Ender Ornek, Cağin Mustafa Ureyen, Alparslan Kurtul, Fatih Oksüz
{"title":"土耳其白喉心肌炎发病多年。","authors":"Ender Ornek, Cağin Mustafa Ureyen, Alparslan Kurtul, Fatih Oksüz","doi":"10.5152/akd.2012.078","DOIUrl":null,"url":null,"abstract":"We would like to thank the author of the letter for kind interest to our article and for sharing their study results. In our case, myocardial infarction (MI) after carbon monoxide (CO) intoxication developed in a patient with underlying coronary artery disease (previous stent implantation) (1). However, in their case MI developed in a young subject with no history of coronary artery disease. They reported that, although successful reperfusion was achieved in infarct related artery, complete recovery of myocardial function cannot be achieved. The causes of these were discussed. We congratulate the authors for this very interesting and important report. Whatever the status of the patient, immediate reperfusion (preferably primary percutaneous intervention if possible) treatment is mandatory as recommended in guidelines in these patients. Major issue is that, reperfusion treatment may not be enough in CO intoxication induced MI. Oxygen administration or hyperbaric oxygen therapy should be considered in patients with CO poisoning and cardiac toxicity (MI). Because, as reported in the case, successful TIMI-3 flow restoration may not completely salvage myocardium. The reason of is that CO has a more generalized toxic effect on myocardium apart from a limited toxic effect localized at infarct related area. CO intoxication may cause acute MI in those with or without preexisting CAD, through various complex mechanisms. CO attaches to the hemoglobin (Hb) and blocks the capacity to carry oxygen. Carboxyhemoglobin may cause MI by severe generalized tissue hypoxia (2). Secondly, CO also has direct toxic effect on myocardial mitochondria (3). Thirdly, CO can trigger thrombus formation due to increased platelet aggregability and polycythemia (2). Consequently, CO intoxication may cause acute MI in those with or without preexisting CAD. We recommend strict electrocardiographic and enzymatic monitoring of all patients in the first hours after CO exposure.","PeriodicalId":55524,"journal":{"name":"Anadolu Kardiyoloji Dergisi-The Anatolian Journal of Cardiology","volume":" ","pages":"279-80"},"PeriodicalIF":0.0000,"publicationDate":"2012-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.5152/akd.2012.078","citationCount":"6","resultStr":"{\"title\":\"Diphtheria myocarditis in Turkey after years.\",\"authors\":\"Ender Ornek, Cağin Mustafa Ureyen, Alparslan Kurtul, Fatih Oksüz\",\"doi\":\"10.5152/akd.2012.078\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We would like to thank the author of the letter for kind interest to our article and for sharing their study results. In our case, myocardial infarction (MI) after carbon monoxide (CO) intoxication developed in a patient with underlying coronary artery disease (previous stent implantation) (1). However, in their case MI developed in a young subject with no history of coronary artery disease. They reported that, although successful reperfusion was achieved in infarct related artery, complete recovery of myocardial function cannot be achieved. The causes of these were discussed. We congratulate the authors for this very interesting and important report. Whatever the status of the patient, immediate reperfusion (preferably primary percutaneous intervention if possible) treatment is mandatory as recommended in guidelines in these patients. Major issue is that, reperfusion treatment may not be enough in CO intoxication induced MI. Oxygen administration or hyperbaric oxygen therapy should be considered in patients with CO poisoning and cardiac toxicity (MI). Because, as reported in the case, successful TIMI-3 flow restoration may not completely salvage myocardium. The reason of is that CO has a more generalized toxic effect on myocardium apart from a limited toxic effect localized at infarct related area. CO intoxication may cause acute MI in those with or without preexisting CAD, through various complex mechanisms. CO attaches to the hemoglobin (Hb) and blocks the capacity to carry oxygen. Carboxyhemoglobin may cause MI by severe generalized tissue hypoxia (2). Secondly, CO also has direct toxic effect on myocardial mitochondria (3). Thirdly, CO can trigger thrombus formation due to increased platelet aggregability and polycythemia (2). Consequently, CO intoxication may cause acute MI in those with or without preexisting CAD. We recommend strict electrocardiographic and enzymatic monitoring of all patients in the first hours after CO exposure.\",\"PeriodicalId\":55524,\"journal\":{\"name\":\"Anadolu Kardiyoloji Dergisi-The Anatolian Journal of Cardiology\",\"volume\":\" \",\"pages\":\"279-80\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2012-05-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://sci-hub-pdf.com/10.5152/akd.2012.078\",\"citationCount\":\"6\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Anadolu Kardiyoloji Dergisi-The Anatolian Journal of Cardiology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5152/akd.2012.078\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"2012/3/13 0:00:00\",\"PubModel\":\"Epub\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Anadolu Kardiyoloji Dergisi-The Anatolian Journal of Cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5152/akd.2012.078","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2012/3/13 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
We would like to thank the author of the letter for kind interest to our article and for sharing their study results. In our case, myocardial infarction (MI) after carbon monoxide (CO) intoxication developed in a patient with underlying coronary artery disease (previous stent implantation) (1). However, in their case MI developed in a young subject with no history of coronary artery disease. They reported that, although successful reperfusion was achieved in infarct related artery, complete recovery of myocardial function cannot be achieved. The causes of these were discussed. We congratulate the authors for this very interesting and important report. Whatever the status of the patient, immediate reperfusion (preferably primary percutaneous intervention if possible) treatment is mandatory as recommended in guidelines in these patients. Major issue is that, reperfusion treatment may not be enough in CO intoxication induced MI. Oxygen administration or hyperbaric oxygen therapy should be considered in patients with CO poisoning and cardiac toxicity (MI). Because, as reported in the case, successful TIMI-3 flow restoration may not completely salvage myocardium. The reason of is that CO has a more generalized toxic effect on myocardium apart from a limited toxic effect localized at infarct related area. CO intoxication may cause acute MI in those with or without preexisting CAD, through various complex mechanisms. CO attaches to the hemoglobin (Hb) and blocks the capacity to carry oxygen. Carboxyhemoglobin may cause MI by severe generalized tissue hypoxia (2). Secondly, CO also has direct toxic effect on myocardial mitochondria (3). Thirdly, CO can trigger thrombus formation due to increased platelet aggregability and polycythemia (2). Consequently, CO intoxication may cause acute MI in those with or without preexisting CAD. We recommend strict electrocardiographic and enzymatic monitoring of all patients in the first hours after CO exposure.