This report examines differences in risk of myocardial infarction and stroke (cardiovascular events) between the cyclooxygenase-2 (COX-2) inhibitors Rofecoxib, Celecoxib, and Valdecoxib, and the traditional nonsteroidal anti-inflammatory agents (NSAIDs) Naproxen and Ibuprofen, as well as Meloxicam, a preferential COX-2 inhibitor. The population studied was the DoD TRICARE beneficiary population greater than age 40 during the study period. In September of 2004, Rofecoxib was removed from the market due to an increased risk of cardiovascular events. In February of 2005, the Food and Drug Administration (FDA) examined the entire class of COX-2 inhibitors and recommended that Valdecoxib also be withdrawn from the market. According to Department of Defense TRICARE prescription records, COX-2 inhibitor prescription numbers were increasing rapidly and more than $7 million was spent on these agents alone in July of 2004. Logistic regression was used to analyze TRICARE prescription and diagnosis data from calendar years 2002, 2003, and 2004 for cardiovascular event risk comparisons among various NSAIDs. Rofecoxib was found to have a significantly increased risk of cardiovascular events when compared with all other medications in the study, including Valdecoxib. Odds ratios for comparison with Valdecoxib, Celecoxib, Meloxicam, Ibuprofen, and Naproxen were 1.09, 1.14, 1.15, 1.28, and 1.23. Valdecoxib showed a significant increase compared to Ibuprofen, Naproxen, and Celecoxib (odds ratios 1.21, 1.16, and 1.06). Ibuprofen showed a significantly decreased risk relative to all medications except Naproxen. When considering only cardiovascular risk, this study suggests prescribers should consider Ibuprofen or Naproxen as the primary agent of choice, with Meloxicam, and Celecoxib as reasonable second choices. Ultimately, the decision must also weigh the patient's risk of gastrointestinal side effects and cost of therapy.

Bakgrund : Vid hjärt- och kärlsjukdomar är kvinnor degraderade, de får sämre behandling jämfört med män, mindre forskning sker på kvinnor och de får oftare fel eller ingen diagnos. I och med att mannen varit normen och referensramen, behandlas även kvinnor efter samma kriterier. Kvinnors symtom på hjärtinfarkt skiljer sig från mannens. Syftet : Syftet med litteraturöversikten var att belysa kvinnors upplevelse av att drabbas av hjärtinfarkt. Metod : Studien genomfördes som en litteraturöversikt. Artiklarna söktes i databaserna Cinahl och PubMed vilket resulterade i elva kvalitativa artiklar. Resultat : Kvinnor upplevde fysiska symtom från olika delar av kroppen, det kan vara från mag-tarmkanalen, extremiteter och bröstregionen. De förnekar symtomen och försöker komma på orsaker till varför de uppstår. Vården ger bristfällig information och tar dem inte på allvar vilket leder till osäkerhet. Kvinnor mår fortfarande dåligt flera månader efter infarkten och har svårt att klara vardagen. De behöver stöd från familjen som kan stötta och finnas till, även om de inte alltid berättar hur de mår. Slutsats : Kvinnor upplever en rad olika symtom när de drabbas av hjärtinfarkt och symtom kan uppstå från olika delar på kroppen, inte bara i bröstregionen. De upplever också att vårdpersonalen ger bristfällig information och inte tar dem på allvar när de söker för sina symtom. Många kvinnor har kvarvarande symtom flera månader efter infarkten. / Background : When it comes to heart disease, women are degraded. Women get worse treatment, more often wrong or no diagnosis and research is less in women. As the man is the norm and reference the women also get treated after the same criteria. Women’s symptoms are different compered to men. Aim : The aim of this study was to explore women’s experiences of suffering from a myocardial infarction. Methods : The design is a literature review. Data collection occurred in the databases Cinahl and PubMed which resulted in eleven qualitative articles. Result s: Women experienced symptoms from different parts of the body, which may be from the gastrointestinal area, extremities and breast region. They deny the symptoms and try to find reasons why they occur. Care provides give lack of information and does not take them seriously, which causes women to feel insecure. Women still feel bad several months after the infarction and have difficulty coping with everyday life. They need support from the family that can give them support and help, although they do not always tell family how they feel. Conclusion : Women experience a variety of symptoms when they suffer from myocardial infarction, and symptoms may start from different parts of the body, not just in the breast region. They also experience that the caregiver provides inadequate information and do not take them seriously when they seek medical care. Many women have remaining symptoms several months after the infarction.

OBJECTIVES The aim of this study was to test the hypothesis that hypothermia and early reperfusion are synergistic for limiting infarct size when an acutely occluded coronary is associated with cardiac arrest. BACKGROUND Cohort studies have shown that 1 in 4 post-cardiac arrest patients without ST-segment elevation has an acutely occluded coronary artery. However, many interventional cardiologists remain unconvinced that immediate coronary angiography is needed in these patients. METHODS Thirty-two swine (mean weight 35 +/- 5 kg) were randomly assigned to 1 of the following 4 treatment groups: group A, hypothermia and reperfusion; group B, hypothermia and no reperfusion; group C, no hypothermia and reperfusion; and group D, no hypothermia and no reperfusion. The left anterior descending coronary artery was occluded with an intracoronary balloon, and ventricular fibrillation was electrically induced. Cardiopulmonary resuscitation was begun after 4 min of cardiac arrest. Defibrillation was attempted after 2 min of cardiopulmonary resuscitation. Resuscitated animals randomized to hypothermia were rapidly cooled to 34 degrees C, whereas those randomized to reperfusion had such after 45 min of left anterior descending coronary artery occlusion. RESULTS At 4 h, myocardial infarct size was calculated. Group A had the smallest infarct size at 16.1 +/- 19.6% (p < 0.05). Group C had an intermediate infarct size at 29.5 +/- 20.2%, whereas groups B and D had the largest infarct sizes at 41.5 +/- 15.5% and 41.1 +/- 15.0%, respectively. CONCLUSIONS Acute coronary occlusion is often associated with cardiac arrest, so treatment of resuscitated patients should include early coronary angiography for potential emergent reperfusion, while providing hypothermia for both brain and myocardial protection. Providing only early hypothermia, while delaying coronary angiography, is not optimal. (J Am Coll Cardiol Intv 2016; 9: 2403-12)

The myocardium is known to release CPK, LDH1 , and GOT in response to ischemia as a result of myocardial infarction. This study was designed to induce the release of cardiac enzymes without adversely effecting the myocardium by perfusion hypothermia, thereby suggesting that these enzymes are not as specific in the diagnosis of myocardial infarction as once thought. Hypothermia was by in vivo perfusion of the left anterior descending coronary artery. Enzyme activity was measured from sera samples spectrophotometrically and electrophoretically. Significant CPK and LDH1 increases were observed in animals perfused between 25 and 19 C. These results indicate that, while heart function remained unchanged, an alteration occurred in the membrane integrity of the myocardial cells.

L'infarctus du myocarde (IDM) est l'une des principales causes de morbi-mortalité dans les pays développés et ce malgré l'amélioration enregistrée ces dernières années dans sa prise en charge thérapeutique. L'obésité est classée comme étant un facteur de risque majeur pour les maladies coronaires par l'American Heart Association, et concerne 14,5 % de la population française (enquête ObEpi-Roche/INSERM, 2009). En utilisant un modèle expérimental d'obésité, la souris ob/ob génétiquement dépourvue en leptine, l'objectif du présent travail de thèse a été d'étudier l'efficacité de stratégies cardioprotectrices comme le postconditionnement (PCD) ischémique ou l'exercice physique chronique contre l'IDM. La première partie de ce travail de thèse a mis en évidence une perte de la cardioprotection par PCD ischémique au cours de l'obésité. L'étude des voies de signalisation aura permis de mettre en évidence l'implication des protéines phosphatases PTEN, MKP3 et PP2C dans l'inefficacité du PCD. La seconde partie de ce travail de thèse a montré un effet cardioprotecteur de l'exercice physique chronique contre l'IDM dans un contexte expérimental d'obésité. Cet effet est associé à une augmentation des défenses enzymatiques antioxydantes, à une amélioration des fonctions mitochondriales, à une activation des voies de signalisation cardioprotectrices RISK et SAFE et enfin à une diminution des protéines phosphatases impliquées dans la régulation négative des acteurs des voies de signalisation cardioprotectrices. La preuve scientifique des bienfaits de l'exercice est aujourd'hui un argument de poids pour poursuivre les efforts entrepris par les pouvoirs publics ces dernières années à travers le Programme National Nutrition Santé pour favoriser la pratique d'une activité physique et sportive et en particulier chez les obèses. / Myocardial infarction (MI) remains the leading cause of morbidity and mortality in the developing countries despite significant therapeutic advances over these last years. Obesity is a major risk factor for coronary heart disease according to the American Heart Association and concern 14.5% of the French population (ObEpi-Roche/INSERM survey, 2009). Using the leptin-deficient ob/ob mice, an animal model of obesity, the aim of the present thesis was to investigate the efficacy of cardioprotective strategies such as ischemic postconditioning (PCD) or chronic physical exercise against MI. In the first part of this thesis, we have found that the cardioprotective effects of PCD vanish with obesity. The investigation of the cardioprotective pathways has revealed that protein phosphatases such as PTEN, MKP3 and PP2C are involved in the inability of PCD to protect the heart. The second part of this thesis has demonstrated for the first time a cardioprotective effect of chronic physical exercise against MI in an experimental model of obesity. This effect was associated with increased antioxidant enzymes, improved mitochondrial function, activation of the cardioprotective RISK and SAFE pathways and finally a decrease in the related protein phosphatases levels. The scientific proofs given by this work underlines the “Programme National Nutrition Santé” developed by the French government to encourage all people and especially obese people to observe physical and sport activities.

Orientador: Marcos Ferreira Minicucci / Resumo: Introdução: As doenças cardiovasculares são as principais causas de mortalidade em todo o mundo. O infarto agudo do miocárdio com supradesnivelamento de segmento ST (IAMCSST) vem apresentando redução da mortalidade após a introdução das terapias de reperfusão. Diversos fatores estão associados a pior prognóstico e foi evidenciado que massa e função muscular podem estar associadas a comorbidades como hipertensão arterial sistêmica, síndrome metabólica, diabetes mellitus, obesidade e morte precoce. A força e massa muscular são regulados por diversos fatores entre os quais podemos destacar a miostatina. A miostatina, conhecida classicamente como regulador negativo da musculatura tem apresentado papel controverso na literatura, sendo por vezes relacionada a perda de massa muscular. Até o presente momento não há estudos investigando o papel da miostatina nas síndromes coronarianas agudas. Objetivo: O objetivo do presente estudo é avaliar a associação dos valores séricos de miostatina, com a massa e função muscular, tempo de internação e mortalidade hospitalar de pacientes com IAMCSST admitidos no Hospital das Clínicas da Faculdade de Medicina de Botucatu. Materiais e métodos: Trata-se de um estudo prospectivo observacional com pacientes admitidos com diagnóstico de IAMCSST no Hospital das Clínicas da Faculdade de Medicina de Botucatu, no período de maio de 2018 a fevereiro de 2019. Foram incluídos pacientes com IAMCSST, que aceitaram participar e foram recrutados nas primeiras 48 ... (Resumo completo, clicar acesso eletrônico abaixo) / Mestre

No Brasil, as doenças cardiovasculares constituem-se nas principais causas de mortalidade, sendo o infarto agudo do miocárdio a entidade nosológica mais freqüente dentre as doenças isquêmicas do coração. Os fatores de risco que predispõem as pessoas a essa doença estão relacionados a hábitos do estilo de vida e história familiar. Assim, esta investigação, de natureza descritiva, pretende identificar os fatores de risco relacionados ao meio ambiente, à biologia humana, estilo de vida, e sistema de saúde de pacientes internados em um hospital privado, até 48 horas após a ocorrência de infarto agudo do miocárdio, identificar o conhecimento quanto aos fatores de risco para o desenvolvimento de novos problemas de saúde e verificar se algumas variáveis, relacionadas aos fatores de risco de pacientes infartados em hospital público e privado, são semelhantes. O referencial teórico foi o Modelo de Campo de Saúde que compõe elementos relacionados ao meio ambiente, biologia humana, estilo de vida e sistema de saúde. Foram entrevistados 31 pacientes internados, em um hospital privado de uma cidade do interior do Estado de São Paulo, no período de janeiro a julho de 2003, após assinatura do termo de consentimento informado. Os resultados revelam que, quanto ao meio ambiente, a maioria dos pacientes era alfabetizada, 11 (35,5%) tinha o primeiro grau completo, 10 (32,2%) eram aposentados e donas-de-casa, 24 (77,4%) trabalhavam em torno de 8 a 10 horas por dia e tinham somente um emprego, e a renda familiar mensal, para 19 (61,3%), encontrava-se na faixa de 5 a 15 ou mais salários-mínimos, 22 (70,9%) eram casados e 15 (48,3%) tinham três ou mais filhos, 21 (67,7%) eram procedentes de Ribeirão Preto e região e todos residiam em zona urbana. Em relação à biologia humana, 19 (61,3%) eram do sexo masculino, aproximadamente metade 17 (54,8%) encontrava-se na faixa etária de 40 a 59 anos, 18 (58,1%) encontravam-se com sobrepeso ou obesidade classes I e II. Quanto aos antecedentes familiares, os dados mais expressivos apontam que 23 (74,2%) apresentavam hipertensão arterial sistêmica, 15 (48,3%) diabetes melittus, 17 (54,8%) infarto agudo do miocárdio e 6 (19,3%) acidente vascular cerebral. Das mulheres entrevistadas, 7 (22,6%) faziam uso algum tipo de terapia de reposição hormonal. No tocante ao estilo de vida relacionado aos hábitos alimentares, 29 (93,6%) utilizavam frituras nas refeições, 14 (45,2%) ingeriam doces e refrigerantes diariamente e 13 (41,9%) tomavam três xícaras ou mais de café ao dia, 18 (58,1%) faziam uso de bebidas alcoólicas, 10 (32,2%) eram fumantes, 9 (29,0%) ex-fumantes e 18 (58,1%) sedentários. Quanto ao estresse, 12 (38,7%) sentiam-se estressados no local de trabalho e 19 (61,3%) dormiam menos que oito horas por noite. Em relação ao sistema de saúde, 16 (51,6%) conheciam o diagnóstico, 12 (38,7%) apresentaram dúvidas acerca da doença, 21 (67,7%) utilizavam os serviços de saúde oferecidos pelo plano de saúde e 17 (54,8%) realizavam tratamento de hipertensão arterial sistêmica e diabetes melittus. Os dados revelam que os pacientes infartados estão expostos a hábitos autocriados que são passiveis de modificação havendo a necessidade de iniciar este processo educativo inclusive no período de internação hospitalar. / The cardiovascular diseases in Brazil, constitute nowadays death’s first cause and myocardial infarction is the most frequent nosological entity amonmg heart isquemical diseases. Among risk factors which predispose people committed by this disease are their life style’s and familiar history’s habits. This descriptive investigation intended to identify the risk factors related to the environment, human biology, life style and health systems of patients admitted in a private hospital, until 48 hours after the myocardial infarction; identify the knowledge’s blanket concerning to the risk factors related to new health problems’ development and verify if some variables are related to the risk factors which are similar to those of admitted patients in private and public hospitals. The theoretical referential used was the Health Model Field which constitutes the elements linked to the environment, human biology, life style an health system. We interviewed 31 internee patients in a private hospital in São Paulo’s interior, from January through July, 2003. Concerning to the environment 93,5% of the patients were literate; among them 11 (35,5%) had completed high school; related to their occupation 10 (32,2%) were retired and housewives; concerning to their working hours and job numbers, 24 (77,4%) work around 8 or 10 hours a day and have only one job; when referring to their familiar monthly income, 19 (61,3%) obtained from 5 to or more minimum salaries; 22 (70,9%) were married and 15 (48,3%) had three or more children; 21 (67,7%) were from Ribeirão Preto and its region and all of them lived in urban areas. When referring to the human biology, 19 (61,3%) were masculine and their ages varied between 40 and 59 years old; 18 (58,1%) were over weighted or fat, belonging to classes I and II; concerned to the familiar preceding, the most expressive data showed that 23 (74,2%) presented systemic arterial hypertension; 15 (48,3%) mellitus diabetes; 17 (54,8%) myocardial infarction and 6 (19,3%) cerebral vascular accident; 7 (22,6%) were feminine and were using hormones. Concerned to their life style, related to the feeding habits, 29 (93,6%) were accustomed to eat fried food; 14 (45,2%) used to eat sweeties and drink soft drinks daily; 13 (41,9%) used to drink 3 or more cups of coffee a day. When referring to the use of alcoholic drinks, 18 (58,1%) used to drink it; 10 (32,2%) were smokers and 9 (29,0%) were ex-smokers; 18 (58,1%) were sedentary. When referring to the stressing environment and sleeping patterns, 12 (38,7%) mention the work place and 19 (61,3%) sleep less than 8 hours a day. Concerning to the health system, 16 (51,6%) knew their diagnosis; 12 (38,7%) presented doubts about their diseases; 21 (67,7%) used the health services offered by their health insurance and 17 (54,8%) were under arterial hypertension and mellitus diabetes treatment. The data showed the patients who suffered by myocardial infarction are exposed to “selfcreated" habits, which may be modified and it is important to mention the necessity of raising educative programs including the patient’s permanence at the hospital.

The incidence and mortality from cardiovascular disease (CVD) in patients with chronic kidney disease (CKD) far exceeds that seen in the general population. Whilst a number of risk factors and associations have been identified in patients with CKD that may contribute to the increased risk of CVD, our understanding of the underlying pathophysiology remains poor. It has previously been reported that uraemic animals sustain larger myocardial infarcts and that this ‘reduced ischaemia tolerance’ may in part explain the excess mortality from CVD seen in CKD patients. The aim of this work was to establish an in vivo model of uraemic myocardial infarction in order to further explore the pathophysiology of uraemic CVD with particular focus on ameliorating myocardial ischaemia-reperfusion injury using ischaemic and pharmacological preconditioning. An increase in myocardial infarct size was demonstrated in the sub-total nephrectomy model of chronic uraemia, confirming previous reports in the literature. However, infarct size was not found to be increased in adenine diet induced renal failure. In addition, it was demonstrated for the first time, that the techniques of ischaemic preconditioning (IPC) and remote ischaemic preconditioning (RIPC) are both efficacious and not attenuated by chronic uraemia induced by sub-total nephrectomy or adenine diet (IPC only). Investigations were undertaken using an agent (a HIF stabiliser, FG4497) to induce pharmacological preconditioning in both animals with renal insufficiency and those without. These studies demonstrate that stabilisation of hypoxia inducible factor (HIF) may be a promising strategy to induce pharmacological preconditioning. It is hoped that this work may lay the foundations for future investigations to determine why sub-totally nephrectomised rats have larger infarcts whilst those with adenine induced renal failure, with a substantially greater degree of renal dysfunction, do not. Moreover, it is hoped that; by demonstrating that uraemia 3 does not prevent or attenuate the myocardial protection afforded by ischaemic preconditioning, the recruitment of patients with CKD will be encouraged to clinical trials of both ischaemic preconditioning and other therapies to limit myocardial infarction.

Background: Previous studies that have examined functional status in relation to vascular events have focused on the short term after events and have measured functional status a limited number of times. The trajectories of functional status before and after vascular events are not well characterized, and the factors influencing these trajectories are not well known. Methods: A comprehensive, structured, narrative review was performed on the topic of trajectories of disability and cognition surrounding vascular events. Then using 2 large population-based epidemiologic cohorts, the Northern Manhattan Study (NOMAS) and the Cardiovascular Health Study (CHS), trajectories of functional status were examined. In Analysis A, in NOMAS, the effect of inflammatory biomarkers (interleukin-6 [IL6], tumor necrosis factor receptor-1 [TNFR1], C-reactive protein [CRP], and lipoprotein-associated phospholipase-A2 [LpPLA2]) on the intercept and slope of functional status was determined over a median of 13 years, measured with yearly assessments by the Barthel index. In Analysis B, in NOMAS, a similar modeling strategy was used to examine whether subclinical ischemic disease on brain MRIs, measured by subclinical brain infarct (SBI) and white matter hyperintensity volume (WMHV), was associated with functional trajectories. In Analysis C, in CHS, participants had yearly assessments of disability with a combined activities of daily living (ADL) and instrumental ADL scale. The slope of change in disability was compared before and after vascular events (stroke and myocardial infarction [MI]). Results: In Analysis A, CRP (-0.41 BI points per 1 SD increase, 95% CI -0.82 to 0.002) and LpPLA2 (-0.40, 95% CI -0.75 to -0.04) were associated with baseline BI but not change over time. TNFR1 was associated with baseline BI (-0.93, 95% CI -1.59 to -0.26) and change over time (-0.36 BI points per year, 95% CI -0.69 to -0.03). In Analysis B, functional change was -0.85 BI points per year (95%CI -1.01 to -0.69); among those with SBI there were -0.88 additional points annually (-1.44 to -0.32). In WMHV models, annual functional change was -1.04 points (-1.2 to -0.88), with -0.74 additional points annually per SD WMHV increase (-0.99 to -0.49). In Analysis C, stroke (0.88, 95% CI 0.57-1.20, p<0.0001) was associated with a greater acute increase in disability than MI (0.20, 0.06-0.35, p=0.006). The annual increase in disability before stroke (0.06 points per year, 0.002-0.12, p=0.04) more than tripled after stroke (0.15 additional points per year, 0.004-0.30, p=0.04). The annual increase in disability before MI (0.04 points per year, 0.004-0.08, p=0.03) did not change significantly after MI (0.02 additional points per year, -0.07-0.11, p=0.7). Conclusions: In these large population-based studies with repeated measures of functional status and disability over long-term follow-up, several trajectories were found. In Analysis A, TNFR1 predicted worse overall functional status as well as accelerated decline over time. In Analysis B, both SBI and WMHV were associated with accelerated decline. In Analysis C, there was a steeper decline in function after stroke but not MI. These findings help to elucidate the course and potential etiologies of long-term functional decline related to vascular events, and they suggest directions for future research in this area.

Efferocytosis, the clearance of apoptotic cells including apoptotic neutrophils by macrophage phagocytosis, is a key cellular mechanism for resolution of inflammation and tissue repair. Cyclin-dependent kinases (CDKs) 7 and 9 phosphorylate RNA polymerase II that is vital for neutrophil transcriptional capacity. CDK inhibitors such as R-roscovitine, and the more selective inhibitor AT7519, induce neutrophil apoptosis and promote resolution of several mouse models of inflammation including acute lung inflammation. The hypothesis investigated here was that AT7519 would promote neutrophil apoptosis (i) in the infarcted heart, leading to macrophage polarisation, angiogenesis, reduced infarct expansion and retention of cardiac function and (ii) in the peritoneum, enhancing resolution of sterile peritonitis. AT7519 (1μM) induced apoptosis of mouse unstimulated-bone marrow derived neutrophils and thioglycollate-stimulated neutrophils in vitro in a time- and caspase-dependent manner, but did not alter activation assessed by calcium flux in response to the synthetic formyl peptide (fMLF) or platelet-activating factor (PAF). Only high concentrations of AT7519 (10 μM) induced monocyte/macrophage apoptosis and this was likely due to saturated phagocytosis of apoptotic neutrophils induced by high concentration of AT7519. Myocardial infarction (MI) was induced by coronary artery ligation in adult male mice and infarct volume was assessed 7 or 21 days later by in vitro optical projection tomography (OPT). The novel use of OPT for this purpose was validated by demonstrating correlation with infarct volume obtained by late-gadolinium enhanced magnetic resonance imaging in vivo and with infarct area assessed by histological staining (Masson’s Trichrome) in tissue sections. AT7519 (30 mg/kg i.p.) increased the number of apoptotic neutrophils (cleaved caspase-3 and Ly6G +ve) in the heart when administered after MI, but this was not associated with any subsequent alteration in macrophage polarisation, vessel density, infarct expansion or structural and functional remodelling of the left ventricle. In contrast, induction of neutrophil apoptosis by AT7519 (30mg/kg i.p.) successfully promoted macrophage polarisation and the resolution of inflammation associated with peritonitis elicited by either 10% thioglycollate or by 1mg zymosan. AT7519 treatment also reduced the number of CD19+ B cells, Foxp3+CD4+ T cells and eosinophils in peritoneal lavage, and prolonged the phase of monocyte recruitment in zymosan-induced peritonitis. In conclusion, AT7519 successfully induced mouse neutrophil apoptosis in vitro, as well as in vivo in experimental MI and peritonitis. Subsequent promotion of inflammation resolution in peritonitis was not matched by improved outcome following MI. Unexpected effects of CDK inhibition on monocytes, T cells and eosinophils that are necessary for myocardial infarct repair may have compromised any beneficial effects resulting from promotion of in situ neutrophil apoptosis. CDK inhibition may therefore have therapeutic potential for the treatment of peritonitis, but not for prevention of infarct expansion and detrimental ventricular remodelling after MI.