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Objectives This study explored the association of ischemic burden, as measured by vasodilator stress cardiovascular magnetic resonance (CMR), with all-cause mortality and the effect of revascularization on all-cause mortality in patients with stable ischemic heart disease (SIHD). Background In patients with SIHD, the association of ischemic burden, derived from vasodilator stress CMR, with all-cause mortality and its role for decision-making is unclear. Methods The registry consisted of 6,389 consecutive patients (mean age: 65 ± 12 years; 38% women) who underwent vasodilator stress CMR for known or suspected SIHD. The ischemic burden (at stress first-pass perfusion imaging) was computed (17-segment model). The effect of CMR-related revascularization (within the following 3 months) on all-cause mortality was retrospectively explored using the electronic regional health system registry. Results During a 5.75-year median follow-up, 717 (11%) deaths were documented. In multivariable analyses, more extensive ischemic burden (per 1-segment increase) was independently related to all-cause mortality (hazard ratio: 1.04; 95% confidence interval: 1.02 to 1.07; p 5 segments, n = 432; 10% vs. 24%; p = 0.01). Conclusions In a large retrospective registry of unselected patients with known or suspected SIHD who underwent vasodilator stress CMR, extensive ischemic burden was related to a higher risk of long-term, all-cause mortality. Revascularization was associated with a protective effect only in the restricted subset of patients with extensive CMR-related ischemia. Further research will be needed to confirm this hypothesis-generating finding.

Introduction: We analysed QT dispersion within the first 6 months postinfarction, its relationship with the main established risk stratifiers and its clinical value. Methods and results: In 55 patients with a first Q-wave myocardial infarction the 12-lead electrocardiogram was scanned and digitised for analysis of QT dispersion (QT maximum–QT minimum) at first day (72 [61–96] ms), first week (69 [47–90] ms), first month (67 [46–88] ms) and sixth month (47 [40–74] ms; P Conclusion: QT dispersion decreases progressively during the first months after myocardial infarction. These changes should be taken into account to define cut-off values of clinical interest in this phase. This variable does not seem related to the classic prognosis predictors. In a nonselected postinfarction population it has a low clinical value.

Introduction: ST-segment elevation on Q-leads after an acute myocardial infarction is related to a greater infarct size. The meaning of a further exercise-induced ST-segment elevation in these patients has not been analyzed. Method: Thirty-six patients with ST-segment elevation on Q-leads were studied after a first acute myocardial infarction. Exercise testing and cardiac catheterization were performed at the first week. Left ventricular volumes (ml/m 2 ); the extent of abnormal wall motion (AWM: chords); contractile reserve (AWM improvement with low dose dobutamine) and coronary patency in the culprit artery were analyzed. Cardiac catheterization was repeated at the sixth month in 20 patients; systolic recovery (AWM improvement), left ventricular volumes and coronary patency were again evaluated. Results: Patients with exercise-induced ST-segment elevation in two or more Q-leads ( n =21) showed lesser contractile reserve (6±6 vs. 12±7 chords, P =0.01) than patients without exercise-induced ST-segment elevation ( n =13). AWM ( F =8.1) and absence of exercise-induced ST-segment elevation ( F =9.5; positive predictive value: 80%; negative predictive value: 68%) were the only independent predictors of contractile reserve. Nevertheless, this electrocardiographic sign was not related to left ventricular volumes, coronary patency or systolic function and it did not predicted late systolic recovery. Conclusions: In patients with baseline ST-segment elevation on Q-leads an exercise-induced ST-segment elevation is independently related to a lesser contractile reserve but not to the evolution of volumes or regional dysfunction during the first 6 months post-infarction. Therefore, the clinical value of this sign seems to be limited to the non-invasive detection of myocardial viability during the early post-infarction phase.