Citations

Purpose of review Cardiac amyloidosis is an infiltrative cardiomyopathy with characteristic echocardiographic findings. Echocardiography is the initial imaging test to identify restrictive cardiomyopathies, and timely diagnosis is important for treatment and prognosis. This review outlines key echocardiographic “red flags,” structural and functional findings, and emerging diagnostic tools that enhance early recognition and monitoring of cardiac amyloidosis. Recent findings Classic echocardiographic red flags for cardiac amyloidosis include increased ventricular wall thickness, biatrial enlargement, pericardial effusion, and a granular myocardial appearance. Tissue Doppler imaging shows reduced mitral annular velocities, while advanced disease presents with restrictive filling patterns. Global longitudinal strain with apical sparing is a hallmark finding that distinguishes cardiac amyloidosis from other cardiomyopathies. Left atrial strain has been proposed as a prognostic marker for thromboembolism in cardiac amyloidosis. Evidence shows variability in strain measurements across different vendors, which is an important consideration when comparing results between institutions in both research and clinical practice. Echocardiography can be used in conjunction with multimodal imaging techniques in order to monitor disease progression. Summary Echocardiography is the initial diagnostic test of choice and several findings can suggest cardiac amyloidosis. Advances in echocardiographic techniques have enabled earlier detection of cardiac involvement and now play a central role in both diagnosis and ongoing treatment monitoring.

This retrospective propensity-matched cohort study assessed the association between sodium-glucose co-transporter-2 inhibitor (SGLT2i) use and cardiovascular outcomes in patients with acute myocardial infarction (AMI) without a history of heart failure. Using the TriNetX U.S. Collaborative Network, we identified 1440 matched patients (720 SGLT2i+ vs 720 SGLT2i−) with preserved ejection fraction and no prior heart failure. Nearly 90% of patients had diabetes. The primary outcome was major adverse cardiovascular events (MACE), defined as a composite of MI, stroke, heart failure, and all-cause mortality. At 1 year, MACE occurred in 17.4% of SGLT2i+ versus 22.0% of SGLT2i− patients (odds ratio [OR] 0.746, 95% CI 0.574-0.969; P = .028), and all-cause mortality occurred in 3.1% versus 7.6%, respectively (OR 0.389, 95% CI 0.234-0.645; P < .001). SGLT2i use was also associated with lower risks of major bleeding. Findings were consistent over long-term follow-up. While the observed associations suggest potential cardioprotective effects of SGLT2i post-MI in patients without heart failure, residual confounding cannot be excluded. The observed reduction in bleeding events is novel and warrants further investigation in prospective studies.

Sodium-glucose co-transporter-2 inhibitors (SGLT2i) have demonstrated benefits in heart failure with preserved ejection fraction (HFpEF), but their impact following acute myocardial infarction (AMI) is less well understood. Using the TriNetX Research Network (TriNetX) multi-center registry (2014–2022), we identified patients with heart failure with preserved ejection fraction (HFpEF)—defined as left ventricular ejection fraction (LVEF) >50% and New York Heart Association (NYHA) class II–IV—not previously treated with sodium-glucose co-transporter 2 inhibitors (SGLT2i) who experienced an acute myocardial infarction (AMI). Patients who initiated SGLT2i within 1-year post-AMI were compared with those who did not. Propensity score matching was used to balance cohorts ( n = 20,423 each; mean age 68.3 ± 11.0 years; 54.5% female) for demographics, comorbidities, and treatment variables. The primary outcome was a composite of major adverse cardiovascular events (MACE), including all-cause mortality, recurrent AMI, acute heart failure, and stroke. Secondary outcomes included cardiac arrest and major bleeding. SGLT2i use was associated with lower rates of MACE (3.7% vs 6.1%; P = .0005), all-cause mortality (0.9% vs 5.6%; P < .0001), and other adverse events at both 30 days and 1 year. In this large, propensity-matched cohort, SGLT2i use post-AMI in HFpEF patients was associated with favorable cardiovascular outcomes. Further studies are needed to confirm these associations.

Purpose: Functional septorhinoplasty is an effective treatment for nasal airway obstruction. Little distinction exists between bilaterally and unilaterally obstructed patients in literature. Our study evaluates outcomes in patients with unilateral nasal airway obstruction compared to those with bilateral nasal airway obstruction as measured by nasal obstruction symptom evaluation scores following functional septorhinoplasty. Materials and Methods: A total of 227 patients underwent functional septorhinoplasty for nasal airway obstruction. Patients were grouped into unilateral (n = 64) and bilateral (n = 163) nasal obstruction cohorts based on patient report and physician assessment. Nasal obstruction symptom evaluation (NOSE) scores were obtained pre-operatively and post-operatively at least 3 months following surgery. Results: Patients with unilateral nasal obstruction had slightly less severe symptoms preoperatively than patients with bilateral obstruction. Average preoperative NOSE scores for patients with unilateral obstruction was 64 (SD = 19) and 72 (SD = 18) for patients with bilateral obstruction ( P = .004). Postoperative NOSE scores following septorhinoplasty were significantly reduced for patients with both unilateral and bilateral nasal obstruction (postoperative NOSE scores unilateral: 17, SD = 16 ; bilateral: 23, SD = 21). There was no statistical significance in outcomes between patients with unilateral or bilateral nasal obstruction groups. Conclusions: Symptoms in patients with unilateral obstruction are similar but slightly less severe than patients with bilateral obstruction. Patients with unilateral and bilateral nasal obstruction experienced a similar degree of improvement in symptom following functional septorhinoplasty.

INTRODUCTION: Early neoplastic progression of Barrett's esophagus (BE) is often treated with endoscopic therapy. Although effective, some patients are refractory to therapy or recur after apparent eradication of the BE. The goal of this study was to determine whether genomic alterations within the treated BE may be associated with persistent or recurrent disease. METHODS: We performed DNA sequencing on pre-treatment esophageal samples from 45 patients who were successfully treated by endoscopic therapy and did not recur as well as pre-treatment and post-treatment samples from 40 patients who had persistent neoplasia and 21 patients who had recurrent neoplasia. The genomic alterations were compared between groups. RESULTS: The genomic landscape was similar between all groups. Patients with persistent disease were more likely to have pre-treatment alterations involving the receptor tyrosine kinase pathway ( P = 0.01), amplifications of oncogenes ( P = 0.01), and deletions of tumor suppressor genes ( P = 0.02). These associations were no longer significant after adjusting for patient age and BE length. More than half of patients with persistent (52.5%) or recurrent (57.2%) disease showed pre-treatment and post-treatment samples that shared at least 50% of their driver mutations. DISCUSSION: Pre-treatment samples were genomically similar between those who responded to endoscopic therapy and those who had persistent or recurrent disease, suggesting there is not a strong genomic component to treatment response. Although it was expected to find shared driver mutations in pre-treatment and post-treatment samples in patients with persistent disease, the finding that an equal number of patients with recurrent disease also showed this relation suggests that many recurrences represent undetected minimal residual disease.

Injection of autologous adipose tissue removed via liposuction has been used clinically for facial contouring, the aging face, furrows, facial atrophy, acne scars, nasolabial folds, chin, and various other surgical defects. Survival rates for autografts of fat have been quoted anywhere from 30% to 80%. Our study uses a reproducible rabbit animal model for autotransplantation of adipose tissue and examines the histopathologic changes that occur to the graft over time. Autogenous subcutaneous fat was removed from a dorsal scapular donor site, treated to stimulate cannula damage as in liposuction, then reinjected at the base of the ear. Histologic examination of the grafts were made at 5, 10, 15, 20, 40, and 100 days after transplantation. Hematoxylin‐eosin sections were graded on degree of fibrosis present (0 to 4+), viable fat (1 to 10), degree of inflammation (0 to 4+), and neovascularization (+ or ‐). Viability of fat decreased from 8.5 to 10 at 5 days to 2 viability at 40 days. Acute inflammation peaked at 10 days, followed by the chronic inflammatory response with macrophages and multinucleated giant cells scavenging the dying fat graft. Neovascularization began at 5 days, peaked at 10 days, and remained constant thereafter only at the edge of the graft. Microcysts appeared at 15 days and increased in number in proportion to the decrease in viable fat. In summary, the temporal histologic events are progressive fibrosis; decreased amount of viable fat; inflammation beginning with a neutrophilic response, later a macrophage and giant cell response; and neovascularization at the periphery of the graft insufficient to maintain graft viability. In our animal model, autografts of fat appear to have limited long‐term viability and are replaced by fibrous tissue. This may have clinical implications in autografting of fat in facial plastic and reconstructive surgery.