BackgroundStudies with other imaging modalities have demonstrated a relationship between contrast transit and cardiac output (CO) and pulmonary vascular resistance (PVR). We tested the hypothesis that the transit time during contrast echocardiography could accurately estimate both CO and PVR compared to right heart catheterization (RHC).Methods27 patients scheduled for RHC had 2D-echocardiogram immediately prior to RHC. 3 ml of DEFINITY contrast followed by a 10 ml saline flush was injected, and a multi-cycle echo clip was acquired from the beginning of injection to opacification of the left ventricle. 2D-echo based calculations of CO and PVR along with the DEFINITY-based transit time calculations were subsequently correlated with the RHC-determined CO and PVR.ResultsThe transit time from full opacification of the right ventricle to full opacification of the left ventricle inversely correlated with CO (r = -0.61, p < 0.001). The transit time from peak opacification of the right ventricle to first appearance in the left ventricle moderately correlated with PVR (r = 0.46, p < 0.01). Previously described echocardiographic methods for the determination of CO (Huntsman method) and PVR (Abbas and Haddad methods) did not correlate with RHC-determined values (p = 0.20 for CO, p = 0.18 and p = 0.22 for PVR, respectively). The contrast transit time method demonstrated reliable intra- (p < 0.0001) and inter-observer correlation (p < 0.001).ConclusionsWe describe a novel method for the quantification of CO and estimation of PVR using contrast echocardiography transit time. This technique adds to the methodologies used for noninvasive hemodynamic assessment, but requires further validation to determine overall applicability.

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Background: Cardiac output can be estimated during retrospectively gated CT coronary angiography by anatomically determining left ventricular volumes; prospective triggering to minimize radiation precludes this methodology. We propose an alternative method for cardiac output estimation based on preclinical models suggesting that cardiac output may be inversely related to contrast washout from the aortic root during timing bolus scanning, as measured by peak aortic root contrast attenuation. Methods: 34 patients had CT coronary angiography timing bolus performed with 20 ml iodixanol at 5.5 ml/s followed by 20 ml normal saline at 5.5 ml/s through an 18-Ga antecubital catheter. Peak aortic root contrast attenuation was correlated to cardiac output calculated by echocardiography using heart rate stroke volume from biplane Simpson's method. Results: Mean age was 58 ± 13 years; body surface area, 2.0 ± 0.5 m 2 . 53% were women. Stroke volume, cardiac output and cardiac index were 67 ± 19 ml, 4.5 ± 1.6 L/min, and 2.2 ± 0.7 L/min/m 2 , respectively. Peak aortic root contrast attenuation was 207 ± 46 HU and correlated to cardiac output and cardiac index with r = -0.64, p < 0.0001 and r = -0.55, p < 0.001, respectively. Regression analysis estimates cardiac output = -0.02 peak aortic root contrast attenuation +9.1. Conclusion: This novel method for cardiac output estimation by CTCA appears feasible. The CT physiologic parameters using the timing test-bolus data moderately correlated with echocardiographic assessment of cardiac output. The calculation of cardiac output adds important hemodynamic data to anatomic information provided by CTCA, and further development of this method may preserve assessment of left ventricular performance in prospective triggering.

A 65-year-old woman with history of trigeminal neuralgia presented with left facial tic douloureux soon followed by substernal chest pain. Electrocardiogram demonstrated T-wave inversions in leads I and aVL, and an initial troponin I of 2.58 ng/ml led to cardiac catheterization. Coronary angiography was normal, but left ventriculogram revealed midanterior and inferior wall dyskinesis (A and B, arrowheads pointing to dyskinetic segments, Online Video 1) consistent with midventricular ballooning syndrome (1). Cardiovascular magnetic resonance imaging using a steady-state cine sequence completed on hospital day 2 similarly demonstrated midventricular ballooning (Online Video 2), but delayed hyperenhancement was not detected in the midventricle or elsewhere on post-contrast images (C).Catecholamine-mediated myocardial stunning is a presumed mechanism for this syndrome. This presentation supports this hypothesis. Attacks of trigeminal neuralgia have long been noted to be associated with catecholamine surge (2). In this case, an episode of tic douloureux ironically led to a pain of the heart, a coeur douloureux. REFERENCES 1. Hurst RT, Askew JW, Reuss CS, et al. Transient midventricular ballooning syndrome: a new variant. J Am Coll Cardiol 2006;48:579 -83. 2. Strittmatter M, Grauer MT, Fischer C, et al. Autonomic nervous system and neuroendocrine changes in patients with idiopathic trigeminal neuralgia. Cephalalgia 1996;16:476-80.