Prediction of Venous Thromboembolism in Diverse Populations Using Machine Learning and Structured Electronic Health Records.

BACKGROUND: Venous thromboembolism (VTE) is a major cause of morbidity and mortality worldwide. Current risk assessment tools, such as the Caprini and Padua scores and Wells criteria, have limitations in their applicability and accuracy. This study aimed to develop machine learning models using structured electronic health record data to predict diagnosis and 1-year risk of VTE. METHODS: We trained and validated models on data from 159 001 participants in the Mount Sinai Data Warehouse. We then externally tested them on 401 723 participants in the UK Biobank and 123 039 participants in All of Us. All data sets contain populations of diverse ancestries and clinical histories. We used these data sets to develop small, medium, and large models with increasing features on a range of optimizing portability to maximizing performance. We make trained models publicly available in click-and-run format at https://doi.org/10.17632/tkwzysr4y6.6. RESULTS: In the holdout and external test sets, respectively, models achieved areas under the receiver operating characteristic curve of 0.80 to 0.83 and 0.72 to 0.82 for VTE diagnosis prediction and 0.76 to 0.78 and 0.64 to 0.69 for 1-year risk prediction, significantly outperforming the Padua score. Models also demonstrated robust performance across different VTE types and patient subsets, including ethnicity, age, and surgical and hospitalization status. Models identified both established and novel clinical features contributing to VTE risk, offering valuable insights into its underlying pathophysiology. CONCLUSIONS: Machine learning models using structured electronic health record data can significantly improve VTE diagnosis and 1-year risk prediction in diverse populations. Model probability scores exist on a continuum, affecting mortality risk in both healthy individuals and VTE cases. Integrating these models into electronic health record systems to generate real-time predictions may enhance VTE risk assessment, early detection, and preventative measures, ultimately reducing the morbidity and mortality associated with VTE.

Primary Prevention of Subclinical Atherosclerosis in Young Adults: JACC Review Topic of the Week.

There is growing evidence that the atherosclerotic process that leads to symptomatic cardiovascular disease (CVD) starts at an early age. In young adults, exposure to low-density lipoprotein-cholesterol and other cardiovascular risk factor (CVRF) mediators, even at levels considered within normal limits, increases the prevalence of subclinical atherosclerosis and is associated with greater risk of cardiovascular events later in life. The optimal CVRF targets to prevent CVD in asymptomatic young individuals (<40 years) are unknown. The randomized controlled PRECAD (Prevent Coronary Artery Disease) trial has been developed to assess the potential benefit of an aggressive control of CVRF in otherwise healthy young adults. The hypothesis of PRECAD is that in subjects aged 20 to 39 years without known CVD, maintaining low-density lipoprotein-cholesterol <70 mg/dL and strict control of blood pressure and glucose will prevent the onset of atherosclerosis and/or its progression. The primary endpoint will be the change in total atherosclerosis burden, a surrogate for CVD.

Severe hypertriglyceridemia: Existing and emerging therapies.

Severe hypertriglyceridemia (sHTG), defined as a triglyceride (TG) concentration ≥ 500 mg/dL (≥ 5.7 mmol/L) is an important risk factor for acute pancreatitis. Although lifestyle, some medications, and certain conditions such as diabetes may lead to HTG, sHTG results from a combination of major and minor genetic defects in proteins that regulate TG lipolysis. Familial chylomicronemia syndrome (FCS) is a rare disorder caused by complete loss of function in lipoprotein lipase (LPL) or LPL activating proteins due to two homozygous recessive traits or compound heterozygous traits. Multifactorial chylomicronemia syndrome (MCS) and sHTG are due to the accumulation of rare heterozygous variants and polygenic defects that predispose individuals to sHTG phenotypes. Until recently, treatment of sHTG focused on lifestyle interventions, control of secondary factors, and nonselective pharmacotherapies that had modest TG-lowering efficacy and no corresponding reductions in atherosclerotic cardiovascular disease events. Genetic discoveries have allowed for the development of novel pathway-specific therapeutics targeting LPL modulating proteins. New targets directed towards inhibition of apolipoprotein C-III (apoC-III), angiopoietin-like protein 3 (ANGPTL3), angiopoietin-like protein 4 (ANGPTL4), and fibroblast growth factor-21 (FGF21) offer far more efficacy in treating the various phenotypes of sHTG and opportunities to reduce the risk of acute pancreatitis and atherosclerotic cardiovascular disease events.

ABCA1 Deficiency: A Rare Cause of Premature Coronary Artery Disease.

ATP-binding cassette transporter A1 (ABCA1) deficiency results in very low high-density lipoprotein cholesterol levels. Complete ABCA1 deficiency, or Tangier disease, is characterized by premature atherosclerotic cardiovascular disease, yellow-orange tonsils, hepatosplenomegaly, peripheral neuropathy, and corneal opacification. Early recognition of this condition can lead to regular monitoring for atherosclerotic cardiovascular symptoms and treatment of major modifiable risk factors. (Level of Difficulty: Beginner.).

Incident CHD and ischemic stroke associated with lipoprotein(a) by levels of Factor VIII and inflammation.

BACKGROUND: Inflammation and coagulation may contribute to the increased risk for atherosclerotic cardiovascular disease (ASCVD) associated with high lipoprotein(a). The association of lipoprotein(a) with ASCVD is stronger in individuals with high versus low high-sensitivity C-reactive protein (hs-CRP), a marker of inflammation. OBJECTIVES: Determine the association of lipoprotein(a) with incident ASCVD by levels of coagulation Factor VIII controlling for hs-CRP. METHODS: We analyzed data from 6,495 men and women 45 to 84 years of age in the Multi-Ethnic Study of Atherosclerosis (MESA) without prevalent ASCVD at baseline (2000-2002). Lipoprotein(a) mass concentration, Factor VIII coagulant activity, and hs-CRP were measured at baseline and categorized as high or low (≥75th or <75th percentile of the distribution). Participants were followed for incident coronary heart disease (CHD) and ischemic stroke through 2015. RESULTS: Over a median follow-up of 13.9 years, there were 390 CHD and 247 ischemic stroke events. The hazard ratio (95%CI) for CHD associated with high lipoprotein(a) (≥40.1 versus <40.1 mg/dL) including adjustment for hs-CRP among participants with low and high Factor VIII was 1.07 (0.80-1.44) and 2.00 (1.33-3.01), respectively (p-value for interaction 0.016). The hazard ratio (95%CI) for CHD associated with high lipoprotein(a) including adjustment for Factor VIII was 1.16 (0.87-1.54) and 2.00 (1.29-3.09) among participants with low and high hs-CRP, respectively (p-value for interaction 0.042). Lp(a) was not associated with ischemic stroke regardless of Factor VIII or hs-CRP levels. CONCLUSION: High lipoprotein(a) is a risk factor for CHD in adults with high levels of hemostatic or inflammatory markers.

Familial Hypercholesterolemia: Challenges for a High-Risk Population: JACC Focus Seminar 1/3.

The availability of statins, ezetimibe, and PCSK9 inhibitors has significantly improved the prognosis of familial hypercholesterolemia (FH). However, a great number of individuals with FH do not achieve guideline-recommended low-density lipoprotein (LDL) cholesterol levels despite maximal lipid-lowering therapy. Novel therapies that lower LDL independent of LDL receptor activity can help mitigate atherosclerotic cardiovascular disease risk in most homozygous FH and many heterozygous FH patients. However, access to novel therapies remains limited for heterozygous FH patients with persistent elevation of LDL cholesterol despite treatment with multiple classes of cholesterol-lowering therapies. Conduction of cardiovascular outcomes clinical trials in patients with FH can be challenging because of difficulty in recruitment and long periods of follow-up. In the future, the use of validated surrogate measures of atherosclerosis may allow for clinical trials with fewer study participants and shorter duration, thereby expediting access to novel treatments for patients with FH.

Clinical Trial Design for Triglyceride-Rich Lipoprotein-Lowering Therapies: JACC Focus Seminar 3/3.

Triglyceride-rich lipoproteins (TRLs) are a source of residual risk in patients with atherosclerotic cardiovascular disease, and are indirectly correlated with triglyceride (TG) levels. Previous clinical trials studying TG-lowering therapies have either failed to reduce major adverse cardiovascular events or shown no linkage of TG reduction with event reduction, particularly when these agents were tested on a background of statin therapy. Limitations in trial design may explain this lack of efficacy. With the advent of new RNA-silencing therapies in the TG metabolism pathway, there is renewed focus on reducing TRLs for major adverse cardiovascular event reduction. In this context, the pathophysiology of TRLs, pharmacological effects of TRL-lowering therapies, and optimal design of cardiovascular outcomes trials are major considerations.

Clinical Trial Design for Lipoprotein(a)-Lowering Therapies: JACC Focus Seminar 2/3.

Lipoprotein(a) [Lp(a)] is a source of residual risk in patients with atherosclerotic cardiovascular disease (ASCVD). Clinical trials of fully human monoclonal antibodies targeting proprotein convertase subtilisin kexin 9 have shown that reductions in Lp(a) concentrations may be a predictor of event reduction with this class of cholesterol-lowering therapy. With the advent of selective therapies targeting Lp(a) such as antisense oligonucleotides, small-interfering RNA-based therapies, and gene editing, lowering of Lp(a) may lead to reduction in ASCVD. The phase 3 Lp(a)HORIZON (Assessing the Impact of Lipoprotein(a) Lowering with TQJ230 on Major Cardiovascular Events in Patients With CVD) outcomes trial is currently testing the effect of pelacarsen, an antisense oligonucleotide, on ASCVD risk. Olpasiran is a small-interfering RNA that is in a phase 3 clinical trial. As these therapies enter clinical trials, challenges in trial design will have to be addressed to optimize patient selection and outcomes.

Impella percutaneous left ventricular assist device as mechanical circulatory support for cardiogenic shock: A retrospective analysis from a tertiary academic medical center.

OBJECTIVES: To describe hemodynamic efficacy and clinical outcomes of Impella percutaneous left ventricular assist device (pLVAD) in patients with cardiogenic shock (CS). BACKGROUND: Percutaneous LVADs are increasingly used in CS management. However, device-related outcomes and optimal utilization remain active areas of investigation. METHODS: All CS patients receiving pLVAD as mechanical circulatory support (MCS) between 2011 and 2017 were identified. Clinical characteristics and outcomes were analyzed. A multivariable logistic regression model was created to predict MCS escalation despite pLVAD. Outcomes were compared between early and late implantation. RESULTS: A total of 115 CS patients (mean age 63.6 ± 13.8 years; 69.6% male) receiving pLVAD as MCS were identified, the majority with CS secondary to acute myocardial infarction (AMI; 67.0%). Patients experienced significant cardiac output improvement (median 3.39 L/min to 3.90 L/min, p = .002) and pharmacological support reduction (median vasoactive-inotropic score [VIS] 25.4 to 16.4, p = .049). Placement of extracorporeal membrane oxygenation (ECMO) occurred in 48 (41.7%) of patients. Higher pre-pLVAD VIS was associated with subsequent MCS escalation in the entire cohort and AMI subgroup (OR 1.27 [95% CI 1.02-1.58], p = .034 and OR 1.72 [95% CI 1.04-2.86], p = .035, respectively). Complications were predominantly access site related (bleeding [9.6%], vascular injury [5.2%], and limb ischemia [2.6%]). In-hospital mortality was 57.4%, numerically greater survival was noted with earlier device implantation. CONCLUSIONS: Treatment with pLVAD for CS improved hemodynamic status but did not uniformly obviate MCS escalation. Mortality in CS remains high, though earlier device placement for appropriately selected patients may be beneficial.

Atrial Fibrillation in Patients Hospitalized With COVID-19: Incidence, Predictors, Outcomes, and Comparison to Influenza.

OBJECTIVES: The goal of this study is to determine the incidence, predictors, and outcomes of atrial fibrillation (AF) or atrial flutter (AFL) in patients hospitalized with coronavirus disease-2019 (COVID-19). BACKGROUND: COVID-19 results in increased inflammatory markers previously associated with atrial arrhythmias. However, little is known about their incidence or specificity in COVID-19 or their association with outcomes. METHODS: This is a retrospective analysis of 3,970 patients admitted with polymerase chain reaction-positive COVID-19 between February 4 and April 22, 2020, with manual review performed of 1,110. The comparator arm included 1,420 patients with influenza hospitalized between January 1, 2017, and January 1, 2020. RESULTS: Among 3,970 inpatients with COVID-19, the incidence of AF/AFL was 10% (n = 375) and in patients without a history of atrial arrhythmias it was 4% (n = 146). Patients with new-onset AF/AFL were older with increased inflammatory markers including interleukin 6 (93 vs. 68 pg/ml; p < 0.01), and more myocardial injury (troponin-I: 0.2 vs. 0.06 ng/ml; p < 0.01). AF and AFL were associated with increased mortality (46% vs. 26%; p < 0.01). Manual review captured a somewhat higher incidence of AF/AFL (13%, n = 140). Compared to inpatients with COVID-19, patients with influenza (n = 1,420) had similar rates of AF/AFL (12%, n = 163) but lower mortality. The presence of AF/AFL correlated with similarly increased mortality in both COVID-19 (relative risk: 1.77) and influenza (relative risk: 1.78). CONCLUSIONS: AF/AFL occurs in a subset of patients hospitalized with either COVID-19 or influenza and is associated with inflammation and disease severity in both infections. The incidence and associated increase in mortality in both cohorts suggests that AF/AFL is not specific to COVID-19, but is rather a generalized response to the systemic inflammation of severe viral illnesses.

Predictors of Hemodynamic Response to Intra-Aortic Balloon Pump Therapy in Patients With Acute Decompensated Heart Failure and Cardiogenic Shock.

OBJECTIVES: There is renewed interest in intra-aortic balloon pump (IABP) use in chronic systolic heart failure (HF) patients with acute decompensation and cardiogenic shock (CS). We sought to identify predictors of early IABP response to guide optimal use in this population. METHODS: We retrospectively analyzed records of chronic systolic HF patients presenting to our center between 2011-2018 with acute decompensated HF who received IABP for CS. An IABP responder was defined as having both an early cardiac output (CO) increase and mean pulmonary artery pressure (MPAP) decrease above the cohort median values. RESULTS: During this period, a total of 218 chronic systolic HF patients received IABP for acute decompensation with CS. The average CO increase was 0.57 ± 0.85 L/min and MPAP reduction was 5.1 ± 7.6 mm Hg. Fifty-six patients (25.7%) were identified as IABP responders, with mean CO increase of 1.21 ± 0.87 L/min and MPAP reduction of 12.1 ± 5.9 mm Hg. Systemic vascular resistance (SVR) >1300 dynes/sec/cm-5 (odds ratio [OR], 5.04; 95% confidence interval [CI], 1.86-13.6; P<.01) and moderate-severe mitral regurgitation (OR, 2.42; 95% CI, 1.25-4.66; P<.01) predicted robust hemodynamic response. CONCLUSIONS: A subset of chronic systolic HF patients had robust hemodynamic response to IABP with significant CO augmentation and MPAP reduction. Higher SVR and moderate-severe mitral regurgitation predicted early hemodynamic response to IABP.

Characterization of Myocardial Injury in Patients With COVID-19.

BACKGROUND: Myocardial injury is frequent among patients hospitalized with coronavirus disease-2019 (COVID-19) and is associated with a poor prognosis. However, the mechanisms of myocardial injury remain unclear and prior studies have not reported cardiovascular imaging data. OBJECTIVES: This study sought to characterize the echocardiographic abnormalities associated with myocardial injury and their prognostic impact in patients with COVID-19. METHODS: We conducted an international, multicenter cohort study including 7 hospitals in New York City and Milan of hospitalized patients with laboratory-confirmed COVID-19 who had undergone transthoracic echocardiographic (TTE) and electrocardiographic evaluation during their index hospitalization. Myocardial injury was defined as any elevation in cardiac troponin at the time of clinical presentation or during the hospitalization. RESULTS: A total of 305 patients were included. Mean age was 63 years and 205 patients (67.2%) were male. Overall, myocardial injury was observed in 190 patients (62.3%). Compared with patients without myocardial injury, those with myocardial injury had more electrocardiographic abnormalities, higher inflammatory biomarkers and an increased prevalence of major echocardiographic abnormalities that included left ventricular wall motion abnormalities, global left ventricular dysfunction, left ventricular diastolic dysfunction grade II or III, right ventricular dysfunction and pericardial effusions. Rates of in-hospital mortality were 5.2%, 18.6%, and 31.7% in patients without myocardial injury, with myocardial injury without TTE abnormalities, and with myocardial injury and TTE abnormalities. Following multivariable adjustment, myocardial injury with TTE abnormalities was associated with higher risk of death but not myocardial injury without TTE abnormalities. CONCLUSIONS: Among patients with COVID-19 who underwent TTE, cardiac structural abnormalities were present in nearly two-thirds of patients with myocardial injury. Myocardial injury was associated with increased in-hospital mortality particularly if echocardiographic abnormalities were present.

Malignant Arrhythmias in Patients With COVID-19: Incidence, Mechanisms, and Outcomes.

BACKGROUND: Patients with coronavirus disease 2019 (COVID-19) who develop cardiac injury are reported to experience higher rates of malignant cardiac arrhythmias. However, little is known about these arrhythmias-their frequency, the underlying mechanisms, and their impact on mortality. METHODS: We extracted data from a registry (NCT04358029) regarding consecutive inpatients with confirmed COVID-19 who were receiving continuous telemetric ECG monitoring and had a definitive disposition of hospital discharge or death. Between patients who died versus discharged, we compared a primary composite end point of cardiac arrest from ventricular tachycardia/fibrillation or bradyarrhythmias such as atrioventricular block. RESULTS: Among 800 patients with COVID-19 at Mount Sinai Hospital with definitive dispositions, 140 patients had telemetric monitoring, and either died (52) or were discharged (88). The median (interquartile range) age was 61 years (48-74); 73% men; and ethnicity was White in 34%. Comorbidities included hypertension in 61%, coronary artery disease in 25%, ventricular arrhythmia history in 1.4%, and no significant comorbidities in 16%. Compared with discharged patients, those who died had elevated peak troponin I levels (0.27 versus 0.02 ng/mL) and more primary end point events (17% versus 4%, P=0.01)-a difference driven by tachyarrhythmias. Fatal tachyarrhythmias invariably occurred in the presence of severe metabolic imbalance, while atrioventricular block was largely an independent primary event. CONCLUSIONS: Hospitalized patients with COVID-19 who die experience malignant cardiac arrhythmias more often than those surviving to discharge. However, these events represent a minority of cardiovascular deaths, and ventricular tachyarrhythmias are mainly associated with severe metabolic derangement. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT04358029.

Comparison of the Hemodynamic Response to Intra-Aortic Balloon Counterpulsation in Patients With Cardiogenic Shock Resulting from Acute Myocardial Infarction Versus Acute Decompensated Heart Failure.

The intra-aortic balloon pump (IABP) neither benefits nor harms patients with acute myocardial infarction (AMI) with cardiogenic shock (CS) but may stabilize those with chronic heart failure who decompensate into CS. We sought to compare its hemodynamic effects in these 2 populations. We performed a retrospective analysis of the hemodynamic effects of IABP for AMI or acute decompensated heart failure (ADHF) patients with hemodynamic evidence of CS. The primary outcome was cardiac output (CO) change following insertion. In total, 205 patients were treated for CS resulting from AMI (73; 35.6%) or ADHF (132; 64.4%). At baseline, both cohorts had significant hemodynamic compromise with mean arterial pressure 75.6 ± 12.3 mm Hg, CO 3.02 ± 0.84 L/min, and cardiac power index 0.26 ± 0.06 W/m2; these parameters were nearly identical between groups though ADHF-CS patients had a higher pre-IABP mean pulmonary artery (PA) pressure than AMI-CS patients. After IABP insertion, ADHF-CS patients had moderate CO augmentation whereas AMI-CS experienced almost no improvement (0.58 ± 0.79 L/min vs 0.12 ± 1.00 L/min; p = 0.0009). Intracardiac filling pressures were reduced by similar amounts in both cohorts. Systemic vascular resistance was reduced in patients with ADHF-CS but not in those with AMI-CS. In conclusion, following IABP insertion, ADHF-CS patients experience roughly a 5-fold greater CO augmentation compared with AMI-CS patients. Pre-IABP PA pressure differences and differential systemic vascular resistance reduction may explain these results and shed light on recent evidence supporting IABP use in ADHF-CS and curbing it in AMI-CS.

Predictors of Survival for Patients with Acute Decompensated Heart Failure Requiring Extra-Corporeal Membrane Oxygenation Therapy.

Chronic systolic heart failure (HF) with acute decompensation can result in cardiogenic shock (CS) requiring short-term mechanical circulatory support. We sought to identify predictors of survival for acute decompensated HF (ADHF) patients requiring veno-arterial extracorporeal membrane oxygenation (VA-ECMO). Patients >18 years old treated at our institution with VA-ECMO from 2009 to 2018 for ADHF with CS were studied. Demographic, hemodynamic, and echocardiographic data were collected. The primary outcome was survival to discharge. Fifty-two patients received VA-ECMO for ADHF with CS; 24 (46.2%) survived. Seventeen (32.7%) had suffered cardiac arrest, and 37 (71.2%) were mechanically ventilated. Mean lactate was 4.33 ± 3.45 mmol/L, and patients were receiving 2.7 ± 1.2 vasopressor/inotropic infusions at ECMO initiation; these did not differ significantly between survivors and nonsurvivors. Pre-ECMO cardiac index was 1.84 ± 0.56L/min/m and 1.94 ± 0.63L/min/m in survivors and nonsurvivors, respectively (p = 0.57). In multivariable analysis, only diabetes mellitus (DM; OR, 13.25; CI, 1.42-123.40; p = 0.02) and mineralocorticoid receptor antagonist use (OR, 0.12; CI, 0.02-0.78; p = 0.03) were independent predictors of mortality. Nineteen (79.2%) survivors required durable ventricular assist device. Among ADHF patients receiving VA-ECMO, DM is a powerful predictor of outcomes while markers of clinical acuity including hemodynamics, vasopressor/inotrope use, and lactate are not. The vast majority of survivors required durable left-ventricular assist devices.

Mortality risk after transcatheter aortic valve implantation: analysis of the predictive accuracy of the Transcatheter Valve Therapy registry risk assessment model.

AIMS: The risk assessment tools currently used to predict mortality in transcatheter aortic valve implantation (TAVI) were designed for patients undergoing cardiac surgery. We aimed to assess the accuracy of the TAVI dedicated risk score in predicting mortality outcomes. METHODS AND RESULTS: Consecutive patients (n=1,038) undergoing TAVI at a single institution from 2014 to 2016 were included. The ACC/TVT registry mortality risk score, the STS-PROM score and the EuroSCORE II were calculated for all patients. In-hospital and 30-day all-cause mortality rates were 1.3% and 2.9%, respectively. The ACC/TVT risk stratification tool scored higher for patients who died in-hospital than for those who survived the index hospitalisation (6.4±4.6 vs. 3.5±1.6, p=0.03, respectively). The ACC/TVT score showed a high level of discrimination, C-index for in-hospital mortality 0.74, 95% CI: (0.59-0.88). There were no significant differences between the performance of the ACC/TVT registry risk score, the EuroSCORE II and the STS-PROM score for in-hospital and 30-day mortality rates. CONCLUSIONS: The ACC/TVT registry risk model is a dedicated tool to aid in the prediction of in-hospital mortality risk after TAVI.

Weight loss outcomes among patients referred after primary bariatric procedure.

BACKGROUND: Bariatric patients may not always obtain long-term care by their primary surgeon. Our aim was to evaluate weight loss outcomes in patients who had surgery elsewhere. METHODS: We conducted a retrospective analysis. Postreferral management included nonsurgical, revision, or conversion. Primary outcomes were percent excess weight loss (%EWL) overall, according to original operation, and based on postreferral management. RESULTS: Between 2001 and 2013, there were 569 patients. Mean follow-up was 3.1 years. Management was 42% nonsurgical, 41% revision, and 17% conversion. Overall, mean %EWL was 45.3%. Based on original surgery type, %EWL was 41.2% for adjustable gastric banding vs 58.3% for Roux-en-Y gastric bypass (P ≤ .0001). Management affected %EWL (41.2% nonsurgical vs 45.3% revision vs 55.1% conversion, P ≤ .0001). CONCLUSIONS: Patients referred after bariatric surgery can achieve satisfactory weight loss. This differs based on surgery type and management strategy.

Long-term outcomes after Roux-en-Y gastric bypass: 10- to 13-year data.

BACKGROUND: Short- and mid-term data on Roux-en-Y gastric bypass (RYGB) indicate sustained weight loss and improvement in co-morbidities. Few long-term studies exist, some of which are outdated, based on open procedures or different techniques. OBJECTIVES: To investigate long-term weight loss, co-morbidity remission, nutritional status, and complication rates among patients undergoing RYGB. SETTING: An academic, university hospital in the United States. METHODS: Between October 2000 and January 2004, patients who underwent RYGB≥10 years before study onset were eligible for chart review, office visits, and telephone interviews. Revisional surgery was an endpoint, ceasing eligibility for study follow-up. Outcomes included weight loss measures and rates of co-morbidity remission, complications, and nutritional deficiencies. RESULTS: RYGB was performed in 328 patients with a mean preoperative body mass index of 47.5 kg/m(2). Of 294 eligible patients, 134 (46%) were contacted for follow-up at ≥ 10 years (10+Year follow-up). Mean percentage excess weight loss (%EWL) was 58.9% at 10+Year. Higher %EWL was achieved by non-super-obese versus super-obese (61.3% versus 52.9%, P = .034). Blood pressure, lipid panel, and hemoglobin A1c improved significantly. At 10 years, remission of co-morbidities was 46% for hypertension and hyperlipidemia and 58% for diabetes mellitus. Thirty patients (9%) had revisional surgery for weight regain. Sixty-four patients (19.5%) had long-term complications requiring surgery. All-cause mortality was 2.7%. Nutritional deficiencies were seen in 87% of patients. CONCLUSIONS: Weight loss after RYGB appears to be significant and sustainable, especially in the non-super-obese. Co-morbidities are improved, with a substantial number in remission a decade later. Nutritional deficiencies are almost universal.