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Summary:The pathogenesis of U-wave inversion and its clinical value are still not clear, although the U wave was described by Einthoven together with the other electrocardiographic (ECG) waves. Not considered a useful diagnostic clue, it is not usually mentioned in ECG reports. In recent years, stimulated by the long QT syndromes and by the discovery of U-wave changes in some pathologic, mostly cardiac states, this neglected wave has attracted new interest. This review focuses on the negativity of the U wave in ischemic heart disease. The discovery of M cells and their electrophysiology has established the cellular basis for repolarization and has contributed to our knowledge of U-wave genesis. Hemodynamic changes during diastole in acute ischemia also furnish interesting elements for the interpretation of U-wave changes, and some experimental and clinical studies, besides designating stretch as a cause of U-wave changes, have also proved their value for more accurate bedside diagnosis and prognosis. They may indicate the extent of myocardial ischemia, the presence of collateral circulation, and the possible territory and vessel involved. When U-wave changes are the first and only sign of ischemia, they may contribute to a decision regarding the hospital admission of a patient without typical ischemic symptoms. Furthermore, U-wave changes during exercise tests increase their sensitivity.

Summary: Pericardial involvement (PI) in acute myocardialinfarction (AMI) is a complication usually considered benign and has therefore received less attention than those more severe. It may be easily missed because it presents few symptoms and signs, which in turn may be confused with those of AMI. Its pathophysiology, diagnosis, and pitfalls are discussed. The GISSI-1 trial revealed a marked reduction of PI in the group treated with thrombolysis. This unexpected finding was later confirmed by the GISSI-2 trial and by other studies, drawing attention to its meaning. Data from the GISSI as well as from other studies have been reviewed and seem to indicate that PI is associated with larger AMIs and with a significant increase in 6-and 12-month mortality. This may be attributed to the consequences of late remodeling of a large infarction. These findings lead to the conclusion that PI should be granted more attention, and that it might identify patients with apoorer long-term outcome.

SummaryBackground: In acute inferior myocardial infarction (AIMI), the ST depression from VI to V4 has been the subject of many papers, while the ST changes in other leads, their association, and the right ventricular (RV) involvement have been studied less.Hypothesis: This study was performed to contribute to the meaning of the ST changes and RV involvement in AIMI.Methods: Seventy-one patients, admitted within 6 h from symptom onset, all thrombolysed, were enrolled. We classified them according to ST patterns and RV involvement. We divided the right coronary artery into three segments, considering the origin of RV branch and the crux as dividing points. We established a coronary score attributing 2 points to each terminal branch. Comparisons were performed between the electrocardiographic (ECG) findings at onset, the creatine phosphokinase (CPK) peaks, the radionuclide ejection fractions, and the coronary angiographies.Results: We found that the ST changes give indications regarding the site, extension, and extent of AIMI; RV involvement can mask posterior extension, points to the right coronary a9 the culprit vessel (loo%), and, with high probability,