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Among patients with unstable angina or myocardial infarction without ST-segment elevation, prasugrel did not significantly reduce the frequency of the primary end point, as compared with clopidogrel, and similar risks of bleeding were observed. (Funded by Eli Lilly and Daiichi Sankyo; TRILOGY ACS ClinicalTrials.gov number, NCT00699998.).

Acute myocardial infarction To the Editor. With regard to the article "Acute myocardial infarction in a 21-year old male with normal selective coronary arteriogram" (Can Med Assoc J 105: 843, 1971) I would like to suggest an alternative diagnosis of "Acute nonspecific (also known as benign, idiopathic or viral) pericarditis." The patient described in the report at no time had any cardiac symptoms other than chest pain. It would be interesting to know if he had even a minimal upper respiratory infection one to three weeks before his admission to hospital. The symptoms of acute nonspecific pericarditis often lead to an erroneous diagnosis of myocardial infarction and it is highly important that the patient not be stigmatized by such an error. It has been estimated that in approximately 25% of patients with non-specific pericarditis there is no friction rub audible while a smaller number have a burning chest pain similar to that of myocardial infarction. The ECG in Fig. 1 "showing changes of recent inferolateral infarction" is not a clear tracing but could also be characteristic of pericarditis including concavity upwards of ST segments, ST segment depression in AVR, and peaking of T waves. In pericarditis the ECG abnormalities are attributed to superficial myocarditis (epicarditis); muscle damage is produced but is less extensive than in myocardial infarct. The one factor in this case favouring acute myocardial infarction is an SGOT report of 298 units since it is much less likely to rise so high in pericarditis. However,

The use of periprocedural cangrelor during PCI was not superior to placebo in reducing the primary end point. The prespecified secondary end points of stent thrombosis and death were lower in the cangrelor group, with no significant increase in the rate of transfusion. Further study of intravenous ADP blockade with cangrelor may be warranted. (ClinicalTrials.gov number, NCT00385138.)

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Cangrelor, when administered intravenously 30 minutes before PCI and continued for 2 hours after PCI, was not superior to an oral loading dose of 600 mg of clopidogrel, administered 30 minutes before PCI, in reducing the composite end point of death from any cause, myocardial infarction, or ischemia-driven revascularization at 48 hours. (ClinicalTrials.gov number, NCT00305162.)

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