Fragmented QRS on surface electrocardiogram is not a reliable predictor of myocardial scar, angiographic coronary disease or long term adverse outcomes.

PURPOSE: Conflicting evidence remains regarding the value of fragmented QRS (fQRS) on surface electrocardiogram (EKG). We present the 5-year outcome of patients with fQRS on EKG and its correlation to SPECT and coronary angiography (CA). METHODS: We retrospectively studied EKG's in 248 consecutive patients undergoing SPECT and CA with known or suspected coronary artery disease (CAD). The presence of fQRS or Q waves in two contiguous EKG leads was correlated with major coronary artery distributions on SPECT and cath. Patients with bundle-branch block, paced-rhythm or absence of EKG within one month of SPECT were excluded. The final EKG data for 238 patients were analyzed and compared with myocardial scar on SPECT and the presence of significant (>50%) coronary stenosis on CA. Predictors of MACE (death, MI, heart failure) were evaluated. Freedom from all-cause mortality was assessed by Kaplan-Meier analysis. RESULTS: Of 238 patients, no significant difference was noted in the presence of scar on SPECT in fQRS (3/77; 3.8%) versus no fQRS (11/161; 6.8%) (P=0.56); or CA based CAD (55/77; 71% fQRS) and no fQRS (99/161, 61.4%) (P=0.20). EKG Q wave presence was similar in both groups: (12/77; 15.5% fQRS), (17/161; 10.5% no fQRS) (P=0.3). Patients with CA based significant LAD disease were 3.680 times more likely to have fQRS (P=0.04), however, fQRS was not significantly associated with MACE (P=0.92) or all-cause mortality (P=0.93). CONCLUSIONS: This study does not support routine assessment of fQRS on surface EKG as a reliable predictor of SPECT myocardial scar, MACE or all-cause mortality over a long period of follow-up.

Effect of alcohol septal ablation in patients with hypertrophic cardiomyopathy on the electrocardiographic pattern.

Alcohol septal ablation (ASA) of patients with hypertrophic cardiomyopathy (HC) allows study of the electrocardiographic effects of myocardial necrosis confined to the base of the interventricular septum, a rare event in atherothrombotic coronary artery disease. Eighty-four consecutive patients were studied after ASA for HC. After excluding 20 with pacing before ASA and 6 with no available preprocedure electrocardiograms, the electrocardiograms of the remaining 58 patients were compared with those of 58 consecutive patients with anterior ST elevation myocardial infarctions who underwent primary intervention for left anterior descending coronary artery (LAD) occlusions. In 25 patients, the occlusions were proximal to the first septal perforator, and in 33 patients, the occlusions were more distal. All electrocardiograms were analyzed with respect to conduction abnormalities and ST-segment changes. Patients with HC developed right bundle branch block significantly more often than those with LAD occlusions (50% vs 14%, p = 0.001) Moreover, patients with HC required postprocedure pacing more frequently (14% vs 2%, p <0.05). A distinctive pattern of ST displacement was found. There was more frequent ST depression in leads I and aVF and greater ST elevation in lead V(1) in patients who underwent ASA, indicating a greater tendency toward a rightward direction than was true in patients with LAD occlusions. In conclusion, in addition to more frequent right bundle branch block after ASA, a distinctive a characteristic pattern of ST-segment deviation similar to but distinct from that produced by proximal LAD occlusion appeared.

Association of size of myocardial scar and persistence of ST-segment elevation after healing of anterior wall myocardial infarction.

Half the patients who survive ST-segment elevation anterior myocardial infarction continue to have ST elevation (STE) 6 months after the event. The mechanism for this and its clinical significance are unclear. There are data to suggest that larger infarcts are more likely to have persistent changes in the ST segment. This study is designed to test this association further using a novel means of assessing the presence and magnitude of myocardial scar using cardiac magnetic resonance imaging (MRI). Delayed imaging by MRI after injection of gadolinium is commonly used to detect myocardial scar through the appearance of delayed contrast hyperenhancement. Consecutive patients referred for myocardial viability imaging were reviewed. The volume of scar as a percentage of anterior wall volume was calculated, and the 26 patients with scar involving >or=10% of the anterior wall were selected for inclusion. All had an electrocardiogram recorded within 15 days of MRI, and none had an intervening cardiac event. Observers unaware of MRI findings independently measured ST-segment changes. Nine patients had STE >1 mm and 17 did not. Mean anterior scar volume in the group without STE was 31.9 +/- 17.1% of the anterior wall volume compared with 50.3 +/- 15.9% in the group with STE >1 mm (p = 0.01). The larger the myocardial scar, the more likely STE was to be present. Only 1 of 10 patients (10%) with scar in the anterior wall <30% had such an elevation compared with 3 of 9 (33%) with scar size of 30% to 49% and 5 of 7 (78%) with scars >or=50%. In conclusion, persistent anterior STE is associated with the size of myocardial scar detected using MRI.

A rare case of tako-tsubo cardiomyopathy complicated by a left ventricular thrombus.

Tako-tsubo cardiomyopathy is a rare stress-related cardiomyopathy usually seen in postmenopausal women after an emotional stressor. Patients generally present with angina-like substernal chest pain. The electrocardiogram (ECG) shows ST segment elevation or T wave inversions across the anterior precordial leads. Cardiac markers are minimally elevated, without evidence of coronary artery disease on angiography. The ventriculogram demonstrates hypokinesis and ballooning of the apex with hyperkinesis of the base. Prognosis is favorable with normalization of wall motion abnormalities within weeks. We present a rare case tako-tsubo cardiomyopathy complicated by a left ventricular mural thrombus. It is thought that this thrombus may have been precipitated by the ventricular dyskinesis. Further research is needed to determine the true incidence of left ventricular thrombus and the role of short-term anticoagulant therapy in this disorder.