{"title":"Focus on trimetazidine in acute coronary syndrome","authors":"L. Gowdak","doi":"10.31887/HM.2018.75/GOWDAK","DOIUrl":"https://doi.org/10.31887/HM.2018.75/GOWDAK","url":null,"abstract":"Trimetazidine is an anti-ischemic agent that acts at the cellular level by shifting the cardiac energy metabolism from β-oxidation of free fatty acids to the more efficient glucose oxidation. In patients with an acute myocardial infarction (AMI) who are treated with thrombolysis and/or a percutaneous coronary intervention (PCI), ischemia-reperfusion injury may occur after reestablishing myocardial blood supply to an ischemic region. In animal models of ischemia-reperfusion injury, trimetazidine markedly reduced casein kinase and lactate dehydrogenase activities and decreased the infarct size. In patients with an AMI, trimetazidine reduced the rate of any form of reperfusion arrhythmias, more so with potentially life-threatening arrhythmias. In the EMPI-FR study (European Myocardial Infarction Project – Free Radicals), in the subset of patients not receiving thrombolysis assessed as per-protocol analysis, there was an 11.9% and 13.8% risk reduction in 35-day mortality and in-hospital mortality, respectively, in patients receiving trimetazidine. More recently, it was shown that trimetazidine, as an adjunctive therapy to PCI, reduced myocardial damage and preserved left ventricular function more than PCI alone. In a large registry of patients with AMI, the use of trimetazidine was associated with significant reductions in all-cause mortality and combined major adverse cardiac events (MACE), a finding that was confirmed in the first meta-analysis to report these benefits in patients with AMI treated with trimetazidine, showing a 67% risk reduction for MACE, which was defined as the composite of death, recurrent nonfatal MI, target vessel revascularization, coronary artery bypass graft, recurrence of angina, and/or hospitalization for heart failure. L Heart Metab. 2018;75:22-27","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"36 1","pages":"22-28"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88562839","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"From atropine eye drops to takotsubo syndrome in an 89-year-old lady","authors":"M. Scali, M. Marzilli","doi":"10.31887/HM.2018.75/SCALI","DOIUrl":"https://doi.org/10.31887/HM.2018.75/SCALI","url":null,"abstract":"A few hours after receiving atropine drops for an eye examination, an 89-year-old lady complained of compressive chest pain that was associated with an ST-segment elevation in the anterolateral and inferior leads. Emergency coronary angiography showed normal coronary arteries; however, contrast ventriculography showed an “apical ballooning” pattern (octopus trap) in end systole that is typical of takotsubo syndrome. The left ventricular function, monitored by a 2D echocardiogram, fully recovered at follow-up. Atropine eye drops can have systemic effects, especially in the elderly, inducing, through a sympathetic imbalance, an acute coronary microvascular dysfunction that may trigger takotsubo syndrome in the absence of classic emotional stress. This case report provides support for the hypothesis that takotsubo syndrome is a manifestation of acute microvascular dysfunction. L Heart Metab. 2018;75:29-32","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"86 1","pages":"29-32"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73014407","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Cardiac energy metabolism in mild and severe ischemia","authors":"G. Lopaschuk","doi":"10.31887/hm.2018.75/lopaschuk","DOIUrl":"https://doi.org/10.31887/hm.2018.75/lopaschuk","url":null,"abstract":"The heart must continuously produce large amounts of adenosine triphosphate (ATP) to maintain contractile function. The majority of this cardiac ATP is derived from mitochondrial oxidative phosphorylation, a process that consumes large amounts of oxygen. Ischemia results in a mismatch between oxygen demand and oxygen supply to the heart, which, in turn, results from a decrease in mitochondrial oxidative phosphorylation and an energy deficient state in the heart muscle. The magnitude of the decrease in mitochondrial oxidative phosphorylation during ischemia depends on the severity of ischemia and the degree to which oxygen supply is impaired. Glycolysis (which does not require oxygen) accelerates during ischemia in an attempt to increase ATP production. During ischemia, there are also changes in the source of energy substrate used to support residual mitochondrial oxidative phosphorylation, which includes an increase in the contribution of fatty acid oxidation, a decrease in glucose oxidation, and residual mitochondrial oxidative metabolism. Increased glycolysis accompanied by a decrease in glucose oxidation during ischemia results in an accumulation of H+ and lactate. Accumulation of these glycolytic byproducts decreases cardiac efficiency and adds to the severity of the oxygen supply-demand mismatch seen during ischemia. Therapeutic strategies that inhibit the contribution of fatty acid oxidation to residual mitochondrial oxidative metabolism will result in an increase in glucose oxidation, an improved coupling between glycolysis and glucose oxidation, a decrease in glycolytic byproduct accumulation, an increase in cardiac efficiency, and a decrease in the severity of ischemic injury. L Heart Metab. 2018;75:33-36","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"61 1","pages":"33-36"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80692663","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acute coronary syndrome: the illusion of treatment!","authors":"M. Marzilli","doi":"10.31887/hm.2018.75/marzilli2","DOIUrl":"https://doi.org/10.31887/hm.2018.75/marzilli2","url":null,"abstract":"Acute coronary syndrome is a critical area for the “illusion of treatment,” which is a phenomenon where there is an unjustified enthusiasm for a treatment by both patients and doctors. Therapeutic illusion is not the only factor driving overtreatment, as treatment decisions are also influenced by reimbursement pressures, quality measures, fear of litigation, and patients’ expectations. Despite the other factors involved in overtreatment, therapeutic illusion is the one contributor that all cardiologists can begin to address immediately by evaluating their own practice, verifying adherence to the guidelines, and applying simple conscious heuristics to more rational evidence-based care. L Heart Metab. 2018;75:19-21","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"9 1","pages":"19-21"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75188122","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The changing face of acute coronary syndromes","authors":"S. A. Yaseen, A. Badri, Wei, C. Shufelt, N. Merz","doi":"10.31887/HM.2018.75/ALYASEEN","DOIUrl":"https://doi.org/10.31887/HM.2018.75/ALYASEEN","url":null,"abstract":"Acute coronary syndrome is a leading cause of ischemic heart disease mortality and morbidity. Despite the rising prevalence of obesity and diabetes, the epidemiology of acute coronary syndrome appears to be shifting with an observed decreased incidence of ST-segment elevation myocardial infarction (STEMI) and hospital mortality accompanied by an increased incidence of non–STEMI across all age groups and in both women and men. Underlying potential contributors to this change include aging of the population, implementation of primary and secondary prevention strategies, which result in changes in atherosclerotic coronary artery disease, and technological improvements that have increased the sensitivity of cardiac diagnostic tests. Appreciation of sex differences in ischemic heart disease, identification of nonobstructive coronary disease, and the diagnosis of coronary microvascular dysfunction as contributors to ischemia with no obstructive coronary artery disease (INOCA) is increasing. Work is ongoing to fill the gaps in knowledge needed for evidence-based guidelines for the changing face of acute coronary syndrome. L Heart Metab. 2018;75:4-8","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"14 1","pages":"4-8"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76131073","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Does unstable angina still exist","authors":"C. Rambarat, I. Elgendy, C. Pepine","doi":"10.31887/HM.2018.75/RAMBARAT","DOIUrl":"https://doi.org/10.31887/HM.2018.75/RAMBARAT","url":null,"abstract":"","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"59 1","pages":"15-18"},"PeriodicalIF":0.0,"publicationDate":"2018-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77116198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Acute coronary syndrome without coronary obstructions: Diagnosis and treatment","authors":"G. Niccoli, G. Scalone, F. Crea","doi":"10.31887/HM.2018.75/NICCOLI","DOIUrl":"https://doi.org/10.31887/HM.2018.75/NICCOLI","url":null,"abstract":"Myocardial infarction with no obstructive coronary atherosclerosis (MINOCA) is a syndrome with different causes. Its prevalence ranges between 5% and 25% of all myocardial infarctions. The prognosis is extremely variable, as it strictly depends on the cause of MINOCA. Clinical history, electrocardiography, cardiac enzymes, echocardiography, coronary angiography, and left ventricular angiography represent first-level diagnostic investigations to identify the causes of MINOCA. This preliminary step helps divide patients presenting with epicardial or microvascular patterns and to perform specific additional tests for an adequate management workflow. This article will focus on the diagnosis and treatment of MINOCA. L Heart Metab. 2018;75:9-14","PeriodicalId":35477,"journal":{"name":"Heart and Metabolism","volume":"21 2 1","pages":"9-14"},"PeriodicalIF":0.0,"publicationDate":"2018-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78043551","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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