Incidence and Clinical Predictors of Pulmonary Embolism in Severe Heart Failure Patients Admitted to a Coronary Care Unit

CHEST Journal ◽  
2005 ◽  
Vol 128 (4) ◽  
pp. 2576-2580 ◽  
Author(s):  
Eduardo S. Darze ◽  
Adriana L. Latado ◽  
Aloyra G. Guimarães ◽  
Rodrigo A.V. Guedes ◽  
Alessandra B. Santos ◽  
...  
2017 ◽  
Vol 8 (17) ◽  
pp. 115-120 ◽  
Author(s):  
Sevda Türen ◽  
Filiz Çetinkaya Işık ◽  
Necibe Uzun Morgül ◽  
Rahime Atakoğlu

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
Y Hsiao ◽  
I Shimizu ◽  
T Wakasugi ◽  
S Jiao ◽  
T Watanabe ◽  
...  

Abstract Background/Introduction Mitochondria are dynamic regulators of cellular metabolism and homeostasis. The dysfunction of mitochondria has long been considered a major contributor to aging and age-related diseases. The prognosis of severe heart failure is still unacceptably poor and it is urgent to establish new therapies for this critical condition. Some patients with heart failure do not respond to established multidisciplinary treatment and they are classified as “non-responders”. The outcome is especially poor for non-responders, and underlying mechanisms are largely unknown. Purpose Studies indicate mitochondrial dysfunction has causal roles for metabolic remodeling in the failing heart, but underlying mechanisms remain to be explored. This study tried to elucidate the role of Mitofusin-1 in a failing heart. Methods We examined twenty-two heart failure patients who underwent endomyocardial biopsy of intraventricular septum. Patients were classified as non-responders when their left-ventricular (LV) ejection fraction did not show more than 10% improvement at remote phase after biopsy. Fourteen patients were classified as responders, and eight as non-responders. Electron microscopy, quantitative PCR, and immunofluorescence studies were performed to explore the biological processes or molecules involved in failure to respond. In addition to studies with cardiac tissue specific knockout mice, we also conducted functional in-vitro studies with neonatal rat ventricular myocytes. Results Twenty-two patients with IDCM who underwent endomyocardial biopsy were enrolled in this study, including 14 responders and 8 non-responders. Transmission electron microscopy (EM) showed a significant reduction in mitochondrial size in cardiomyocytes of non-responders compared to responders. Quantitative PCR revealed that transcript of mitochondrial fusion protein, Mitofusin-1, was significantly reduced in non-responders. Studies with neonatal rat ventricular myocytes (NRVMs) indicated that the beta-1 adrenergic receptor-mediated signaling pathway negatively regulates Mitofusin-1 expression. Suppression of Mitofusin-1 resulted in a significant reduction in mitochondrial respiration of NRVMs. We generated left ventricular pressure overload model with thoracic aortic constriction (TAC) in cardiac specific Mitofusin-1 knockout model (c-Mfn1 KO). Systolic function was reduced in c-Mfn1 KO mice, and EM study showed an increase in dysfunctional mitochondria in the KO group subjected to TAC. Conclusions Mitofusin-1 becomes a biomarker for non-responders with heart failure. In addition, our results suggest that therapies targeting mitochondrial dynamics and homeostasis would become next generation therapy for severe heart failure patients. Funding Acknowledgement Type of funding source: None


2005 ◽  
Vol 99 (3) ◽  
pp. 409-413 ◽  
Author(s):  
Stamos Kyrzopoulos ◽  
Stamatis Adamopoulos ◽  
John T. Parissis ◽  
John Rassias ◽  
George Kostakis ◽  
...  

2017 ◽  
Vol 17 (1) ◽  
Author(s):  
Tamrat Befekadu Abebe ◽  
Eyob Alemayehu Gebreyohannes ◽  
Akshaya Srikanth Bhagavathula ◽  
Yonas Getaye Tefera ◽  
Tadesse Melaku Abegaz

2012 ◽  
Vol 53 (5) ◽  
pp. 306-312 ◽  
Author(s):  
Masashi Kamioka ◽  
Hitoshi Suzuki ◽  
Shinya Yamada ◽  
Yoshiyuki Kamiyama ◽  
Shu-ichi Saitoh ◽  
...  

2014 ◽  
Vol 20 (10) ◽  
pp. S190-S191
Author(s):  
Takaharu Hayashi ◽  
Yoshihiro Asano ◽  
Yasushi Sakata ◽  
Seiji Takashima

2021 ◽  
pp. 112972982110596
Author(s):  
Eunice Vieira Cavalcante Silva ◽  
Marcelo Eidi Ochiai ◽  
Kelly Regina Novaes Vieira ◽  
Antonio Carlos Pereira Barretto

Background: During decompensated heart failure, the use of intravenous inotropes can be necessary. With peripheral venous access, prolonged inotrope infusion can cause phlebitis. However, traditional central venous catheters have possible complications. Peripherally inserted central catheters (PICCs) may be an alternative to traditional catheters. Aim: Our objective was to compare the incidence of phlebitis between patients with PICC and those with peripheral venous access catheter indwelling. Methods: In a randomized clinical trial, the patients were randomized to PICC and control groups, with 40 patients in each group. The inclusion criteria were hospitalized patients with advanced heart failure, ejection fraction of <0.45, and platelet count of >50,000/mm3 and current use of continuous intravenous infusion of dobutamine. The patients were randomly assigned to receive a PICC or keep their peripheral venous access. The primary end point was the occurrence of phlebitis. Results: The PICC and control groups included 40 patients each. The median age was 61.5 years; ejection fraction, 0.24; and dobutamine dose, 7.73 µg/(kg min). Phlebitis occurred in 1 patient (2.5%) in the PICC group and in 38 patients (95.0%) in the control group, with an odds ratio of 0.10% (95% confidence interval: 0.01%–1.60%, p < 0.001). Conclusion: In conclusion, in severe heart failure patients who received intravenous dobutamine, PICC use reduced the incidence of phlebitis when compared to patients with peripheral venous access. Therefore, the PICC use should considered over peripheral venous access for prolonged intravenous therapy in heart failure patients.


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