ABSTRACT
Abstract Objective: Transcatheter aortic valve replacement has been an alternative to invasive treatment for symptomatic severe aortic stenosis in high risk patients. The primary endpoint was 30-day and 1-year mortality from any cause. Secondary endpoints were to compare the clinical and echocardiographic variation pre-and post- transcatheter aortic valve replacement, and the occurrence of complications throughout a 4-year follow-up period. Methods: This prospective cohort, nestled to a multicenter study (Registro Brasileiro de Implante de Bioprótese por Cateter), describes the experience of a public tertiary center in transcatheter aortic valve replacement. All patients who underwent this procedure between October 2011 and February 2016 were included. Results: Fifty-eight patients underwent transcatheter aortic valve replacement. The 30-day all-cause mortality was 5.2% (n=3) and after 1 year was 17.2% (n=10). A significant improvement in New York Heart Association functional classification was observed when comparing pre-and post- transcatheter aortic valve replacement (III or IV 84.4% versus 5.8%; P<0.001). A decline in peak was observed (P<0.001) and mean (P<0.001) systolic transaortic gradient. The results of peak and mean post-implant transaortic gradient were sustained after one year (P=0.29 and P=0.36, respectively). Left ventricular ejection fraction did not change significantly during follow-up (P=0.41). The most frequent complications were bleeding (28.9%), the need for permanent pacemaker (27.6%) and acute renal injury (20.6%). Conclusion: Mortality and complications in this study were consistent with worldwide experience. Transcatheter aortic valve replacement had positive clinical and hemodynamic results, when comparing pre-and post-procedure, and the hemodynamic profile of the prosthesis was sustained throughout follow-up.
Subject(s)
Humans , Male , Female , Aged , Aged, 80 and over , Aortic Valve Stenosis/surgery , Transcatheter Aortic Valve Replacement/methods , Severity of Illness Index , Brazil , Heart Valve Prosthesis/adverse effects , Echocardiography , Prospective Studies , Risk Factors , Treatment Outcome , Transcatheter Aortic Valve Replacement/adverse effectsABSTRACT
A angiotensina (Ang) II e aldosterona induzem hipertensão arterial por mecanismos em parte mediados pela imunidade adaptativa, envolvendo linfócitos T auxiliares respondedores (Tresp). Os linfócitos T reguladores (Treg) são capazes de suprimir os efeitos pró-inflamatórios do sistema imune. O presente estudo avaliou se a transferência adotiva de Treg é capaz de prevenir a hipertensão e a lesão vascular induzidas pela AngII ou pela aldosterona, em dois protocolos distintos. No protocolo com Ang II, camundongos machos C57BL/6 sofreram a injeção endovenosa de Treg ou Tresp, sendo depois infundidos com Ang II (1ug/kg/min), ou salina (grupo controle) por 14 dias. No protocolo com aldosterona, um outro conjunto de animais sofreu injeções de Treg ou Tresp, sendo depois infundido com aldosterona (600ug/kg/d) ou salina (grupo controle), pelo mesmo intervalo de tempo. O grupo tratado com aldosterona recebeu salina 1% na água. Tanto o grupo Ang II como aldosterona apresentaram elevação da pressão arterial sistólica (43% e 31% respectivamente), da atividade da NADPH oxidase na aorta (1,5 e 1,9 vezes, respectivamente) e no coração (1,8 e 2,4 vezes, respectivamente) e uma redução da resposta vasodilatadora à acetilcolina (de 70% e 56%, respectivamente), quando comparados com os respectivos controles (P<0,05). Adicionalmente, a administração de Ang II proporcionou um aumento rigidez vascular (P<0,001), na expressão de VCAM-1 nas artérias mesentéricas (P<0,05), na infiltração aórtica de macrófagos e linfócitos T (P<0,001) e nos níveis plasmáticos das citocinas inflamatórias interferon (INF)-y, interleucina (IL)-6, Tumor necrosis factor (TNF)-a e IL-10 (P<0,05). Ang II causou uma queda de 43% no número de células Foxp3+ no córtex renal, enquanto que a transferência adotiva de Treg aumentou as células Foxp3+ em duas vezes em comparação com o controle. A administração de Treg preveniu o remodelamento vascular induzido pela aldosterona, observado na relação média/lúmen...
Angiotensin (Ang) II and aldosterone (aldo) induce hypertension through mechanisms in part mediated by adaptive immunity and T responder lymphocytes. T regulatory (Treg) lymphocytes suppress pro-inflammatory mediators of the immune system. We questioned whether Treg adoptive transfer will blunt Ang II or aldo-induced hypertension and vascular injury, by evaluating two distinct protocols. In the Ang II protocol, male C57BL/6 mice were injected i.v. with Treg or T responder cells, and then infused with Ang II (1ug/kg/min) or saline, for 14 days. In the aldosterone protocol, another set of animals was injected with Treg or T responder cells, and then infused with aldosterone (600ug/kg/d) or saline, for the same period. The aldosterone group received saline 1% in drinking water. Both Ang II and aldosterone treated mice presented an increase in systolic blood pressure (43% and 31% respectively), of NADPH oxidase activity in aorta (1.5 and 1.9 fold, respectively) and heart (1.8 and 2.4 fold respectively) and an impaired vasodilatory response do acetylcholine (by 70% and 56% respectively), when compared to their controls (P<0.05). In addition, Ang II administration resulted in increased vascular stiffness (P<0.001), mesenteric artery vascular cell adhesion molecule (VCAM-1) expression (P<0.05), aortic macrophage and T cell infiltration (P<0.001), and the plasma levels of the inflammatory cytokines INF-y, IL-6, TNF-a, and IL-10 (P<0,05). And II caused a 43% decrease in the number of Foxp3+ cells in the renal cortex, while Treg adoptive transfer increased Foxp3+ cells 2-fold compared to control. Treg administration prevented aldosterone-induced vascular remodelling, as observed by media to lumen ratio and media cross sectional area analysis of mesenteric arteries (P<0,05). All the above were prevented by Treg but not by T responder cell adoptive transfer. These results demonstrate that Treg suppress Ang II of aldo-mediated vascular injury and BP elevation...