Usefulness of electrocardiographic parameters as compared with computed tomography measures of left atrial volume enlargement: from the ROMICAT trial.

INTRODUCTION: The 12-lead surface electrocardiogram (ECG) is commonly used as a noninvasive modality to assess for left atrial enlargement (LAE), but data comparing ECG against cardiac computed tomography (CT) for LAE is lacking. We aimed to determine the diagnostic performance of 6 ECG criteria for LAE as compared with CT left atrial volume (LAV) and index to body surface area (LAVI) as the reference standard. MATERIALS AND METHODS: In 339 patients (age: mean ± mean, 53 ± 12 years; 63% male), we evaluated the quantitative ECG parameters of P duration, P to PR segment ratio, P wave area, and P terminal force in lead V1. We also assessed qualitatively the morphology of bifid and biphasic P waves. Patients were stratified into top and lowest quartile of LAV and LAVI by CT. RESULTS: Of the 6 ECG criteria, patients with P duration greater than 110 milliseconds had a 2½-fold increase likelihood of being in the top quartile of LAV (adjusted odds ratio [OR], 2.51; P = .01) and LAVI (adjusted OR, 2.74; P = .007) as measured by CT. For this ECG criterion, the sensitivity and specificity were 71% and 55% for CT LAE by LAV and 61% and 55% for LAVI. The remaining ECG parameters of LAE assessed (P to PR segment ratio, P terminal force in lead V1, P wave area, bifid, and biphasic P wave) were not associated with LAE by CT-based LAV or LAVI (all P ≥ .20). DISCUSSION: Only P duration greater than 110 milliseconds was independently associated with LAE based on CT-derived LA volume and index. However, none of the established ECG parameters of LAE have sufficient diagnostic accuracies for predicting volumetric enlargement by CT, thus limiting its clinical utility.

Performance of electrocardiographic criteria for left ventricular hypertrophy as compared with cardiac computed tomography: from the Rule Out Myocardial Infarction Using Computer Assisted Tomography trial.

OBJECTIVE: Cardiac computed tomography (CT) is a state-of-the-art technology that provides an accurate noninvasive method to quantify left ventricular mass for analysis of left ventricular hypertrophy (LVH). We aimed to examine seven ECG-based LVH criteria against two CT indexation criteria for LVH: a CT-specific body surface area cutoff and the obesity-independent height criteria. METHODS: In 333 patients (mean age 53 +/- 12 years, 61% men), 64-slice contrast-enhanced CT was performed and 12-lead surface ECG within 24 h. Left ventricular mass was measured at end-diastole. Using both CT indexation criteria, the cohort was subdivided into patients with LVH and without LVH. The seven ECG criteria for LVH were the Cornell voltage index, Cornell voltage duration product, Cornell/strain index, Sokolow-Lyon index, Romhilt-Estes scores at least 4 and at least 5, and Gubner-Ungerleider. RESULTS: The ECG parameters had high specificities (85-97%) and variable low sensitivities (4-43%) when compared to either CT criteria of LVH. The three Cornell-based methods performed the best (test-positive likelihood ratio: 4.5-6.7), followed by the Sokolow-Lyon and Romhilt-Estes scores (test-positive likelihood ratio: 2.3-4.0). With the exception of the Gubner-Ungerleider criterion, the other six ECG criteria were associated with at least one of the CT-based LVH (adjusted odds ratio 2.4-9.5) and had incremental predictive value beyond that of hypertension history. CONCLUSION: Using cardiac CT as a gold standard for LVH assessment, ECG criteria for LVH have high specificities with the three Cornell-based criteria providing the best test performance for identifying patients with LVH.

Administration of tissue plasminogen activator for acute ischemic stroke in a rural Wisconsin hospital.

BACKGROUND: Tissue plasminogen activator (tPA) has provided a means to improve functional outcome of patients in the treatment of acute ischemic stroke. METHODS: A retrospective chart analysis of ischemic stroke patients presenting from January 1995 to April 2007 to a particular hospital emergency department located in Ladysmith, Wis was conducted. The following factors were analyzed: door-to-tPA time, National Institutes of Health Stroke Scores (NIHSS) at admission and discharge, complication rates, disposition status, contraindications for receiving tPA, and specialties of physicians involved with stroke care. RESULTS: During this time period, data was available for 108 patients diagnosed with ischemic stroke treated by physicians in 3 specialties (family practice, internal medicine, and emergency medicine). Of these patients, 18 were treated with tPA for an overall tPA administration rate of 16.2%. Onset of symptoms >3 hours prior to presentation was the most common contraindication to tPA administration. Door-to-tPA time was <60 minutes in 38.9% of cases. Patients treated with tPA were more likely to be discharged home and were less likely to expire within the following month; however, these differences did not reach statistical significance. CONCLUSIONS: This study provides evidence that tPA can be safely administered in rural hospitals. Physicians working in rural emergency departments are able to diagnose and manage acute ischemic stroke within the guidelines established by the National Institute of Neurologic Disorders and Stroke (NINDS) without increased complication rates. Making tPA available in rural communities increases access to treatment and improves outcomes of patients with acute ischemic stroke.

Low-level endotoxin induces potent inflammatory activation of human blood vessels: inhibition by statins.

BACKGROUND: Low-level endotoxemia (ie, >or=50 pg/mL) in apparently healthy subjects was recently identified as a powerful, independent risk factor for atherosclerosis. METHODS AND RESULTS: We treated human saphenous veins (HSVs) with low levels of endotoxin. Release of the proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemoattractant protein-1 (MCP-1) was measured by ELISA. Superoxide was determined by using the fluorescent probe dihydroethidium (HE), and monocyte binding was assessed with calcein-labeled U-937 cells. Three- to 4-fold increases in MCP-1 and IL-8 release were observed at endotoxin concentrations of 100 pg/mL; these increases were inhibited by the 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor atorvastatin. Studies in cultured endothelial cells suggest that the mechanism is related to inhibition of isoprenylation (ie, geranylgeranylation) rather than cholesterol formation. Endotoxin produced dose-dependent increases in HE fluorescence that were inhibited by the superoxide dismutase mimics Tiron and MnTBAP. Endotoxin potently induced U-937 cell binding to HSV; binding was inhibited by both Tiron and atorvastatin. Toll-like receptor-4 expression was detected in cultured HSV endothelial and smooth muscle cells and in intact HSV. CONCLUSIONS: Clinically relevant levels of endotoxin, as reported in ambulatory populations, have profound inflammatory effects on intact HSV. Inhibition of endotoxin-induced vascular inflammation might contribute to the beneficial effects of statins in treating atherosclerosis.