Even a low comorbidity burden predicts poor outcome in chronic heart failure.

BACKGROUND: Patients with heart failure (HF) often have multiple cardiovascular risk factors (CVRF) and comorbidities (CMB). We evaluated the impact of additive CMB and CVRF in HF prognosis. METHODS: We retrospectively analyzed ambulatory patients with systolic dysfunction between January 2012 and May 2018. Follow-up: until January 2021. Endpoint: all-cause death. CVRF analyzed: Arterial hypertension, Diabetes mellitus and smoking. CMB evaluated: coronary artery disease, non-coronary atherosclerotic disease, respiratory disease, dementia, anemia, chronic kidney disease, inflammatory/autoimmune disease, active cancer and atrial fibrillation. Classification according to the number of CVRF and/or CMB: < 2 and ≥ 2. The independent prognostic impact of CVRF/CMB burden was assessed with multivariate Cox-regression. RESULTS: Most patients had ≥ 2 CMB (67.9%). Regarding CVRF, 14.9% presented none, 40.2% had one and 32.1% had two. During a median 49-month follow-up, 419 (49.1%) patients died. Mortality was higher among patients with ≥2 CVRF (56.1 vs 43.4% in those with <2) and in those with ≥2 CMB (57.7 vs 31.0%). While patients with one CMB had similar mortality than those with none. Patients with ≥2 CMB had higher long-term mortality risk: HR=2.47 (95% CI: 1.95-3.14). In patients with ≥2CVRF: HR of dying = 1.39 (1.14- 1.70). When taken together there was a clear survival disadvantage for patients with ≥ 2 CVRF/CMB - adjusted HR: 2.20 (1.45-3.34). CONCLUSION: The presence of only 2 CVRF/CMB more than doubles the patients´ risk of dying. CVRF and CMB should be assessed as part of routine patient management.

Benzodiazepine use and mortality in chronic heart failure.

INTRODUCTION: The prognostic implications of using benzodiazepines (BZD) in heart failure (HF) patients are still unknown. OBJECTIVES: This study aimed to assess the association of BZD use with all­cause death in ambulatory, chronic HF patients. PATIENTS AND METHODS: We investigated a retrospective cohort of ambulatory HF patients with left ventricular systolic dysfunction (LVSD). The patients were followed up from their first medical appointment until January 2021 and all­cause mortality was the primary end point. The Cox regression analysis was used to assess the association between BZD use and all­cause mortality. Subgroup analyses were performed considering age, sex, body mass index (BMI), respiratory disease, chronic kidney disease (CKD), and New York Heart Association (NYHA) class. Multivariable models were built to account for confounders. RESULTS: We studied 854 patients (69% men), of mean (SD) age 71 (13) years, of whom 51% had severe LSVD, and 242 (28.3%) regularly used BZD. During a median follow­up of 46 months, 443 patients (51.9%) died. BZD use predicted no crude survival disadvantage in the entire investigated group and in the subgroup analysis according to sex, respiratory disease, BMI, and NYHA class. BZD use was not mortality­associated among patients aged 75 years and younger. However, in those older than 75 years the hazard ratio (HR) of all­cause death was 1.3 (95% CI, 0.99-1.69; P = 0.06). BZD use seemed safe in the patients without CKD, but in those with CKD it was associated with worse survival (HR, 1.33; 95% CI, 1.02-1.73). In a multivariable­adjusted analysis, the use of BZD was independently associated with increased death risk (HR, 1.36; 95% CI, 1.06-1.75). CONCLUSIONS: The patients medicated with BZD presented a 36% higher risk of dying. BZD should probably be used with caution, particularly in older HF patients and in those with CKD.

Low stress hyperglycemia ratio predicts worse prognosis in diabetic acute heart failure patients.

INTRODUCTION: Acute blood glucose but not glycated hemoglobin (HbA1c) predicts poor outcome in acute heart failure (HF). The stress hyperglycemia ratio (SHR) has been proposed as a prognostic predictor in various clinical settings. OBJECTIVES: We assessed the prognostic implications of the SHR in acute HF patients with and without diabetes. METHODS: We performed a retrospective analysis of an acute HF registry conducted between 2009 and 2010. Estimated average glucose (eAG) was calculated as (28.7×HbA1c)-46.7 and SHR as acute blood glucose divided by eAG. The primary endpoint was all-cause mortality. Follow-up was three months. Patients were grouped by SHR tertiles (≤0.88, 0.89-1.16, and >1.16). Cox regression analysis was used to test the association of SHR (cut-off 0.88) with all-cause mortality. Analysis was stratified according to the presence of diabetes. Multivariate models were built accounting for acute blood glucose and for eAG (models 1 and 2, respectively). RESULTS: We studied 599 patients, mean age 76±12 years, of whom 62.1% had reduced ejection fraction and 50.9% had diabetes. Median acute blood glucose, eAG and SHR were 136 (107-182) mg/dl, 131 (117-151) mg/dl, and 1.02 (0.20-3.34), respectively. During follow-up 102 (17.0%) died. In patients with diabetes, those in the lowest SHR tertile had a hazard ratio (HR) of 2.24 (95% CI: 1.05-5.22) (model 1) and 2.34 (1.25-4.38) (model 2). In patients without diabetes, the HR of three-month death in the lowest SHR tertile was 0.71 (95% CI: 0.36-1.39) and 1.02 (0.58-1.81). Significant interaction was observed between diabetes and SHR. CONCLUSIONS: In HF patients with diabetes, a SHR ≤0.88 was associated with a more than twofold higher three-month mortality risk. No such association was found in non-diabetic patients. The presence of diabetes influences the association of the SHR with mortality.

The prognostic impact of magnesium in acute heart failure is different according to the presence of diabetes mellitus.

Background: Hypermagnesemia predicts mortality in chronic heart failure (HF); however, in acute HF, magnesium does not seem to be outcome-associated. Diabetes mellitus (DM) frequently associates with altered magnesium status. We hypothesized that DM might influence the prognostic impact of magnesium in acute HF. Methods: This is a retrospective cohort study of hospitalized patients with acute HF. Patients without data on admission serum magnesium were excluded. Follow-up: 1 year from hospital admission. Primary end point: all-cause mortality. Patients were divided according to median serum magnesium (1.64 mEq/L). The Kaplan-Meier survival method was used to determine survival curves according to magnesium levels. The analysis was stratified according to the presence of DM. A multivariable Cox regression analysis was used to study the prognostic impact of magnesium. Results: We studied 606 patients. The mean age was 76 ± 12 years, 44.1% were male, 50.7% had DM, and 232 (38.3%) died during follow-up. Median magnesium was 1.64 (1.48-1.79) mEq/L. Patients with magnesium ≥1.64 mEq/L had higher 1-year mortality [141 (46.4%) vs 91 (30.1%), P < .001]. After adjustments for age, sex, history of atrial fibrillation, systolic blood pressure, heart rate, ischemic etiology, B-type natriuretic peptide, estimated glomerular filtration rate, alcohol consumption, antihyperglycaemic agents or glycated hemoglobin, admission glycemia, New York Heart Association class IV, and severe left ventricle systolic dysfunction, serum magnesium ≥1.64 mEq/L was associated with higher mortality only in patients with DM: HR 1.89 (95% confidence interval: 1.19-3.00), P = .007, and 1.27 (95% confidence interval: 0.83-1.94) and P = .26 for non-DM patients. The results were similar if magnesium was analyzed as a continuous variable. Per 0.1 mEq/L increase in magnesium levels, patients with DM had 13% increased risk of 1-year mortality. Conclusions: Higher magnesium levels were associated with worse prognosis only in HF patients with DM.

The ratio of furosemide dosage to urinary sodium concentration predicts mortality in patients with chronic stable heart failure.

INTRODUCTION: The urinary sodium (UNa) concentration is associated with outcomes in patients with acute heart failure (HF). Its impact in individuals with chronic HF is unknown. OBJECTIVES: This study examined the combined effect of diuretic dosage and UNa concentration in chronic HF. PATIENTS AND METHODS: The research sample for this retrospective cohort study consisted of ambulatory patients receiving optimized therapy and followed in an HF clinic. The patients were recruited between 2009 and 2012. The exclusion criteria were therapeutic adjustments or hospital admissions in the previous 2 months and renalreplacement therapy. The patients were followed for 5 years; the endpoint was all­cause mortality. The association between the ratio of furosemide dosage to UNa concentration and 5­year mortality was studied using a receiver operating characteristic (ROC) curve. The  patients were cross­classified according to daily furosemide dosage (with the cutoff set at 80 mg) and UNa concentration (80 mEq/l). Multivariable Cox regression analysis was used to assess the prognostic impact of the ratio. RESULTS: We analyzed 283 patients with chronic HF (70.3% male; mean age, 69 years). During follow­up, 134 patients died. The median furosemide dosage was 80 mg/day and the mean UNa concentration was 85 mEq/l. Based on the ROC curve, the best cutoff for the ratio of daily furosemide dosage to UNa concentration was 0.8. Patients with a ratio of 0.8 or higher had an adjusted hazard ratio for 5­year mortality of 2.85 (95% CI, 1.78-4.58). Patients with a UNa excretion rate of less than 80 mEq/l who wereadministered 80 mg or more of furosemide per day were found to have a worse prognosis (HR, 4.15; 95% CI, 2.31-7.45) when compared with those with a UNa excretion rate of 80 mEq/l or more and less than 80 mg furosemide per day. CONCLUSIONS: Combining the diuretic dosage and measurement of UNa excretion can be used to refine risk stratification in chronic HF. The furosemide­to­UNa ratio can be a surrogate marker for diuretic resistance and has a prognostic impact in chronic HF.

Ralstonia mannitollylitica endocarditis: A case report.

Ralstonia mannitolilytica (R. mannitolilytica.) is an emerging aerobic Gram-negative bacteria causing infection among immunocompromised patients. R. mannitolilytica, has been described in hospital outbreaks, mainly as bloodstream infection, but also as meningitis, hemoperitoneum infection and post renal transplant infection. We describe the first reported case of R. mannitolilytica infective endocarditis.

The Influence of Gender in The Prognostic Impact of Diabetes mellitus in acute Pulmonary Embolism.

Diabetes mellitus (DM) predicts ominous outcomes in acute pulmonary embolism (PE). The influence of gender on the prognostic impact of DM in PE is unknown. We did a retrospective analysis of a cohort of patients hospitalized with PE between 2006 and 2013. The exclusion criteria were age <18, non-pulmonary veins thromboembolism, recurrent PE, chronic thromboembolic pulmonary hypertension, no radiologic confirmation of PE, and active neoplasia. The primary endpoint was all-cause mortality. The follow-up was from diagnosis until October 2017. We assessed the prognostic impact of DM using a multivariate Cox regression analysis. The analysis was stratified according to gender. The interaction between gender and DM in the outcome of patients with PE was tested. We studied 577 PE patients (median age 65 years, 36.9% men, 19.8% diabetic). The genders were similar regarding the prevalence of DM, the extension and location of PE, and the thrombolytic therapy or brain natriuretic peptide (BNP) value. Diabetics presented higher all-cause mortality (Hazard ratio (HR) = 2.33 (95% confidence Interval (CI) 1.513.61)) when compared with non-diabetics. However, when analysis was stratified according to gender, DM was independently associated with a worse prognosis only in women (HR = 2.31 (95% CI 1.453.65)), while in men the HR was 1.10 (95% CI 0.592.04). The interaction between gender and DM was significant (p = 0.04). Gender influences the prognostic impact of DM in acute PE. Diabetic women with PE have twice the long-term mortality risk, while DM is not mortality-associated in men.

Methicillin-Resistant Staphylococcus aureus and Candida albicans Secondary Bloodstream Co-Infection in a Patient with Tubular Oesophageal Duplication.

Gastrointestinal duplications are rare congenital anomalies usually found incidentally in asymptomatic adult patients. We report a case of methicillin-resistant Staphylococcus aureus and Candida albicans secondary bloodstream co-infection in a 57-year-old male patient with a communicating tubular oesophageal duplication. The patient completed 21 days of medical treatment with vancomycin and anidulafungin and remained well without any complications, over 2 years of follow-up. LEARNING POINTS: Tubular oesophageal duplications are rare and often asymptomatic.Candida spp. seem to facilitate Staphylococcus aureus concomitant infection.Bloodstream infection due to uncommon agents should prompt further and exhaustive investigation of the source of infection.

Proteus mirabilis endocarditis.

A 62-year-old man was admitted to the emergency department due to fever and acute heart failure. A transthoracic echocardiogram revealed severe aortic valve obstruction. He was an hepatic transplant recipient and was medicated with everolimus. He underwent mitral and aortic valve replacement with prosthetic valves 4 years ago. Due to his medical background, therapy and clinical presentation, empirical therapy for infective endocarditis was started. Transoesophageal echocardiogram showed severe aortic valve regurgitation but no other findings suggestive of endocarditis. Computed tomography (CT) revealed pulmonary infiltrates compatible with infection and no evidence of septic embolisation. Multiple sets of blood cultures were negative. Proteus mirabilis was isolated in bronchial lavage and antibiotic therapy was adjusted. The patient underwent aortic valve replacement, with no macroscopic findings suggestive of endocarditis. P. mirabilis was isolated in the surgically removed valve. Dual antibiotic therapy was successfully administered for 6 weeks.