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1.
Telemed J E Health ; 29(8): 1203-1210, 2023 08.
Artigo em Inglês | MEDLINE | ID: mdl-36595519

RESUMO

Background: Telemedical transmission of prehospital electrocardiograms (ECGs) to a target clinic may improve clinical workflows and speed of intervention. However, whether ECG transmission delays prehospital workflows remains controversial. Therefore, we aimed to clarify whether ECG transmission prolongs prehospital scene time in patients diagnosed with acute coronary syndrome (ACS). Methods: We retrospectively included all patients diagnosed with ACS by prehospital emergency physicians from July 2016 to June 2019 at a single academic center. The primary endpoint was the effect of ECG transmission on prehospital scene time. The secondary endpoints were the effects of ECG diagnosis on prehospital scene time and quality of care. Multivariable regression was used to account for patients' age, physician specialty, completion of specialty training, and whether emergencies occurred throughout the day or night shifts as potential confounders. Results: A total of 1,106 cases were included, of which 154 ECG transmissions were performed. ECG transmission prolonged prehospital scene time by an average of 3 min: adjusted regression coefficient [95% confidence interval (95% CI)]: 3.24 (1.7-4.8), p < 0.001. Prehospital treatment time was not influenced by prehospital ECG-based diagnosis (ST-elevation myocardial infarction [STEMI] vs. non-ST-elevation ACS [NSTE-ACS]): adjusted regression coefficient (95% CI): 0.7 (-1.3 to 2.7), p = 0.490. Emergency physicians adhered to local standard operating procedures in 739 of 1,007 (73%) patients diagnosed with NSTE-ACS and 93 of 99 (94%) patients diagnosed with STEMI. A STEMI diagnosis compared with NSTE-ACS was associated with five times higher odds of adhering to standard operating procedures (odds ratio [95% CI]: 5.6 [2.7-14.6], p < 0.001). Conclusion: The observed delay of ∼3 min in the prehospital scene time by ECG transmission is clinically irrelevant. For patients prehospitally diagnosed with NSTE-ACS who do not meet STEMI criteria, adherence to standard operating procedures seems unjustifiably low and should be improved.


Assuntos
Síndrome Coronariana Aguda , Serviços Médicos de Emergência , Infarto do Miocárdio , Infarto do Miocárdio com Supradesnível do Segmento ST , Telemedicina , Humanos , Infarto do Miocárdio/diagnóstico , Infarto do Miocárdio com Supradesnível do Segmento ST/diagnóstico , Estudos Retrospectivos , Serviços Médicos de Emergência/métodos , Fatores de Tempo , Eletrocardiografia
2.
Vascul Pharmacol ; 44(5): 326-32, 2006 May.
Artigo em Inglês | MEDLINE | ID: mdl-16530020

RESUMO

INTRODUCTION: Growth factor therapy provides a therapeutic alternative for "no option" patients with coronary disease. Fibroblast Growth Factor-2 (FGF-2) predominantly stimulates angiogenesis, the growth of new capillaries, whereas Monocyte Chemoattractant Protein-1 (MCP-1) is considered an arteriogenic agent. We hypothesised a synergetic effect of FGF-2 and MCP-1 in ischemic myocardium. METHODS: A severe coronary stenosis was created in pigs. After one week, chronic ischemia was confirmed by angiography, echocardiography, reduced ejection fraction, and increase of marker enzymes. FGF-2, MCP-1, both, or vector only were then injected intramyocardially as plasmid DNA in the impaired area. Regional contractility and number of capillaries and arterial vessels were evaluated after three months. RESULTS: FGF-2, FGF-2+MCP-1, and vector, but not MCP-1 alone improved regional contractility at rest, whereas only FGF-2 alone ameliorated function under stress conditions. Angiogenesis in the ischemic area was stimulated by FGF-2 compared to MCP-1. In contrast, MCP-1 induced arteriogenesis relative to FGF-2. CONCLUSION: Differences for vessel growth and regional function were apparent between FGF-2 and MCP-1. This contrast could allow the speculation that development of a flow reserve in chronically ischemic myocardium is linked to angiogenesis rather than to arteriogenesis. No additional benefits were seen following combined therapy.


Assuntos
Quimiocina CCL2/biossíntese , Estenose Coronária/terapia , Fator 2 de Crescimento de Fibroblastos/biossíntese , Terapia Genética , Peptídeos e Proteínas de Sinalização Intercelular/biossíntese , Contração Miocárdica , Isquemia Miocárdica/terapia , Neovascularização Fisiológica , Animais , Capilares/crescimento & desenvolvimento , Quimiocina CCL2/genética , Doença Crônica , Estenose Coronária/metabolismo , Estenose Coronária/fisiopatologia , Vasos Coronários/crescimento & desenvolvimento , Modelos Animais de Doenças , Fator 2 de Crescimento de Fibroblastos/genética , Vetores Genéticos , Peptídeos e Proteínas de Sinalização Intercelular/genética , Isquemia Miocárdica/metabolismo , Isquemia Miocárdica/fisiopatologia , Miocárdio/metabolismo , Suínos
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