The Impact of Beta-Blocker Maintenance on Decompensated Heart Failure: A Systematic Review and Meta-Analysis.

BACKGROUND: Acute Heart Failure (HF) is related to a significant hospital mortality rate and functional impairment in many patients. However, there is still a lack of studies that support the use of Beta-blockers (BB) in the management of decompensated HF. OBJECTIVE: This study aimed to evaluate the impact on mortality of maintaining BB in patients with decompensated HF. METHODS: A systematic review and meta-analysis was performed, using the databases PubMed, Cochrane Library, SCIELO and BVS, selecting only cohort studies and Randomized Clinical Trials (RCTs) from the last 10 years, which have been selected based on inclusion and exclusion criteria. RESULTS: An 86% reduction in the risk of in-hospital death was found (RR=0.14, 95% CI: 0.10- 0.18) in patients with HF who maintained the use of BB during hospitalization. A second analysis found a 44% (RR=0.56, 95% CI: 0.47-0.66) lower chance of in-hospital death in the group that previously used BB. Regarding the analysis of mortality after hospital discharge, only studies that have evaluated the use of BB in HF with reduced ejection fraction pointed to a reduction in mortality. Furthermore, some articles have found a relationship between the reduction in readmissions and the use of post-discharge BB. CONCLUSION: There is still no consensus regarding the use of BB in patients hospitalized with decompensated HF. In view of the limitations of the data found in the present study, the need for more RCTs that address this topic is emphasized in order to resolve this uncertainty in the management of cardiovascular patients.

Beta-adrenergic blocker inhibits oral carcinogenesis and reduces tumor invasion.

PURPOSE: Beta-adrenergic signaling can influence cancer progression and the use of beta blockers as adjuvant drugs in oncologic patients has been suggested. However, the involvement of beta-adrenergic blockers in tumorigenesis is poorly understood. This study investigated the action of beta-adrenergic blocker propranolol on tumor onset using a preclinical model of chemically induced oral cancer. METHODS: Thirty-two male Wistar rats were subjected to daily subcutaneous injection of beta-blocker propranolol (10 mg/kg; SubQ), while another 32 rats received only a PBS injection (sham group). One week after starting propranolol treatment, all rats were submitted to chemical induction of oral carcinogenesis with 4-nitroquinoline-1-oxide (4NQO). After 16 weeks, they were assessed for occurrence of oral squamous cell carcinoma (OSCC), in addition to measurement of tumor volume and thickness, and tissue levels of cytokines IL-6, TNF-alpha and IL-10 in the tumor microenvironment. RESULTS: Propranolol treatment reduced the occurrence of OSCC by 31%, 95% CI ( - 127, 216). Beta-adrenergic blocker significantly decreased thickness of OSCC when compared with PBS. Rats treated with propranolol exhibited a lower tumor volume when compared with control rats, but this result did not reach statistical significance. Tumors from propranolol-treated rats exhibited reduced concentrations of pro-inflammatory cytokines IL-6 and TNF-α. There was no difference in the IL-10 levels between tumors from propranolol- and sham-treated rats. CONCLUSION: Beta-adrenergic signaling may be one of the mechanisms associated with chemically induced oral carcinogenesis.

Carvedilol as primary prophylaxis for gastric variceal bleeding in portal hypertension model in rats / Carvedilol como profilaxia de sangramento em varizes gástricas em modelo de hipertensão portal em ratos

ABSTRACT Background: Portal hypertension (PH) can be measured indirectly through a hepatic vein pressure gradient greater than 5 mmHg. Cirrhosis is the leading cause for PH and can present as complications ascites, hepatic dysfunction, renal dysfunction, and esophagogastric varices, characterizing gastropathy. Aim: To evaluate the use of carvedilol as primary prophylaxis in the development of collateral circulation in rats submitted to the partial portal vein ligament (PPVL) model. Method: This is a combined qualitative and quantitative experimental study in which 32 Wistar rats were divided into four groups (8 animals in each): group I - cirrhosis + carvedilol (PPVL + C); group II - cirrhosis + vehicle (PPVL); group III - control + carvedilol (SO-sham-operated + C); group IV - control + vehicle (SO-sham-operated). After seven days of the surgical procedure (PPVL or sham), carvedilol (10 mg/kg) or vehicle (1 mL normal saline) were administered to the respective groups daily for seven days. Results: The histological analysis showed no hepatic alteration in any group and a decrease in edema and vasodilatation in the PPVL + C group. The laboratory evaluation of liver function did not show a statistically significant change between the groups. Conclusion: Carvedilol was shown to have a positive effect on gastric varices without significant adverse effects.

RESUMO Racional: A hipertensão portal (HP), medida indiretamente através do gradiente pressórico da veia hepática >5 mmHg, tem como principal causa etiológica a cirrose. Possui como complicações a ascite, disfunção hepática, disfunção renal e varizes esofagogástricas, que caracterizam o quadro de gastropatia. Objetivo: Avaliar o uso do carvedilol como profilaxia primária no desenvolvimento da circulação colateral em ratos submetidos ao modelo de ligadura parcial de veia porta (LPVP). Método: Estudo experimental qualitativo e quantitativo no qual foram utilizados 32 ratos Wistar, divididos em quatro grupos (n=8): grupo I - cirrose + carvedilol (LPVP+C); grupo II - cirrose + veículo (LPVP); grupo III - controle + carvedilol (SO - sham-operated+C); grupo IV - controle + veículo (SO - sham-operated). Após transcorridos sete dias do procedimento cirúrgico, foi administrado carvedilol (10 mg/kg) e veículo (1mL) para os respectivos grupos por sete dias consecutivos. Resultados: A análise histológica não mostrou alteração hepática em nenhum grupo e diminuição de edema e vasodilatação no grupo LPVP+C. A avaliação laboratorial da função hepática não mostrou alteração com significância estatística entre os grupos. Conclusão: Carvedilol mostrou ser fármaco com efeito positivo no sangramento das varizes gástricas e sem efeitos adversos significantes.

Atenolol prevents the formation of expansive hematoma after rhytidoplasty / O atenolol previne a formação de hematoma expansivo após ritidoplastia

Objective: To evaluate the perioperative use of atenolol in reducing the incidence of hematoma after rhytidoplasty. Methods: Between January 2007 and February 2013, 80 patients were randomized into two groups: Group A (n = 26) received perioperative atenolol in order to maintain heart rate (PR) around 60 per minute; Group B (n = 54) did not receive atenolol. Both groups underwent the same anesthetic and surgical technique. We monitored blood pressure (BP), HR, hematoma formation and the need for drainage. Patients were followed-up until the 90th postoperative day. The variables were compared between the groups using the ANOVA test. Continuous variables were presented as mean ± standard deviation and the differences were compared with the Student's t test. Values of p d" 0.05 were considered significant. Results: In group A the mean BP (110-70mmHg ± 7.07) and HR (64 / min ± 5) were lower (p d" 0.05) than in group B (135-90mmHg ± 10.6) and (76 / min ± 7.5), respectively. There were four cases of expansive hematoma in group B, all requiring reoperation for drainage, and none in group A (p d" 0,001). Conclusion: The perioperative use of atenolol caused a decrease in blood pressure and heart rate and decreased the incidence of expanding hematoma after rhytidectomy. .

Objetivo: avaliar o uso perioperatório do atenolol na redução da incidência de hematoma pós-ritidoplastia. Métodos: entre janeiro de 2007 e fevereiro de 2013 foram randomizados 80 pacientes em dois grupos: Grupo A (n=26) recebeu atenolol perioperatório com objetivo de manter frequência de pulso (FP) ± 60 por minuto, Grupo B (n=54) não recebeu atenolol. Ambos os grupos foram submetidos à mesma técnica anestésico-cirúrgica. A pressão arterial (PA) e FP, formação de hematoma e a necessidade de drenagem foram monitorizados. Houve seguimento até o 90º dia de pós-operatório. As variáveis foram analisadas entre os dois grupos utilizando-se o teste de ANOVA. As variáveis contínuas foram apresentadas como média (± Desvio-padrão) e as diferenças foram comparadas utilizando-se o t de Student. Foram considerados significantes os valores p<0,05. Resultados: as médias no grupo A de PA (110-70mmHg ± 7,07) e FP (64 /min ± 5) foram menores (p<0,05) em relação ao grupo B (135-90mmHg ± 10,6) e (76/min ± 7,5), respectivamente. Houve quatro casos de hematoma expansivo no grupo B, todos com necessidade de reoperação para a sua drenagem e nenhum no grupo A (p<0,001). Conclusão: o uso do atenolol perioperatório promoveu a redução de pressão arterial e frequência de pulso e diminuiu a incidência de hematoma expansivo pós-ritidoplastia. .