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[PMID]:28966326
[Au] Autor:Katoh M; Takeda N; Arimoto T; Abe H; Oda K; Osuga Y; Fujii T; Komuro I
[Ad] Endereço:Department of Cardiovascular Medicine, Graduate School of Medicine, The University of Tokyo.
[Ti] Título:Bevacizumab-Related Microvascular Angina and Its Management with Nicorandil.
[So] Source:Int Heart J;58(5):803-805, 2017 Oct 21.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Bevacizumab, an inhibitor of vascular endothelial growth factor (VEGF)-A, is currently used to treat patients with ovarian or colon cancer. While several cardiovascular toxicities related to bevacizumab-containing regimens have been reported, the effect of bevacizumab on the coronary microcirculation has not been fully elucidated. Here we report a case of 54-year-old female patient who developed microvascular angina after a series of bevacizumab-containing chemotherapeutic regimen. The discontinuation of bevacizumab and nicorandil administration was effective in alleviating her chest discomfort and the ischemic changes on her ECG. This highlights the possibility that coronary microvascular angina can be induced in patients treated with bevacizumab-containing chemotherapy. It should also be noted that nicorandil can be effective in managing microvascular angina.
[Mh] Termos MeSH primário: Bevacizumab/efeitos adversos
Angina Microvascular/tratamento farmacológico
Nicorandil/administração & dosagem
[Mh] Termos MeSH secundário: Inibidores da Angiogênese/efeitos adversos
Inibidores da Angiogênese/uso terapêutico
Bevacizumab/uso terapêutico
Angiografia Coronária
Circulação Coronária/efeitos dos fármacos
Relação Dose-Resposta a Droga
Eletrocardiografia/efeitos dos fármacos
Feminino
Seguimentos
Seres Humanos
Angina Microvascular/induzido quimicamente
Angina Microvascular/diagnóstico
Meia-Idade
Neoplasias Ovarianas/tratamento farmacológico
Vasodilatadores/administração & dosagem
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Angiogenesis Inhibitors); 0 (Vasodilator Agents); 260456HAM0 (Nicorandil); 2S9ZZM9Q9V (Bevacizumab)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-537


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[PMID]:28966311
[Au] Autor:Fukui Y; Nozawa T; Ihori H; Sobajima M; Nakadate T; Matsuki A; Nonomura M; Fujii N; Inoue H; Kinugawa K
[Ad] Endereço:Second Department of Internal Medicine, Graduate School of Medicine, University of Toyama.
[Ti] Título:Nicorandil Attenuates Ischemia-Reperfusion Injury Via Inhibition of Norepinephrine Release From Cardiac Sympathetic Nerve Terminals.
[So] Source:Int Heart J;58(5):787-793, 2017 Oct 21.
[Is] ISSN:1349-3299
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:A large amount of norepinephrine (NE) released from cardiac sympathetic nerve terminals might accelerate myocardial ischemic injury. Nicorandil (NICO), K channel opener, could attenuate cardiac NE release from the sympathetic nerve terminals during ischemia. The present study aimed to investigate the effects of NICO-induced attenuation of cardiac NE release on myocardial ischemia-reperfusion (I/R) injury in rats, by comparison with the effect of cardiac sympathetic denervation on I/R injury.Cardiac interstitial NE (iNE) concentrations were determined using a microdialysis method. Rats were divided into 3 groups; control, NICO, and denervation groups. Cardiac sympathetic denervation was performed by painting 10% phenol on the left ventricular epicardium 7 days before producing ischemia. The left coronary artery was ligated for 30 minutes and then re-perfused for 120 minutes. NICO (50 µg/kg/minute) was infused intravenously starting 20 minutes before the coronary occlusion to the end of the ligation.The infarct size of the left ventricle was smaller in rats treated with NICO than in control rats (20.2 ± 3.0 versus 50.6 ± 14.7%, P < 0.01). Sympathetic denervation also reduced infarct size (28.5 ± 10.4 %, P < 0.01), which was not significantly different from that in the NICO group. At the end of 30-minute ischemia, iNE increased markedly in control rats (0.1 ± 0.1 to 20.6 ± 5.3 × 10 pg/mL), whereas the increase was completely inhibited in denervated rats. NICO markedly attenuated the increase (4.9 ± 3.0 × 10 pg/mL, P < 0.01) during ischemia.NICO-induced attenuation of neural NE release during ischemia might, at least in part, contribute to myocardial protection against I/R injury.
[Mh] Termos MeSH primário: Ventrículos do Coração/inervação
Traumatismo por Reperfusão Miocárdica/tratamento farmacológico
Miocárdio/metabolismo
Nicorandil/farmacologia
Norepinefrina/antagonistas & inibidores
Fibras Simpáticas Pós-Ganglionares/metabolismo
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Ventrículos do Coração/metabolismo
Ventrículos do Coração/patologia
Masculino
Traumatismo por Reperfusão Miocárdica/metabolismo
Traumatismo por Reperfusão Miocárdica/fisiopatologia
Norepinefrina/metabolismo
Ratos
Ratos Wistar
Fibras Simpáticas Pós-Ganglionares/efeitos dos fármacos
Complexo Vitamínico B/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
12001-76-2 (Vitamin B Complex); 260456HAM0 (Nicorandil); X4W3ENH1CV (Norepinephrine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171102
[Lr] Data última revisão:
171102
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171003
[St] Status:MEDLINE
[do] DOI:10.1536/ihj.16-391


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[PMID]:28609713
[Au] Autor:Zhang F; Xuan Y; Cui J; Liu X; Shao Z; Yu B
[Ad] Endereço:Department of Cardiology, The Affiliated Hospital of Xuzhou Medical University, PR China.
[Ti] Título:Nicorandil modulated macrophages activation and polarization via NF-κb signaling pathway.
[So] Source:Mol Immunol;88:69-78, 2017 Aug.
[Is] ISSN:1872-9142
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Nicorandil, a drug with both nitrate-like and ATP-sensitive potassium (K ) channel-activating properties, has been well demonstrated in various aspects of myocardial infarction (MI), especially in inhibiting cell apoptosis and increasing coronary flow. However, the role of nicorandil in regulating inflammation and angiogenesis following myocardial infarction is still unrevealed. In the present study, we explored the effect of nicorandil on macrophage phenotype transition and inflammation regulation and the potential underlying mechanisms. For the phenotype transition and phagocytosis ability of macrophages detection, flow cytometry analysis was used. The inflammation factors were measured with ELISA and qRT-PCR. Western blot was used to assess the levels of NF-κb and its target genes and VEGF expression. The tube formation ability of endothelial cells was examined on matrigel. We discovered that nicorandil can obviously inhibit the differentiation of monocytes into mature macrophages and decrease M1 phenotype transition both in peritoneal macrophages and cultured macrophage cell line in normal or hypoxia and serum deprivation (H/SD) conditions. Meanwhile, nicorandil can induce an anti-inflammatory M2 phenotype. Thereby, nicorandil regulated macrophages switching to M1/M2 status. Our data further showed that NF-κb and the expression of its target genes were pivotal players in the regulation of macrophages phenotype. Besides, we also showed that nicorandil can promote the tube formation and VEGF expression in endothelial cells. We concluded that nicorandil may serve as an effective modulator of NF-κb signaling pathway during the pathogenesis of MI via regulating M1/M2 status and promoting angiogenesis.
[Mh] Termos MeSH primário: Anti-Hipertensivos/farmacologia
Ativação de Macrófagos/efeitos dos fármacos
Macrófagos/citologia
Nicorandil/farmacologia
Canais de Potássio/agonistas
Fator de Transcrição RelA/antagonistas & inibidores
[Mh] Termos MeSH secundário: Animais
Apoptose/imunologia
Diferenciação Celular/efeitos dos fármacos
Linhagem Celular
Sobrevivência Celular/imunologia
Células Endoteliais da Veia Umbilical Humana/fisiologia
Seres Humanos
Inflamação/tratamento farmacológico
Camundongos
Camundongos Endogâmicos C57BL
Neovascularização Fisiológica/efeitos dos fármacos
Fagocitose/imunologia
Espécies Reativas de Oxigênio/metabolismo
Fator de Transcrição RelA/metabolismo
Fator A de Crescimento do Endotélio Vascular/biossíntese
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Antihypertensive Agents); 0 (Potassium Channels); 0 (Reactive Oxygen Species); 0 (Rela protein, mouse); 0 (Transcription Factor RelA); 0 (VEGFA protein, human); 0 (Vascular Endothelial Growth Factor A); 260456HAM0 (Nicorandil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171009
[Lr] Data última revisão:
171009
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170614
[St] Status:MEDLINE


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[PMID]:28594895
[Au] Autor:Roy Chowdhury U; Bahler CK; Holman BH; Fautsch MP
[Ad] Endereço:Department of Ophthalmology, Mayo Clinic, Rochester, Minnesota, United States of America.
[Ti] Título:ATP-sensitive potassium (KATP) channel openers diazoxide and nicorandil lower intraocular pressure by activating the Erk1/2 signaling pathway.
[So] Source:PLoS One;12(6):e0179345, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Elevated intraocular pressure is the most prevalent and only treatable risk factor for glaucoma, a degenerative disease of the optic nerve. While treatment options to slow disease progression are available, all current therapeutic and surgical treatments have unwanted side effects or limited efficacy, resulting in the need to identify new options. Previous reports from our laboratory have established a novel ocular hypotensive effect of ATP-sensitive potassium channel (KATP) openers including diazoxide (DZ) and nicorandil (NCD). In the current study, we evaluated the role of Erk1/2 signaling pathway in KATP channel opener mediated reduction of intraocular pressure (IOP). Western blot analysis of DZ and NCD treated primary normal trabecular meshwork (NTM) cells, human TM (isolated from perfusion cultures of human anterior segments) and mouse eyes showed increased phosphorylation of Erk1/2 when compared to vehicle treated controls. DZ and NCD mediated pressure reduction (p<0.02) in human anterior segments (n = 7 for DZ, n = 4 for NCD) was abrogated by U0126 (DZ + U0126: -9.7 ± 11.5%, p = 0.11; NCD + U0126: -0.1 ± 11.5%, p = 1.0). In contrast, U0126 had no effect on latanoprostfree acid-induced pressure reduction (-52.5 ± 6.8%, n = 4, p = 0.001). In mice, DZ and NCD reduced IOP (DZ, 14.9 ± 3.8%, NCD, 16.9 ± 2.5%, n = 10, p<0.001), but the pressure reduction was inhibited by U0126 (DZ + U0126, 0.7 ± 3.0%; NCD + U0126, 0.9 ± 2.2%, n = 10, p>0.1). Histologic evaluation of transmission electron micrographs from DZ + U0126 and NCD + U0126 treated eyes revealed no observable morphological changes in the ultrastructure of the conventional outflow pathway. Taken together, the results indicate that the Erk1/2 pathway is necessary for IOP reduction by KATP channel openers DZ and NCD.
[Mh] Termos MeSH primário: Diazóxido/farmacologia
Pressão Intraocular/efeitos dos fármacos
Ativação do Canal Iônico/efeitos dos fármacos
Canais KATP/metabolismo
Sistema de Sinalização das MAP Quinases/efeitos dos fármacos
Nicorandil/farmacologia
[Mh] Termos MeSH secundário: Adulto
Idoso
Idoso de 80 Anos ou mais
Animais
Butadienos/farmacologia
Células Cultivadas
Ativação Enzimática/efeitos dos fármacos
Seres Humanos
Lactente
Camundongos Endogâmicos C57BL
Meia-Idade
Nitrilos/farmacologia
Hipotensão Ocular/fisiopatologia
Perfusão
Fosforilação/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Butadienes); 0 (KATP Channels); 0 (Nitriles); 0 (U 0126); 260456HAM0 (Nicorandil); O5CB12L4FN (Diazoxide)
[Em] Mês de entrada:1709
[Cu] Atualização por classe:170918
[Lr] Data última revisão:
170918
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170609
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0179345


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[PMID]:28379216
[Au] Autor:Ravindran S; Swaminathan K; Ramesh A; Kurian GA
[Ad] Endereço:Vascular Biology Lab, SASTRA University, Thanjavur, India.
[Ti] Título:Nicorandil attenuates neuronal mitochondrial dysfunction and oxidative stress associated with murine model of vascular calcification.
[So] Source:Acta Neurobiol Exp (Wars);77(1):57-67, 2017.
[Is] ISSN:1689-0035
[Cp] País de publicação:Poland
[La] Idioma:eng
[Ab] Resumo:Evidences suggest that the presence of chronic kidney disease (CKD) is associated with cerebrovascular diseases related cognitive decline in dialysis patients. As mitochondrial dysfunction is implicated in neurodegenerative disorders, we hypothesized that changes in brain mitochondria occur due to vascular calcification induced by renal failure and the opening of the mitochondrial potassium channel using nicorandil may prevent its dysfunction. Brain tissues from rats with vascular calcification were studied. Nicorandil (7.5 mg/kg b.wt.) was given either concomitantly or after the induction of calcification. The brain tissues were evaluated for antioxidant capacity, mitochondrial enzymes and oxidative phosphorylation efficiency along with the progression of calcification. The results suggested that renal failure, elevated the calcium, phosphorus product in the brain. The brain cytoplasm and mitochondrial fractions showed an elevated TBARS and a corresponding decline in the antioxidant enzymes, indicating a sev ere oxidative stress. The elevated brain mitochondrial enzymes like NADH dehydrogenase, and succinate dehydrogenase in the disease control groups, reversed to the near control level after nicorandil treatment. We observed that nicorandil was more effective when given after calcification. It reduced the biochemical alterations associated with calcium and phosphorous toxicity in the brain, by preserving mitochondria, the key target for treating neurodegenerative diseases.
[Mh] Termos MeSH primário: Mitocôndrias/efeitos dos fármacos
Doenças Mitocondriais/tratamento farmacológico
Nicorandil/uso terapêutico
Estresse Oxidativo/efeitos dos fármacos
Calcificação Vascular/prevenção & controle
Complexo Vitamínico B/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Aorta/patologia
Cálcio/metabolismo
Catalase/metabolismo
Esquema de Medicação
Depuradores de Radicais Livres/metabolismo
Antígenos de Histocompatibilidade Classe I/metabolismo
Testes de Função Renal
Peroxidação de Lipídeos/efeitos dos fármacos
Mitocôndrias/metabolismo
Mitocôndrias/ultraestrutura
Doenças Mitocondriais/etiologia
Nicorandil/farmacologia
Fósforo/metabolismo
Ratos
Ratos Wistar
Insuficiência Renal Crônica/complicações
Insuficiência Renal Crônica/diagnóstico
Substâncias Reativas com Ácido Tiobarbitúrico/metabolismo
Calcificação Vascular/etiologia
Complexo Vitamínico B/farmacologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Free Radical Scavengers); 0 (Histocompatibility Antigens Class I); 0 (Thiobarbituric Acid Reactive Substances); 12001-76-2 (Vitamin B Complex); 260456HAM0 (Nicorandil); 27YLU75U4W (Phosphorus); EC 1.11.1.6 (Catalase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1704
[Cu] Atualização por classe:170414
[Lr] Data última revisão:
170414
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170406
[St] Status:MEDLINE


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[PMID]:28285861
[Au] Autor:Liang LN; Zhong X; Zhou Y; Hou ZQ; Hu HR; Zhu FF; Chen JB; Ji XF; Shang DY
[Ad] Endereço:Department of Emergency, Shandong Provincial Hospital affiliated to Shandong University, No. 324, Jingwu Road, Jinan 250021, Shandong, China.
[Ti] Título:Cardioprotective effect of nicorandil against myocardial injury following cardiac arrest in swine.
[So] Source:Am J Emerg Med;35(8):1082-1089, 2017 Aug.
[Is] ISSN:1532-8171
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:INTRODUCTION: Nicorandil, a vasodilatory drug used to treat angina, was reported to protect against myocardial ischemia-reperfusion injury in various animal models. However, its cardioprotective action following cardiac arrest is unknown. We examined the cardioprotective effects of nicorandil in a porcine model of cardiac arrest and resuscitation. METHODS: Ventricular fibrillation was induced electrically for 4min in anesthetized domestic swine, followed by cardiopulmonary resuscitation. Sixteen successfully resuscitated animals were randomized to saline control (n=8) or nicorandil (n=8) groups. Nicorandil (150µg/kg) was administered by central intravenous injection at onset of restoration of spontaneous circulation (ROSC), followed by 3µg/kg/min infusion until reperfusion end. Sham-operated animals received surgery only (n=4). Hemodynamic parameters were monitored continuously. Blood samples were taken at baseline, 5, 30, 180, and 360min after ROSC. Left ventricular ejection fraction was assessed by echocardiography at baseline and 6h after ROSC. The animals were euthanized 6h after ROSC, and the cardiac tissue was removed for analysis. RESULTS: 6 h after ROSC, nicorandil had significantly improved all hemodynamic variables (all P<0.05) except the maximum rate of left ventricular pressure decline and heart rate (P>0.05) compared with the control group. Control animals showed elevated cardiac troponin I and lactate levels compared with sham animals, which were significantly decreased following nicorandil treatment (P<0.05). In the saline control group, the adenosine triphosphate (ATP) content was largely reduced but subsequently rescued by nicorandil (P<0.05). Histopathologic injury was reduced with nicorandil treatment. Nicorandil reduced cardiomyocyte apoptosis as evidenced by reduced terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL)-positive cells, decreased Bax and caspase-3 expression, and increased Bcl-2 expression in the myocardium (all P<0.05). CONCLUSION: Nicorandil exhibited cardioprotective effects on myocardial injury following cardiac arrest via improvement in post-resuscitation myocardial dysfunction and energy metabolism, reduction in myocardial histopathologic injury, and antiapoptotic effects.
[Mh] Termos MeSH primário: Cardiotônicos/farmacologia
Parada Cardíaca/patologia
Nicorandil/farmacologia
Traumatismo por Reperfusão/prevenção & controle
Fibrilação Ventricular/patologia
[Mh] Termos MeSH secundário: Animais
Modelos Animais de Doenças
Injeções Intravenosas
Masculino
Suínos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Cardiotonic Agents); 260456HAM0 (Nicorandil)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170314
[St] Status:MEDLINE


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[PMID]:28245258
[Au] Autor:Asensio-López MC; Soler F; Pascual-Figal D; Fernández-Belda F; Lax A
[Ad] Endereço:Cardiología Clínica y Experimental, Laboratorios de Investigación Biomédica, Universidad de Murcia en Campus de El Palmar, Murcia, Spain.
[Ti] Título:Doxorubicin-induced oxidative stress: The protective effect of nicorandil on HL-1 cardiomyocytes.
[So] Source:PLoS One;12(2):e0172803, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The primary cardiotoxic action of doxorubicin when used as antitumor drug is attributed to the generation of reactive oxygen species (ROS) therefore effective cardioprotection therapies are needed. In this sense, the antianginal drug nicorandil has been shown to be effective in cardioprotection from ischemic conditions but the underlying molecular mechanism to cope with doxorubicin-induced ROS is unclear. Our in vitro study using the HL-1 cardiomyocyte cell line derived from mouse atria reveals that the endogenous nitric oxide (NO) production was stimulated by nicorandil and arrested by NO synthase inhibition. Moreover, while the NO synthase activity was inhibited by doxorubicin-induced ROS, the NO synthase inhibition did not affect doxorubicin-induced ROS. The inhibition of NO synthase activity by doxorubicin was totally prevented by preincubation with nicorandil. Nicorandil also concentration-dependently (10 to 100 µM) decreased doxorubicin-induced ROS and the effect was antagonized by 5-hydroxydecanoate. The inhibition profile of doxorubicin-induced ROS by nicorandil was unaltered when an L-arginine derivative or a protein kinase G inhibitor was present. Preincubation with pinacidil mimicked the effect of nicorandil and the protection was eliminated by glibenclamide. Quantitative colocalization of fluorescence indicated that the mitochondrion was the target organelle of nicorandil and the observed response was a decrease in the mitochondrial inner membrane potential. Interference with H+ movement across the mitochondrial inner membrane, leading to depolarization, also protected from doxorubicin-induced ROS. The data indicate that activation of the mitochondrial ATP-sensitive K+ channel by nicorandil causing mitochondrial depolarization, without participation of the NO donor activity, was responsible for inhibition of the mitochondrial NADPH oxidase that is the main contributor to ROS production in cardiomyocytes. Impairment of the cytosolic Ca2+ signal induced by caffeine and the increase in lipid peroxidation, both of which are indicators of doxorubicin-induced oxidative stress, were also prevented by nicorandil.
[Mh] Termos MeSH primário: Doxorrubicina/farmacologia
Miócitos Cardíacos/efeitos dos fármacos
Miócitos Cardíacos/metabolismo
Nicorandil/farmacologia
Estresse Oxidativo/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Cálcio/metabolismo
Linhagem Celular
Peroxidação de Lipídeos/efeitos dos fármacos
Camundongos
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Óxido Nítrico/metabolismo
Óxido Nítrico Sintase/metabolismo
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Reactive Oxygen Species); 260456HAM0 (Nicorandil); 31C4KY9ESH (Nitric Oxide); 80168379AG (Doxorubicin); EC 1.14.13.39 (Nitric Oxide Synthase); SY7Q814VUP (Calcium)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170828
[Lr] Data última revisão:
170828
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170301
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0172803


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[PMID]:28143616
[Au] Autor:Meena DS; Meena CB; Parvez J
[Ad] Endereço:Department of Cardiology, Swai Man Singh Medical College, Jaipur, Rajasthan, India. dr.daulatsinghmeena@gmail.com.
[Ti] Título:Hypertrophic obstructive cardiomyopathy with multiple coronary arteries to right ventricular microfistulas: a case report and review of the literature.
[So] Source:J Med Case Rep;11(1):24, 2017 Jan 31.
[Is] ISSN:1752-1947
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Coronary artery microfistulas are a rare anomaly; their association with hypertrophic cardiomyopathy is even rarer and can lead to serious cardiac complications owing to coronary steal phenomena such as angina pectoris, myocardial infarction, congestive heart failure, ventricular and supraventricular arrhythmias, syncope, and sudden death. CASE PRESENTATION: A 32-year-old Indian woman presented to our institute with severe angina on exertion and multiple episodes of pre-syncope. Echocardiography revealed hypertrophic obstructive cardiomyopathy. Coronary angiography showed no significant atherosclerotic lesions; however, it revealed multiple microfistulas originated from all three major coronary arteries and draining into her right ventricle. This finding was confirmed by the rapid filling of the pulmonary artery after dye was injected into her left coronary artery during a cardiac catheterization study and by a significant oxygen step up of 15 % seen from her right atria to right ventricle during oximetry analysis. We treated our patient's condition with medical therapy including metoprolol and nicorandil. She improved and angina grade had decreased from class III to class II on a follow-up visit 1 month after discharge. CONCLUSIONS: In this case report and literature review, we highlight an unusual but important association that can lead to symptomatic worsening of angina in young patients with hypertrophic cardiomyopathy owing to coronary steal phenomena.
[Mh] Termos MeSH primário: Angina Pectoris/complicações
Cardiomiopatia Hipertrófica/patologia
Angiografia Coronária
Vasos Coronários/patologia
Ventrículos do Coração/patologia
Fístula Vascular/patologia
[Mh] Termos MeSH secundário: Adulto
Angina Pectoris/diagnóstico por imagem
Angina Pectoris/tratamento farmacológico
Antiarrítmicos/uso terapêutico
Cardiomiopatia Hipertrófica/diagnóstico por imagem
Cardiomiopatia Hipertrófica/tratamento farmacológico
Feminino
Seres Humanos
Metoprolol/uso terapêutico
Nicorandil/uso terapêutico
Síncope
Resultado do Tratamento
Fístula Vascular/diagnóstico por imagem
Fístula Vascular/tratamento farmacológico
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 260456HAM0 (Nicorandil); GEB06NHM23 (Metoprolol)
[Em] Mês de entrada:1706
[Cu] Atualização por classe:170623
[Lr] Data última revisão:
170623
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170202
[St] Status:MEDLINE
[do] DOI:10.1186/s13256-016-1161-7


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[PMID]:28125542
[Au] Autor:Kwon O; Park DW
[Ad] Endereço:Department of Cardiology, Asan Medical Center, College of Medicine, University of Ulsan, Seoul, Korea.
[Ti] Título:Nicorandil for maximal hyperemia: a theoretical advantage awaiting clinical significance.
[So] Source:Coron Artery Dis;28(2):95-97, 2017 03.
[Is] ISSN:1473-5830
[Cp] País de publicação:England
[La] Idioma:eng
[Mh] Termos MeSH primário: Hiperemia
Nicorandil
[Mh] Termos MeSH secundário: Reserva Fracionada de Fluxo Miocárdico
Seres Humanos
Vasodilatadores
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Vasodilator Agents); 260456HAM0 (Nicorandil)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170127
[St] Status:MEDLINE
[do] DOI:10.1097/MCA.0000000000000455


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[PMID]:28100342
[Au] Autor:Wang ZQ; Chen MX; Liu DL; Zheng WX; Cao XZ; Chen H; Huang MF; Luo ZR
[Ad] Endereço:Department of Cardiology, Fuzhou General Hospital of Nanjing Military Command, Xiamen University, Fuzhou 350025, China.
[Ti] Título:[The effect on myocardial perfusion and clinical outcome of intracoronary nicorandil injection prior to percutaneous coronary intervention in ST-segment elevation myocardial infarction].
[So] Source:Zhonghua Xin Xue Guan Bing Za Zhi;45(1):26-33, 2017 Jan 25.
[Is] ISSN:0253-3758
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:To investigate the effect of intracoronary administration of nicorandil prior to primary percutaneous coronary intervention (PPCI) on myocardial perfusion and short-term clinical outcomes in patients with ST-segment elevation myocardial infarction (STEMI). A total of 158 patients with STEMI undergoing PPCI from January 2014 to December 2015 in Fuzhou General Hospital were enrolled consecutively in this prospective controlled randomized trial. Patients were assigned into three groups with random number table: the nicorandil group (patients received intracoronary administration of 6 mg nicorandil after guide wire or balloon successfully crossed the target lesion, =53), the nitroglycerin group (patients received intracoronary administration of 300 µg nitroglycerin after after guide wire or balloon successfully crossed the target lesion, =52) and the control group(patients received routine treatment, =53). The primary outcomes were myocardial perfusion, including the levels of corrected TIMI frame count (cTFC), and the incidence of no reflow or slow flow after PPCI. The secondary outcomes included the incidence of major adverse cardiovascular events (MACE) during hospitalization (all-cause death, reperfusion arrhythmia within 2 hours after PPCI, angina within 24 hours after PPCI, new heart failure or worsening cardiac function, and repeat revascularization) and within 3 months of follow-up (all-cause death, nonfatal myocardial infarction, repeat revascularization, post-infarction angina, and re-hospitalization for congestive heart failure). The age of enrolled patients was (62.9±11.3) years old, and 130 cases (82.3%) of them were male. The median time of symptom-onset to balloon was 4.50 (3.20, 6.43) hours. There were significantly difference in cTFC immediately after PPCI((21.68±7.43)frames, (24.74±8.66)frames, and(27.06±10.40)frames), incidence of no reflow or slow flow after PPCI(5.7%(3/53), 13.5%(7/52), and 22.6%(12/53)), ST-segment resolution at 2 hours after procedure(90.6%(48/53), 84.6%(44/52), and 74.5%(38/53)), and reperfusion arrhythmia at 2 hours after procedure(15.1%(8/53), 36.6%(19/52), and 34.0%(18/53)) among the 3 groups( <0.01 or 0.05). In the multivariate logistic regression models, intracoronary administration of nicorandil could lower the cTFC level ( =0.17, 95% 0.10-0.41, =0.001), acted as a protecting factor on lowering the incidence of no reflow or slow flow ( =0.13, 95% 0.02-0.96, =0.045) and reperfusion arrhythmia ( =0.26, 95% 0.09-0.74, =0.012), as well as facilitating the ST-segment resolution at 2 hours after procedure ( =4.62, 95% 1.14-18.82, =0.033). However, observed parameters were similar between intracoronary administration of nitroglycerin group compared with control group (all >0.05). MACE within 3 months of follow-up were similar among the 3 groups(all >0.05). Intracoronary administration of nicorandil prior to balloon dilation can significantly improve the myocardial perfusion and reduce the occurrence of reperfusion arrhythmia during PPCI for STEMI, but does not affect the short-term prognosis in STEMI patients.
[Mh] Termos MeSH primário: Infarto do Miocárdio/tratamento farmacológico
Nicorandil/uso terapêutico
Intervenção Coronária Percutânea
Vasodilatadores/uso terapêutico
[Mh] Termos MeSH secundário: Idoso
Angioplastia Coronária com Balão
Arritmias Cardíacas
Feminino
Seres Humanos
Masculino
Meia-Idade
Nitroglicerina
Prognóstico
Estudos Prospectivos
Infarto do Miocárdio com Supradesnível do Segmento ST
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RANDOMIZED CONTROLLED TRIAL
[Nm] Nome de substância:
0 (Vasodilator Agents); 260456HAM0 (Nicorandil); G59M7S0WS3 (Nitroglycerin)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170727
[Lr] Data última revisão:
170727
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170120
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.0253-3758.2017.01.006



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