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Aims In systemic light-chain (AL) amyloidosis, quantification of right ventricular (RV) amyloid burden has been limited and the pathogenesis of RV dysfunction is poorly understood. Using 18F-florbetapir positron emission tomography/computed tomography (PET/CT), we aimed to quantify RV amyloid; correlate RV amyloid with RV structure and function; determine the independent contributions of RV, left ventricular (LV), and lung amyloid to RV function; and associate RV amyloid with major adverse cardiac events (MACE: death, heart failure hospitalization, cardiac transplantation). Methods and results We prospectively enrolled 106 participants with AL amyloidosis (median age 62 years, 55% males) who underwent 18F-florbetapir PET/CT, magnetic resonance imaging, and echocardiography. 18F-florbetapir PET/CT identified RV amyloid in 63% of those with and 40% of those without cardiac involvement by conventional criteria. RV amyloid burden correlated with RV ejection fraction (EF), RV free wall longitudinal strain (FWLS), RV wall thickness, RV mass index, N-terminal pro-brain natriuretic peptide, troponin T, LV amyloid, and lung amyloid (each P < 0.001). In multivariable analysis, RV amyloid burden, but not LV or lung amyloid burden, predicted RV dysfunction (EF P = 0.014; FWLS P < 0.001). During a median follow-up of 28 months, RV amyloid burden predicted MACE (P < 0.001). Conclusion This study shows for the first time that 18F-florbetapir PET/CT identifies early RV amyloid in systemic AL amyloidosis prior to alterations in RV structure and function. Increasing RV amyloid on 18F-florbetapir PET/CT is associated with worse RV structure and function, predicts RV dysfunction, and predicts MACE. These results imply a central role for RV amyloid in the pathogenesis of RV dysfunction. [ABSTRACT FROM AUTHOR]

Background: Echocardiographic deformation-based ratios and novel multi-parametric scores have been suggested to discriminate transthyretin cardiac amyloidosis (ATTR-CM) from other causes of increased left ventricular wall thickness among patients referred for ATTR-CM evaluation. Their relative predictive accuracy has not been well studied. We sought to (1) identify echocardiographic parameters predictive of ATTR-CM and (2) compare the diagnostic accuracy of these parameters in patients with suspected ATTR-CM referred for technetium-99m-pyrophosphate scintigraphy. Methods: Echocardiograms from 598 patients referred to 3 major amyloidosis centers for technetium-99m-pyrophosphate to detect ATTR-CM were analyzed, including longitudinal strain (LS) analysis. Deformation ratios (septal apex to base ratio, relative apical sparing, ejection fraction to global LS), a multi-center European increased wall thickness score, and Mayo Clinic derived ATTR score (transthyretin cardiac amyloidosis score) were calculated. A logistic regression model was used to identify the parameters that best associated with a diagnosis of ATTR-CM. Comparison of the diagnostic capacity of the parameters was performed by receiver operating characteristic curves and the area under the curve (AUC). Results: Over half of the subjects (54.2%) were diagnosed with ATTR-CM (78% were men, median age of 76 years). Age, inferolateral wall thickness, and basal LS were the strongest predictors of ATTR-CM, AUC of 0.87 (95% CI: 0.83, 0.90), superior to the increased wall thickness score AUC of 0.78 (95% CI: 0.73, 0.83; P =0.004). An inferolateral wall thickness of ≥14 mm (AUC: 0.73) was as accurate as the published cut-offs for transthyretin cardiac amyloidosis score and septal apex to base (AUC: 0.72 and 0.69, P =0.8 and P =0.1, respectively), and was superior to ejection fraction to global LS and relative apical sparing (AUC: 0.64 and 0.53, P <0.001, respectively). A cut-off of ≥−8% for average basal LS (AUC: 0.76, CI: 0.72–0.79) had a similar area under the curve to transthyretin cardiac amyloidosis score (TCAS) (P =0.2); outperforming the other indices (P <0.01). Conclusion: Inferolateral wall thickness and average basal LS performed as well as or better than more complex echo ratios and multiparametric scores to predict ATTR-CM. [ABSTRACT FROM AUTHOR]

Intravenous drug use (IVDU) and associated infective endocarditis (IE) has been on the rise in the US since the beginning of the opioid epidemic. IVDU-IE has high morbidity and mortality, and treatment can be lengthy. We aim to quantify the association between IVDU and length of stay (LOS) in IE patients. The National Inpatient Sample database was used to identify IE patients, which was then stratified into IVDU-IE and non-IVDU-IE groups. Weighted values of hospitalizations were used to generate national estimates. Multivariable linear and logistic regression analyses were applied to estimate the effects of IVDU on LOS. We identified 1,114,257 adult IE patients, among which 123,409 (11.1%) were IVDU-IE. Compared to non-IVDU-IE patients, IVDU-IE patients were younger, had fewer comorbidities, and had an overall longer LOS (median [interquartile range]: 10 [5-20] versus 7 [4-13] d, P < 0.001), with a greater percentage of patients with a LOS longer than 30 d (13.7% versus 5.7%, P < 0.001). After adjusting for multiple demographic and clinical factors, IVDU was independently associated with a 1.25-d increase in LOS (beta-coefficient = 1.25, 95% confidence interval [CI]: 0.95-1.54, P < 0.001) and 35% higher odds of being hospitalized for more than 30 d (odds ratio = 1.35, 95% CI: 1.27-1.44, P < 0.001). Among IE patients, being IVDU has associated with a longer LOS and a higher risk of prolonged hospital stay. Steps toward the prevention of IE in the IVDU population should be taken to avoid an undue burden on the healthcare system. [ABSTRACT FROM AUTHOR]

Aims: In systemic light-chain (AL) amyloidosis, quantification of right ventricular (RV) amyloid burden has been limited and the pathogenesis of RV dysfunction is poorly understood. Using 18F-florbetapir positron emission tomography/computed tomography (PET/CT), we aimed to quantify RV amyloid; correlate RV amyloid with RV structure and function; determine the independent contributions of RV, left ventricular (LV), and lung amyloid to RV function; and associate RV amyloid with major adverse cardiac events (MACE: death, heart failure hospitalization, cardiac transplantation)., Methods and Results: We prospectively enrolled 106 participants with AL amyloidosis (median age 62 years, 55% males) who underwent 18F-florbetapir PET/CT, magnetic resonance imaging, and echocardiography. 18F-florbetapir PET/CT identified RV amyloid in 63% of those with and 40% of those without cardiac involvement by conventional criteria. RV amyloid burden correlated with RV ejection fraction (EF), RV free wall longitudinal strain (FWLS), RV wall thickness, RV mass index, N-terminal pro-brain natriuretic peptide, troponin T, LV amyloid, and lung amyloid (each P < 0.001). In multivariable analysis, RV amyloid burden, but not LV or lung amyloid burden, predicted RV dysfunction (EF P = 0.014; FWLS P < 0.001). During a median follow-up of 28 months, RV amyloid burden predicted MACE (P < 0.001)., Conclusion: This study shows for the first time that 18F-florbetapir PET/CT identifies early RV amyloid in systemic AL amyloidosis prior to alterations in RV structure and function. Increasing RV amyloid on 18F-florbetapir PET/CT is associated with worse RV structure and function, predicts RV dysfunction, and predicts MACE. These results imply a central role for RV amyloid in the pathogenesis of RV dysfunction., Competing Interests: Conflict of interest: O.F.C.: Research fellowship from the International Society of Amyloidosis and Pfizer. S.A.M.C.: Investigator-initiated research grant from Pfizer. A.J.Y.: Consulting fees from AbbVie, Adaptive Biotechnologies, Amgen, Bristol-Myers Squibb, Celgene, GlaxoSmithKline, Janssen, Karyopharm, Oncopeptides, Regeneron, Sanofi, and Takeda. V.S.: Research support from Takeda, Celgene, Janssen, and Prothena and scientific advisory board for Caelum Biosciences. F.L.R.: Consulting fees from AstraZeneca and research support from Pfizer, Alnylam, and Ionis/Akcea. H.L.: Consulting fees from Celgene, Takeda, Janssen, Prothena, Pfizer, and Juno and research support from Amgen, Spectrum, and Takeda. R.Y.K.: Grant funding from Alnylam Pharmaceuticals. M.F.D.C.: Research grant from Spectrum Dynamics and Gilead and consulting fees from Sanofi and General Electric. R.H.F.: Consulting fees from Ionis Pharmaceuticals, Alnylam Pharmaceuticals, and Caelum Biosciences and research funding from GlaxoSmithKline and Akcea. S.D.: Consulting fees from Pfizer and GE HealthCare and investigator-initiated grant from Pfizer, Attralus, GE HealthCare, Phillips, and Siemens. The other authors do not have any conflicts of interest related to this study to declare., (© The Author(s) 2024. Published by Oxford University Press on behalf of the European Society of Cardiology. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background Aortic dissection (AD) during pregnancy and puerperium is a rare catastrophe with devastating consequences for both parent and fetus. Population-level incidence trends and outcomes remain relatively undetermined. Methods and Results We queried a US population-based health care database, the National Inpatient Sample, and identified all patients with a pregnancy-related AD hospitalization from 2002 to 2017. In total, 472 pregnancy-related AD hospitalizations (mean age, 30.9±0.6 years) were identified from 68 514 000 pregnancy-related hospitalizations (0.69 per 100 000 pregnancy-related hospitalizations), with 107 (22.7%) being type A and 365 (77.3%) being type B. The incidence of AD appeared to increase over the 16-year study period but was not statistically significant ( P for trend >0.05). Marfan syndrome, primary hypertension, and preeclampsia/eclampsia were found in 21.9%, 14.4%, and 11.5%, respectively. On multivariable logistic regression analysis, Marfan syndrome was associated with the highest risk of developing AD during pregnancy and puerperium (adjusted odds ratio, 3469.36 [95% CI, 1767.84-6831.75]; P <0.001). The in-hospital mortalities of AD, type A AD, and type B AD were 7.3%, 4.3%, and 8.1%, respectively. Length of hospital stay for the AD, type A AD, and type B AD groups were 7.7±0.8, 10.4±1.9, and 6.9±0.9 days, respectively. Conclusions We quantified population-level incidence and in-hospital mortality in the United States and observed an increase in the incidence of pregnancy-related AD. In contrast, its in-hospital mortality appears lower than that of non-pregnancy-related AD.