often more difficult in these scenarios. Although car- diac enzymes were elevated for a slightly longer time period after presentation in patients with myocarditis, enzymatic markers of active myonecrosis had re- solved in most patients in the 2 groups 48 hours afterward, suggesting a transient nature of myonecro- sis and lack of ongoing damage in this group. Acknowledgment: We would like to thank the Vac- cine Healthcare Centers Network (Washington, DC) for case management, the astute clinicians for diligent assistance in case investigation, and our patients in this case series. 1. Dec GW Jr, Waldman H, Southern J, Fallon JT, Hutter AM Jr, Palacios I. Viral myocarditis mimicking acute myocardial infarction. J Am Coll Cardiol 1992;20: 85– 89. 2. Miklozek CL, Crumpacker CS, Royal HD, Come PC, Sullivan JL, Abelmann WH. Myocarditis presenting as acute myocardial infarction. Am Heart J 1988; 115:768 –776. 3. Baboonian C, Treasure T. Meta-analysis of the association of enteroviruses with human heart disease. Heart 1997;78:539 –543. 4. Kuhl U, Pauschinger M, Bock T, Klingel K, Schwimmbeck CP, Seeberg B, Krautwurm L, Poller W, Schultheiss HP, Kandolf R. Parvovirus B19 infection mimicking acute myocardial infarction. Circulation 2003;108:945–950. 5. Halsell JS, Riddle JR, Atwood JE, Gardner P, Shope R, Poland GA, Gray GC, Ostroff S, Eckart RE, Hospenthal DR, et al. Myopericarditis following smallpox vaccination among vaccinia-naive US military personnel. JAMA 2003;289:3283– 3289. 6. Eckart RE, Love SS, Atwood JE, Arness MK, Cassimatis DC, Campbell CL, Boyd SY, Murphy JG, Swerdlow DL, Collins LC, et al. Incidence and follow-up of inflammatory cardiac complications after smallpox vaccination. J Am Coll Cardiol 2004;44:201–205. 7. Grabenstein JD, Winkenwerder W Jr. US military smallpox vaccination program experience. JAMA 2003;289:3278 –3282. 8. Centers for Disease Control and Prevention. Cardiac-related events during the civilian smallpox vaccination program—United States, 2003. Morbid Mortal Weekly Rep 2003;52:492– 496. Effect of Transcatheter Atrial Septal Defect Closure in Children on Left Ventricular Diastolic Function Alessandro Giardini, MD, Phillip Moore, MD, Michael Brook, MD, Valerie Stratton, RDCS, and Theresa Tacy, MD The acute impact of transcatheter atrial septal defect (ASD) closure on left ventricular (LV) diastolic function was assessed in 15 consecutive children, and pre- and postclosure data were compared with those in a matched group of controls. The data indicate that transcatheter ASD closure leads to an immediate im- provement in LV diastolic function as assessed by septal myocardial Doppler tissue imaging and LV inflow velocity propagation. The improvement in LV diastolic properties correlates with the degree of right ventricular volume overload. 2005 by Excerpta Medica Inc. (Am J Cardiol 2005;95:1255–1257) I n patients with atrial septal defects (ASDs), right ventricular volume overload causes an alteration of chamber geometry and of left ventricular (LV) func- tion on the basis of adverse ventricular interdepen- dence. 1–3 Transcatheter ASD closure can acutely re- model cardiac chamber geometry, leading to improved LV systolic performance. 1–3 The aim of the present study was to evaluate the acute effects of transcatheter ASD closure on LV diastolic function using Doppler tissue imaging (DTI) and M-mode color Doppler echocardiography. ••• From October 2002 to January 2004, a total of 188 patients underwent transcatheter ASD closure at our institution. In 29 patients (median age 0.5 years, range 0.02 to 3.3), the procedure was guided by transtho- racic echocardiography, and in 113 patients (median age 43 years, range 9.8 to 84), it was guided by intracardiac echocardiography using a 10Fr intracar- diac probe. In 46 patients (median age 5 years, range 1 to 14), the procedure was guided by transesophageal echocardiography during general anesthesia. DTI and M-mode color Doppler assessment of LV diastolic function were performed in 15 patients who under- went transesophageal echocardiography, and they rep- resented the study population. In all patients, Amplatzer devices (AGA Medical Corporation, Golden Valley, Minnesota) were used (median device diameter 16 mm, range 10 to 23), and no residual shunts were noted immediately after clo- sure. No patient had additional valvular or vascular heart disease. Echocardiographic assessments were performed immediately before and 5 minutes after device deployment using a transesophageal multiplane probe (Acuson, Siemens Medical Solutions USA, Inc., Mountain View, California) from the 4- or 2-chamber view. The method of measuring the LV inflow prop- agation velocity (LVIPV) was modified from the method described by Garcia et al. 4 Doppler color gain was set at subsaturation levels in all study participants. The image plane was adjusted to view the maximum length of LV inflow. An M-mode cursor was positioned through the center of the inflow, with the cursor line parallel with flow. The maximum detectable mean ve- locity moving away from the transducer (Nyquist limit) was reduced serially until the first isovelocity line of the mitral E-wave front could be clearly identified. LVIPV From the Pediatric Cardiology and Adult Congenital Unit, University of Bologna, Bologna, Italy; and the Division of Pediatric Cardiology, Department of Pediatrics, University of California, San Francisco, San Francisco, California. Dr. Tacy’s address is: Division of Pediatric Cardiology, University of California, San Francisco, 505 Parnassus Ave., San Francisco, California 94143-0214. E-mail: tatacy@ pedcard.ucsf.edu. Manuscript received August 24, 2004; revised manuscript received and accepted January 14, 2005. 1255 ©2005 by Excerpta Medica Inc. All rights reserved. 0002-9149/05/$–see front matter The American Journal of Cardiology Vol. 95 May 15, 2005 doi:10.1016/j.amjcard.2005.01.062