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.
on behalf of GISSI-AF Investigators* Background-Left atrial (LA) dilation precedes or appears early after the onset of atrial fibrillation (AF) and factors in perpetuating the arrhythmia. Angiotensin receptor blockers were proposed for reversing LA remodeling. We evaluated the effect of valsartan on LA remodeling in patients with a recent episode of AF and the effect of LA size on AF recurrence (AFr). Methods and Results-LA and left ventricular (LV) echocardiographic variables were measured at baseline and 6 and 12 months in 340 patients from GISSI-AF, a trial testing valsartan prevention of AFr. Reversal of remodeling was considered as a decrease in LA size over 12 months. Changes in patients with and without recurrence and the relationship to duration of AFr were analyzed. Patients were 68.4Ϯ8.8 years old, with history of hypertension (85.3%) and cardioversion in the previous 2 weeks (87.4%) or Ն2 AFr in the previous 6 months (40.4%). Baseline LA maximal volume (LAVmax) was severely increased (Ͼ40 mL/m 2 ); LV dimensions and function were relatively normal. Over 12 months, 54.4% of patients had AFr. LAVmax was unchanged by rhythm, time, or randomized treatment. Higher baseline LAVmax and lower LA emptying fraction were linearly related to increasing AFr duration during follow-up. T he hypothesis that long-term renin-angiotensin system (RAS) inhibition could reverse the left atrial (LA) remodeling process and thereby contribute to the prevention of atrial fibrillation recurrence (AFr) was formally tested in the double-blind, randomized, Gruppo Italiano per lo Studio della Sopravvivenza nell'Infarto Miocardico-Atrial Fibrillation (GISSI-AF) trial. 1,2 The entirely neutral results of the study were somewhat surprising, 3 given the wealth of positive evidence. Data from experimental AF implicated RAS in the remodeling associated with atrial electric heterogeneity, ab- Received March 7, 2011; accepted August 9, 2011 Clinical Perspective on p 728 Conclusions-GISSI-AFPost hoc analyses of clinical trials in patients with left ventricular dysfunction showed that ACE inhibitors and angiotensin receptor blockers (ARBs) reduced the onset of new AF, 10,11 and, in prospective studies of patients after cardioversion of paroxysmal and persistent AF, RAS inhibitors in addition to amiodarone prevented recurrences of AF. 12 We report the results from the GISSI-AF echo study that explored whether the expected effect of valsartan to reverse LA remodeling would prevent AF recurrences. In addition, left atrial volume (LAV) and LV anatomy and function were assessed to estimate left ventricular resistance to LA emptying. MethodsThe GISSI-AF trial was a double-blind, randomized, placebocontrolled, multicenter study that enrolled 1442 patients in sinus rhythm with a history of AF to test whether the ARB valsartan could reduce the recurrence of AF (see Expanded Methods, Patients in the GISSI-AF Main Study, in the online-only Data Supplement). The primary end points were time to the first recurrence of AF and the proportion of patients w...
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,
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