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Results for “Heart failure with reduced ejection fraction”

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At least 19 recordsLinked to original sources

PubMed2026

Nurse-led titration models of care for heart failure reduced ejection fraction: a systematic narrative review of characteristics, patient outcomes, and healthcare resource utilization.

AIMS: Nurse-led titration (NLT) models of care assist with delivery of guideline directed medical therapy for patients with heart failure with reduced ejection fraction (HFrEF). Effectiveness of NLT is established but there is limited information of characteristics of models, patient outcomes and healthcare resource utilization. To build upon the existing evidence by providing a systematic narrative review of the literature of NLT of medications for patients with HFrEF. This review syntheses characteristics of NLT models of care, patient outcomes and healthcare resource utilization. METHODS AND RESULTS: A systematic narrative literature review with systematic search strategy, identification of results, thematic analysis and narrative synthesis. A search was conducted from 2012 to 2025 in Medline, Cinahl complete, Embase and Cochrane. Sixteen studies of NLT models of care were identified from 1944 screened records. Characteristics of models of care were participation of nurses, multidisciplinary teams, follow-up and common features of service delivery. Patient outcomes of mortality were favourable for those that received NLT. There is some evidence of changes in healthcare resource utilization; studies in which the NLT groups received more HF nurse visits and greater HF medication use also reported reduced rehospitalizations. CONCLUSION: Findings reinforce the published benefits of NLT. Additional studies examining adverse events and quality-of-life outcomes are needed to strengthen the evidence base. Several studies suggest a shift in resource use with NLT, highlighting the need for an economic evaluation to inform a cost-effective model of care.

Humans↗

PubMedDate not supplied

Contribution of systolic and diastolic abnormalities to heart failure with a normal and a reduced ejection fraction.

Heart failure (HF) has traditionally been divided into HF with a reduced ejection fraction (EF; systolic HF) and HF with a normal EF (diastolic HF). Both groups have reductions in exercise tolerance, neurohumoral activation, and abnormal left ventricular (LV) filling dynamics and impaired relaxation. Although the normal EF indicates that pump performance is adequately compensated, some of the patients with HF and a normal EF have reduced longitudinal systolic velocity indicating cardiac muscular contractile dysfunction. Regardless of EF, the severity of HF and its prognosis and degree of exercise intolerance are closely related to the degree of diastolic filling abnormalities. Patients with HF and a reduced EF have ventricular dilatation and elongated myocytes, whereas patients with HF and a normal EF do not. Thus, patients with HF have diastolic abnormalities regardless of EF and many patients with HF and a normal EF have contractile abnormalities despite preserved systolic pump performance. Heart failure with a normal EF and a reduced EF differs in the systolic LV pump performance and the type of remodeling. The mechanism of the differing remodeling responses is not known, but aging, sex differences, and diabetes may contribute.

Cardiac Output, Low↗

PubMed2026

Exerkine dysregulation links visceral adiposity to skeletal muscle impairment in end-stage heart failure with reduced ejection fraction: proteomic evidence for a cardio-adipose-muscle axis.

BACKGROUND: Heart failure with reduced ejection fraction (HFrEF) is associated with profound alterations in body composition, skeletal muscle dysfunction, and impaired exercise capacity. Exerkines representing exercise-responsive signaling molecules released by skeletal muscle, adipose tissue, and other organs may mediate systemic metabolic communication between tissues. However, their role in advanced HFrEF and their relationship with adiposity and skeletal muscle characteristics remain poorly understood. METHODS: We studied 73 patients with end-stage HFrEF and 16 healthy controls. Body composition was assessed using computed tomography, including visceral (VAT), subcutaneous (SAT), and epicardial adipose tissue (EAT), as well as skeletal muscle quantity (psoas muscle index, PMI) and quality (psoas muscle density, PMD). Functional performance was evaluated using handgrip strength (HGT) and the 6-min walk test (6MWT). Circulating exerkines were quantified using the Olink technology. Associations between proteins and clinical variables were assessed using age- and creatinine-adjusted linear models with false discovery rate correction. RESULTS: Among patients with HFrEF, 36% were obese and 38% exhibited central obesity independent of BMI. Muscle strength and muscle quality were strongly associated with functional capacity. VAT correlated with muscle mass but not with muscle quality or performance. Compared with controls, HFrEF patients demonstrated elevated inflammatory and metabolic stress-related exerkines including CXCL8, CCL2, IL-6, TNF, IL-15, GDF15, FGF21, ANGPTL4, CTSB, DCN, and resistin. In contrast, proteins associated with muscle integrity and regenerative signaling (myostatin, BDNF, IL-7, SPARC) were significantly reduced. In HFrEF patients leptin strongly correlated with adiposity measures. Metabolic stress mediators (GDF15, IL-15, FGF21, CTSB) were inversely associated with muscle quality and functional performance, whereas myostatin positively correlated with muscle quality, strength, and exercise capacity. BDNF was inversely associated with frailty. CONCLUSIONS: Advanced HFrEF is characterized by a dysregulated exerkine network linking adiposity, skeletal muscle quality, and functional performance. Four biologically coherent axes were identified: a leptin-driven adiposity axis, a metabolic stress-muscle quality axis, a myostatin-related muscle function axis, and a neurotrophic frailty axis. These findings support the presence of a systemic cardio-adipose-muscle signaling network in end-stage HFrEF and identify candidate molecular mediators of sarcopenia and functional decline.

Humans↗

PubMed2026

Efficacy and Safety of the Kidney Function-Based Finerenone Dosing Strategy Used in FINEARTS-HF.

BACKGROUND: Given that mineralocorticoid receptor antagonists have the potential to impair renal function and induce hyperkalemia, close monitoring of estimated glomerular filtration rate (eGFR) and serum potassium levels is essential to ensure the safe administration of this therapy. OBJECTIVES: In this prespecified analysis, the authors evaluated the efficacy and safety of the kidney function-based finerenone dosing strategy used in the FINEARTS-HF trial. METHODS: In FINEARTS-HF, patients with an eGFR of 25 to 60 mL/min/1.73 m2 at baseline were stratified at randomization to the low-dose group and started on 10 mg of finerenone once daily (titrated to a maximum 20 mg/d) or matching placebo, whereas those with an eGFR >60 mL/min/1.73 m2 at baseline were stratified to the high-dose group and started on 20 mg of finerenone once daily (titrated to a maximum 40 mg/d) or matching placebo. The primary outcome was the composite of total (first and recurrent) heart failure events and cardiovascular death. RESULTS: Among 5,986 (99.8%) analyzable patients, 3,159 were assigned to the higher eGFR/high-dose stratum and 2,827 to the lower eGFR/low-dose stratum group. The mean ± SD achieved dose was 32.3 ± 9.1 mg (finerenone) and 34.4 ± 7.8 mg (placebo) in the higher eGFR/high-dose stratum, and 15.6 ± 4.3 mg (finerenone) and 16.7 ± 4.0 mg (placebo) in the lower eGFR/low-dose stratum. The effect of finerenone on the primary outcome was consistent across the 2 dosing strata (higher eGFR/high-dose stratum: rate ratio: 0.77 [95% CI: 0.63-0.94] vs lower eGFR/low-dose stratum: rate ratio: 0.87 [95% CI: 0.74-1.03]; P for interaction = 0.34). Consistent benefits were observed for the components of the primary outcome and all-cause death. Safety was also consistent between dosing strata, except for hypokalemia, where the reduction in the odds of hypokalemia with finerenone compared to placebo was greater in the higher eGFR/high-dose stratum (P-interaction < 0.01). CONCLUSIONS: In FINEARTS-HF, an eGFR-based dosing strategy allowed effective and safe use of finerenone in patients with heart failure with mildly reduced ejection fraction/ heart failure with preserved ejection fraction with a baseline eGFR as low as 25 mL/min/1.73 m2. We recommend that clinicians implement the trial-validated dosing strategy and incorporate appropriate uptitration to the target dose to ensure optimal therapeutic outcomes. (FINEARTS-HF [Study to Evaluate the Efficacy (Effect on Disease) and Safety of Finerenone in Participants With Heart Failure and Left Ventricular Ejection Fraction (Proportion of Blood Expelled Per Heart Stroke) Greater or Equal to 40%; NCT04435626).

Aged↗

PubMed2006

ACC/AHA guideline update: treatment of heart failure with reduced left ventricular ejection fraction.

Heart failure (HF) affects approximately 5 million persons in the United States each year. HF is predominantly a disease of the elderly: Approximately 80% of patients hospitalized with HF are older than age 65. Approximately one-half of older adult patients with CHF have a decreased ejection fraction. Elderly patients with HF and a reduced LVEF have a higher mortality than elderly patients with HF with a normal LVEF. Despite numerous excellent studies showing the efficacy of appropriate drugs in reducing mortality in patients with HF and a reduced LVEF, these medications are underutilized in the treatment of HF. This article discusses the latest guidelines from the American College of Cardiology/American Heart Association for the treatment of patients with HF and a reduced LVEF.

Aged↗

PubMed2006

Outcome of heart failure with preserved ejection fraction in a population-based study.

BACKGROUND: The importance of heart failure with preserved ejection fraction is increasingly recognized. We conducted a study to evaluate the epidemiologic features and outcomes of patients with heart failure with preserved ejection fraction and to compare the findings with those from patients who had heart failure with reduced ejection fraction. METHODS: From April 1, 1999, through March 31, 2001, we studied 2802 patients admitted to 103 hospitals in the province of Ontario, Canada, with a discharge diagnosis of heart failure whose ejection fraction had also been assessed. The patients were categorized in three groups: those with an ejection fraction of less than 40 percent (heart failure with reduced ejection fraction), those with an ejection fraction of 40 to 50 percent (heart failure with borderline ejection fraction), and those with an ejection fraction of more than 50 percent (heart failure with preserved ejection fraction). Two groups were studied in detail: those with an ejection fraction of less than 40 percent and those with an ejection fraction of more than 50 percent. The main outcome measures were death within one year and readmission to the hospital for heart failure. RESULTS: Thirty-one percent of the patients had an ejection fraction of more than 50 percent. Patients with heart failure with preserved ejection fraction were more likely to be older and female and to have a history of hypertension and atrial fibrillation. The presenting history and clinical examination findings were similar for the two groups. The unadjusted mortality rates for patients with an ejection fraction of more than 50 percent were not significantly different from those for patients with an ejection fraction of less than 40 percent at 30 days (5 percent vs. 7 percent, P=0.08) and at 1 year (22 percent vs. 26 percent, P=0.07); the adjusted one-year mortality rates were also not significantly different in the two groups (hazard ratio, 1.13; 95 percent confidence interval, 0.94 to 1.36; P=0.18). The rates of readmission for heart failure and of in-hospital complications did not differ between the two groups. CONCLUSIONS: Among patients presenting with new-onset heart failure, a substantial proportion had an ejection fraction of more than 50 percent. The survival of patients with heart failure with preserved ejection fraction was similar to that of patients with reduced ejection fraction.

Aged↗

PubMed2026

New Evidence in Heart Failure: 2026 Update.

Heart failure (HF) remains a major cause of morbidity, mortality, impaired quality of life and healthcare expenditure worldwide. The global burden of HF continues to increase due to population aging, improved survival, and the growing prevalence of cardiovascular, renal, and metabolic comorbidities. Simultaneously, the pace of scientific progress in HF has accelerated considerably. Recent advances have refined our understanding of HF epidemiology, prognosis, and disease trajectories, including emerging concepts of HF improvement, remission, and recovery. The Second Universal Definition of HF has also updated the classification framework, moving beyond the traditional ejection fraction-based categories. HF is now broadly classified into two major phenotypes: heart failure with reduced ejection fraction (HFrEF) and heart failure with preserved ejection fraction (HFpEF). Novel mechanistic insights highlight the role of inflammation, immune activation, metabolic dysfunction, mitochondrial biology, and multisystem interactions in HF progression. There has also been significant progress in the characterization and management of major comorbidities, including chronic kidney disease (CKD), diabetes, obesity, atrial fibrillation (AF), pulmonary hypertension, frailty, malnutrition, and cancer. Diagnostic innovations include novel biomarkers, multi-omics technologies, artificial intelligence-based approaches, advanced imaging techniques, congestion assessment tools, and emerging digital health solutions. Important advances have occurred in specific HF aetiologies, including cardiomyopathies, cardiac amyloidosis (CA), myocarditis, arrhythmia-induced cardiomyopathy (AiCM), and Chagas cardiomyopathy. Therapeutic developments continue to reshape HF management across the spectrum of left ventricular ejection fraction. Recent evidence has focused on optimization of guideline-directed medical therapy in HFrEF, expansion of evidence-based therapies in HFpEF, and growing roles for sodium-glucose cotransporter-2 inhibitors, finerenone, incretin-based therapies, and transcatheter valve interventions. Collectively, these advances support the transition from a predominantly phenotype-based approach towards a more personalized and biologically informed model of HF care, with the potential to further improve outcomes across the entire HF spectrum.

Journal Article↗

PubMed2006

Costs for heart failure with normal vs reduced ejection fraction.

BACKGROUND: Among the elderly population, heart failure (HF) with normal ejection fraction (EF) is more common than classic HF with low EF. However, there are few data regarding the costs of HF with normal EF. In a prospective, population-based cohort of elderly participants, we compared the costs and resource use of patients with HF and normal and reduced EF. METHODS: A total of 4549 participants (84.5% white; 40.6% male) in the National Heart, Lung, and Blood Institute Cardiovascular Health Study were linked to Medicare claims from 1992 through 1998. By protocol echo examinations or clinical EF assessments, 881 participants with HF were characterized as having abnormal or normal EF. We applied semiparametric estimators to calculate mean costs per subject for a 5-year period. RESULTS: There were 495 HF participants with normal EF (186 prevalent at study entry and 309 incident during the study period) and 386 participants with abnormal EF (166 prevalent and 220 incident). Participants with abnormal EF had more cardiology encounters and cardiac procedures. However, compared with abnormal EF participants, the 5-year costs for normal EF participants were similar in both the prevalent ($33,023 with abnormal EF and $32,580 with normal EF; P=.93) and incident ($49,128 with abnormal EF and $45,604 with normal EF; P=.55) groups. In models accounting for comorbid conditions, the costs with normal and abnormal EF remained similar. CONCLUSIONS: Over a 5-year period, patients with HF and normal EF consume as many health care resources as those with reduced EF. These data highlight the substantial financial burden of HF with normal EF among the elderly population.

Aged↗

PubMed2025

Finerenone-Related Risk of Hypotension in Heart Failure With Mildly Reduced or Preserved Ejection Fraction.

BACKGROUND: The nonsteroidal mineralocorticoid receptor antagonist finerenone reduces clinical events in heart failure with mildly reduced ejection fraction/preserved ejection fraction; however, the implications of treatment-related hypotension are unknown. OBJECTIVES: The authors investigated predictors of systolic blood pressure (SBP) <100 mm Hg and investigator-reported hypotension and their associations with randomized treatment and clinical outcomes in the FINEARTS-HF (Study to Evaluate the Efficacy [Effect on Disease] and Safety of Finerenone in Participants With Heart Failure and Left Ventricular Ejection Fraction [Proportion of Blood Expelled Per Heart Stroke]) trial. METHODS: FINEARTS-HF was a randomized, placebo-controlled trial of finerenone in symptomatic patients with chronic heart failure (left ventricular ejection fraction ≥40%). Predictors of SBP <100 mm Hg and hypotension were identified using Cox models. Associations between SBP <100 mm Hg and hypotension, treatment, and clinical outcomes were evaluated using time-updated Cox models. The primary outcome was a composite of total heart failure events and cardiovascular death. RESULTS: Among the 5,815 participants with available data, post-baseline SBP <100 mm Hg occurred in 899 (538 with finerenone vs 361 with placebo; odds ratio: 1.60; 95% CI: 1.38-1.85) and investigator-reported hypotension in 364 patients (225 with finerenone vs 139 with placebo; odds ratio: 1.67; 95% CI: 1.34-2.08). Participants experiencing SBP <100 mm Hg had lower baseline SBP, were older, had higher N-terminal pro-B-type natriuretic peptide levels, a history of smoking, and no diabetes. Treatment-related risk of the primary endpoint was reduced in patients with no/before SBP <100 mm Hg (rate ratio: 0.78; 95% CI: 0.67-0.90) and appeared to attenuate afterwards (rate ratio: 0.99; 95% CI: 0.70-1.39), although no formal statistical interaction was observed (Pinteraction = 0.33). CONCLUSIONS: In this prespecified analysis of the FINEARTS-HF trial, finerenone led to higher rates of post-baseline SBP <100 mm Hg and investigator-reported hypotension. Although hypotension should not prompt automatic treatment discontinuation, these patients should be carefully monitored. (Study to Evaluate the Efficacy (Effect on Disease) and Safety of Finerenone in Participants With Heart Failure and Left Ventricular Ejection Fraction (Proportion of Blood Expelled Per Heart Stroke) Greater or Equal to 40% [FINEARTS-HF]; NCT04435626).

Humans↗

PubMed2004

[Natriuretic peptides--new diagnostic markers in heart disease].

In patients with heart failure, increased wall stretch due to volume and pressure overload leads to an increase in circulating natriuretic peptides (ANP and BNP and their N-terminal fragments NT-proANP and NT-proBNP). Plasma BNP levels commonly considered normal (< 20 pg/ml) are influenced by age, sex, and also by genetic factors. ANP and BNP are synthesized and released by atrial and ventricular myocytes (Figure 1). In subjects with acute dyspnea, a BNP plasma concentration of 100 pg/ml has been established as a cutoff value for the diagnosis of heart failure yielding a very high negative predictive value coupled with an acceptable positive predictive value (Figure 3). However, recent evidence suggests that much more subtle elevations of plasma BNP may also indicate an increased long-term risk of cardiovascular events and death (Figure 2). In acute heart failure, natriuretic peptides correlate with ventricular pressure and volume overload, as well as with NYHA functional class. They can, however, not reliably discriminate between heart failure due to reduced ejection fraction and heart failure with preserved systolic function (Figure 4). Thus, elevated BNP or NT-proBNP levels always demand further clarification of heart failure etiology using echocardiography as the method of choice. As indicated by the algorithm for a BNP-based differential diagnosis of acute heart failure symptoms (Figure 5), a variety of noncardiac causes may also lead to moderate elevations of the markers (BNP plasma concentrations of 100-400 pg/ml). In addition, normal marker levels may be observed in > 20% of patients with long-term stable heart failure. Thus, increased plasma concentrations of natriuretic peptides are not strictly specific for heart diseases and also lack sensitivity in the chronic compensated state. Diuretics, angiotensin-converting enzyme (ACE) inhibitors, angiotensin receptor antagonists, and spironolactone have been shown to decrease BNP and NT-proBNP in parallel with clinical and hemodynamic improvement. In patients hospitalized for decompensated heart failure, predischarge plasma BNP levels reflect the risk of future death and rehospitalization (Figure 6). Although adjusting heart failure treatment to reduce plasma NT-proBNP levels may improve outcome, a general recommendation for monitoring drug therapy using this marker should not be derived from this observation. General practitioners may, in the future, use BNP or NT-proBNP as a rule-out test for heart failure and preselect patients for further diagnostic work-up on the basis of an elevated plasma level. Within the framework of the German network for heart failure the multicentric "Handheld-BNP Study" will clarify, whether echocardiography using low-price simple handcarried devices could be used as an alternative or, more likely, as a complementary diagnostic tool to further improve heart failure diagnosis in primary care.

Biomarkers↗

PubMed2005

Benefit of cardiac resynchronization therapy to a patient with a narrow QRS complex and ventricular dyssynchrony identified by tissue synchronization imaging.

This report described an 81-year-old woman with severe symptomatic heart failure, reduced ejection fraction, mitral regurgitation, and an electrocardiographic QRS width of 118 ms who had ventricular dyssynchrony identified by echocardiographic tissue synchronization imaging. Because of her severe heart failure symptoms on maximal medical therapy, referral to implant a defibrillator, and mechanical dyssynchrony, she underwent cardiac resynchronization-defibrillator therapy with lateral left ventricular lead placement. This resulted in an immediate 30% increase in stroke volume and 35% decrease in mitral regurgitation. Echocardiographic tissue synchronization imaging may play a role in identifying mechanical dyssynchrony in patients with narrow QRS duration who may potentially benefit from cardiac resynchronization therapy.

Aged, 80 and over↗

PubMed1991

Effect of enalapril on survival in patients with reduced left ventricular ejection fractions and congestive heart failure.

BACKGROUND: Patients with congestive heart failure have a high mortality rate and are also hospitalized frequently. We studied the effect of an angiotensin-converting-enzyme inhibitor, enalapril, on mortality and hospitalization in patients with chronic heart failure and ejection fractions less than or equal to 0.35. METHODS: Patients receiving conventional treatment for heart failure were randomly assigned to receive either placebo (n = 1284) or enalapril (n = 1285) at doses of 2.5 to 20 mg per day in a double-bind trial. Approximately 90 percent of the patients were in New York Heart Association functional classes II and III. The follow-up averaged 41.4 months. RESULTS: There were 510 deaths in the placebo group (39.7 percent), as compared with 452 in the enalapril group (35.2 percent) (reduction in risk, 16 percent; 95 percent confidence interval, 5 to 26 percent; P = 0.0036). Although reductions in mortality were observed in several categories of cardiac deaths, the largest reduction occurred among the deaths attributed to progressive heart failure (251 in the placebo group vs. 209 in the enalapril group; reduction in risk, 22 percent; 95 percent confidence interval, 6 to 35 percent). There was little apparent effect of treatment on deaths classified as due to arrhythmia without pump failure. Fewer patients died or were hospitalized for worsening heart failure (736 in the placebo group and 613 in the enalapril group; risk reduction, 26 percent; 95 percent confidence interval, 18 to 34 percent; P less than 0.0001). CONCLUSIONS: The addition of enalapril to conventional therapy significantly reduced mortality and hospitalizations for heart failure in patients with chronic congestive heart failure and reduced ejection fractions.

Blood Pressure↗

PubMed2025

Mode of Death in Patients With Heart Failure With Mildly Reduced or Preserved Ejection Fraction: The FINEARTS-HF Randomized Clinical Trial.

IMPORTANCE: The mode of death in patients with heart failure with mildly reduced ejection fraction (HFmrEF) or heart failure with preserved ejection fraction (HFpEF) remains poorly understood and may vary by EF. OBJECTIVE: To evaluate the mode of death according to EF and the treatment effect of finerenone on cause-specific mortality in patients with HFmrEF/HFpEF. DESIGN, SETTING, AND PARTICIPANTS: This was a prespecified secondary analysis of the Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients With Heart Failure (FINEARTS-HF) randomized clinical trial, which evaluated clinical outcomes in 6001 patients with HF and EF greater than or equal to 40% randomly assigned to finerenone or placebo. The mode of death in relation to baseline EF categories (<50%, ≥50-<60%, and ≥60%) was examined, and the effect of randomized treatment on cause-specific death in Cox regression models was assessed. Data analysis was conducted between September 2024 and January 2025. INTERVENTIONS: Finerenone vs placebo. MAIN OUTCOMES AND MEASURES: Mode of death as centrally adjudicated by a clinical end points committee. RESULTS: Of 1013 patients (16.9%; median [IQR] age, 76 [69-82] years; 594 male [58.6%]) who died during median (IQR) follow-up of 32 (23-36) months, mode of death was ascribed to cardiovascular causes in 502 (49.6%), noncardiovascular causes in 368 (36.3%), and undetermined cause in 143 (14.1%). Of cardiovascular deaths, 215 (42.8%) were due to sudden death, 163 (32.4%) to HF, 48 (9.6%) to stroke, 25 (5.0%) to myocardial infarction, and 51 (10.2%) to other cardiovascular causes. The proportion of all-cause, cardiovascular, and sudden death was higher in those with EF less than 50%. The proportion of deaths related to HF was similar across EF categories, and the proportion of deaths due to myocardial infarction, stroke, and other cardiovascular causes was low regardless of EF. Randomization to finerenone did not significantly reduce death or cause-specific death compared with placebo in any EF category. CONCLUSIONS AND RELEVANCE: Among patients with HFmrEF/HFpEF in the FINEARTS-HF randomized clinical trial, higher proportions of cardiovascular and overall mortality in those with EF less than 50% were related principally to higher proportions of sudden death. A clear treatment effect of finerenone on cardiovascular or cause-specific mortality was not identified, although the trial was likely underpowered for these outcomes. TRIAL REGISTRATION: ClinicalTrials.gov Identifier: NCT04435626.

Humans↗

PubMed1982

Reliable estimation of peak left ventricular systolic pressure by M-mode echographic-determined end-diastolic relative wall thickness: identification of severe valvular aortic stenosis in adult patients.

In compensated hearts, left ventricular systolic pressure (LVSP) can be estimated from the ratio of LV wall thickness to chamber radius (RWT). To determine the clinical value of such estimates, we examined echocardiography RWT in an unscreened series of 81 individuals with aortic valve disease, hypertension, or normal hearts. Despite the presence, in many subjects, of symptoms of congestive heart failure, reduced ejection fraction, or coronary disease, end-diastolic RWT (RWTD) correlated well with peak LVSP (r = 0.77); 45 of 55 patients with LVSP greater than or equal to 140 mm Hg had RWTD greater than or equal to 0.45, while 26 of 26 with LVSP less than 140 mm Hg had lower values (p less than 0.005). RWTD was greater than or equal to 0.50 in 30 of 34 patients with LVSP greater than or equal to 180 mm Hg and in 6 of 21 with LVSP 140 to 180 mm Hg. RWTD correctly estimated LVSP range in 26 of 27 severe aortic stenosis (AS) patients and, combined with echocardiographic aortic valve calcification, correctly recognized the presence or absence of severe AS in 99% of the series. The RWTD for any given LVSP was higher in patients on antihypertensive treatment and lower in patients with severe aortic regurgitation. In contrast to series based on patients with normal LV function, end-systolic RWT correlated poorly with LVSP.

Adult↗

PubMed2026

Large-Scale Proteomic Profiling of Incident Heart Failure and Its Subtypes in Older Adults.

BACKGROUND: Heart failure (HF) and its main subtypes, heart failure with preserved ejection fraction (HFpEF) and heart failure with reduced ejection fraction (HFrEF), impose an enormous health burden on elders. Assessment of the circulating proteome to illuminate pathogenesis could open new opportunities for treatment. METHODS: We conducted a plasma proteomics screen of incident HF and its subtypes in 2 older population-based cohorts, the CHS (Cardiovascular Health Study) and the AGES-RS (Aging, Gene/Environment Susceptibility-Reykjavik Study). The 2 studies used SomaLogic platforms, with 4404 aptamers in common. Multivariable Cox models were fit to evaluate individual-protein associations with HF, HFpEF, and HFrEF separately in each cohort, and study-specific associations were combined by fixed-effects meta-analysis. Replication was performed in the ARIC (Atherosclerosis Risk in Communities) cohort. Two-sample Mendelian randomization of HF and its subtypes, along with colocalization analysis, was performed to support causal inference. RESULTS: Among 8599 participants, 1590 experienced incident HF (536 HFpEF, 471 HFrEF). There were 119 proteins associated with HF, 15 proteins with HFpEF, and 11 proteins with HFrEF, at Bonferroni-corrected significance. Among these, 9 have never previously been identified for cardiovascular diseases, and another 61 represent new associations with incident HF or its subtypes. Of these 70 proteins, 55 of the 66 available replicated externally. Mendelian randomization analysis revealed 7 proteins genetically associated with HF at nominal significance; 2 were separately associated with HFpEF, and another 2 with HFrEF. Seven of these 9 proteins (NPDC1 [neural proliferation differentiation and control protein 1], APOF [apolipoprotein F], LMAN2 [lectin, mannose-binding 2], ADIPOQ [adiponectin], CD14 [cluster of differentiation 14], ARHGAP1 [Rho GTPase-activating protein 1], C9 [complement 9]) showed new, possibly causal associations, although we did not detect evidence for colocalization. CONCLUSIONS: In this large-scale proteomic study involving 3 longitudinal cohorts of older adults, we identified and replicated 55 novel protein markers of HF or its subtypes, and 7 new, possibly causal proteins. These proteins may enhance risk prediction, improve understanding of pathobiology, and help prioritize targets for therapeutic development of these foremost disorders in elders.

Humans↗

PubMed2003

Renal insufficiency is an independent predictor of mortality after percutaneous coronary intervention.

The present study was designed to evaluate whether the presence of renal disease during percutaneous coronary intervention (PCI) is associated with worse outcomes at 1 year in a multicenter study. The incidence of death, myocardial infarction, coronary artery bypass grafting, repeat PCI, and repeat revascularization were prospectively collected on 4,602 patients (6,542 lesions) in 2 waves of patients who underwent PCI in 17 centers between July 1997 and June 1999. Renal disease was defined as the presence of an increased creatinine level in a patient with a history or presence of renal failure treated with low protein diet or dialysis. Patients with renal disease (n = 192) were older and more likely to have diabetes, heart failure, reduced ejection fraction, known coronary disease, and multivessel disease than patients without renal disease (n = 4,410). Rates of stenting were equivalent (68.2% vs 73.0%, p = NS). Patients with renal disease had lower angiographic success (84.9% vs 92.8%, p <0.001) and higher mortality, both in-hospital (5.7% vs 1.2%, p <0.001) and at 1 year (19.7% vs 4.4%, p <0.0001). After adjusting for clinical, demographic, and angiographic differences, renal disease remained an independent predictor of in-hospital (odds ratio 3.81, 95% confidence interval 1.70 to 8.58) and 1-year (risk ratio 2.46, 95% confidence interval 1.64 to 3.68) mortality. Renal disease conferred additional mortality risk in established high-risk clinical subgroups. In conclusion, after adjusting for a higher frequency of co-morbidities, renal disease remains a strong and independent predictor of increased in-hospital and 1-year mortality after PCI and is additive to other clinical markers of worse outcome.

Aged↗

PubMed1995

ACE inhibitors and calcium antagonists in the treatment of congestive heart failure.

The increased mortality after myocardial infarction is related to the risk of reinfarction, sudden death, and the development and progression of heart failure; in congestive heart failure it is due to the progression of heart failure and sudden death. ACE inhibitors have been proven to prevent cardiovascular events, especially the progression of heart failure, in postinfarct patients with reduced ejection fraction and heart failure in the SAVE and AIRE trials. In patients with congestive heart failure, ACE inhibitor treatment has prevented cardiovascular death and reduced morbidity due to progressive heart failure in the SOLVD trials. In post-myocardial infarction patients, the calcium antagonist nifedipine did not affect mortality or morbidity; diltiazem improved prognosis in patients without congestive heart failure and in patients with non-Q-wave infarction; and verapamil improved prognosis by prevention of reinfarction and sudden death. Combination treatment with both verapamil, which has pronounced antiischemic properties and prevents sudden death and reinfarction, and an ACE inhibitor, which prevents the progression of heart failure, is a possibility for future cardiovascular therapy that should be evaluated.

Angiotensin-Converting Enzyme Inhibitors↗

PubMed2006

Leg flow-mediated arterial dilation in elderly patients with heart failure and normal left ventricular ejection fraction.

BACKGROUND: flow-mediated arterial dilation (FMAD), an indicator of endothelial function, is reduced in patients with heart failure and reduced left ventricular ejection fraction (HFREF). Many elderly patients with heart failure exhibit a normal left ventricular ejection fraction (HFNEF). It is unknown whether FMAD is severely reduced in the elderly with HFNEF. METHODS AND RESULTS: 30 participants >60 yr of age, 11 healthy, 9 with HFNEF, and 10 with HFREF, underwent a cardiovascular magnetic resonance (CMR) assessment of FMAD in the superficial femoral artery followed within 48 h by symptom-limited exercise with expired gas analysis. Elderly patients with HFREF and HFNEF had severely reduced peak oxygen consumption (Vo(2 peak); 12 +/- 2 and 13 +/- 1 ml.kg(-1).min(-1), respectively) vs. their healthy age-matched contemporaries (20 +/- 3 ml.kg(-1).min(-1)). FMAD was 3.8 +/- 1.3% (0.85 +/- 0.22 mm(2)) in patients with HFREF; it was 12.1 +/- 3.6% (3.1 +/- 1.2 mm(2)) and 13.7 +/- 5.9% (3.9 +/- 1.7 mm(2)), respectively, in patients with HFNEF and age-matched healthy older individuals. After adjustment for age and gender, the association of FMAD with Vo(2) was high in healthy and HFREF subjects (P = 0.05 and 0.02, respectively) but less so in HFNEF participants (P = 0.58). CONCLUSIONS: elderly patients with HFNEF do not exhibit marked reduction in leg FMAD. These data suggest that mechanisms other than impaired femoral arterial endothelial function contribute to the severe exercise intolerance experienced by these individuals.

Aged↗