Browsing by Subject "Myocardial infarction"
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- PublicationOpen AccessDiagnostic application of postmortem cardiac troponin I pericardial fluid/serum ratio in sudden cardiac death(MDPI, 2021-03-30) Valverde-Vázquez, María del Rocio; Pérez Cárceles, María Dolores; Osuna, Eduardo; Noguera Velasco, José Antonio; Hernández del Rincón, Juan Pedro; Hernández Romero, Diana; Ciencias SociosanitariasIn approximately 5% of unexpected deaths, establishing a conclusive diagnosis exclusively on the basis of anatomo-pathological findings in a classic autopsy is difficult. Postmortem biomarkers have been actively investigated as complementary indicators to help to reach valid conclusions about the circumstances of death. Several studies propose either the pericardial fluid or peripheral veins as a location for troponin determination, but the optimum sampling site is still a matter of debate. Our objective was to evaluate the association between the ratio of troponin values in the pericardial fluid and serum (determined postmortem) and the diagnosis of acute myocardial infarction (AMI) in the context of sudden cardiac death. We included 175 forensic cases. Two groups were established: AMI deaths (48; 27.4%) and the control group (127; 72.6%). The cardiac Troponin I (cTnI) values in the pericardial fluid and the troponin ratio were found to be associated with the cause of death. Univariate regression analyses showed that both age and the cTnI ratio were significantly associated with the diagnosis of AMI death. In a multivariate analysis, adjusting for confounding factors, the age and cTnI ratio were independent predictors of death from myocardial infarction. We performed a receiver operating characteristic (ROC) curve for the cTnI ratio for AMI death and selected a cut-off point. Our biomarker was found to be a valuable and highly effective tool for use in the forensic field as a complementary method to facilitate diagnosis in nonconclusive autopsies.
- PublicationOpen AccessEarly Anti-inflammatory and Pro-angiogenic Myocardial Effects of Intravenous Serelaxin Infusion for 72 H in an Experimental Rat Model of Acute Myocardial Infarction(2017-12) Sanchez Mas, Jesus; Lax Pérez, Antonio Manuel; Asensio Lopez, Maria del Carmen; Fernandez del Palacio, Maria J; de Boer, Rudolf; Pascual Figal, Domingo A.; MedicinaSprague Dawley rats were subjected to acute myocardial infarction (AMI) by permanent ligation of the left anterior descending coronary artery. At the time of AMI, a subcutaneous mini-osmotic pump was implanted and animals were randomized into three groups, according to the intravenous therapy received during the first 72 h: placebo-treated (saline), serelaxin10-treated (SRLX10 = 10 μg/kg/day), or serelaxin30-treated (SRLX30 = 30 μg/kg/day). Treatment with SRLX30 reduced the expression of inflammatory cytokines and chemokines, as well as the infiltration of macrophages, and increased the expression of pro-angiogenic markers and vessel density in the infarcted myocardium after 7 days. SRLX30 did not reduce early myocardial fibrosis but reduced myocardial levels of sST2 and galectin-3. No significant effects were observed with SRLX10 treatment. A significant correlation was observed between plasma levels of serelaxin and effect measures. The results suggest serelaxin has a protective effect in early processes of cardiac remodeling after AMI.
- PublicationOpen AccessGalectin-3 expression in cardiac remodeling after myocardial infarction(2014-03) Sanchez Mas, Jesus; Lax Pérez, Antonio Manuel; Asensio Lopez, Maria del Carmen; Fernandez del Palacio, Maria J; Caballero, Luis; Garrido, Iris P; Pastor, Francisco; Januzzi, James L; Pascual Figal, Domingo A.; Medicina
- PublicationOpen AccessHistological differences in healing following experimental transmural infarction in rats(Murcia : F. Hernández, 2010) Aljinović, Jure; Vukojevic, Katarina; Košta, Vana; Marinović Guić, Maja; Saraga-Babić, Mirna; Grković, IvicaMechanisms of cardiac regeneration following transmural myocardial infarction were analysed in rat hearts using immunohistochemistry for α-SMA, caspase-3, Ki-67 and nestin markers. Seven weeks after experimental myocardial infarction, two different types of healing processes were revealed in rats with and without aneurysmatic bulging of the left ventricular wall. Besides thinning of the ventricular wall, three zones characterized both types of scars: the scar zone (divided into central and peripheral parts), the peri-infarct zone and the border zone. The main difference between the types of scars was the presence of a central necrotic zone inside the aneurysmatic wall, while connective tissue with myofibroblasts characterized the same zone in nonbulging wall. Apoptotic caspase-3 positive cells were found in the granulation tissue of the border zone in aneurysmatic scar, while in non-bulging scar they characterized all three zones. Proliferating Ki-67 positive cells displayed reverse expression pattern compared to apoptotic cells. Quantification of α-SMA positive cells revealed 60% α-SMA positive cells inside the central part of the aneurysmatic scar zone and 39% in invaginating areas, versus 19% in non-invaginating areas of the peripheral zone, but only 30% in the peripheral part of the non-bulging scar zone. Nestin positive cells were found in both types of scars, but with different distribution. These results suggest that even seven weeks after myocardial infarction, the healing processes in non-bulging scars are in chronic phase, while aneurysmatic scars are still in subacute phase. Histological differences in scar healing might be important for functional properties of the heart wall and for heart recovery prognosis.
- PublicationOpen AccessIsoflurane post-conditioning stimulates the proliferative phase of myocardial recovery in an ischemia-reperfusion model of heart injury in rats(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2014) Agnić, Ivan; Vukojevic, Katarina; Saraga-Babić, Mirna; Filipović, Natalija; Grković, IvicaSummary. The application of isoflurane in a postconditioning manner, during early reperfusion following a period of coronary occlusion, has numerous beneficial effects on the ischemic myocardium, including reduction of infarct size. It does so by stimulating a sequence of well studied anti-apoptotic pro-survival mechanisms in a similar manner to various ‘ischemic’ pre-/postconditioning approaches which achieve their cardio protective effects in both laboratory and clinical situations. Proliferation of newly formed blood vessels, resulting in formation of highly vascularized granulation tissue, is an essential stage of infarct healing. It can be evaluated by detecting various angiogenic factors, including vascular endothelial growth factor (VEGF) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) or by quantification of expression of vascular smooth muscle progenitors, such as Nestin. Expression of these three markers was used to evaluate the effect of early isoflurane post-conditioning in ischemia-reperfusion type cardiac injury. A large reduction in infarct size (59.3% of control), and marked increase of expression of VEGF (43.4%), PECAM1/CD31 (136%) and Nestin (77.9%) was found in experimental animals when compared to control animals that did not receive isoflurane treatment. Hence, based on our results, we can emphasize two morphologically detectable benefits of isoflurane post-conditioning: a marked reduction in infarct size and much better organization/vascularization of necrotic tissue.
- PublicationRestrictedMidterm clinical and echocardiographic results with patch glue repair of left ventricular free wall rupture(Lippincott, Williams & Wilkins, 2003-09-09) Cánovas López, Sergio; Lim, Eric; Dalmau, María J.; Bueno, María; Buendía, Jose; Hornero, Fernando; Gil, Oscar; García, Rafael; Paya, Rafael; Pérez, Jose; Echanove, Ildefonso; Montero, Jose; Cirugía, Pediatría y Obstetricia y GinecologíaBackground— Left ventricular free wall rupture (LVFWR) is a dramatic complication after myocardial infarction. We present our mid-term clinical and echocardiographic results of LVFWR with an epicardial patch without cardiopulmonary bypass. Methods— From February 1993 to May 2001, 17 patients underwent surgery for LVFWR. The mean age±SD of 12 males and 5 females was 68±10 years. All patients presented for emergency surgery with cardiac tamponade confirmed on echocardiography. After opening the chest and identification of the site of rupture, a Goretex patch was fashioned and applied with enbucrilate surgical glue. Results— Effective control of bleeding was achieved in all cases. There were no on-table deaths. The operative (30 day) mortality was 23.5% (4/17). One death occurred because of patch failure, two because of cardiogenic shock, and one from pneumonia. On follow-up at a median of 2.2 years (interquartile range, 1.1 to 4.3 years), two further deaths occurred, one from myocardial infarction and another of undetermined etiology. Echocardiography did not reveal any evidence of restriction to left ventricular free wall motion. Conclusions— Patch glue repair is expedient, simple and effective; with no adverse effects on mid-term ventricular dynamics. In view of superior published results to infarctectomy and repair with extra corporeal circulation, it should be considered to be the initial procedure of choice for the surgical repair of LVFWR.
- PublicationRestrictedMineralocorticoid receptor antagonists modulate galectin-3 and interleukin-33/ST2 signaling in left ventricular systolic dysfunction after acute myocardial infarction(Elsevier, 2015-01) Lax Pérez, Antonio Manuel; Sánchez Mas, Jesús; Asensio Lopez, Maria del Carmen; Fernandez del Palacio, Maria J; Caballero, Luis; Garrido, Iris P; Pastor Pérez, Francisco J; Januzzi, James L; Pascual Figal, Domingo A; MedicinaObjectives: This study aimed to evaluate the specific role of the 2 available mineralocorticoid receptor antagonists (MRAs), eplerenone and spironolactone, on the modulation of galectin-3 (Gal-3) and interleukin (IL)-33/ST2 signaling in an experimental model of left ventricular systolic dysfunction after acute myocardial infarction (MI). Background: The molecular mechanisms of benefits of MRAs in patients with left ventricular systolic dysfunction after MI not well understood. Methods: MI and left ventricular systolic dysfunction were induced by permanent ligation of the anterior coronary artery in 45 male Wistar rats, randomly assigned to no therapy (MI group, n = 15) or to receive MRAs (100 mg/kg/day) for 4 weeks; either eplerenone (n = 15) or spironolactone (n = 15) was used. A sham group was used as a control (n = 8). Elements of the pathway for Gal-3 including transforming growth factor (TGF)-β and SMAD3, as well as that for IL-33/ST2 (including IL-33 and soluble ST2 [sST2]) were analyzed in the infarcted and noninfarcted myocardium by quantitative real-time reverse transcription polymerase chain reaction. Expression of markers of fibrosis (collagen types I and III, tissue inhibitor of metalloproteinase-1) and inflammation (IL-6, tumor necrosis factor-α, monocyte chemotactic protein-1) was also examined. Results: In the infarcted myocardium, compared with sham animals, the MI group had higher concentrations of Gal-3, TGF-β, SMAD3, IL-33, and sST2, as well as higher concentrations of markers of fibrosis and inflammation. Treatment with MRAs down-regulated Gal-3, TGF-β, and SMAD3 and enhanced IL-33/ST2 signaling with lower expression of sST2; protective IL-33 up-regulation was unaffected by MRAs. Modulation of Gal-3 and IL-33/ST2 signaling induced by MRAs correlated with lower expression levels of fibrosis and inflammatory markers. No differences were found between eplerenone and spironolactone. In the noninfarcted myocardium, compared with sham animals, the MI group exhibited a higher expression of Gal-3 and IL-33, but no signs of inflammation or fibrosis were observed; in the presence of MRAs, IL-33 expression was significantly up-regulated, but Gal-3 was unaffected. Conclusions: MRAs play a pivotal role in the Gal-3 and IL-33/ST2 modulation in post-MI cardiac remodeling.
- PublicationOpen AccessRelación entre sexualidad e infarto agudo de miocardio desde una perspectiva fenomenológica(Universidad de Murcia. Servicio de publicaciones, 2022) Niño Peñaranda, Claudia Jazmin; Ballesteros Pinzón, Gersson AndrésIntroducción: La sexualidad ha estado presente a lo largo de la vida del ser humano e incluye aspectos como actividad sexual, identidad, roles, orientación, erotismo, etc. Para personas que han sufrido un infarto agudo de miocardio (IAM), la sexualidad se ve afectada por factores psicológicos, físicos e incluso sociales. Por ello, el objetivo de la presente investigación es describir el significado de la sexualidad para la persona que ha sufrido IAM desde una perspectiva fenomenológica. Material y método: Estudio cualitativo con enfoque fenomenológico, cuya muestra estuvo conformada por 19 personas que sufrieron infarto agudo de miocardio y que fueron atendidas por el servicio de urgencias o medicina interna de una institución de cuarto nivel de complejidad en la ciudad de Bucaramanga (Colombia). Se aplicaron entrevistas a profundidad que fueron codificadas mediante el programa Atlas.ti versión 6.1 y su análisis se llevó a cabo mediante el modelo Colaizzi. Resultados: La sexualidad para la persona que ha sufrido infarto agudo de miocardio se asocia a múltiples situaciones que no solo se relacionan con el acto sexual, sino que también involucran además las relaciones afectivas, compartir con su pareja, familia y amigos, entendiéndose que de esta experiencia se desencadenan aspectos negativos y positivos que afectan la expresión de la sexualidad o la potencializan. Conclusión: El significado de la sexualidad para la persona con infarto agudo de miocardio está dado por las emociones, cuidados, educación, creencias y cambios en la sexualidad, lo cual impacta en el proceso de recuperación de su enfermedad y calidad de vida.
- PublicationOpen AccessSpatio-temporal expression patterns of microRNAs in remodelling and repair of the infarcted heart(F. Hernández y Juan F. Madrid. Universidad de Murcia: Departamento de Biología Celular e Histología, 2015) Chiarella-Redfern, H.H.; Rayner, K.J.; Suuronen, E.J.MicroRNAs (miRNAs) are small, nonmessenger RNAs, 20-22 nucleotides in size, which regulate gene expression at the post-transcriptional level. Typically, miRNAs target the 3’ untranslated region (3'UTR) of mRNA transcripts leading to mRNA degradation or translational repression. The known dysregulation of miRNAs during cardiac ischemia and the crucial role of miRNA-dependent regulation of angiogenesis, fibrosis and hypertrophy present interesting therapeutic opportunities for repairing and regenerating the heart after myocardial infarction (MI). An understanding of the expression pattern and localization of deleterious and beneficial miRNAs during cardiac ischemia is necessary for the development of therapeutics designed to specifically treat the affected tissue and cell populations. This review focuses on the role and localization of key miRNAs implicated in MI while highlighting how their manipulation may promote cardiac repair.
- PublicationOpen AccessSulfur dioxide ameliorates rat myocardial fibrosis by inhibiting endoplasmic reticulum stress(Universidad de Murcia. Departamento de Biología Celular e Histología, 2018) Wang, Xin Bao; Cui, Hong; Du, Jun BaoMyocardial remodeling occurs after myocardial infarction (MI), the leading cause of mortality worldwide. Although myocardial fibrosis plays an important role in the process of myocardial remodeling, there is not yet an effective method of reducing it. The aim of the present study was to determine the effects of sulfur dioxide (SO2) on myocardial fibrosis and the possible mechanisms of these effects. SO2 treatment reduced the extent of myocardial fibrosis and post-MI levels of collagens I and III in the left-ventricular myocardium. SO2 also improved MI-induced thinning of the left ventricular wall while enlarging the left ventricular internal diameter. SO2 was able to reduce matrix metalloproteinase (MMP)-9 activity and increase tissue matrix metalloproteinase inhibitor (TIMP)-1 content in myocardium after MI. However, the mechanism underlying these effects of SO2 on myocardial fibrosis are unknown. Western blot analysis of endoplasmic reticulum (ER) stress-related proteins showed that glucose-regulated protein 78, C/EBP homologous protein, caspase-12, and phosphorylated eukaryotic initiation factor 2α expression levels were significantly increased in MI rats and decreased by SO2 treatment. The ER stress promoter dithiothreitol reversed these effects of SO2. In conclusion, SO2 alleviated myocardial fibrosis in MI rats through a mechanism related to inhibition of excessive ER stress.
- PublicationOpen AccessThe expression of Smad signaling pathway in myocardium and potential therapeutic effects(Universidad de Murcia. Departamento de Biología Celular e Histología, 2017) Duan, Yongjian; Zhu, Wei; Liu, Min; Ashraf, Muhammad; Xu, MeifengMyocardial infarction (MI) is a lifethreatening disease. The expression of Smad proteins in the ischemic myocardium changes significantly following myocardial infarction, suggesting a close relationship between Smad proteins and heart remodeling. Moreover, it is known that the expression of Smads is regulated by transforming growth factor-β (TGF-β) and bone morphogenetic proteins (BMP). Based on these findings, regulating the expression of Smad proteins by targeting TGF-β and BMP in the ischemic myocardium may be considered to be a possible therapeutic strategy for the treatment of myocardial infarction
- PublicationRestrictedYin-Yang 1 transcription factor modulates ST2 expression during adverse cardiac remodeling post-myocardial infarction(Elsevier, 2019-05) Asensio López, María del Carmen; Lax Pérez, Antonio Manuel; Fernández del Palacio, María J; Sassi, Yassine; Hajjar, Roger J; Januzzi, James L; Bayes Genis, Antoni; Pascual Figal, Domingo A; MedicinaBackground: The cardioprotective effects of metformin remain poorly defined. Interleukin (IL)-33/ST2L signaling is a novel cardioprotective pathway, which is antagonized by the soluble isoform sST2. No data exist about the regulation of ST2 expression. This study aimed to evaluate the pathophysiological implication of Yin-Yang 1 (Yy1) transcription factor in cardiac remodeling and the expression of the soluble ST2 isoform. Methods and results: Myocardial infarction (MI) was induced in Wistar rats randomly receiving metformin or saline solution by permanent ligation of the left anterior coronary artery. In addition, a model of cardiomyocyte "biochemical strain" was used. Metformin administration improved post-MI cardiac remodeling, an effect that was associated with increased IL-33 and reduced sST2 levels in the myocardium. The anti-remodeling effects of metformin were also associated with a decrease in the transcription factor Yy1 intranuclear level and lower levels of phosphorylated HDAC4 within the cytoplasmic space. These effects were also observed in a cardiomyocyte biochemical strain model, where Yy1 silencing or HDAC4 inhibition blocked sST2 production in cardiomyocytes. Metformin blocked the HDAC4 phosphorylation induced by MI, preventing its export from the nucleus to the cytosol. The presence of dephosphorylated HDAC4 in the nucleus acted as a co-repressor of Yy1, repressing sST2 expression. Conclusion: The transcription factor Yy1 regulates sST2 expression, and repression of Yy1 by metformin results in lower levels of sST2 that are associated with favorable myocardial remodeling. The manipulation of YY1 or its co-repressor HDAC4 emerge as new targets to modulate ST2/IL33 signaling and prevent adverse cardiac remodeling.