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Background: In severely symptomatic patients with obstructive hypertrophic cardiomyopathy (HCM), the VALOR-HCM (A Study to Evaluate Mavacamten in Adults With Symptomatic Obstructive Hypertrophic Cardiomyopathy Who Are Eligible for Septal Reduction Therapy) trial showed that mavacamten reduced the eligibility for septal reduction therapy with sustained improvement in left ventricular outflow tract gradients. Mavacamten also resulted in favorable cardiac remodeling, including improvement in biomarkers (eg, N-terminal pro-B-type natriuretic peptide and troponin T). However, the impact of mavacamten on left atrial (LA) function is unknown., Objectives: The aim of this study was to assess serial changes in LA strain measures in patients enrolled in the VALOR-HCM trial., Methods: VALOR-HCM included 112 symptomatic patients with obstructive HCM (mean age 60 years; 51% male). Patients assigned to receive mavacamten at baseline (n = 56) continued therapy for 56 weeks and those assigned to placebo transitioned to mavacamten (n = 52) from week 16 to week 56. Echocardiographic LA strain (reservoir, conduit, and contraction) was measured by using a vendor-neutral postprocessing software., Results: At baseline, the mean LA volume index (LAVI) and LA strain values (conduit, contraction, and reservoir) were 41.3 ± 16.5 mL/m 2 , -11.8% ± 6.5%, -8.7% ± 5.0%, and 20.5% ± 8.7%, respectively (all worse than reported normal). LAVI significantly improved by -5.6 ± 9.7 mL/m 2 from baseline to week 56 (P < 0.001). There was a significant (P < 0.05) improvement in absolute LA strain values from baseline to week 56 (conduit [-1.7% ± 6%], contraction [-1.2% ± 4.5%], and reservoir [2.8% ± 7.7%]). Patients originally receiving placebo had no differences in LA measurements up to week 16. There was no significant improvement in LA strain values (conduit [-0.9% ± 3.8%], contraction [-0.4% ± 3.4%], and reservoir [1.4% ± 6.1%]; all; P = NS) from baseline to week 56 in patients with history of atrial fibrillation., Conclusions: In VALOR-HCM, mavacamten resulted in an improvement in LAVI and LA strain at week 56, suggesting sustained favorable LA remodeling and improved function, except in the atrial fibrillation subgroup. Whether the advantageous LA remodeling associated with long-term treatment with mavacamten results in a favorable impact on the observed high burden of atrial tachyarrhythmias in HCM remains to be proven. (A Study to Evaluate Mavacamten in Adults With Symptomatic Obstructive Hypertrophic Cardiomyopathy Who Are Eligible for Septal Reduction Therapy [VALOR-HCM]; NCT04349072)., Competing Interests: Funding Support and Disclosures Bristol Myers Squibb policy on data sharing is provided at https://www.bms.com/researchers-and-partners/independent-research/data-sharing-request-process.html. The VALOR-HCM study was funded by Bristol Myers Squibb. Dr Desai has received consulting fees from Bristol Myers Squibb, Cytokinetics, Tenaya, Edgewise, and Viz.AI; and has done research support to Cleveland Clinic from Bristol Myers Squibb, Cytokinetics, and Tenaya. Drs Wolski and Nissen work for the Cleveland Clinic Coordinating Center for Clinical Research and are employees of the Cleveland Clinic, which received payments for the current research from Bristol Myers Squibb. Dr Geske has received consulting fees from Bristol Myers Squibb. Dr Owens has received consulting fees from Bristol Myers Squibb, Cytokinetics, Pfizer, BioMarin, Tenaya, Lexicon, Stealth, Edgewise, Renovacor; and has received grant support for research from Bristol Myers Squibb. Dr Saberi has received consulting fees from Bristol Myers Squibb and Cytokinetics. Dr Wang has received research grants (to institution) from Bristol Myers Squibb, Cytokinetics, and Abbott Vascular; has been on the consulting/advisory board from Bristol Myers Squibb; has held steering committee roles for Bristol Myers Squibb and Cytokinetics; and has received speaker fees from Bristol Myers Squibb. Dr Lakdawala has received consulting fees from Bristol Myers Squibb, Pfizer, Tenaya, Cytokinetics, and Akros; and has received research support from Bristol Myers Squibb and Pfizer. Drs Sherrid, Tower-Rader, and Naidu have received consulting fees from Bristol Myers Squibb and Cytokinetics. Dr Fermin has received consulting and speaker fees from Bristol Myers-Squibb and BridgeBio; and has received consulting fees from Pfizer. Drs Lampl and Sehnert are employed and have stock ownership at Bristol Myers Squibb. All other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Pericardial diseases have gained renewed clinical interest, leading to a renaissance in the field. There have been many recent advances in pericardial diseases in both multimodality cardiac imaging of diagnoses, such as recurrent, transient constrictive and effusive-constrictive pericarditis, and targeted therapeutics, especially anti-interleukin (IL)-1 agents that affect the inflammasome as part of autoinflammatory pathophysiology. There remains a large educational gap for clinicians, leading to variability in evaluation and management of these patients. The latest pericardial imaging (American Society of Echocardiography, European Association of Cardiovascular Imaging) and clinical guidelines (European Society of Cardiology) are >8-10 years of age and may not reflect current practice. Recent clinical trials involving anti-IL-1 agents in recurrent pericarditis, including anakinra (AIRTRIP), rilonacept (RHAPSODY), and goflikicept have demonstrated their efficacy. The present document represents an international position statement from world leaders in the pericardial field, focusing on novel concepts and emphasizing the role of multimodality cardiac imaging as well as new therapeutics in pericardial diseases., Competing Interests: Funding Support and Author Disclosures Dr Klein has received research grants from Kiniksa Pharmaceuticals and Cardiol Therapeutics, and is on advisory boards for Kiniksa Pharmaceuticals, Cardiol Therapeutics, and Pfizer. Dr Cremer has received research grants from Kiniksa Pharmaceutics and Novartis, and is on advisory boards for Kiniksa Pharmaceutics and Swedish Orphan Biovitrum. Antonio Abbate has received consulting fees from Cardiol Therapeutics, Kiniksa Pharmaceuticals, Implicit Biosciences, Novo Nordisk, Olatec, R-Pharm, Serpin Pharma, and Swedish Orphan Biovitrum. Dr Asher has received royalties from Wolters-Kluwer Publishing Company. Dr Brucato’s institution has received funding from Kiniksa Pharmaceuticals as an investigative site, unrestricted research grants from Swedish Orphan Biovitrum and ACARPIA, and travel and accommodation for advisory committee from Swedish Orphan Biovitrum and Kiniksa. Dr Hoit is speaker for Philips Medical. Dr Kwon has received a research grant from the National Heart, Lung, and Blood Institute of the National Institutes of Health (1R01HL170090-01) and has research agreements with Circle cvi42 and Myocardial Solutions. Dr LeWinter has received a research grant from and is on an advisory board for Kiniksa Pharmaceuticals. Dr Lin is on an advisory board for Kiniksa Pharmaceuticals. Dr Luis is a consultant for Medtronic, Kiniksa Pharmaceuticals, Cardiol Therapeutic, and Swedish Orphan Biovitrum Pharmaceuticals; Dr Ordovas has received a research grant from the American College of Radiology; Dr Schenone is on the speaking bureau for Bristol Myers Squibb; Dr Weber is on advisory boards for Kiniksa Pharmaceuticals, Novo Nordisk, and Horizon Therapeutics; Dr Imazio is on advisory boards for Kiniksa Pharmaceuticals and Cardiol Therapeutics. The other authors have reported that they have no relationships relevant to the contents of this paper to disclose., (Copyright © 2024 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Frequently, multimodality imaging is indispensable in the care of patients with pericardial disease. With cardiac magnetic resonance imaging, pericardial inflammation can be characterized as acute, subacute, or chronic. This spectrum of inflammation is variably associated with reduced compliance of the pericardium, which may result in constrictive pathophysiology, typically well-defined with echocardiography. This interplay between inflammation and hemodynamics is often optimally characterized with multimodality imaging and has redefined the approach of pericardiologists to diagnose, prognosticate, and tailor individual therapies., (Copyright © 2020 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

By assessing nonhospitalized asymptomatic patients, community-based studies inform the prevalence, key clinical characteristics, and outcomes associated with diastolic dysfunction. As the number of parameters to define and grade diastolic function continues to increase, there has been a shift to a focus on readily obtainable measurements with minimal interobserver variability. In this regard, mitral inflow and annular tissue Doppler velocities, as well as measurement of left atrial volume index, are the most feasible and reproducible. Within communities, variations in definitions have limited generalizability regarding the prevalence and risks associated with diastolic dysfunction. Nevertheless, community-based studies have established important associations with hypertension, obesity, and diabetes. Randomized controlled trials of treatment in heart failure with preserved ejection fraction have been disappointing. Importantly, diastolic dysfunction is consistently associated with higher mortality, which emphasizes the importance of early recognition and initiation of appropriate preventative treatments., (Copyright © 2020. Published by Elsevier Inc.)

Thoracic aortic calcification (TAC) is associated with adverse cardiovascular outcomes, and for the cardiovascular imager, is predominantly encountered in 4 settings: 1) incidentally, for example, during a coronary artery calcium scan; 2) as part of dedicated screening; 3) in the evaluation of an embolic event; or 4) in procedural planning. This review focuses on TAC in these contexts. Within atherosclerosis, TAC is common, variable in extent, and begins in the intima with a patchy distribution. In metabolic disorders, aortitis, and radiation-associated cardiovascular disease, calcification preferentially involves the media and is often more concentric. As an incidental finding, atherosclerotic TAC provides limited incremental discriminative value, and current data do not support screening. After an embolic event, the demonstration of thoracic atheroma provides diagnostic clarity, but has limited treatment implications. Before any procedure, the plan often changes if the most severe form of TAC, a porcelain aorta, is discovered., (Copyright © 2018 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

Objectives: This study hypothesized that regurgitation severity, as determined by using the regurgitant volume index, would better delineate differential cardiac dysfunction in asymptomatic patients with moderate to severe aortic regurgitation (AR) and mitral regurgitation (MR)., Background: Frequent surveillance echocardiography is considered appropriate in asymptomatic patients with moderate to severe AR and MR. However, the evidence to support this practice and to define the appropriate frequency is limited., Methods: This was an observational cohort study of consecutive patients with moderate to severe asymptomatic AR or MR who underwent exercise echocardiography. Our cohort included 130 patients with moderate to severe asymptomatic MR and 130 patients with moderate to severe asymptomatic AR who were matched according to age and regurgitant volume index. All patients underwent yearly echocardiographic follow-up studies. Regurgitation severity was determined according to regurgitant volume index, with a level ≥30 ml/m(2) considered a marker of severe regurgitation., Results: During follow-up, regardless of etiology, patients with severe regurgitation demonstrated increasing left ventricular volume indexes (4.2 ± 1.5 ml/m(2) per year; p = 0.01) and decreasing left ventricular ejection fractions (1.3 ± 0.4% per year; p = 0.002). In patients with moderate regurgitation, left ventricular volumes and ejection fractions did not significantly change. In addition, patients with severe regurgitation experienced a similar drop in contractility (end-systolic pressure/end-systolic volume ratio and single-beat pre-load recruitable stroke work) during follow-up independent of regurgitation etiology. Contractility parameters did not change in patients with moderate regurgitation., Conclusions: These asymptomatic patients with moderate AR or MR had stable cardiac function during 3 years of follow-up; thus, frequent echocardiography without a change in clinical status may not be necessary. In the setting of severe regurgitation, further cardiac deterioration occurred at a similar rate and manner irrespective of whether the dysfunction was related to AR or MR., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)