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ABSTRACT: Cardiac CT provides volumetric data that enables characterization of the myocardium.
We evaluated intraobserver, interobserver, and interstudy reproducibility of left ventricular (LV) and right ventricular (RV) mass quantification with cardiac CT.
Thirty-eight patients who underwent cardiac CT twice within 365 days were included in this analysis. Functional reconstructions in 10% steps throughout the R-R interval and axial 1.5-mm sections were used. Semiautomatic contour detection was used to trace epicardial and endocardial borders in all cardiac phases for calculation of LV and RV ejection fraction, end-diastolic volume, end-systolic volume, cardiac output, stroke volume, and ventricular mass. For each study 2 observers measured LV and RV mass twice.
LV mass parameters derived from semiautomatic contour detection algorithm had excellent intraobserver (r = 1.00), interobserver (r = 0.99), and interstudy (r = 0.99) reproducibility (P < 0.0001). Average end-diastolic LV mass was 146.2 ± 42.9 g at the first CT study and 146.8 ± 44.4 g at the second study. For measuring RV mass, reproducibility was good on all levels (r = 0.78, r = 0.78, and r = 0.68, respectively, with an average end-diastolic mass of 25.7 ± 5.8 g at the first study and 24.4 ± 4.8 g at the second study.
Quantification of LV mass at cardiac CT with the threshold-based, region-growing semiautomatic segmentation analysis software evaluated here is highly observer independent and reproducible. This largely holds true for the estimation of RV mass as well; however, further improvements are needed to optimize reproducibility for RV mass quantification.
Journal of cardiovascular computed tomography 08/2011; 5(5):317-24.
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ABSTRACT: External or internal shocks administered to terminate ventricular arrhythmias as a part of electrophysiology or implantable cardioverter-defibrillator testing, can inadvertently cardiovert atrial fibrillation (AF). Moreover, anticoagulation therapy is often withheld in these patients in anticipation of an invasive procedure. The risk of embolic events during these procedures has not been well described. Accordingly, the present study was a prospective evaluation of the incidence of left atrial (LA) thrombus and AF cardioversion among patients undergoing ventricular arrhythmia assessment. Transesophageal echocardiography was routinely performed on 44 consecutive patients in AF with subtherapeutic anticoagulation undergoing electrophysiology or implantable cardioverter-defibrillator testing. Arrhythmia induction was not performed when LA thrombus was present. The incidence and clinical predictors of thrombus, the inadvertent cardioversion of AF, and adverse events related to the procedure were assessed during the subsequent 4 to 6 weeks. Left atrial thrombus was observed in 12 patients (27%). Sinus rhythm was restored in 29 patients (91%), at least transiently, who underwent testing with a shock delivered. No adverse neurologic or hemorrhagic complications were observed. Univariate analysis identified no predictors of LA thrombus or cardioversion to sinus rhythm. In conclusion, LA thrombus and cardioversion to sinus rhythm are common among patients with AF undergoing an evaluation of ventricular arrhythmias. Transesophageal echocardiography performed before the procedure in patients with subtherapeutic anticoagulation is warranted to minimize embolic complications. This strategy appears to be a safe method to guide diagnostic testing in this patient population.
The American journal of cardiology 11/2009; 104(9):1256-8. · 3.58 Impact Factor
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ABSTRACT: We evaluated a prototype SPECT system integrated with multidetector row CT (MDCT) for obtaining complementary information on coronary anatomy and hemodynamic lesion significance. Twenty-five consecutive patients with known or suspected coronary artery disease (CAD) underwent routine SPECT myocardial perfusion imaging (MPI). All patients also underwent repeat MPI with a mobile SPECT unit which could be attached to a 64-slice MDCT system. Coronary CT angiography (cCTA) was performed without repositioning the patient. Investigational MPI was compared with routine MPI for detection of myocardial perfusion defects (PD). Two observers diagnosed presence or absence of CAD based on MPI alone, cCTA alone, and based on combined MPI and cCTA with fused image display. In 22/24 patients investigative MPI corresponded with routine MPI (r = 0.80). Stenosis >or= 50% at cCTA was detected in 6/24 patients. Six out of 24 patients had PD at regular MPI. Three of these six patients had no significant stenosis at cCTA. Three out of 19 patients with normal MPI studies had significant stenosis at cCTA. Our initial experience indicates that the integration of SPECT MPI with cCTA is technically feasible and enables the comprehensive evaluation of coronary artery anatomy and myocardial perfusion with a single instrumental setup.
European Radiology 10/2008; 19(4):845-56. · 3.22 Impact Factor
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ABSTRACT: To evaluate the sensitivity of the serum cardiac troponin I level in detecting stress test-induced myocardial ischemia, the authors conducted a prospective study including patients admitted for chest pain to the telemetry floor of Our Lady of Mercy Medical Center at Bronx, NY. Consecutive 134 telemetry patients that agreed to participate in this study were included. All of these patients had a nuclear stress test and were divided into various groups based on the prestress test probability of having coronary artery disease. To assess serum cardiac troponin I levels, blood samples were drawn before and after stress testing and compared with the stress test results. Overall, 30 patients (22%) had reversible perfusion defects on stress images, and none (0%) had increased serum cardiac troponin I levels. One patient of 18 patients (6%) in group C with negative stress test results had an elevated serum cardiac troponin I level after the stress test, but none of group A or group B patients had elevated troponin I levels. These data show that serum cardiac troponin I levels do not increase with stress test-induced myocardial ischemia.
Heart Disease 4(4):216-9.
