared with control subjects. FMD, 8-isoPGF2α, and p66Shc expression were not affected by IGC. DNA hypomethylation and histone 3 acetylation were found on the p66Shc promoter of patients with T2D, and IGC did not change such adverse epigenetic remodeling. Persistent downregulation of methyltransferase DNMT3b and deacetylase SIRT1 may explain the observed p66Shc-related epigenetic changes. MAGE and AUCpp but not HbA1c were independently associated with the altered epigenetic profile on the p66Shc promoter. Hence, glucose fluctuations contribute to chromatin remodeling and may explain persistent vascular dysfunction in patients with T2D with target HbA1c levels.
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- Ghadri, JR, et al.
(författare)
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Pheochromocytoma triggers takotsubo syndrome
- 2019
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Ingår i: European heart journal. - : Oxford University Press (OUP). - 1522-9645 .- 0195-668X. ; 40:24, s. 1990-1990
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Tidskriftsartikel (refereegranskat)
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| 20. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. Cardiovascular interventions. - 1941-7632. ; 12:2, s. e007796-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 21. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Hypertension (Dallas, Tex. : 1979). - 1524-4563. ; 73:3, s. 506-507
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 22. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. Heart failure. - 1941-3297. ; 12:2, s. e005869-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 23. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. Cardiovascular imaging. - 1942-0080. ; 12:2, s. e008809-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 24. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. Genomic and precision medicine. - 2574-8300. ; 12:2, s. e002439-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 25. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. - 1524-4539. ; 139:5, s. 571-572
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 26. |
- Hill, JA, et al.
(författare)
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Medical Misinformation
- 2019
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Ingår i: Circulation. Cardiovascular quality and outcomes. - 1941-7705. ; 12:2, s. e005496-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 27. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing. - : Springer Science and Business Media LLC. - 1572-8595. ; 55:1, s. 1-3
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 28. |
- Hill, JA, et al.
(författare)
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Medical misinformation: Vet the message!
- 2019
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Ingår i: Journal of electrocardiology. - : Elsevier BV. - 1532-8430 .- 0022-0736. ; 53, s. 112-113
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 29. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: Cardiovascular research. - : Oxford University Press (OUP). - 1755-3245 .- 0008-6363.
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Tidskriftsartikel (refereegranskat)
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| 30. |
- Hill, JA, et al.
(författare)
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Medical Misinformation: Vet the Message!
- 2019
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Ingår i: Cardiovascular drugs and therapy. - : Springer Science and Business Media LLC. - 1573-7241 .- 0920-3206. ; 33:3, s. 275-276
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 31. |
- Hill, JA, et al.
(författare)
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Medical Misinformation: Vet the Message!
- 2019
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Ingår i: International journal of cardiology. - : Elsevier BV. - 1874-1754 .- 0167-5273. ; 277, s. 1-2
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 32. |
- Hill, JA, et al.
(författare)
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Medical Misinformation: Vet the Message!
- 2019
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Ingår i: Journal of the American Heart Association. - 2047-9980. ; 8:3, s. e011838-
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 33. |
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| 34. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: European heart journal. Quality of care & clinical outcomes. - : Oxford University Press (OUP). - 2058-1742 .- 2058-5225. ; 5:2, s. 83-84
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 35. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: European heart journal. Cardiovascular pharmacotherapy. - : Oxford University Press (OUP). - 2055-6845 .- 2055-6837. ; 5:2, s. 62-63
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 36. |
- Hill, JA, et al.
(författare)
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Medical misinformation: Vet the message!
- 2019
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Ingår i: Heart rhythm. - : Elsevier BV. - 1556-3871 .- 1547-5271. ; 16:3, s. 332-333
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 37. |
- Hill, JA, et al.
(författare)
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Medical Misinformation: Vet the Message!
- 2019
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Ingår i: Journal of cardiovascular pharmacology. - 1533-4023. ; 73:2, s. 61-62
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 38. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: European journal of heart failure. - : Wiley. - 1879-0844 .- 1388-9842. ; 21:3, s. 264-265
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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| 39. |
- Hill, JA, et al.
(författare)
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Medical misinformation: vet the message!
- 2019
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Ingår i: Cardiovascular research. - : Oxford University Press (OUP). - 1755-3245 .- 0008-6363. ; 115:14, s. E187-E188
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Tidskriftsartikel (refereegranskat)
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| 43. |
- Lohmann, C, et al.
(författare)
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Atherosclerotic mice exhibit systemic inflammation in periadventitial and visceral adipose tissue, liver, and pancreatic islets.
- 2009
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Ingår i: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 207:2, s. 360-367
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVE: Atherosclerosis is a chronic inflammatory disease of major conduit arteries. Similarly, obesity and type 2 diabetes mellitus are associated with accumulation of macrophages in visceral white adipose tissue and pancreatic islets. Our goal was to characterize systemic inflammation in atherosclerosis with hypercholesterolemia, but without obesity. METHODS AND RESULTS: We compared 22-week-old apolipoprotein E knockout (ApoE(-/-)) with wild-type mice kept for 14 weeks on a high cholesterol (1.25%) diet (CD, n=8) and 8-week-old ApoE(-/-) with wild-type mice kept on a normal diet (ND, n=8). Hypercholesterolemic, atherosclerotic ApoE(-/-) mice on CD exhibited increased macrophages and T-cells in plaques and periadventitial adipose tissue that revealed elevated expression of MIP-1alpha, IL-1beta, IL-1 receptor, and IL-6. Mesenteric adipose tissue and pancreatic islets in ApoE(-/-) mice showed increased macrophages. Expression of IL-1beta was enhanced in mesenteric adipose tissue of ApoE(-/-) mice on CD. Furthermore, these mice exhibited steatohepatitis with macrophage and T-cell infiltrations as well as increased MIP-1alpha and IL-1 receptor expression. Blood glucose, insulin and total body weight did not differ between the groups. CONCLUSIONS: In hypercholesterolemic lean ApoE(-/-) mice, inflammation extends beyond atherosclerotic plaques to the periadventitial and visceral adipose tissue, liver, and pancreatic islets without affecting glucose homeostasis.
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| 44. |
- Merlini, M, et al.
(författare)
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Reduced nitric oxide bioavailability mediates cerebroarterial dysfunction independent of cerebral amyloid angiopathy in a mouse model of Alzheimer's disease
- 2017
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Ingår i: American journal of physiology. Heart and circulatory physiology. - : American Physiological Society. - 1522-1539 .- 0363-6135. ; 312:2, s. H232-H238
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Tidskriftsartikel (refereegranskat)abstract
- In Alzheimer’s disease (AD), cerebral arteries, in contrast to cerebral microvessels, show both cerebral amyloid angiopathy (CAA) -dependent and -independent vessel wall pathology. However, it remains unclear whether CAA-independent vessel wall pathology affects arterial function, thereby chronically reducing cerebral perfusion, and, if so, which mechanisms mediate this effect. To this end, we assessed the ex vivo vascular function of the basilar artery and a similar-sized peripheral artery (femoral artery) in the Swedish-Arctic (SweArc) transgenic AD mouse model at different disease stages. Furthermore, we used quantitative immunohistochemistry to analyze CAA, endothelial morphology, and molecular pathways pertinent to vascular relaxation. We found that endothelium-dependent, but not smooth muscle-dependent, vasorelaxation was significantly impaired in basilar and femoral arteries of 15-mo-old SweArc mice compared with that of age-matched wild-type and 6-mo-old SweArc mice. This impairment was accompanied by significantly reduced levels of cyclic GMP, indicating a reduced nitric oxide (NO) bioavailability. However, no age- and genotype-related differences in oxidative stress as measured by lipid peroxidation were observed. Although parenchymal capillaries, arterioles, and arteries showed abundant CAA in the 15-mo-old SweArc mice, no CAA or changes in endothelial morphology were detected histologically in the basilar and femoral artery. Thus our results suggest that, in this AD mouse model, dysfunction of large intracranial, extracerebral arteries important for brain perfusion is mediated by reduced NO bioavailability rather than by CAA. This finding supports the growing body of evidence highlighting the therapeutic importance of targeting the cerebrovasculature in AD. NEW & NOTEWORTHY We show that vasorelaxation of the basilar artery, a large intracranial, extracerebral artery important for cerebral perfusion, is impaired independent of cerebral amyloid angiopathy in a transgenic mouse model of Alzheimer’s disease. Interestingly, this dysfunction is specifically endothelium related and is mediated by impaired nitric oxide–cyclic GMP bioavailability. Listen to this article’s corresponding podcast at http://ajpheart.podbean.com/e/cerebroarterial-dysfunction-in-swedish-arctic-ad-mice/ .
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