BACKGROUND: Depression often interferes with self-management and treatment of medical conditions. This may result in serious medical complications and escalated health-care cost. OBJECTIVES: Study distribution of heart failure (HF) cases estimates the prevalence of depression and its effects on HF-related hospital costs by ethnicity and gender. METHODS: Secondary data files of California Hospital Discharge System for he year 2010 were examined. For patients with a HF diagnosis, details regarding depression, demographics, comorbid conditions, and hospital costs were studied. Age-adjusted HF rates and depression were examined for whites, blacks, Hispanics, and Asians/Pacific Islanders (AP) by comparing HF patients with depression (HF+D) versus HF without depression (HFND). RESULTS: HF cases (n = 62,685; average age: 73) included nearly an equal number of males and females. HF rates were higher (P < 0.001) among blacks compared to Hispanics, AP, and whites and higher among males than females. One-fifth of HF patients had depression, higher among females and whites compared to males and other ethnic groups. Further, HF hospital costs for blacks and AP were higher (P < 0.001) compared to other groups. The cost for HF+D was 22% higher compared to HFND, across all gender and ethnic groups, largely due to higher comorbidities, more admissions, and longer hospitalization. CONCLUSION: Depression, ethnicity, and gender are all associated with increased hospital costs of HF patients. The higher HF and HF+D costs among blacks, AP, and males reflect additional burden of comorbidities (hypertension and diabetes). Prospective studies to assess if selective screening and treating depression among HF patients can reduce hospital costs are warranted.

Introduction: Point-of-care ultrasound (POCUS) performed by emergency physicians (EP) has emerged as an effective alternative to radiology department ultrasounds for the diagnosis of lower extremity deep vein thrombosis (DVT). Systematic reviews suggested good sensitivity and specificity overall for EP-performed POCUS for DVT diagnosis, yet high levels of heterogeneity were reported.

Methods: In this systematic review and meta-analysis, we aimed to provide the most up-to-date estimates of the accuracy of EP-performed POCUS for diagnosis of DVT and to explore potential correlations with test performance. We performed systematic searches in MEDLINE and Embase for original, primary data articles from January 2012–June 2021 comparing the efficacy of POCUS performed by EPs to the local standard. Quality Assessment of Diagnostic Accuracy Studies-2 for individual articles are reported. We obtained summary measures of sensitivity, specificity, and their corresponding 95% confidence intervals (CI) using bivariate mixed-effects regression models. We performed meta-regression, subgroup, and sensitivity analyses as planned in the protocol CRD42021268799 submitted to PROSPERO.

Results: Fifteen publications fit the inclusion criteria, totaling 2,511 examinations. Pooled sensitivity and specificity were 90% (95% CI 82%–95%) and 95% (CI 91%–97%), respectively. Subgroup analyses by EP experience found significantly better accuracy for exams performed by EP specialists (93%, CI 88%–97%) vs trainees (77%, CI 60%–94%). Specificity for EP specialists (97%, CI 94%–99%) was higher than for trainees (87%, CI 76%–99%, P = 0.01). Three-point compression ultrasound (CUS) was more sensitive than two-point CUS but was only statistically significant when limited to EP specialists (92% vs 88%, P = 0.07, and 95% vs 88%, P = 0.02, respectively).

Conclusion: Point-of-care ultrasound performed by emergency physicians is sensitive and specific for the diagnosis of suspected DVT when performed by trained attending EPs. Three-point compression ultrasound examination may be more sensitive than two-point CUS.

Background

Conventional hemodynamic parameters may not accurately predict symptomatic improvement after percutaneous mitral valvuloplasty (PMV). Changes in left heart chamber compliance following adequate relief o0066 mitral stenosis (MS) may be useful in determining functional capacity after PMV. This study aims to determine the acute effects of PMV on compliance of the left heart and whether its changes relate to the patient's functional capacity.

Methods

One-hundred thirty-seven patients with severe MS undergoing PMV were enrolled. Left atrial (C_a ) and left ventricular (C_v ) compliance were invasively estimated and net atrioventricular compliance (C_av ) was calculated before and immediately after the procedure. B-type natriuretic peptide (BNP) levels were obtained before and 24 hr after the procedure. The primary endpoint was functional status at 6-month follow-up, and the secondary endpoint was a composite of death, mitral valve (MV) replacement, repeat PMV, new onset of atrial fibrillation, or stroke in patients in whom PMV was successful.

Results

The mean age was 43 ± 12 years, and 119 patients were female (87%). After PMV, C_a and C_av improved significantly from 5.3 [IQR 3.2-8.2] mL/mmHg to 8.7 [5.3-19.2] mL/mmHg (P < 0.001) and 2.2 [1.6-3.4] to 2.8 [2.1-4.1] mL/mmHg (P < 0.001), respectively, whereas C_v did not change (4.6 [3.2-6.8] to 4.4 [3.1-5.6]; P = 0.637). Plasma BNP levels significantly decreased after PMV, with no correlation between its variation and changes in left chamber compliance. At 6-month follow-up, NYHA functional class remained unchanged in 32 patients (23%). By multivariable analyses, changes in C_a immediately after PMV (adjusted OR 1.42; 95% CI 95% 1.02 to 1.97; P = 0.037) and younger age (adjusted OR 0.95; CI 95% 0.92-0.98; P = 0.004), predicted improvement in functional capacity at 6-month follow-up, independent of postprocedural data. The secondary endpoint were predicted by post-PMV mean gradient (adjusted HR 1.363; 95% CI 95% 1.027-1.809; P = 0.032), and lack of functional improvement at 6-month follow-up (adjusted HR 4.959; 95% 1.708-14.403; P = 0.003).

Conclusions

C_a and C_av increase significantly after PMV with no change in C_v . The improvement of C_a is an important predictor of functional status at 6-month follow up, independently of other hemodynamic data. Postprocedural mean gradient and lack of short-term symptomatic improvement were predictors of adverse outcome.

Objective

Ischemic mitral regurgitation (MR) is common, but its response to percutaneous coronary intervention (PCI) is poorly understood. This study tested the utility of myocardial perfusion imaging (MPI) for the stratification of MR response to PCI.

Methods

MPI and transthoracic echocardiography (echo) were performed among patients undergoing PCI. MPI was used to assess stress/rest myocardial perfusion. MR was assessed via echo (performed before and after PCI).

Results

A total of 317 patients with abnormal myocardial perfusion on MPI underwent echo 25±39 days before PCI. MR was present in 52%, among whom 24% had advanced (≥moderate) MR. MR was found to be associated with left ventricular (LV) chamber dilation on MPI and echo (both P<0.001). The magnitude of global LV perfusion deficits increased in relation to MR severity (P<0.01). Perfusion differences were greatest for global summed rest scores, which were 1.6-fold higher among patients with advanced MR versus those with mild MR (P=0.004), and 2.4-fold higher versus those without MR (P<0.001). In multivariate analysis, advanced MR was found to be associated with a fixed perfusion defect size on MPI [odds ratio 1.16 per segment (confidence interval 1.002-1.34), P=0.046], independent of LV volume [odds ratio 1.10 per 10 ml (confidence interval 1.04-1.17), P=0.002]. Follow-up via echo (1.0±0.6 years) demonstrated MR to decrease (≥1 grade) in 31% of patients and increase in 12% of patients. Patients with increased MR after PCI had more severe inferior perfusion defects on baseline MPI (P=0.028), whereas defects in other distributions and LV volumes were similar (P=NS).

Conclusion

The extent and distribution of single-photon emission computed tomography-evidenced myocardial perfusion defects impact MR response to revascularization. An increased magnitude of inferior fixed perfusion defects predicts post-PCI progression of MR.

In light of the adverse prognosis related to severe mitral regurgitation, heart failure, or sudden cardiac death in a subset of patients with mitral valve prolapse (MVP), identifying those at higher risk is key. For the first time in decades, researchers have the means to rapidly advance discovery in the field of MVP thanks to state-of-the-art imaging techniques, novel omics methodologies, and the potential for large-scale collaborations using web-based platforms. The National Heart, Lung, and Blood Institute recently initiated a webinar-based workshop to identify contemporary research opportunities in the treatment of MVP. This report summarizes 3 specific areas in the treatment of MVP that were the focus of the workshop: 1) improving management of degenerative mitral regurgitation and associated left ventricular systolic dysfunction; 2) preventing sudden cardiac death in MVP; and 3) understanding the mechanisms and progression of MVP through genetic studies and small and large animal models, with the potential of developing medical therapies.

Objectives

The aim of this study was to assess the incidence, mechanisms, and outcomes of mitral regurgitation (MR) after percutaneous mitral valvuloplasty (PMV).

Background

Significant MR continues to be a major complication of PMV, with a wide range in clinical presentation and prognosis.

Methods

Consecutive patients with mitral stenosis undergoing PMV were prospectively enrolled. MR severity was evaluated by using quantitative echocardiographic criteria, and its mechanism was characterized by 3-dimensional transesophageal echocardiography, divided broadly into 4 categories based on the features contributing to the valve damage. B-type natriuretic peptide levels were obtained before and 24 h after the procedure. Endpoints estimated cardiovascular death or mitral valve (MV) replacement due to predominant MR.

Results

A total of 344 patients, ages 45.1 ± 12.1 years, of whom 293 (85%) were women, were enrolled. Significant MR after PMV was found in 64 patients (18.6%). The most frequent mechanism of MR was commissural, which occurred in 22 (34.4%) patients, followed by commissural with posterior leaflet in 16 (25.0%), leaflets at central scallop or subvalvular damage in 15 (23.4%), and central MR in 11 (17.2%). During the mean follow-up period of 3 years (range 1 day to 10.6 years), 60 patients reached the endpoint. The event-free survival rates were similar among patients with mild or commissural MR, whereas patients with damaged central leaflet scallop or subvalvular apparatus had the worst outcome, with an event-free survival rate at 1 year of only 7%. Long-term outcome was predicted by net atrioventricular compliance (C_n) at baseline and post-procedural variables, including valve area, mean gradient, and magnitude of decrease in B-type natriuretic peptide levels, adjusted for the mechanism of MR.

Conclusions

Significant MR following PMV is a frequent event, mainly related to commissural splitting, with favorable clinical outcome. Parameters that express the relief of valve obstruction and the mechanism by which MR develops were predictors of long-term outcomes.

Nonsyndromic mitral valve prolapse (MVP) is a common degenerative cardiac valvulopathy of unknown etiology that predisposes to mitral regurgitation, heart failure and sudden death. Previous family and pathophysiological studies suggest a complex pattern of inheritance. We performed a meta-analysis of 2 genome-wide association studies in 1,412 MVP cases and 2,439 controls. We identified 6 loci, which we replicated in 1,422 cases and 6,779 controls, and provide functional evidence for candidate genes. We highlight LMCD1 (LIM and cysteine-rich domains 1), which encodes a transcription factor and for which morpholino knockdown of the ortholog in zebrafish resulted in atrioventricular valve regurgitation. A similar zebrafish phenotype was obtained with knockdown of the ortholog of TNS1, which encodes tensin 1, a focal adhesion protein involved in cytoskeleton organization. We also showed expression of tensin 1 during valve morphogenesis and describe enlarged posterior mitral leaflets in Tns1(-/-) mice. This study identifies the first risk loci for MVP and suggests new mechanisms involved in mitral valve regurgitation, the most common indication for mitral valve repair.