Acute myocardial infarction caused by coronary tumour embolism.

C-reactive protein have different relations to subsequent mortality and myocardial infarction after acute coronary syndrome: a GUSTO-IV substudy. A. FAMI Study Investigators. High-sensitivity C-reactive protein is within normal levels at the very onset of first ST-segment elevation acute myocardial infarc-tion in 41% of cases: a multiethnic case-control study. value of C-reactive protein and cardiac troponin I in primary percutaneous interventions for ST-elevation myo-cardial infarction. Late microvascular obstruction after acute myocardial infarction: relation with cardiac and inflammatory markers. Lip GY. A multimarker risk stratification approach to non-ST elevation acute coronary syndrome: implications of troponin T, CRP, NT-proBNP, and fibrin D-dimer levels. Ambrose JA. Early prognostic usefulness of C-reactive protein added to the Thrombolysis In Myocardial Infarction risk score in acute coronary syndromes. Clinical utiliry of C-reactive protein measured at admission, hospital discharge, and 1 month later to predict outcome in patients with acute coronary artery disease. The RISCA (recurrence and inflammation in the acute coronary syndromes) study. Prognostic value of biomar-kers during and after non-ST-segment elevation acute coronary syndrome. Predictive value of C-reactive protein and troponin T in patients with unstable angina: a comparative analysis. CAPTURE Investigators. Chimeric c7E3 AntiPlatelet Therapy in Unstable angina REfractory to standard treatment trial. A point-of-care platelet function assay and C-reactive protein for prediction of major cardiovascular events after drug-eluting stent im-plantation. Clinical relevance of C-reactive protein during follow-up of patients with acute coronary syndromes in the Aggrastat-to-Zocor Trial. A 78-year-old male patient with advanced lung cancer and liver metas-tasis was admitted to our hospital because of persistent and critical hyperkalaemia (5.1–7.1 mEq/L), probably caused by tumour lysis syndrome. He had a history of myocardial infarction and arteriosclerosis obliterans. Echocardiography showed akinesis of the cardiac apex, and severe hypokinesis of the inferior wall, reflecting old infarction. His hyperkalaemia was accompanied by elevated levels of aminotrans-ferases and lactate dehydrogenase. Because his disease was an incurable malignancy, palliative care was chosen for his treatment. Although no electrocardiographic abnormalities associated with hyperkalaemia were detected during hospitalization, he suffered sudden death due to ventricular fibrillation. The clinicians suspected that the uncontrolled hyperkalaemia had induced this fatal arrhythmia. An autopsy was performed in which the lung cancer (pleomorphic carcinoma) with extensive blood-borne metastases was confirmed. Fresh myocardial necrosis was found to be superimposed on an area of fibrosis corresponding to old infarction in the left anterior wall (Panel A, arrowheads). This finding suggested that the precise cause of death was not …