Reperfusion Therapy For Myocardial Infarction Research Articles

Shaping the Future of Cardiac Wellness: Exploring Revolutionary Approaches in Disease Management and Prevention

Cardiovascular diseases (CVDs) remain a leading cause of morbidity and mortality worldwide. Effective prevention and management strategies are essential to reduce the burden of CVDs. This review summarizes recent advances in the prevention and management of CVDs. In terms of prevention, lifestyle modifications, such as diet, exercise, and smoking cessation, remain important strategies. Pharmacological interventions, including statins, antiplatelet agents, and antihypertensive medications, have also shown benefits. Innovative approaches, such as genetic testing and risk stratification, targeted prevention strategies, and the use of mobile health technology, are being explored. In terms of management, acute management strategies, such as reperfusion therapy for myocardial infarction, acute heart failure management, and stroke management, have improved outcomes. Chronic management strategies, including medical therapy for heart failure, arrhythmia management, and device therapy for heart failure, have also shown benefits. Innovative approaches, such as precision medicine and personalized treatment, the use of artificial intelligence in diagnosis and treatment, and advances in traditional Chinese and regenerative medicine, are being investigated. While recent advances in the prevention and management of CVDs are promising, challenges remain in implementing these strategies, including cost-effectiveness, access to care, and resistance to change in clinical practice. Continued research and innovation are essential to reduce the burden of CVDs and improve patient outcomes.

Efficacy of tanshinone IIA in rat models with myocardial ischemia-reperfusion injury: a systematic mini-review and meta-analysis.

Myocardial ischemia-reperfusion injury (MIRI) refers to severe damage to the ischemic myocardium following the restoration of blood flow, and it is a major complication of reperfusion therapy for myocardial infarction. Notably, drugs such as metoprolol have been utilized to reduce ischemia-reperfusion injury. Tanshinone IIA is a major constituent extracted from Salvia miltiorrhiza Bunge. Recently, tanshinone IIA has been studied extensively in animal models for controlling MIRI. Therefore, we conducted a meta-analysis on the application of tanshinone IIA in rat models with MIRI to evaluate the therapeutic effects of tanshinone IIA. A comprehensive search was conducted across PubMed, Web of Science, Embase, the Cochrane Library, the China National Knowledge Infrastructure database, the Wanfang database, and the Chinese Scientific Journal Database to gather studies on tanshinone IIA intervention in rat models with MIRI.We employed SYRCLE's risk of bias tool to assess study quality. The primary outcome indicators were superoxide dismutase (SOD) and malondialdehyde (MDA). Myocardial infarction area was a secondary outcome indicator. This study was registered at PROSPERO (registration number CRD 42022344447). According to the inclusion and exclusion criteria, 15 eligible studies were selected from 295 initially identified studies. In rat models with MIRI, tanshinone IIA significantly increased SOD levels while reducing MDA levels and myocardial infarction area. Moreover, the duration of myocardial ischemia influenced the effectiveness of tanshinone IIA. However, additional high-quality research studies are needed to establish the efficacy and definitive guidelines for the use of tanshinone IIA. Animal studies demonstrated that tanshinone IIA exerted a significant therapeutic effect when the ischemia duration was less than 40 minutes. Tanshinone IIA was found to be more effective when administered via intravenous, intraperitoneal, and intragastric routes at doses above 5 mg/kg. Additionally, treatment with tanshinone IIA at all stages-prior to myocardial ischemia, after ischemia but before reperfusion, prior to ischemia and after reperfusion, and after reperfusion-showed satisfactory results. Tanshinone IIA enhanced SOD activity and reduced MDA levels, thereby ameliorating oxidative stress damage during MIRI. Additionally, it reduced the myocardial infarction area, indicating its effectiveness in mitigating MIRI-induced damage in rats and demonstrating a myocardial protective effect. These findings contribute valuable insights for developing MIRI treatment strategies.

Leonurine pretreatment protects the heart from myocardial ischemia-reperfusion injury.

Myocardial ischemia-reperfusion (I/R), an important complication of reperfusion therapy for myocardial infarction, is characterized by hyperactive oxidative stress and inflammatory response. Leonurine (4-guanidino-n-butyl syringate, SCM-198), an alkaloid extracted from Herbaleonuri, was previously found to be highly cardioprotective both in vitro and in vivo. Our current study aimed to investigate the effect of SCM-198 preconditioning on myocardial I/R injury in vitro and in vivo, respectively, as well as to decipher the mechanism involved. Rats were pretreated with SCM-198 before subjected to 45 min of myocardial ischemia, which was followed by 24 h of reperfusion. Primary neonatal rat cardiac ventricular myocytes (NRCMs) were exposed to hypoxia (95% N2 + 5% CO2) for 12 h, and then to 12 h reoxygenation so as to mimic I/R. The enzymatic measurements demonstrated that SCM-198 reduced the release of infarction-related enzymes, and the hemodynamic and echocardiography measurements showed that SCM-198 restored cardiac functions, which suggested that SCM-198 could significantly reduce infarct size, maintaining cardiomyocyte morphology, and that SCM-198 pretreatment could significantly reduce cardiomyocytes apoptosis. Moreover, we demonstrated that SCM-198 could exert a cardioprotective effect by reducing reactive oxygen species (ROS) level and Akt phosphorylation while reducing the phosphorylation of p38 and JNK. In addition, the upregulation of p-Akt, Bcl-2/Bax induced by SCM-198 treatment were blocked by PI3K inhibitor LY294002, and the total protein level of Akt was not affected by SCM-198 pretreatment. Our experimental results indicated that SCM-198 could have a cardioprotective effect on I/R injury, which confirmed the utility of SCM-198 preconditioning as a strategy to prevent I/R injury.

Dexmedetomidine alleviates myocardial ischemia–reperfusion injury by down-regulating miR-34b-3p to activate the Jagged1/Notch signaling pathway

BackgroundMyocardial ischemia/reperfusion (I/R) injury is a fatal event that usually occurs after reperfusion therapy for myocardial infarction. Dexmedetomidine (Dex) has been shown to be beneficial in the treatment of myocardial infarction, however, its underlying mechanism for regulating I/R injury is unclear. MethodsH9c2 cell and rat models of I/R injury were established via oxygen-glucose deprivation reoxygenation (OGD/R) and occlusion of the left anterior descending branch of coronary artery, respectively. Flow cytometry, MTT, or DHE assay detected cell activity, ROS, or apoptosis, respectively. The expression levels of miR-34b-3p and related mRNAs were determined using qRT-PCR. Related protein expression levels were detected by Western blotting and ELISA test. The interaction between miR-34b-3p and Jagged1 was assessed by dual luciferase reporter and RIP assays. The morphology of cardiac tissue was examined by TTC, HE, and TUNEL labeling. ResultsDex markedly inhibited the inflammatory damage and apoptosis caused by OGD/R in H9c2 cells. MiR-34b-3p and Jagged1 levels were increased and decreased in myocardial I/R injury model, respectively, while Dex reversed this effect. Moreover, miR-34b-3p was firstly reported to directly bind and decrease Jagged1 expression, thereby inhibiting Notch signaling pathway. Transfection of agomiR-34b-3p or Jagged1 silencing eliminated Dex’s defensive impact on OGD/R-induced cardiomyocytes damage. Dex relieved the myocardial I/R injury of rats via inhibiting miR-34b-3p and further activating Notch signaling pathway. ConclusionDex protected myocardium from I/R injury via suppressing miR-34b-3p to activate Jagged1-mediated Notch signaling pathway. Our findings revealed a novel mechanism underlying of Dex on myocardial I/R injury.

A Novel Insight Into the Fate of Cardiomyocytes in Ischemia-Reperfusion Injury: From Iron Metabolism to Ferroptosis.

Ischemia-reperfusion injury (IRI), critically involved in the pathology of reperfusion therapy for myocardial infarction, is closely related to oxidative stress the inflammatory response, and disturbances in energy metabolism. Emerging evidence shows that metabolic imbalances of iron participate in the pathophysiological process of cardiomyocyte IRI [also termed as myocardial ischemia-reperfusion injury (MIRI)]. Iron is an essential mineral required for vital physiological functions, including cellular respiration, lipid and oxygen metabolism, and protein synthesis. Nevertheless, cardiomyocyte homeostasis and viability are inclined to be jeopardized by iron-induced toxicity under pathological conditions, which is defined as ferroptosis. Upon the occurrence of IRI, excessive iron is transported into cells that drive cardiomyocytes more vulnerable to ferroptosis by the accumulation of reactive oxygen species (ROS) through Fenton reaction and Haber–Weiss reaction. The increased ROS production in ferroptosis correspondingly leads cardiomyocytes to become more sensitive to oxidative stress under the exposure of excess iron. Therefore, ferroptosis might play an important role in the pathogenic progression of MIRI, and precisely targeting ferroptosis mechanisms may be a promising therapeutic option to revert myocardial remodeling. Notably, targeting inhibitors are expected to prevent MIRI deterioration by suppressing cardiomyocyte ferroptosis. Here, we review the pathophysiological alterations from iron homeostasis to ferroptosis together with potential pathways regarding ferroptosis secondary to cardiovascular IRI. We also provide a comprehensive analysis of ferroptosis inhibitors and initiators, as well as regulatory genes involved in the setting of MIRI.

TCT-204 Consequences of Covid-19 Policy on Myocardial Infarction Reperfusion Therapy and Prognosis in a High-Volume PCI Center in Chile

TCT-204 Consequences of Covid-19 Policy on Myocardial Infarction Reperfusion Therapy and Prognosis in a High-Volume PCI Center in Chile

CGMP and mitochondrial K+ channels-Compartmentalized but closely connected in cardioprotection.

The 3',5'-cGMP pathway triggers cytoprotective responses and improves cardiomyocyte survival during myocardial ischaemia and reperfusion (I/R) injury. These beneficial effects were attributed to NO-sensitive GC induced cGMP production leading to activation of cGMP-dependent protein kinase I (cGKI). cGKI in turn phosphorylates many substrates, which eventually facilitate opening of mitochondrial ATP-sensitive potassium channels (mitoKATP ) and Ca2+ -activated potassium channels of the BK type (mitoBK). Accordingly, agents activating mitoKATP or mitoBK provide protection against I/R-induced damages. Here, we provide an up-to-date summary of the infarct-limiting actions exhibited by the GC/cGMP axis and discuss how mitoKATP and mitoBK, which are present at the inner mitochondrial membrane, confer mito- and cytoprotective effects on cardiomyocytes exposed to I/R injury. In view of this, we believe that the functional connection between the cGMP cascade and mitoK+ channels should be exploited further as adjunct to reperfusion therapy in myocardial infarction. LINKED ARTICLES: This article is part of a themed issue on cGMP Signalling in Cell Growth and Survival. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v179.11/issuetoc.

Consequences of COVID-19 Pandemic on Myocardial Infarction Reperfusion Therapy and Prognosis in a High-Volume PCI Center in Chile

Background: Characterize the clinical profile, treatment, and evolution of patients with acute myocardial infarction (AMI) during the coronavirus disease 2019 (COVID-19) pandemic and compare them to a historical cohort. Methods: This was a case-control study comprising of AMI patients who were transferred to a high-volume percutaneous coronary intervention (PCI) hospital between March 3 and July 15, 2020 (n=96), and a historical cohort of patients who were transferred during the same weeks in 2019 (n=269). Results: Differing results during pandemic vs pre-pandemic included age (63±12 vs 68±12 years, p 12 hours from onset of symptoms (44.4% vs 0%, p<0.01), median door-to-device time (4 vs 3 hours, p<0.01), primary PCI (97% vs 71%, p<0.01), cardiogenic shock (19.8% vs 4.1%, p<0.01), mechanical complication (10.4% vs 1.7%, p<0.01), follow-up mortality at 30-days (19.8% vs 1.4% p<0.01) and cardiovascular deaths (12.5% vs 1.4%, p<0.01). During the outbreak, 40% of patients had positive COVID-19 status, which was a predictor for 30-day overall mortality (RR 2.90;95% CI 1.14-7.36). Conclusions: We observed a 67.4% reduction in AMI patient referrals during the pandemic. AMI patients exhibited delays in consults and treatment, higher morbidity and increased mortality. COVID-19 positivity was associated with a worse 30-day overall survival.

Consequences of COVID-19 pandemic on myocardial infarction reperfusion therapy and prognosis.

To characterize the clinical profile of patients with AMI during the COVID-19 pandemic, comparing them with a historical cohort. A case-control study of 96 patients with AMI transferred to a high-volume percutaneous coronary intervention (PCI) hospital between March and July 2020, and a historical cohort of 269 patients transferred during the same period in 2019. When comparing patients transferred during the pandemic with those of the historical cohort, the former were younger (63 ± 12 vs 68 ± 12 years, p < 0.01), had a higher frequency of hypertension (66 vs 45%, p < 0.01) and of smoking (40% vs 25%, p < 0.01). Also, during COVID-19 outbreak a higher proportion of patients had ST-elevation AMI consulting > 12 hours from the onset of symptoms (44 vs 0%, p < 0.01), a higher median door-to-device time (4 vs 3 hours, p < 0.01), a higher use of primary percutaneous coronary intervention (97 vs 71%, p < 0.01), and higher frequencies of cardiogenic shock (20 vs 4%, p < 0.01) and mechanical complications (10% vs 2%, p < 0.01). Patients during COVID pandemic had a higher thirty-day overall (20 vs 1.4%, p < 0.01) and cardiovascular mortality (13 vs 1%, p < 0.01). During the outbreak, 40% of patients had positive COVID-19 status, which was a predictor for thirty-day overall mortality (Risk ratio 2.90; 95% confidence intervals 1.14-7.36). During the pandemic patients with AMI exhibited delays in consultations and treatment, higher morbidity, and increased mortality. COVID-19 positivity was associated to worse thirty-day overall survival.

Reperfusion therapy for acute myocardial infarction with st elevation

The article is devoted to the development of new strategies for reperfusion therapy in myocardial infarction, based on the prolongation of the use of primary and salvage PCI in the acute period in patients with an initially increased risk of death in the absence of the possibility of timely implementation, as well as interventions 12–24 hours after successful thrombolysis, directed to prevent the development of relapses of ischemia and reocclusion.

Co‑expression of tissue kallikrein1 and tissue inhibitor of matrix metalloproteinase1 improves myocardial ischemia‑reperfusion injury by promoting angiogenesis and inhibiting oxidative stress.

Myocardial ischemia/reperfusion (I/R) injury is a serious complication of reperfusion therapy for myocardial infarction. At present, there is not an effective treatment strategy available for myocardial I/R. The present study aimed to investigate the effects of human tissue kallikrein 1 (hTK1) and human tissue inhibitors of matrix metalloproteinase 1 (hTIMP1) gene co-expression on myocardial I/R injury. A rat model of myocardial I/R injury and a cell model with hypoxia/reoxygenation (H/R) treatment in cardiac microvascular endothelial cells (CMVECs) were established, and treated with adenovirus (Ad)-hTK1/hTIMP1. Following which, histological and triphenyl-tetrazolium-chloride staining assays were performed. Cardiac function was tested by echocardiographic measurement. The serum levels of oxidative stress biomarkers in rats and the intracellular reactive oxygen species (ROS) levels in CMVECs were measured. Additionally, experiments, including immunostaining, reverse transcription-quantitative PCR, western blotting, and MTT, wound healing, Transwell and tube formation assays were also performed. The results of the present study demonstrated that Ad-hTK1/hTIMP1 alleviated myocardial injury and improved cardiac function in myocardial I/R model rats. Ad-hTK1/hTIMP1 also significantly enhanced microvessel formation, decreased matrix metalloproteinase (MMP)2 and MMP9 expression, and reduced oxidative stress in myocardial I/R model rats. Furthermore, Ad-hTK1/hTIMP1 significantly enhanced proliferation, migration and tube formation in H/R-treated CMVECs. Additionally, Ad-hTK1/hTIMP1 significantly decreased intracellular ROS production and γ-H2A.X variant histone expression levels in H/R-treated CMVECs. In conclusion, the results of the present study demonstrated that co-expression of hTK1 and hTIMP1 genes displayed significant protective effects on myocardial I/R injury by promoting angiogenesis and suppressing oxidative stress; therefore, co-expression of hTK1 and hTIMP1 may serve as a potential therapeutic strategy for myocardial I/R injury.

Metformin exerts cardioprotection via attenuating mitochondrial fission in cardiac ischaemia-reperfusion injury in rats

Abstract Background Cardiac ischemia/reperfusion (I/R) injury following myocardial infarction reperfusion therapy is a phenomenon that results in further cardiomyocytes death and impaired cardiac contractility. Although metformin has been shown to exert cardioprotection in addition to glycemic control, its effect on cardiac I/R injury are still controversy, and the comparative doses of metformin in cardiac I/R injury have never been investigated. Purpose We hypothesized that metformin given acutely prior to cardiac ischaemia exerts cardioprotection in rats with cardiac I/R injury via attenuating cardiac mitochondrial dysfunction, leading to improved left ventricular (LV) function. Methods Forty Male Wistar rats were subjected to cardiac I/R injury. Four treatment groups were investigated. The first group received saline as a control group. The second to the fourth groups received metformin at 100, 200, and 400 mg/kg intravenously, respectively. During the I/R protocols, the LV function, arrhythmia score, and mortality rate were determined. At the end, the hearts were rapidly removed to determine infarct size, cardiac mitochondrial function, cardiac mitochondrial dynamics, and cardiac apoptosis. Results Metformin 200 mg/kg exerted the highest level of cardioprotection through the attenuated incidence of arrhythmia, decreased infarct size (Fig. 1), improved cardiac mitochondrial function, and decreased mitochondrial fission (Fig. 1) and cardiac apoptotic markers, leading to improved cardiac function during I/R injury. Although Metformin at all doses effectively decreased infarct size, improved cardiac mitochondrial function and LV function, Metformin at 200 mg/kg exerted the best efficacy (Fig. 1). Conclusions Metformin exerts cardioprotection by attenuating mitochondrial dysfunction and decreased mitochondrial fission, leading to decreased infarct size and ultimately improved LV function after acute cardiac I/R injury in rats. These findings also indicate the potential biphasic effects of metformin on infarct size which are dose-dependent. Figure 1 Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): National Science and Technology Development Agency Thailand (NC), and Thailand Research Fund (SCC)

An international survey in Latin America on the practice of interventional cardiology during the COVID-19 pandemic, with aparticular focus on myocardial infarction.

IntroductionA reduction in the number of interventional cardiology procedures has emerged as a result of the COVID-19 pandemic. A survey was performed to quantify this decrease and the impact on the management of myocardial infarction in Latin America.MethodsA telematic survey was conducted for all countries in Latin America. Diagnostic catheterisations, coronary and structural interventions, as well as the incidence and delay to reperfusion therapy of myocardial infarction (STEMI), were recorded. Two periods were compared: from 24 February to 8 March 2020 (pre-COVID-19) and another 2‑week period that varied according to country (COVID-19).ResultsResponses were obtained from 79 centres in 20 countries. There was a significant decrease in the number of diagnostic procedures (−65.2%), coronary interventions (−59.4%), structural therapeutics (−86.1%) and STEMI care (−51.2%). A decrease was noted in the incidence of STEMI, but also a delay in the time to STEMI reperfusion. While there was a variation in activity in interventional cardiology between countries, patient behaviour was rather homogeneous.ConclusionsA significant reduction in healthcare activity has been noted during the COVID-19 pandemic, including STEMI care, with the risk of increased mortality and/or morbidity following STEMI. Healthcare providers should encourage patients with suspected symptoms of STEMI to call for emergency care to ensure rapid diagnosis and timely reperfusion treatment.Electronic supplementary materialThe online version of this article (10.1007/s12471-020-01440-y) contains supplementary material which is available to authorized users.

Electroacupuncture preconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting mitophagy mediated by the mTORC1-ULK1-FUNDC1 pathway

Myocardial ischemia/reperfusion (I/R) is an important complication of reperfusion therapy for myocardial infarction, and trimetazidine is used successfully for treatment of ischemic cardiomyopathy by regulating mitochondrial function. Moreover, electroacupuncture (EA) preconditioning was demonstrated to be cardioprotective in both in vivo rodent models and in patients undergoing heart valve replacement surgery. However, the mechanisms have not been well elucidated. Mitophagy, mediated by the mTORC1-ULK1-FUNDC1 (mTOR complex 1-unc-51-like autophagy-activating kinase 1-FUN14 domain-containing 1) pathway, can regulate mitochondrial mass and cell survival effectively to restrain the development of myocardial ischemia/reperfusion injury (MIRI). In this study, we hypothesized that EA preconditioning ameliorated MIRI via mitophagy. To test this, rapamycin, an mTOR inhibitor, was used. The results showed that EA preconditioning could reduce the infarct size and risk size, and decrease the ventricular arrhythmia score and serum creatine kinase-myocardial band isoenzyme (CK-MB), lactate dehydrogenase (LDH), and cardiac troponin T (cTnT) in MIRI rats. Moreover, it also attenuated MIRI-induced apoptosis and mitophagy accompanied by elevated mTORC1 level and decreased ULK1 and FUNDC1 levels. However, these effects of EA preconditioning were blocked by rapamycin, which aggravated MIRI, reduced adenosine triphosphate (ATP) production, and antagonized infarct size reduction. In conclusion, our results indicated that EA preconditioning protected the myocardium against I/R injury by inhibiting mitophagy mediated by the mTORC1-ULK1-FUNDC1 pathway.

PDRPS7 protects cardiac cells from hypoxia/reoxygenation injury through inactivation of JNKs.

Myocardial ischemia/reperfusion (I/R) injury is a major complication of reperfusion therapy in myocardial infarction. Ischemic myocardium produces a variety of peptides. We recently identified PDRPS7 as a novel peptide in cardiomyocytes that can be induced by hypoxia. However, the role of PDRPS7 is unknown. Here, we investigated the effects of PDRPS7 on hypoxia/reoxygenation (H/R)‐induced injury in rat cardiomyoblast H9c2 cells and NRCMs. We found that PDRPS7 improved cell survival and attenuated lactate dehydrogenase leakage following H/R in H9c2 cells and NRCMs. PDRPS7 also alleviated H/R‐induced pulsation reduction in NRCMs. Moreover, H/R‐induced cell apoptosis was decreased in the presence of PDRPS7. H/R‐induced reactive oxygen species generation was reduced by PDRPS7; in addition, PDRPS7 did not impact H2O2‐induced cell injury. Signaling analysis demonstrated that H/R increased the phosphorylation levels of JNKs, ERKs, and p38 mitogen‐activated protein kinases. However, PDRPS7 only attenuated H/R‐induced JNK phosphorylation, but not phosphorylation of ERKs and p38. PDRPS7 protected cardiomyocytes from apoptosis by inhibiting JNK phosphorylation and c‐Jun phosphorylation pathways, markedly upregulating anti‐apoptotic Bcl‐2 expression and inhibiting that of pro‐apoptotic Bax and cleaved caspase‐3. Importantly, pharmacological activation of JNKs diminished the protective effect of PDRPS7 in terms of cell survival against H/R stimulation. In summary, our study identified PDRPS7 as a novel cardioprotective peptide against H/R challenge and this action was mediated, at least in part, through inactivation of JNKs.

Adenosine receptors as therapeutic targets for the treatment of myocardial infarction and its complications. Part I. Myocardial infarction

Abstract Adenosine is an endogenous compound with cardioprotective properties that acts via A1, A2A, A2B and A3 plasma membrane receptors. Over the last several decades, the mechanisms underlying adenosine’s protective effects in the ischemic myocardium were investigated. They are the basis for ischemic preconditioning and postconditioning procedures that protect the heart from ischemia/reperfusion injury. The promising results of animal model studies have encouraged a large group of researchers to conduct clinical trials assessing the benefits of adenosine as an adjunct to reperfusion therapy in myocardial infarction. This review describes the mechanisms behind the cardioprotective effect of adenosine and presents current reports on its clinical utility in the treatment of myocardial infarction.

The Effect of Media Campaigns, Patient Characteristics, and Presenting Symptoms on Prehospital Delay in Myocardial Infarction Patients: A Prospective Cohort Study

Delays in reperfusion therapy for myocardial infarction (MI) are associated with increased mortality and morbidity, and most of this delay is due to delay in patients initiating contact with emergency services. This study assesses the impact of the Australian National Heart Foundation media campaign and identifies patient characteristics and presenting symptoms that may contribute to delay. This prospective cohort study identified patients with a diagnosis of MI admitted to a single tertiary metropolitan hospital in Perth, Western Australia from July 2013 to January 2014. Patients were interviewed and responses were categorised to determine their reasons for delaying treatment and the impact of mass media campaigns. Delay times were analysed using multivariable linear regression models for the Whole Cohort (all patients admitted to the tertiary hospital, including patients from rural and peripheral hospitals) and the Direct Admission Cohort (patients admitted directly to the tertiary hospital). Of 376 patients, 255 patients provided consent, and symptom onset-time was available for 175 patients. While almost two thirds of the cohort was aware of media campaigns, awareness was not associated with decreased prehospital delay. Median delay was 3.9hours for the Whole Cohort and 3.5hours for the Direct Admission Cohort. Delay was associated with being widowed, symptom onset on a weekday compared with weekend, past medical history of MI and coronary artery bypass graft, private compared with ambulance transport to hospital, and lack of symptoms of sweating and weakness. In addition, for the Direct Admission Cohort, age and income were also associated with delay. This study did not find an association between awareness of media campaigns and delay. This study identified important characteristics and presenting symptoms that are associated with delay, and possibly relevant to future media campaigns.

Reperfusion Therapy of Myocardial Infarction: From Classic to Modern Fibrinolysis

Reperfusion Therapy of Myocardial Infarction: From Classic to Modern Fibrinolysis

Lymphocyte Communication in Myocardial Ischemia/Reperfusion Injury.

Myocardial ischemia/reperfusion (I/R) is an important complication of reperfusion therapy for myocardial infarction (MI). It is a complex process involving metabolic and immunological factors. To date, no effective treatment has been identified. Recent Advances: Previous research has focused on the role of innate immune cells in I/R injury. In recent years, increasing evidence has accumulated for an important role for adaptive immune cells, particularly T lymphocytes. Data from ST elevation MI patients have identified prognostic significance for lymphocyte counts, particularly postreperfusion lymphopenia. Dynamic changes in circulating CD4+ T cell subsets occurring early after reperfusion are associated with development of I/R injury in the form of microvascular obstruction. Transcoronary gradients in cell counts suggest sequestration of these cells into the reperfused myocardium. These findings support existing data from mouse models indicating a role for CD4+ T cells in I/R injury. It is clear, however, the effects of lymphocytes in the ischemic myocardium are time and subset specific, with some having protective effects, while others are pathogenic. An understanding of the cellular events that lead to accumulation of lymphocytes in the myocardium, and their actions once there, is key to manipulating this process. Chemokines produced in response to ischemia and cellular injury have an important role, while lymphocyte-derived cytokines are critical in the balance between inflammation and healing. Further research into the involvement of lymphocytes in myocardial I/R injury may allow development of targeted therapies, opening a new avenue of considerable therapeutic potential. Antioxid. Redox Signal. 26, 660-675.

Reperfusion therapy of myocardial infarction in Mexico: A challenge for modern cardiology.

Mexico has been positioned as the country with the highest mortality attributed to myocardial infarction among the members of the Organization for Economic Cooperation and Development. This rate responds to multiple factors, including a low rate of reperfusion therapy and the absence of a coordinated system of care. Primary angioplasty is the reperfusion method recommended by the guidelines, but requires multiple conditions that are not reached at all times. Early pharmacological reperfusion of the culprit coronary artery and early coronary angiography (pharmacoinvasive strategy) can be the solution to the logistical problem that primary angioplasty rises. Several studies have demonstrated pharmacoinvasive strategy as effective and safe as primary angioplasty ST-elevation myocardial infarction, which is postulated as the choice to follow in communities where access to PPCI is limited. The Mexico City Government together with the National Institute of Cardiology have developed a pharmaco-invasive reperfusion treatment program to ensure effective and timely reperfusion in STEMI. The model comprises a network of care at all three levels of health, including a system for early pharmacological reperfusion in primary care centers, a digital telemedicine system, an inter-hospital transport network to ensure primary angioplasty or early percutaneous coronary intervention after fibrinolysis and a training program with certification of the health care personal. This program intends to reduce morbidity and mortality associated with myocardial infarction.