Contemporary experience of percutaneous management of complex aortic and ventricular pseudoaneurysms associated to perivalvular leak: A case series and review of literature.

BACKGROUND: Percutaneous closure of aortic and ventricular pseudoaneurysms (PSA) has only been reported on a case report and series basis. In previous case reports, percutaneous closure has been performed successfully in patients of prohibitive surgical risk. This case series aims to show feasibility of percutaneous closure of aortic and ventricular pseudoaneurysm secondary to perivalvular leak (PVL) in a small patient population and the utility of multimodality imaging as an integral tool in procedural planning. This is the largest complex case series to date describing the feasibility and success rate of complex PSA closure, with a follow-up period of up to 4 years. MATERIAL AND METHODS: We performed institutional review and systemic literature review to identify all paravalvular leak cases with associated pseudoaneurysm formation for which a closure procedure was performed. Ten patients were identified. Pooled analysis for cases from institutional review (n = 10) and systemic literature review (n = 39) was performed. The success rate was 100 %. At 30-days, the mortality was 0 %. CONCLUSION: In paravalvular leak patients with subsequent pseudoaneurysm formation, exhaustive imaging evaluation is required for closure. However, it can be achievable with favorable rates of success.

3D print and multi-modality imaging guided transcatheter closure of multiple left ventricular pseudoaneurysms.

Left ventricular pseudoaneurysm (PSA) after surgical aortic valve replacement (AVR) is a known but uncommon complication. It is associated with risks such as thromboembolism and life-threatening rupture. Surgical repair has traditionally been utilized in low-risk patients but transcatheter closure has become a promising therapeutic option. This case report describes the utility of multimodality imaging in pre-, intra-, and post-procedural evaluation of transcatheter PSA closure and is among the first to demonstrate the utility of 3D print model.

DSPECT-specific normative limits for left ventricular size and function.

BACKGROUND: Differences in spatial resolution and image filtering between the solid-state DSPECT and traditional Anger SPECT (ASPECT) cameras are likely to result in differences in LV measurements. However, DSPECT-specific normal values are not available. The traditional approach of using patients deemed to have a low (< 5%) probability of coronary artery disease for the derivation of normative values has a number of limitations. We used healthy organ-donor subjects without known disease or medication use for derivation of normal values. METHODS: Subjects were 92 consecutive kidney or liver donors who underwent single-day rest (5 mCi)-stress (15 mCi) Tc-99m sestamibi-gated SPECT myocardial perfusion imaging (MPI) on the DSPECT camera for pre-operative evaluation and had normal perfusion and LV function. Exclusion criteria included any known cardiac disease or medications. LV measurements were made on the post-stress supine stress images using QGS®. RESULTS: Of 92 subjects (mean age 54.4 ± 15.0 and 39% men), mean EF ± 2SD for women and men was 77.2% ± 14.1% and 70.0 % ± 14.7%, respectively. Mean end-diastolic volume ± 2SD for women and men was 67.0 ± 32.2 mL and 99.6 ± 51.6 mL (indexed 38.3 ± 17.2 mL/m2 and 48.1 ± 25.9 mL/m2), respectively. Mean end-systolic volume ± 2SD for women and men was 16.1 ± 15.7 mL and 31.2 ± 29.2 mL (indexed 9.2 ± 8.8 mL/m2 and 15.0 ± 14.2 mL/m2), respectively. Mean LV wall volume ± 2SD for women and men was 95.9 ± 26.0 mL and 112.0 ± 48.8 mL (indexed 55.0 ± 13.8 mL/m2 and 54.1 ± 24.6 mL/m2), respectively. CONCLUSION: We report DSPECT-specific LV measurements from normal subjects from which limits of normality can be derived for clinic use. Organ donors who undergo pre-operative MPI are a suitable cohort for the derivation of normal values.

Increased Mortality in Patients With Preoperative and Persistent Postoperative Pulmonary Hypertension Undergoing Mitral Valve Surgery for Mitral Regurgitation: A Cohort Study.

Background Preoperative pulmonary hypertension (PH) is associated with excess mortality among patients with severe mitral regurgitation undergoing mitral valve surgery (MVS). However, the links between PH phenotype, pulmonary vascular remodeling, and persistent postoperative PH are not well understood. We aimed to describe the associations between components of pulmonary hemodynamics as well as postoperative residual PH with longitudinal mortality in patients with severe mitral regurgitation who received MVS. Methods and Results Patients undergoing MVS for severe mitral regurgitation from 2011 to 2016 were retrospectively identified within our health system (n=488). Mean pulmonary artery pressure and other hemodynamic variables were determined by presurgical right-heart catheterization. Postoperative pulmonary artery systolic pressure was assessed on echocardiogram 42 to 365 days post-MVS. Longitudinal survival over a mean 3.9 years of follow-up was evaluated using Cox proportional hazards modeling to compare survival after adjustment for demographics, surgical characteristics, and comorbidities. Pre-MVS prevalence of PH was high at 85%. After adjustment, each 10-mm Hg increase in preoperative mean pulmonary artery pressure was associated with a 1.38-fold increase in risk of death (95% CI, 1.13-1.68). Elevated preoperative pulmonary vascular resistance, transpulmonary gradient, and right atrial pressure were similarly associated with increased mortality. Among 231 patients with postoperative echocardiogram, evidence of PH on echocardiogram (pulmonary artery systolic pressure ≥35 mm Hg) was associated with increased risk of death (hazard ratio [HR], 2.02 [95% CI, 1.17-3.47]); however, this was no longer statistically significant after adjustment (HR, 1.55 [95% CI, 0.85-2.85]). Conclusions In patients undergoing MVS for mitral regurgitation, preoperative PH, and postoperative PH were associated with increased mortality.

Association between cumulative social risk, particulate matter environmental pollutant exposure, and cardiovascular disease risk.

BACKGROUND: Long-term exposure to pollution has been shown to increase risk of cardiovascular disease (CVD) and mortality, and may contribute to the increased risk of CVD among individuals with higher social risk. METHODS: Data from the community-based Heart Strategies Concentrating on Risk Evaluation (HeartSCORE) study were used to quantify Cumulative Social Risk (CSR) by assigning a score of 1 for the presence of each of 4 social risk factors: racial minority, single living, low income, and low educational status. 1-year average air pollution exposure to PM2.5 was estimated using land-use regression models. Associations with clinical outcomes were assessed using Cox models, adjusting for traditional CVD risk factors. The primary clinical outcome was combined all-cause mortality and nonfatal CVD events. RESULTS: Data were available on 1933 participants (mean age 59 years, 66% female, 44% Black). In a median follow up time of 8.3 years, 137 primary clinical outcome events occurred. PM2.5 exposure increased with higher CSR score. PM2.5 was independently associated with clinical outcome (adjusted hazard ratio [HR]: 1.19 [95% CI: 1.00, 1.41]). Participants with ≥2 CSR factors had an adjusted HR of 2.34 (1.48-3.68) compared to those with CSR = 0. The association was attenuated after accounting for PM2.5 (HR: 2.16; [1.34, 3.49]). Mediation analyses indicate that PM2.5 explained 13% of the risk of clinical outcome in individuals with CSR score ≥ 2. CONCLUSION: In a community-based cohort study, we found that the association of increasing CSR with higher CVD and mortality risks is partially accounted for by exposure to PM2.5 environmental pollutants.

Association between ideal cardiovascular health and markers of subclinical cardiovascular disease.

BACKGROUND: Ideal cardiovascular health (CVH) was proposed by the American Heart Association to promote population health. We aimed to characterize the association between ideal CVH and markers of subclinical cardiovascular disease (CVD). HYPOTHESIS: We hypothesized that ideal CVH is associated with several markers of subclinical CVD. METHODS: We used data from the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) study. We assigned 1 for each of the ideal CVH factors met. Endothelial function, expressed as Framingham reactive hyperemia index (fRHI), was measured using the EndoPAT device. Coronary artery calcium (CAC) and carotid intima-media thickness (CIMT) were quantified using electron beam computed tomography and carotid ultrasonography, respectively. RESULTS: A total of 1933 participants (mean [SD] age: 59 [7.5] years, 34% male, 44% black) were included. The mean number of ideal CVH factors met was 2.3 ± 1.3, with blacks having significantly lower score compared to whites (2.0 ± 1.2 vs 2.5 ± 1.4, respectively; P < 0.001). Seven hundred and eighty-nine participants (41%) achieved ≥3 ideal CVH factors. Participants with ≥3 ideal CVH factors (compared to those with <3 factors) had an average of 107 (95% confidence interval [CI]: 50-165) Agatston units lower CAC, 0.04 (0.01-0.06) mm lower CIMT, and 0.07 (0.02-0.12) units higher fRHI, after adjusting for age, sex, race, income, education, and marital status. Participants with ≥3 ideal CVH factors had 50% lower odds (95% CI: 28%-66%) of having CAC >100 Agatston units. CONCLUSION: In a community-based study with low prevalence of ideal CVH, even achieving three or more ideal CVH factors were associated with lower burden of subclinical CVD, indicating the utility of this construct for disease prevention.

Association of obstructive sleep apnea with microvascular endothelial dysfunction and subclinical coronary artery disease in a community-based population.

Studies have reported an association between obstructive sleep apnea (OSA) and cardiovascular disease (CVD) morbidity and mortality. Proposed mechanisms include endothelial dysfunction and atherosclerosis. We aimed to investigate the associations of OSA with endothelial dysfunction and subclinical atherosclerotic coronary artery disease (CAD), and assess the impact of race on these associations. We used data from the Heart Strategies Concentrating on Risk Evaluation (Heart SCORE) study, a community-based prospective cohort with approximately equal representation of black and white participants. OSA severity was measured in 765 individuals using the apnea-hypopnea index (AHI). Endothelial dysfunction was measured using the Endo-PAT device, expressed as Framingham reactive hyperemia index (F_RHI). Coronary artery calcium (CAC), a marker of subclinical CAD, was quantified by electron beam computed tomography. There were 498 (65%) female participants, 282 (37%) black individuals, and 204 (26%) participants with moderate/severe OSA (AHI ≥15). In univariate models, moderate/severe OSA was associated with lower F_RHI and higher CAC, as well as several traditional CVD risk factors including older age, male sex, hypertension, diabetes, higher body mass index, and lower high-density lipoprotein cholesterol levels. In a multivariable model, individuals with moderate/severe OSA had 10% lower F_RHI and 35% higher CAC, which did not reach statistical significance ( p=0.08 for both comparisons). There was no significant interaction of race on the association of OSA with F_RHI or CAC ( p-value >0.1 for all comparisons). In a community-based cohort comprised of black and white participants, moderate/severe OSA was modestly associated with endothelial dysfunction and subclinical atherosclerotic CAD. These associations did not vary by race.