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Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is an angiopathy caused by mutations in the NOTCH3 gene. Typical microvascular changes are found throughout the arterial tree, but the documented disease expression is confined to the central nervous system. In an ongoing CADASIL study, we noted a number of patients with early acute myocardial infarction (before the age of 50 years), as well as patients with electrocardiogram (ECG) abnormalities. We analyzed these data to determine whether myocardial ischemia is associated with NOTCH3 mutations. ECGs were recorded in mutated (n = 41) and nonmutated (n = 22) individuals from 15 genetically confirmed CADASIL families, and blindly classified according to the Minnesota code. Cardiologic history was assessed and cardiovascular disease risk factors were determined. Evidence for myocardial infarction was defined as a positive history for acute myocardial infarction and/or a Minnesota Code 1 (Q-waves) on ECG. We examined CADASIL myocardial tissue ultrastructurally and immunohistochemically for evidence of microangiopathy. We found that almost 25% (10/41) of mutation carriers had evidence of myocardial infarction, versus none of the 22 nonmutation carriers (p = 0.011). Five had a medical history of acute myocardial infarction, and 5 had current pathologic Q-waves on ECG. Acute myocardial infarction occurred at a mean age of 39.6 +/- 5.22 years, and predated major neurologic symptoms of CADASIL in all cases. Pathologic examination of myocardial tissue revealed typical CADASIL arteriopathic changes of the coronary microvasculature. To our knowledge, this is the first study showing that NOTCH3 mutation carriers may be at increased risk of early acute myocardial infarction, expanding CADASIL disease expression beyond the central nervous system to include the heart.
In a significant proportion of patients with sustained ventricular tachycardia (VT) following anterior myocardial infarction, the areas of slow conduction are activated early during cardiac depolarization. Therefore, they may not be detected by the standard time-domain analysis of the signal-averaged electrocardiogram (SAECG) which is limited to the terminal part of the QRS complex. Spectral turbulence analysis of the SAECG is a new frequency domain technique which examines the whole QRS complex and may improve identification of patients with sustained VT following anterior infarction. We compared the results of time-domain and spectral turbulence analyses of the SAECG in 53 postinfarction patients with sustained VT and in 53 age-, gender- and infarct site-matched patients without VT. The receiver operator characteristic curves have shown that the time-domain analysis resulted in better identification of patients with VT following inferior than following anterior infarction (e.g., at the sensitivity level of 90%, the corresponding values of specificity were 96 and 90%, respectively), whereas the spectral turbulence analysis performed better in the anterior site of infarction. When both time-domain and spectral turbulence analyses were combined, the accuracy of the SAECG for identification of patients with VT following anterior infarction improved, reaching a specificity of 97% at the sensitivity level of 90%. In conclusion (1) spectral turbulence analysis of the SAECG results in better identification of patients with VT following anterior than following inferior infarction, and (2) the combination of time-domain and spectral turbulence analyses of the SAECG may improve identification of patients with VT following anterior infarction.
BACKGROUND: Patency of infarct-related artery in patients who suffered an acute myocardial infarction (AMI) has been shown to be associated with improved survival. Ventricular tachyarrhythmias induced by programmed electrical stimulation may be predictive of arrhythmic events and sudden death. HYPOTHESIS: The study was undertaken to assess the possible effect of a patent infarct-related coronary artery on induced ventricular tachyarrhythmias during programmed ventricular stimulation in survivors of AMI. METHODS: In this prospective study, programmed electrical stimulation was performed before hospital discharge (14 +/- 2 days) in 79 patients who survived an AMI. Patients were subdivided into two groups: Group I with patent infarct-related coronary artery (n = 64) and Group 2 with occluded infarct-related artery (n = 15) at coronary angiography performed at 14 +/- 2 days. These two groups were comparable in terms of mean left ventricular ejection fraction, location of infarct-related artery, number of diseased vessels, peak creatine kinase value, and infarct location. RESULTS: Ventricular arrhythmias were induced in 21 patients ( 32.6%) of Group I and 4 patients (26.6%) of Group 2. This difference was not statistically significant. CONCLUSION: This study suggests that ventricular arrhythmias induced by programmed ventricular stimulation in survivors of AMI did not differ whether the infarct-related artery was patent or occluded. Other factors may play a role in electrical instability as assessed by programmed ventricular stimulation.
PURPOSE: To compare global and regional myocardial infarction (MI) measurements on clinical gadolinium-enhanced magnetic resonance (MR) images using human manual contouring and a computer algorithm previously validated by histopathology, and to study the degree to which visual assessment and human contouring of infarct extent agreed with the computer algorithm. MATERIALS AND METHODS: Infarct size in 20 patients was measured by human manual contouring and with an automated feature analysis and combined thresholding (FACT) computer algorithm. Short-axis slices were divided into myocardial sectors for regional analysis. Extent of infarction was also graded visually by consensus of expert readers and compared to human and computer contouring. RESULTS: Despite good correlations (R = 0.93-0.95) between human contouring and the FACT algorithm, human contouring overestimated infarct size by 3.8% of the left ventricle (23.8% of the MI) area (P < 0.001). Human contouring also overestimated the circumferential extent, transmural extent, and extent of infarction within a sector by 7.1%, 18.2%, and 27.9%, respectively (all P < 0.001). Both consensus reading and human contouring overestimated infarct grades compared with the FACT algorithm (P = 0.002 and P < 0.001). CONCLUSION: Clinically relevant overestimation of MI can occur in visual interpretation and in human manual contouring, particularly with respect to extent of infarction on a regional basis.