Patient and Physician Determinants of Implantable Cardioverter Defibrillator Use in the Heart Failure Population

Recent studies report surprisingly low rates of implantable cardioverter defibrillator (ICD) placement for primary prevention against sudden cardiac death among patients with heart failure and left ventricular systolic dysfunction. Reasons for the low rates of utilization are not well understood. The authors examined ICD implantation rates at a university-based tertiary care center and used multivariable analysis to identify independent factors associated with ICD utilization. The ICD implantation rate for 850 eligible patients was 70%. Forty-seven (18%) patients refused implantation; women were twice as likely to refuse compared to men (8% vs 4%, P=.013). Race was not associated with utilization. On multivariable analysis, independent predictors of implantation included having a heart failure specialist (odds ratio [OR], 8.13; P<.001) or general cardiologist (OR, 2.23; P=.13) managing care, age range 70 to 79 (OR, 0.55; P<.001) or 80 and older (OR, 0.26; P<.001), female sex (OR, 0.49; P<.001), QRS interval (OR, 1.016; P<.001), diastolic blood pressure (OR, 0.979; P=.011), cerebrovascular disease (OR, 0.44; P=.007), and dementia (OR, 0.13; P=.002). Our registry of patients with cardiomyopathy and heart failure reveals that high rates of utilization are possible. Factors closely associated with ICD utilization include type of physician coordinating care, age, and comorbidities. Congest Heart Fail. 2010;16:141–146. © 2010 Wiley Periodicals, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/78684/1/j.1751-7133.2009.00139.x.pd

A Web Application for Self-Monitoring Improves Symptoms in Chronic Systolic Heart Failure

Objective: The objective of this study was to determine if a Web application that promoted mindfulness of the progress of the chronic disease through self-monitoring improved quality of life in heart failure. Materials and Methods: This was a prospective single-center single-group study. Participants were instructed how to use the Web application and to perform self-monitoring daily for 12 weeks. A comprehensive physical exam, assessment of New York Heart Association (NYHA) class, the Minnesota Living with Heart Failure Questionnaire (MLHFQ), and an evaluation of self-management were performed in person at baseline and at 12 weeks. Results: Participants consisted of older (mean, 59 years), predominantly female (63%) adults with NYHA class II or III symptoms. NYHA classification (preintervention versus postintervention, 2.5±0.13 versus 2.0±0.13; p=0.0032) and MLHFQ score (55.7±4.6 versus 42.6±5.1, respectively; p=0.0078) improved over 12 weeks of self-monitoring. A trend toward improvement was also demonstrated in weight (preintervention versus postintervention, 209±9.6 pounds versus 207±9.4 pounds; by paired t test, p=0.389), number of times exercised per week (1.29±0.5 versus 2.5±0.6, respectively; p=0.3), and walk distance (572±147 yards versus 845±187 yards, respectively; p=0.119). Jugular venous distention (preintervention versus postintervention, 8.1±0.6?cm versus 6.7±0.3?cm; p=0.083) and peripheral edema (29.2% versus 16.7%, respectively; p=0.375) decreased after 12 weeks of self-monitoring via the Web application. Conclusions: A Web application for self-monitoring heart failure over 12 weeks improved both NYHA classification and MLHFQ score. The trend in improved physical activity and physical exam support these outcomes. The number of patients reporting a sodium-restricted diet increased over the 12 weeks, which may have led to the positive findings.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/140281/1/tmj.2014.0095.pd

Treatment of Heart Failure with Preserved Ejection Fraction

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90240/1/phco.31.3.312.pd

Improving Heart Failure Self-Management Support by Actively Engaging Out-of-Home Caregivers: Results of a Feasibility Study

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/72336/1/j.1751-7133.2008.07474.x.pd

Changing Preferences for Survival After Hospitalization With Advanced Heart Failure

ObjectivesThis study was designed to analyze how patient preferences for survival versus quality-of-life change after hospitalization with advanced heart failure (HF).BackgroundAlthough patient-centered care is a priority, little is known about preferences to trade length of life for quality among hospitalized patients with advanced HF, and it is not known how those preferences change after hospitalization.MethodsThe time trade-off utility, symptom scores, and 6-min walk distance were measured in 287 patients in the ESCAPE (Evaluation Study of Congestive Heart Failure and Pulmonary Artery Catheter Effectiveness) trial at hospitalization and again during 6 months after therapy to relieve congestion.ResultsWillingness to trade was bimodal. At baseline, the median trade for better quality was 3 months' survival time, with a modest relation to symptom severity. Preference for survival time was stable for most patients, but increase after discharge occurred in 98 of 145 (68%) patients initially willing to trade survival time, and was more common with symptom improvement and after therapy guided by pulmonary artery catheters (p = 0.034). Adjusting days alive after hospital discharge for patients' survival preference reduced overall days by 24%, with the largest reduction among patients dying early after discharge (p = 0.0015).ConclusionsPreferences remain in favor of survival for many patients despite advanced HF symptoms, but increase further after hospitalization. The bimodal distribution and the stability of patient preference limit utility as a trial end point, but support its relevance in design of care for an individual patient

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease