Cardiac anxiety, particularly anxiety-related avoidance of exercise, is an important prognostic factor for a MACE in patients after myocardial infarction, independent of cardiac disease severity and depressive symptoms.

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Using both precordial and transesophageal echocardiography, we studied 72 consecutive patients with a recent unequivocal transient ischemic attack or nondisabling stroke to determine the relative value of the two techniques for detecting potential intracardiac sources of cerebral emboli. Group 1 (n=53) patients had no clinical cardiac abnormality, and group 2 (n=19) patients had abnormal cardiac findings upon clinical examination. In group 1, precordial echocardiography detected an abnormality in only one patient (aortic valve thickening) but transesophageal echocardiography denned morphologic abnormalities in five patients (one with a left atrial appendage mass lesion, one with aortic dissection, one with mitral valve prolapse, one with a mitral leaflet mass lesion, and one with aortic valve thickening). In group 2, both precordial and transesophageal echocardiographic studies were normal in 13 patients, while both were abnormal in the remaining six patients. Five of these six patients had pathologic left atrial and/or left ventricular dilatation, but only transesophageal echocardiography defined a left atrial appendage thrombus in two of the six. The sixth patient had mitral chordal rupture, seen on both precordial and transesophageal echocardiography. In addition, in 32 of the 72 patients transesophageal echocardiography identified widespread thoracic aortic atherosclerotic plaques not visualized by precordial echocardiography. We conclude that transesophageal echocardiography significantly increases the yield in visualizing potential intracardiac sources of emboli compared with precordial echocardiography. However, the precise clinical value of the former in the management of such patients requires further study as the number of abnormal transesophageal echocardiographic findings is not high and a causative relation with transient ischemic attacks cannot be proven. (Stroke 1990^21:560-565)

A 20 year-old healthy female volunteer participated in a clinical Phase I and IIa safety and efficacy trial with candidate malaria vaccine PfLSA-3-rec adjuvanted with aluminium hydroxide. Eleven weeks after the third and last immunization she was experimentally infected by bites of Plasmodium falciparum-infected mosquitoes. When the thick blood smear became positive, at day 11, she was treated with artemether/lumefantrine according to protocol. On day 16 post-infection i.e. two days after completion of treatment, she woke up with retrosternal chest pain. She was diagnosed as acute coronary syndrome and treated accordingly. She recovered quickly and her follow-up was uneventful. Whether the event was related to the study procedures such as the preceding vaccinations, malaria infection or antimalarial drugs remains elusive. However, the relation in time with the experimental malaria infection and apparent absence of an underlying condition makes the infection the most probable trigger. This is in striking contrast, however, with the millions of malaria cases each year and the fact that such complication has never been reported in the literature. The rare occurrence of cardiac events with any of the preceding study procedures may even support a coincidental finding.Apart from acute coronary syndrome, myocarditis can be considered as a final diagnosis, but the true nature and patho-physiological explanation of the event remain unclear.