Background: There is no effective method to predict paravalvular regurgitation prior to transcatheter aortic valve replacement (TAVR). Methods: We retrospectively analyzed pre-TAVR computed tomography (CT) scans of 20 patients who underwent TAVR for severe, calcific aortic stenosis and subsequently printed 3-dimensional (3D) aortic root models of each patient. Models were printed using Ninjaflex thermoplastic polyurethane (TPU) (Ninjatek Manheim, PA) and TPU 95A (Ultimaker, Netherlands) on Ultimaker 3 Extended 3D printer (Ultimaker, Netherlands). The models were implanted at nominal pressure with same sized Sapien balloon-expandable frames (Edwards Lifesciences, CA) as received in-vivo. Ex-vivo implanted TAVR models (eTAVR) were scanned using Siemens SOMATOM flash dual source CT (Siemens, Malvern, PA) and then analyzed with Mimics software (Materialize NV, Leuven, Belgium) to evaluate relative stent appositions. eTAVR were then compared to post-TAVR echocardiograms for each patient to assess for correlations of identified and predicted paravalvular leak (PVL) locations. Results: A total of 20 patients (70% male) were included in this study. The median age was 77.5 (74-83.5) years. Ten patients were characterized to elicit mild (9/10) or moderate (1/10) PVL, and 10 patients presented no PVL. In patients with echocardiographic PVL, eTAVR 3D model analyses correctly identified the site of PVL in 8/10 cases. In patients without echocardiographic PVL, eTAVR 3D model analyses correctly predicted the lack of PVL in 9/10 cases. Conclusion: 3D printing may help predict the potential locations of associated PVL post-TAVR, which may have implications for optimizing valve selection and sizing.

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BackgroundLeft atrial (LA) dilation provides a substrate for mitral regurgitation (MR) and atrial arrhythmias. ECG can screen for LA dilation but standard approaches do not assess LA geometry as a continuum, as does non-invasive imaging. This study tested ECG-quantified P wave area as an index of LA geometry.Methods and Results342 patients with CAD underwent ECG and CMR within 7 (0.1±1.4) days. LA area on CMR correlated best with P wave area in ECG lead V1 (r = 0.42, p<0.001), with lesser correlations for P wave amplitude and duration. P wave area increased stepwise in relation to CMR-evidenced MR severity (p<0.001), with similar results for MR on echocardiography (performed in 86% of patients). Pulmonary arterial (PA) pressure on echo was increased by 50% among patients in the highest (45±14 mmHg) vs. the lowest (31±9 mmHg) P wave area quartile of the population. In multivariate regression, CMR and echo-specific models demonstrated P wave area to be independently associated with LA size after controlling for MR, as well as echo-evidenced PA pressure. Clinical follow-up (mean 2.4±1.9 years) demonstrated ECG and CMR to yield similar results for stratification of arrhythmic risk, with a 2.6-fold increase in risk for atrial fibrillation/flutter among patients in the top P wave area quartile of the population (CI 1.1–5.9, p = 0.02), and a 3.2-fold increase among patients in the top LA area quartile (CI 1.4–7.0, p = 0.005).ConclusionsECG-quantified P wave area provides an index of LA remodeling that parallels CMR-evidenced LA chamber geometry, and provides similar predictive value for stratification of atrial arrhythmic risk.

Mitral regurgitation (MR) is common with coronary artery disease (CAD), as altered myocardial substrate can impact valve performance. SPECT myocardial perfusion imaging (MPI) enables assessment of myocardial perfusion alterations. This study examined perfusion pattern in relation to MR. 2377 consecutive patients with known or suspected CAD underwent stress MPI and echocardiography (echo) within 1.6±2.3 days. MR was present on echo in 34% of patients, among whom 13% had advanced (≥moderate) MR. MR prevalence was higher among patients with abnormal MPI (44% vs. 29%, p<0.001), corresponding to increased global ischemia (p<0.001). Regional perfusion varied in left ventricular (LV) segments adjacent to each papillary muscle: Adjacent to the anterolateral papillary muscle, magnitude of baseline and stress-induced anterior/anterolateral perfusion abnormalities was greater among patients with MR (both p<0.001). Adjacent to the posteromedial papillary muscle, baseline inferior/inferolateral perfusion abnormalities were greater with MR (p<0.001), whereas stress inducibility was similar (p=0.39). In multivariate analysis, stress-induced anterior/anterolateral and rest inferior/inferolateral perfusion abnormalities were independently associated with MR (both p<0.05) even after controlling for perfusion in reference segments not adjacent to the papillary muscles. MR severity increased in relation to magnitude of perfusion abnormalities in each territory adjacent to the papillary muscles, as evidenced by greater prevalence of advanced MR among patients with ≥moderate anterior/anterolateral stress perfusion abnormalities (10.7% vs. 3.6%), with similar results when MR was stratified based on rest inferior/inferolateral perfusion (10.4% vs. 3.0%, both p<0.001). In conclusion, findings demonstrate that myocardial perfusion pattern in LV segments adjacent to the papillary muscles influences presence and severity of MR.

Purpose Left ventricular (LV) remodeling and myocardial fibrosis have been linked to adverse heart failure outcomes. Mid wall late gadolinium enhancement (MW-LGE) on cardiac magnetic resonance (CMR) imaging is well-associated with non-ischemic cardiomyopathy (NICM), but prevalence in ischemic cardiomyopathy (ICM) and association with remodeling are unknown. Methods The population comprised patients with systolic dysfunction (LVEF≤40%). CMR was used to identify MW-LGE, conventionally defined as fibrosis of the mid-myocardial or epicardial aspect of the LV septum. Results 285 patients were studied. MW-LGE was present in 12%, and was 10-fold more common with NICM (32%) vs. ICM (3%, p<0.001). However, owing to higher prevalence of ICM, 15% of patients with MW-LGE had ICM. LV wall stress was higher (p=0.02) among patients with, vs. those without, MW-LGE despite similar systolic blood pressure (p=0.24). In multivariate analysis, MW-LGE was associated with CMR-quantified LV end-diastolic volume (p=0.03) independent of LVEF and mass. Incorporation of clinical and imaging variables demonstrated MW-LGE to be associated with higher LV end-diastolic volume (OR=1.13 [CI 1.004–1.27] per 10 ml/m2, p=0.04) after controlling for presence of NICM (OR=16.0 [CI 5.8–44.1], p<0.001). Conclusions While more common in NICM, MW-LGE can occur in ICM and is a marker of LV chamber dilation irrespective of cardiomyopathic etiology.