Primary care heart failure service identifies a missed cohort of heart failure patients with reduced ejection fraction.

AIMS: We explored whether a missed cohort of patients in the community with heart failure (HF) and left ventricular systolic dysfunction (LVSD) could be identified and receive treatment optimization through a primary care heart failure (PCHF) service. METHODS AND RESULTS: PCHF is a partnership between Inspira Health, National Health Service Cardiologists and Medtronic. The PCHF service uses retrospective clinical audit to identify patients requiring a prospective face-to-face consultation with a consultant cardiologist for clinical review of their HF management within primary care. The service is delivered via five phases: (i) system interrogation of general practitioner (GP) systems; (ii) clinical audit of medical records; (iii) patient invitation; (iv) consultant reviews; and (v) follow-up. A total of 78 GP practices (864 194 population) have participated. In total, 19 393 patients' records were audited. HF register was 9668 (prevalence 1.1%) with 6162 patients coded with LVSD (prevalence 0.7%). HF case finder identified 9725 additional patients to be audited of whom 2916 patients required LVSD codes adding to the patient medical record (47% increase in LVSD). Prevalence of HF with LVSD increased from 0.7% to 1.05%. A total of 662 patients were invited for consultant cardiologist review at their local GP practice. The service found that within primary care, 27% of HF patients identified for a cardiologist consultation were eligible for complex device therapy, 45% required medicines optimization, and 47% of patients audited required diagnosis codes adding to their GP record. CONCLUSION: A PCHF service can identify a missed cohort of patients with HF and LVSD, enabling the optimization of prognostic medication and an increase in device prescription.

Volume status and diuretic therapy in systolic heart failure and the detection of early abnormalities in renal and tubular function.

OBJECTIVES: This study sought to determine the pharmacodynamic effect of modulation of volume status by withdrawal and reinstitution of diuretic treatment on markers of renal and tubular function. BACKGROUND: Decreased renal perfusion and increased congestion are associated with renal dysfunction in patients with heart failure. METHODS: In this study, 30 patients with chronic systolic heart failure in a presumed euvolemic state and on standard oral furosemide therapy (40 to 80 mg) were examined. At baseline, subjects were withdrawn from their loop diuretics. After 72 h, their furosemide regimen was reinstated, and patients were studied again 3 days later. Serum creatinine, atrial and B-type natriuretic peptide, urinary kidney injury molecule (KIM)-1, urinary N-acetyl-beta-D-glucosaminidase (NAG), and serum as well as urinary neutrophil gelatinase-associated lipocalin (NGAL) were determined at various time points. RESULTS: Diuretic withdrawal resulted in increases in atrial and B-type natriuretic peptide (both p < 0.05). Serum creatinine was unaffected. Both urinary KIM-1 (p < 0.001) and NAG (p = 0.010) concentrations rose significantly, after diuretic withdrawal, whereas serum and urinary NGAL were not significantly affected. After reinitiation of furosemide, both urinary KIM-1 and NAG concentrations returned to baseline (both p < 0.05), but NGAL values were unaffected. CONCLUSIONS: Subclinical changes in volume status by diuretic withdrawal and reinstitution are associated with increases and decreases of markers of tubular dysfunction in stable heart failure. Diuretic therapy may favorably affect renal and tubular function by decreasing congestion.

Performing repeated noninvasive bedside measures of volume response to intravenous furosemide in acute pulmonary edema: a feasibility assessment.

Optimizing responses to intravenous furosemide (ivF) in acute pulmonary edema is limited by current insensitive noninvasive means of volume assessment. We conducted a pilot study to assess the feasibility of performing repeated measures of echocardiographic and bioimpedance analysis (BIA) parameters and test their response as noninvasive markers of volume response to ivF. We also aimed to identify the most potentially sensitive markers of this response. Patients receiving ivF for a clinical diagnosis of acute cardiogenic pulmonary edema were studied. Echocardiographic and BIA parameters were measured at 0, 0.5, 1, 2, and 3 h after ivF. Intraobserver variability for each parameter was determined. Thirty-one patients were enrolled who were receiving 40-100 mg of ivF. Transmitral (MV) early peak velocity following Valsalva maneuver and transtricuspid (TV) early peak velocity reduced significantly (P= 0.012 and 0.010, respectively), whereas MV deceleration time increased significantly (P= 0.006) in response to ivF. Short-axis inferior vena cava diameter (SIVC) in expiration and inspiration and SIVC corrected for body surface area in expiration and inspiration reduced significantly following ivF (P= 0.039, 0.020, 0.032, and 0.016, respectively). BIA estimates of extracellular water decreased significantly (P= 0.001), whereas impedance (Z) at currents of 5, 50, 100, and 200 kHz increased following ivF; the changes were significant with all but the last parameter (P < 0.0001, 0.006, 0.010, and 0.051, respectively). Maximal change from baseline for each parameter was greater than its respective intraobserver variability. Performing repeated measures of echocardiographic and BIA parameters is feasible in this unstable group of patients. The above panel of parameters could potentially be used to track volume response to ivF and, thus, to optimize treatment in acute pulmonary edema.