Jouni, H

Abstract Funding Acknowledgements Type of funding sources: None. Background Atrial fibrillation (AF) is known to cause dilation in both the mitral (MA) and the tricuspid (TA) annuli. Few studies have investigated MA dynamics and function in AF compared to sinus rhythm (SR). However, no study addressed this issue in TA. Hence, we set forth to describe TA dynamics in AF and SR and its relationship with severity of tricuspid regurgitation (TR). Methods 3D echocardiographic imaging data were acquired from adult patients in AF or SR with varying degrees of TR between 2018 and 2020. TA was automatically tracked throughout the cardiac cycle using a commercially available software (TomTec 4MV software; Figure 1) over 4-6 cardiac cycles per patient. Time to minimal area as percentage of the R-R interval was recorded in each of the cycles. Absolute change in TA area was calculated as the difference between maximal and minimal TA area in each cardiac cycle and was averaged over 4-6 cycles per patient. This measurement was used to reflect the dynamic range of TA deformation during the cardiac cycle. Right atrial (RA) and right ventricular (RV) volumes and longitudinal strain were also measured (speckle tracking, 4-ch view). Results A total of 70 patients were studied (35 AF; 35 SR; 54% males in each group). Patients with AF were older [median (IQR) of 81 (72-86) years vs. 69 (59-78) years in SR, p < 0.001], had larger maximal TA area and circumference (p < 0.001 for both), larger RA size (p < 0.001), lower RA reservoir strain (p < 0.001) and RV free-wall strain (p < 0.001). Absolute change in TA area was significantly decreased in AF [2.3 (1.7-2.7) cm2] vs. 3.1 (2.3-3.5) cm2 in SR, p = 0.002. Patients with ≥ moderate TR (n = 41, 59%) had lower absolute change in TA area [2.4 (1.7-3.1) cm2 vs. 2.8 (2.2-3.5) cm2 in < moderate TR, p = 0.05]. Female sex was associated with lower absolute change in TA area [2.3 (1.7-3.2) cm2 vs. 2.7 (2.2-3.6) cm2 in males, p = 0.02] on univariate analysis. AF patients had more frequently ≥ moderate TR [28 AF vs. 13 SR, p < 0.001]. On multivariate analysis including sex, rhythm, TR severity, RA and RV strains, and averaged maximal TA area, independent factors associated with lower absolute change in TA area were AF, ≥ moderate TR, and larger maximal TA area (p < 0.05 for all). Time to minimal TA size was achieved in (0-40%) of the R-R interval in 70% of patients in SR compared to only 41% of patients in AF (Figure 2) and in 73% in patients with < moderate TR compared to 43% in patients with ≥ moderate TR. Conclusion AF is associated with blunted TA dynamics resulting in lower decrease in TA size and with a heterogenous timing of minimal TA size throughout the cardiac cycle. The blunted and discoordinated annular contraction may reduce systolic tricuspid valve competence and be involved in the pathophysiology of functional TR. Future studies are needed to confirm this hypothesis and evaluate the effect of restoration of SR on TA dynamics and time to minimal TA size. Abstract Figure 1Abstract Figure 2

Abstract Introduction Coronary artery calcification (CAC) is associated with and identifies patients at higher risk of major adverse cardiovascular events (MACE). However, the prevalence, characteristics, and outcomes of cancer patients with CAC on CT before or after chest radiation therapy (RT) are not well addressed. Methods Retrospective cohort study of all breast cancer patients who underwent chest RT at Mayo Clinic Rochester in 2010. All pre-RT CTs were reviewed and the extent of CAC was recorded in addition to history of pre-RT atherosclerotic risk factors (hypertension (HTN), diabetes mellitus (DM), dyslipidemia, and smoking), history of pre-RT cardiovascular disease (CVD), and RT dosage. MACE (sudden cardiac death (SCD), acute coronary syndrome (ACS), and stroke), and CAC progression in follow-up were recorded. CAC extent was quantified before and on 5-year follow-up CT scan in all patients, and a positive change was considered progression. Patients were divided into 2 groups based on the presence of CAC before RT: present (group 1) or absent (group 2). Results Our cohort was comprised of 244 breast cancer patients who received chest RT. A total of 39 patients (16.9%) had evidence of CAC on CT prior to RT. Compared with patients without CAC before RT (n=205), those with CAC before RT were found to be older (71.8±7.7 vs 58.9±11.3, p<0.01), had higher pre-RT history of HTN (84.6% vs 47.8%); p<0.01), DM (20.5% vs 4.4%; p<0.01), dyslipidemia (74.2% vs 40%; p<0.01), CAD (23.1% vs 3.9%; p<0.01), and stroke (7.69% vs 1.45%; p=0.04). Following RT, patients in group 1 were more likely to exhibit ACS (33.3% vs 2.9%; p<0.01), and stroke (22.6% vs 5.2%; p<0.01). Multinomial logistic regression identified pre-RT CAD pre-RT CAC (β=1.01 (0.33–1.69), OR=7.60 (1.93–29.93); p=0.02) pre-RT CAD (β=0.78 (0.06–1.49), OR=4.74 (1.14–19.74); p=0.03) as independent predictors for the development of MACE after RT. Progression in CAC after RT was found in 61.9% of all patients (13/21) who developed MACE. Conclusion MACE in breast cancer patients undergoing RT can be predicted before RT based on the CV risk factor and disease profile. The strongest predictor for MACE, however, is evidence of CAC before RT. These data provide a unique window for the identification and follow-up of breast cancer RT patients who have a risk of MACE. Funding Acknowledgement Type of funding source: None

We investigated whether disclosure of coronary heart disease (CHD) genetic risk influences perceived personal control (PPC) and genetic counseling satisfaction (GCS). Participants (n = 207, age: 45–65 years) were randomized to receive estimated 10‐year risk of CHD based on a conventional risk score (CRS) with or without a genetic risk score (GRS). Risk estimates were disclosed by a genetic counselor who also reviewed how GRS altered risk in those randomized to CRS+GRS. Each participant subsequently met with a physician and then completed surveys to assess PPC and GCS. Participants who received CRS+GRS had higher PPC than those who received CRS alone although the absolute difference was small (25.2 ± 2.7 vs 24.1 ± 3.8, p = 0.04). A greater proportion of CRS+GRS participants had higher GCS scores (17.3 ± 5.3 vs 15.9 ± 6.3, p = 0.06). In the CRS+GRS group, PPC and GCS scores were not correlated with GRS. Within both groups, PPC and GCS scores were similar in patients with or without family history (p = NS). In conclusion, patients who received their genetic risk of CHD had higher PPC and tended to have higher GCS. Our findings suggest that disclosure of genetic risk of CHD together with conventional risk estimates is appreciated by patients. Whether this results in improved outcomes needs additional investigation.