{
    "abstract": "We assessed the extent and the time course of the acute phase response following myocardial cell necrosis and its relationship with the presence of preinfarction unstable angina (UA).\nElevated levels of acute phase proteins have been reported in patients with UA and in patients with acute myocardial infarction (MI).\nC-Reactive Protein (CRP), serum amyloid A protein (SAA) and interleukin-6 (IL-6) were measured in 36 patients with MI admitted within 3 h from symptoms onset. All patients had normal levels of creatine kinase and of troponin T on admission, rising above diagnostic levels within 6 to 12 h. Blood samples for CRP, SAA and IL-6 measurements were taken on admission, at 6, 24, 48, 72 h and at discharge.\nTwenty of the 36 patients studied presented an unheralded MI (Group 1); the remaining 16 patients had symptoms of unstable angina in the preceding 7 days (Group 2). Group 2 patients have much higher levels of CRP and SAA on admission (median values 8.8 vs. 3 mg/L and 28 vs. 3.4 mg/L, respectively, all p<0.001). Following the necrotic insult, despite similar infarct size and clinical signs of reperfusion, Group 2 patients had strikingly higher peaks of IL-6 (median values 85.2 vs. 19 pg/ml, p<0.05), CRP (50 vs. 31.4 mg/L, p<0.05) and SAA (228 vs. 45 mg/L, p<0.001).\nOur data demonstrated that the acute phase response is greatly enhanced in patients with preinfarction UA compared with those presenting with an unheralded MI. The significant differences in acute phase response observed in these two clinical presentations of MI indicate a major difference in their underlying pathogenetic components.",
    "authors": [
        {
            "affiliation": "Department of Cardiology, Catholic University, Rome, Italy.",
            "firstname": "G",
            "initials": "G",
            "lastname": "Liuzzo"
        },
        {
            "affiliation": null,
            "firstname": "L M",
            "initials": "LM",
            "lastname": "Biasucci"
        },
        {
            "affiliation": null,
            "firstname": "J R",
            "initials": "JR",
            "lastname": "Gallimore"
        },
        {
            "affiliation": null,
            "firstname": "G",
            "initials": "G",
            "lastname": "Caligiuri"
        },
        {
            "affiliation": null,
            "firstname": "A",
            "initials": "A",
            "lastname": "Buffon"
        },
        {
            "affiliation": null,
            "firstname": "A G",
            "initials": "AG",
            "lastname": "Rebuzzi"
        },
        {
            "affiliation": null,
            "firstname": "M B",
            "initials": "MB",
            "lastname": "Pepys"
        },
        {
            "affiliation": null,
            "firstname": "A",
            "initials": "A",
            "lastname": "Maseri"
        }
    ],
    "conclusions": null,
    "copyrights": null,
    "doi": "10.1016/s0735-1097(99)00432-5",
    "journal": "Journal of the American College of Cardiology",
    "keywords": [],
    "methods": null,
    "publication_date": "1999-11-30",
    "pubmed_id": "10577559",
    "results": "Twenty of the 36 patients studied presented an unheralded MI (Group 1); the remaining 16 patients had symptoms of unstable angina in the preceding 7 days (Group 2). Group 2 patients have much higher levels of CRP and SAA on admission (median values 8.8 vs. 3 mg/L and 28 vs. 3.4 mg/L, respectively, all p<0.001). Following the necrotic insult, despite similar infarct size and clinical signs of reperfusion, Group 2 patients had strikingly higher peaks of IL-6 (median values 85.2 vs. 19 pg/ml, p<0.05), CRP (50 vs. 31.4 mg/L, p<0.05) and SAA (228 vs. 45 mg/L, p<0.001).",
    "title": "Enhanced inflammatory response in patients with preinfarction unstable angina.",
    "xml": "<Element 'PubmedArticle' at 0x788502fea7a0>"
}