Background: Patients with lymphedema and lipedema share physical exam findings that may lead to misdiagnosis. Poor mobility is common in patients with obesity and patients with lymphedema and lipedema. This may constitute a risk factor for venous thromboembolism (VTE). Our objective was to evaluate the association of VTE in obese patients with lymphedema and lipedema. Methods: The National Inpatient Sample (NIS) was searched from 2016 to 2020 to identify hospital admissions of obese female patients with lymphedema and lipedema. Patients were analyzed in the context of presence or absence of VTE while adjusting for complex cluster sampling techniques. Predictors of VTE were accessed by multivariable regression. Results: Lymphedema was identified in 189,985 patients and lipedema in 50,645 patients. VTE was observed in 3.12% (n = 374,210) of patients with obesity. In patients with obesity, VTE was more common in patients with lymphedema than without (2.6% vs 1.6%; p < 0.01). Similarly, VTE was more common in patients with lipedema than without (0.6% vs 0.4%; p < 0.01). After multivariable logistic regression, VTE events in obese patients with lymphedema were higher versus without (OR 1.6; CI 1.08-2.43; p = 0.02). Similarly, VTE events were more common in obese patients with lipedema versus obese patients without lipedema (OR 1.20; CI 1.03-1.41; p = 0.02). Conclusions: In this hypothesis-generating study, lymphedema and lipedema show a positive association with VTE after adjusting for baseline patient characteristics such as obesity, which is a known independent risk factor for VTE. Mechanisms whereby lymphedema and lipedema are associated with VTE should be investigated.

Hypoattenuated leaflet thickening (HALT) has been recognized as one of the complica-tions after transcatheter aortic valve implantation and may promote structural valve degeneration and increase the risk of cerebrovascular events. The 2 main types of avail-able transcatheter heart valves (THVs), the balloon-expandable (BE) and the self -expand-ing (SE), are interchangeably used in clinical practice despite substantial design differences. There is unclear evidence on whether these 2 different THV models are achieving similar or different rates of subclinical leaflet thrombosis/HALT. A systematic search of electronic databases was conducted to identify studies that reported the inci-dence of HALT between SE THVs and BE THVs. The Mantel-Haenszel method was used to calculate the 95% confidence interval and pooled risk ratio with a random-effects model. A total of 126 records were identified, of which 22 studies comprising 14,401 patients were included in our final analysis. Among 5,951 patients receiving SE THVs, 194 (3.2%) developed HALT, compared with 8,450 patients receiving BE THVs, of whom 484 (5.7%) developed HALT. There was a statistically significant decrease in the risk of devel-oping HALT in patients receiving SE THVs compared with those receiving BE THVs (risk ratio 0.75, 95% confidence interval 0.59 to 0.95, I2 32%, p = 0.02). In conclusion, could potentially reduce the risk of HALT/subclinical leaflet thrombosis. (c) 2023 Elsev-ier Inc. All rights reserved.

BACKGROUND The impact of pre-existing atrial fibrillation (AF) on outcomes after noncardiac surgery is not clear. OBJECTIVES We aimed to study the impact of AF on the risk of adverse outcomes after noncardiac surgery in a nationwide cohort. METHODS We identified Medicare beneficiaries admitted for noncardiac surgery from 2015 to 2019 and divided the study cohort into 2 groups: with and without AF. Noncardiac surgery was classified into vascular, thoracic, general, genitourinary, gynecological, orthopedics and neurosurgery, breast, head and neck, and transplant. We used propensity score matching on exact age, sex, race, urgency and type of surgery, revised cardiac risk index (RCRI) and CHA(2)DS(2)-VASc score, and tight caliper on other comorbidities. The study outcomes were 30-day mortality, stroke, myocardial infarction, and heart failure. We examined the incremental utility of AF in addition to RCRI to predict adverse events after noncardiac surgery. RESULTS The study cohort included 8,635,758 patients who underwent noncardiac surgery (16.4% with AF). Patients with AF were older, more likely to be men, and had higher prevalence of comorbidities. After propensity score matching, AF was associated with higher risk of mortality (OR: 1.31; 95% CI: 1.30-1.32), heart failure (OR: 1.31; 95% CI: 1.30-1.33), and stroke (OR: 1.40; 95% CI: 1.37-1.43) and lower risk of myocardial infarction (OR: 0.81; 95% CI: 0.79-0.82). Results were consistent in subgroup analysis by sex, race, type of surgery, and all strata of RCRI and CHA(2)DS(2)-VASc score. AF improved the discriminative ability of RCRI (C-statistic 0.73 to 0.76). CONCLUSION Pre-existing AF is independently associated with postoperative adverse outcomes after NCS. (C) 2022 by the American College of Cardiology Foundation.

Background Rheumatic immune mediated inflammatory diseases (IMIDs) are associated with high risk of acute coronary syndrome. The long-term prognosis of acute coronary syndrome in patients with rheumatic IMIDs is not well studied. Methods and Results We identified Medicare beneficiaries admitted with a primary diagnosis of myocardial infarction (MI) from 2014 to 2019. Outcomes of patients with MI and concomitant rheumatic IMIDs including systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis, dermatomyositis, or psoriasis were compared with propensity matched control patients without rheumatic IMIDs. One-to-three propensity-score matching was done for exact age, sex, race, ST-segment-elevation MI, and non-ST-segment-elevation MI variables and greedy approach on other comorbidities. The study primary outcome was all-cause mortality. The study cohort included 1 654 862 patients with 3.6% prevalence of rheumatic IMIDs, the most common of which was rheumatoid arthritis, followed by systemic lupus erythematosus. Patients with rheumatic IMIDs were younger, more likely to be women, and more likely to present with non-ST-segment-elevation MI. Patients with rheumatic IMIDs were less likely to undergo coronary angiography, percutaneous coronary intervention or coronary artery bypass grafting. After propensity-score matching, at median follow up of 24 months (interquartile range 9-45), the risk of mortality (adjusted hazard ratio [HR], 1.15 [95% CI, 1.14-1.17]), heart failure (HR, 1.12 [95% CI 1.09-1.14]), recurrent MI (HR, 1.08 [95% CI 1.06-1.11]), and coronary reintervention (HR, 1.06 [95% CI, 1.01-1.13]) (P<0.05 for all) was higher in patients with versus without rheumatic IMIDs. Conclusions Patients with MI and rheumatic IMIDs have higher risk of mortality, heart failure, recurrent MI, and need for coronary reintervention during follow-up compared with patients without rheumatic IMIDs.

Background: Chronic inflammatory diseases (CIDs) are considered risk enhancing factors for coronary heart disease (CHD). However, sparse data exist regarding relative CHD risks across CIDs. Objective: Determine relative differences in CHD risk across multiple CIDs: psoriasis, rheumatoid arthritis (RA), systemic lupus erythematosus (SLE), human immunodeficiency virus (HIV), systemic sclerosis (SSc), and inflammatory bowel disease (IBD). Methods: The cohort included patients with CIDs and controls without CID in an urban medical system from 2000 to 2019. Patients with CIDs were frequency-matched with non-CID controls on demographics, hypertension, and diabetes. CHD was defined as myocardial infarction (MI), ischemic heart disease, and/or coronary revascularization based on validated administrative codes. Multivariable-adjusted Cox models were used to determine the risk of incident CHD and MI for each CID relative to non-CID controls. In secondary analyses, we compared CHD risk by disease severity within each CID. Results: Of 17,049 patients included for analysis, 619 had incident CHD (202 MI) over an average of 4.4 years of follow-up. The multivariable-adjusted risk of CHD was significantly higher for SLE [hazard ratio (HR) 1.9, 95% confidence interval (CI) 1.2, 3.2] and SSc (HR 2.1, 95% CI 1.2, 3.9). Patients with SLE also had a significantly higher risk of MI (HR 3.6, 95% CI 1.9, 6.8). When CIDs were categorized by markers of disease severity (C-reactive protein for all CIDs except HIV, for which CD4 T cell count was used), greater disease severity was associated with higher CHD risk across CIDs. Conclusions: Patients with SLE and SSc have a higher risk of CHD. CHD risk with HIV, RA, psoriasis, and IBD may only be elevated in those with greater disease severity. Clinicians should personalize CHD risk and treatment based on type and severity of CID.

Introduction: Inflammation plays an important role in the pathogenesis of coronary heart disease (CHD). Chronic inflammatory diseases (CIDs) may serve as models to provide insights into the relationships between immune dysfunction, inflammation, and CHD. To investigate this further, we analyzed the risk of incident CHD across different CIDs. Methods: We created a cohort of individuals with CIDs and non-CID controls (frequency-matched on demographics and CHD risk factors), free of baseline CHD, receiving regular outpatient care in a large medical system from 2000 to 2019. CIDs included psoriasis, rheumatoid arthritis (RA), systemic sclerosis (SSc), systemic lupus erythematosus (SLE), human immunodeficiency virus (HIV), and inflammatory bowel disease (IBD). CHD was defined as myocardial infarction (MI), angina, or coronary revascularization. We used adjusted hazards models to determine incident CHD risk for each CID relative to controls. We also analyzed incident CHD risk by severity of inflammation (baseline C-reactive protein) or immune dysfunction (baseline CD4 T cell level in HIV). Results: Of 18,129 individuals with CIDs and 18,988 controls, there were 1,011 incident CHD events over a median of 3.5 years. After adjusting for demographics and CHD risk factors, CHD risk was significantly elevated in SLE [hazard ratio (HR) 2.85, 95% confidence interval (CI) 2.19-3.71, p<0.01], SSc (HR 2.14, 95% CI 1.54-2.99, p<0.01), HIV (HR 1.38, 95% CI 1.12-1.69, p<0.01), and RA (HR 1.22, 95% CI 1.00-1.49, p=0.05). Findings were similar with MI as the lone outcome. When CIDs were categorized by inflammation or immune dysfunction, there was a pattern of higher CHD risk with higher levels of inflammation/immune dysfunction across CIDs (Figure). Conclusions: Our results show that SLE, SSc, HIV, and RA were associated with significantly elevated risks of incident CHD and MI. Higher levels of inflammation or immune dysfunction were associated with heightened CHD risk within CIDs.

OBJECTIVES The purpose of this study was to compare the risks of incident heart failure (HF) among a variety of chronic inflammatory diseases (CIDs) and to determine whether risks varied by severity of inflammation within each CID. BACKGROUND Individuals with ODs are at elevated risk for cardiovascular diseases, but data are limited regarding risk for HF. METHODS An electronic health records database from a large urban medical system was examined, comparing individuals with ODs with frequency-matched controls without ODs, all of whom were receiving regular outpatient care. Rates of incident HF were determined by using the Kaplan-Meier method and subsequently used multivariate-adjusted proportional hazards models to compare HF risks for each CID. Exploratory analyses determined HF risks by proxy measurement of CID severity. RESULTS Of 37,636 patients (n = 18,278 patients with ODs; and n = 19,358 controls without CIDs) there were 960 incident HF cases over a median of 3.6 years. Risks for incident HF were significantly or borderline significantly elevated for patients with systemic sclerosis (hazard ratio [HR]: 7.26; 95% confidence interval [CI]: 5.72 to 9.21; p < 0.01), systemic lupus erythematosus (HR: 3.15; 95% CI: 2.41 to 4.11; p < 0.01), rheumatoid arthritis (HR: 1.39; 95% CI: 1.13 to 1.71; p < 0.01), and human immunodeficiency virus (HR: 1.28; 95% CI: 0.99 to 1.66; p = 0.06). There was no association between psoriasis or inflammatory bowel disease and incident HF, although patients with those CIDs with higher levels of C-reactive protein had higher risks for HF than controls. CONCLUSIONS Systemic sclerosis and systemic lupus erythematosus were associated with the highest risks of HF, followed by rheumatoid arthritis and HIV. Measurements of inflammation were associated with HF risk across different CIDs. (C) 2020 by the American College of Cardiology Foundation.

BACKGROUND:Structural left atrial and ventricular abnormalities on the electrocardiogram (ECG) and transthoracic echocardiogram (TTE) at the time of ischemic stroke have been associated with morbidity and mortality. Yet, the prognostic impact of the same in embolic stroke of undetermined source (ESUS), a relevant subtype of ischemic stroke with a unique pathophysiology, has not been well studied to date. Our aim was to assess the predictive impact of left atrio-ventricular ECG and TTE abnormalities on one-year hospital readmission after ESUS from an ongoing single center prospective stroke registry in the U.S. METHODS:We identified 369 ESUS patients who had at least 1 year of complete follow-up between 2013 and 2018. We examined the association of abnormal left atrio-ventricular findings on ECG and TTE, as well as basic demographic and clinical characteristics, measured at index admission with time to 1-year hospital readmission using Kaplan-Meier curves, log-rank tests, and Cox proportional hazards regression. RESULTS:Recurrent ischemic stroke and cardiovascular causes constituted 60% of all readmissions. Patients with left atrial dilation on TTE were more likely to readmitted within 1 year (HR 1.51; 95% CI, 1.04-2.21). Bundle branch block, pathologic Q-wave, and troponin elevation curves diverged, but were not significantly associated with readmission (log-rank p=0.34, p=0.08, p=0.42, respectively). CONCLUSIONS:Following ESUS, left atrial dilation on TTE was associated with 1-year overall hospital readmission, of which cardiovascular and cerebrovascular ischemic events, and heart failure were a notable proportion. Our data support ongoing studies of atrial cardiopathy in ESUS patients.

This study investigated the relationship between ankle–brachial index (ABI) and risk for heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF). ABI has previously been associated with mortality, cardiovascular disease (CVD), and overall HF but the relationship between ABI and risk of HF stratified by EF has not been well characterized. We analyzed data from 6553 participants (53% female; mean age 62 ± 10 years) enrolled in the Multi-Ethnic Study of Atherosclerosis (MESA) who were free of known clinical CVD/HF at baseline (2000–2002) and had baseline ABI measured. Participants were classified as low (≤ 0.90), borderline-low (0.91–1.00), normal (1.01–1.40), and high (> 1.40) ABI. Incident hospitalized HF was determined over a median follow-up of 14 years; we classified HF events (n = 321) as HFrEF with EF < 50% (n = 155, 54%) or HFpEF with EF ⩾ 50% (n = 133, 46%). Low ABI was associated with incident HFrEF (hazard ratio (HR): 2.02, 95% CI 1.19–3.40, p = 0.01) and had no significant association with HFpEF (HR: 0.67, 95% CI 0.30–1.48, p = 0.32). Borderline-low and high ABI were not significantly associated with HFrEF or HFpEF. Cubic spline analyses showed association with both low and high ABI for HFrEF and high ABI for HFpEF. A 1 SD lower ABI (for ABI < 1.1) was associated with incident HFrEF in multivariable analysis (HR: 1.27, 95% CI 1.05–1.54) but was not significant after additionally adjusting for interim myocardial infarction (HR: 1.21, 95% CI 0.99–1.48). Low ABI was associated with higher risk for incident HFrEF but not HFpEF in persons free of known CVD. Future studies of a larger size are needed for high ABI analyses.

HomeCirculationVol. 139, No. 24Prolonged Ventricular Asystole Free AccessCase ReportPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessCase ReportPDF/EPUBProlonged Ventricular AsystoleA Premature Diagnosis? Sameer Prasada, MD, Arvind Nishtala, MD, MPH and Nora Goldschlager, MD Sameer PrasadaSameer Prasada Sameer Prasada, MD, NMH Department of Medicine, 676 N St. Clair St, Arkes Pavilion, Ste 2300, Chicago, IL 60611. Email E-mail Address: [email protected] Department of Medicine (S.P.), Feinberg School of Medicine, Northwestern University, Chicago, IL. , Arvind NishtalaArvind Nishtala Division of Cardiology, Department of Medicine (A.N.), Feinberg School of Medicine, Northwestern University, Chicago, IL. and Nora GoldschlagerNora Goldschlager Division of Cardiology, Department of Medicine, University of California San Francisco (N.G.). Department of Medicine, Division of Cardiology, San Francisco General Hospital, CA (N.G.). Originally published10 Jun 2019https://doi.org/10.1161/CIRCULATIONAHA.119.041051Circulation. 2019;139:2798–2801ECG ChallengeAn 81-year-old man with coronary artery disease and recently diagnosed bladder cancer underwent a transurethral bladder tumor resection under general anesthesia, during which he was observed to have >7 seconds of ventricular asystole. He remained hemodynamically stable and regained a normal sinus rhythm without intervention. He had not received any parasympathomimetic agents such as neostigmine or other pharmacological agents that affect cardiac rhythm. In the postanesthesia care unit, his heart rate was 54 bpm, blood pressure was 179/78 mm Hg, respiratory rate was 17 breaths per minute, and oxygen saturation was 100% on room air. Cardiovascular, pulmonary, and neurological examinations performed in the postanesthesia care unit were normal. During routine history gathering, he reported no symptoms of exertional intolerance, chest pressure, shortness of breath, dizziness, lightheadedness, or syncope.The simultaneously recorded leads II and V5 of the ECG of his intraoperative event are shown in Figure 1. His baseline ECG is shown in Figure 2. What is the intraoperatively recorded rhythm, and what is its pathophysiology? Is pacemaker implantation indicated?Download figureDownload PowerPointFigure 1. Simultaneously recorded leads II and V5 rhythm strip demonstrating 7.2 seconds of ventricular asystole during surgery.Download figureDownload PowerPointFigure 2. Baseline ECG showing first-degree atrioventricular block, right bundle-branch block, and left anterior fascicular block.Please turn the page to read the diagnosis.Response to ECG ChallengeThe rhythm strip in Figure 1 shows sinus rhythm; then, after a premature ventricular depolarization, 5 nonconducted P waves occur at a rate of 47 bpm, with a 7.2-second period of ventricular asystole. Sinus rhythm with intact atrioventricular conduction (PR interval, ≈220 milliseconds) resumes after a junctional escape complex that terminates the pause in ventricular rhythm. The patient's baseline ECG (Figure 2) is notable for PR interval prolongation to 220 milliseconds, right bundle-branch block, and left anterior fascicular block.This type of paroxysmal atrioventricular block (AVB) has been defined as a sudden-onset, pause-dependent phase 4 block.1 As Figure 3 shows, the premature ventricular depolarization (arrow) conducts in a retrograde fashion, resetting the sinus node and resulting in a pause, and causes PP prolongation (from 1020–2620 milliseconds).Download figureDownload PowerPointFigure 3. Annotated rhythm strip demonstrating paroxysmal atrioventricular block caused by phase 4 conduction block.Our patient with underlying conduction system abnormalities on baseline ECG is highly likely to have a diseased His-Purkinje system, with both diminished resting membrane potential during phase 4 of the action potential and a proclivity for spontaneous diastolic depolarization.2,3 The pause generated by the premature ventricular depolarization allows extra time for diastolic depolarization of His-Purkinje myocytes during phase 4 of their action potential (Figure 4).1Download figureDownload PowerPointFigure 4. Purkinje myocyte transmembrane potentials (TMP) showing mechanism of phase 4 block. After a premature beat (dot), there is a spontaneous diastolic decrease in TMP from the resting value (arrow). When TMP crosses the threshold potential, paroxysmal atrioventricular block or phase 4 block ensues, and the subsequent impulse (star) is blocked. HPS indicates His-Purkinje system. Adapted from Lee et al1 with permission. Copyright © 2009, Elsevier.The pause may continue long enough for the transmembrane potential to reach a critical threshold in this diseased region of the His-Purkinje system. Depolarization to this threshold causes action potentials of reduced amplitude that propagate very slowly as a result of decreased voltage-gated sodium channel availability.1,2 This prevents anterograde conduction to the ventricles. Therefore, the ventricular pause is critical to the development of paroxysmal AVB, also known as phase 4 block.The prolonged ventricular asystole continues for 7.2 seconds until a junctional escape complex (dot in Figure 3) occurs that resets the transmembrane potential of these diseased fibers to their maximum value. After this, an appropriately timed sinus impulse (star) conducts to that region.In addition to premature depolarizations, other triggers for paroxysmal AVB include spontaneous slowing of sinus rate and termination of supraventricular tachycardias with subsequent pause in rhythm.1Paroxysmal AVB is underdiagnosed and frequently missed because of, as the name suggests, its episodic and unpredictable nature. The differential diagnosis typically includes vagally mediated AVB; electrocardiographic intervals can help facilitate distinction. During ventricular asystole, paroxysmal AVB is typically associated with sinus acceleration. In Figure 3, the PP interval shortens from 1320 to 1260 milliseconds. In contrast, vagally mediated AVB is associated with prolongation of the PP interval during ventricular asystole. In addition, vagally mediated AVB often occurs with progressive prolongation of PR intervals, whereas paroxysmal AVB typically has stable and normal PR intervals in the complexes preceding the onset of block. Finally, vagally mediated AVB is not initiated by a pause after a premature beat.The management of paroxysmal AVB or phase 4 block has not been defined or addressed in published guidelines. Because of the irreversibility of this conduction tissue disease, pacemaker implantation is warranted. Our patient had a dual-chamber pacemaker placed to prevent future high-grade AVB.DisclosuresNone.Footnoteshttps://www.ahajournals.org/journal/circSameer Prasada, MD, NMH Department of Medicine, 676 N St. Clair St, Arkes Pavilion, Ste 2300, Chicago, IL 60611. Email sameer.[email protected]eduReferences1. Lee S, Wellens HJ, Josephson ME. Paroxysmal atrioventricular block.Heart Rhythm. 2009; 6:1229–1234. doi: 10.1016/j.hrthm.2009.04.001CrossrefMedlineGoogle Scholar2. Shenasa M, Josephson ME, Wit AL. Paroxysmal atrioventricular block: Electrophysiological mechanism of phase 4 conduction block in the His-Purkinje system: a comparison with phase 3 block.Pacing Clin Electrophysiol. 2017; 40:1234–1241. doi: 10.1111/pace.13187CrossrefMedlineGoogle Scholar3. Rosenbaum MB, Elizari MV, Levi RJ, Nau GJ. Paroxysmal atrioventricular block related to hypopolarization and spontaneous diastolic depolarization.Chest. 1973; 63:678–688.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Bun S, Asarisi F, Heme N, Squara F, Scarlatti D, Taghji P, Deharo J, Moceri P and Ferrari E (2022) Prevalence and Clinical Characteristics of Patients with Pause-Dependent Atrioventricular Block, Journal of Clinical Medicine, 10.3390/jcm11020449, 11:2, (449) June 11, 2019Vol 139, Issue 24 Advertisement Article InformationMetrics © 2019 American Heart Association, Inc.https://doi.org/10.1161/CIRCULATIONAHA.119.041051PMID: 31180745 Originally publishedJune 10, 2019 PDF download Advertisement SubjectsArrhythmiasElectrophysiology