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BackgroundLoperamide at supratherapeutic doses can cause cardiac toxicity, presenting as cardiogenic shock, prolonged QT, malignant arrhythmias, or in severe cases sudden cardiac death. Surreptitious loperamide use is difficult to diagnose. We present an interesting case of loperamide use presenting with polymorphic ventricular tachycardia, cardiogenic shock.Case summaryA 25-year-old female presented with multiple syncopal episodes for 12 months with an electrocardiogram showing a Brugada-like pattern for which she underwent implantable cardioverter-defibrillator placement. One day following the procedure, she developed cardiogenic shock and was transferred to our tertiary care centre. Extensive workup was unrevealing. She responded well to supportive management, recovering from shock and was transferred to the floor. Unfortunately, she again developed cardiogenic shock, ultimately leading to cardiac arrest. Given the unclear cause for her cardiovascular symptoms, futher medication history was obtained. It was revealed that she was taking 100–150 tablets of loperamide per day. The decision was made to treat with intralipid emulsion therapy empirically given the strong suspicion for loperamide toxicity. The patient recovered well with supportive care. Loperamide levels returned elevated at 190 ng/mL. Repeated studies showed improvement of the conduction block, resolution of arrhythmias, and recovery of right and left ventricular function.DiscussionAcute loperamide toxicity can present as biventricular failure, with difficult-to-control arrhythmias. It requires a high index of suspicion. Treatment for loperamide toxicity is mainly supportive, lipid emulsion therapy can be considered in severe or refractory cases.

Hydroxychloroquine is a disease-modifying antirheumatic drug used for various rheumatological conditions. Its long-term use is well-known to have toxic effects on cardiac muscle cells. We present a biopsy-proven case of hydroxychloroquine-induced cardiotoxicity with detailed histopathological and imaging findings. The patient was referred to our heart failure clinic for concerns of reduction in left ventricular ejection fraction despite being on guideline-directed medical therapy. She had been diagnosed with rheumatoid arthritis, pulmonary hypertension and then subsequently heart failure with reduced ejection fraction 5 years ago. The evaluation included right heart catheterisation, cardiac MRI and endomyocardial biopsy. Light and electron microscopy showed myocyte hypertrophy and vacuolar change, abnormal mitochondria, myeloid bodies and curvilinear bodies. These findings were specific for hydroxychloroquine-induced cardiomyopathy. This case highlights the importance of clinical monitoring, early suspicion and consideration of drug-induced toxicities as a culprit for heart failure.

There is paucity of data regarding durable left ventricular assist device (LVAD) outcomes in patients with chronic kidney disease (CKD) stages 3-5 and CKD stage 5 on dialysis (end-stage renal disease [ESRD]).We conducted a retrospective study of Medicare beneficiaries with ESRD and a 5% sample of patients with CKD with an LVAD (2006-2018) to determine 1-year outcomes using the United States Renal Data System database. The LVAD implantation, comorbidities, and outcomes were identified using appropriate International Classification of Diseases, 9th and 10th edition codes. We identified 496 patients with CKD and 95 patients with ESRD who underwent LVAD implantation. The patients with ESRD were younger (59 years vs 66 years; P.001), had more Blacks (40% vs 24.6%, P = .009), compared with the CKD group. The 1-year mortality (49.5% vs 30.9%, P.001) and index mortality (27.4% vs 16.7%, P = .014) rates were higher for patients with ESRD. A subgroup analysis showed significantly higher mortality in ESRD vs CKD 3 (49.5% vs 30.2%, adjusted P = .009), but no significant difference in mortality between stage 3 vs 4/5 (30.2% vs 30.8%, adjusted P = .941). There was no significant difference in secondary outcomes (bleeding, stroke, and sepsis/infection) during follow-up between the 2 groups.Patients with ESRD undergoing LVAD implantation had significantly higher index and 1-year mortality rates compared with patients with CKD.

Summary Background Evaluation of patients with acute decompensated heart failure includes symptom review, biomarker measurement and comorbidity assessment. Early objective evaluation of functional status is generally not performed. Aim To investigate whether a simple low-impact functional assessment and measurement of sarcopenia would be safe, feasible and predictive of hospital length of stay and all-cause 30-day hospital readmission. Methods We administered 3-minute bicycle ergometry and hand grip strength tests at admission and discharge to patients for whom a decision to admit for heart failure management was made in the emergency department. Associations were examined between test results and length of stay and 30-day readmission. Exclusion criteria included acute coronary syndrome, hypoxia, end-stage renal disease, dementia/delirium and inability to sit at bedside. The Kansas City Cardiomyopathy Questionnaire-12, the Patient Health Questionnaire-2 and the visual analogue scale for dyspnoea were administered at admission, the visual analogue scale at discharge and the Kansas City Cardiomyopathy Questionnaire-12 at 30 days. Results Fifty patients were enrolled: 58% were female; the mean age was 66.2 ± 12.5 years; 24% had heart failure with preserved ejection fraction. Bicycle ergometry variables did not correlate with outcomes. Change in handgrip strength correlated with readmission, but not after adjustment (rpartial = 0.14; P = 0.35). Total diuretic dose correlated with length of stay; only discharge visual analogue scale and baseline lung disease had significant adjusted correlations with readmission. Conclusions Functional assessment in the emergency department of patients admitted for heart failure did not predict outcomes. However, the prognostic value of these assessments for decision-making about disposition (admission or discharge) may still be warranted.

Background Targeted treatment for decompensated right heart failure (RHF) with or without left heart failure is lacking. Vasopressin antagonists (vaptans) may offer an option by increasing urine output and fluid mobilization when used in acute decompensated RHF without impacting blood pressure or renal function, both common complications of loop diuretics. Methods and results We searched electronic medical records from 2 institutions over 4 years for patients with RHF treated with vaptans. Urine output, creatinine, BUN and sodium, 1 day pre- versus 1 day post-vaptan initiation were compared. Baseline (admission) pre-vaptan values for patients with RHF who met inclusion criteria (n = 112) were RAP, median (interquartile range) = 19 (13–24) mmHg; cardiac index, mean ± standard deviation = 1.8 ± 0.4 L/min/m2; BNP, 1078 (523–1690) pg/ml; creatinine clearance of 51 (39–69) ml/min, BUN, 37 (26–54) mg/dl, and serum [Na+] 132 (126–135) mEq/L. Most patients (n = 103/112) received intravenous inotrope (prior to vaptan, n = 91). Overall length of stay was 27 (16–43) days. Vaptan treatment (90% tolvaptan, 10% conivaptan) was associated with increased 24 h urine output, 1517 (906–2394) vs 2337 (1425–3744) mL, p = 0.005, and [Na+], 127 (124–130) vs 130 (126–135) mEq/L, p = 0.001, without significant change in Cr or BUN. Furosemide IV dose equivalent decreased or remained unchanged in 75% of patients at 24 h and 64% at 72 h compared to the 24 h prior to vaptan use. Conclusion Vaptans were associated with a significant increase in urine output and serum sodium with an apparent reduction or stabilization of furosemide equivalent dosing in the early treatment period in patients with decompensated RHF. Vaptans may offer a management option for patients failing conventional diuretic-based treatment.

Subgroup analyses of major randomized clinical trials in heart failure are published frequently, but their impact on medical knowledge and practice guidelines has not been previously reported. In a novel analysis, we determined number of citations, impact factors, number of authors, and citations in guidelines of both parent trials and sub‐studies; we also qualitatively assessed whether the analyses were described as post‐hoc and non‐pre‐specified. A total of 229 sub‐studies evaluating outcomes in patient subgroups were published (median 6, range 0–36 per trial). The number of subjects in the parent trials positively correlated with number of sub‐studies (rho = 0.51, P = 0.009). The subgroups are frequently not pre‐specified. The impact factors of sub‐studies were lower in comparison to the parent trials as were the number of citations two years after the publication date; in addition, parent trials were cited more frequently in European and American professional guidelines compared with the sub‐studies. We maintain that the sub‐studies derived from major heart failure trials are frequently published, but their contribution to clinical guidelines and medical knowledge are highly debatable.

The Hospital Readmissions Reduction Program provides incentives to hospitals to reduce early readmissions for heart failure (HF), acute myocardial infarction (AMI), and pneumonia (PNE).To examine the contribution of each diagnosis to readmissions penalty size, data were obtained from the Center for Medicare and Medicaid Services, American Hospital Association, and United States Census Bureau including number of cases; readmissions payment adjustment factor (values1 indicate a penalty for excess readmissions), excess readmission ratio (ERR, or ratio of adjusted predicted readmission based on comorbidities, frailty, and individual patient demographics to expected probability of readmission at an average hospital) for each diagnosis, hospital teaching status, bed number, and zip code socioeconomic status. Of 2,228 hospitals with ≥25 cases per diagnosis, 1,636 received a penalty. Univariate correlation coefficients between penalty and ERR were -0.66, -0.61, and -0.43 for HF, PNE, and AMI, respectively (all P.001). Correlation between ERRs was greatest for PNE and HF (0.30; P.001) and weakest for PNE and AMI (0.12; P.001). In regression analyses, the HF ERR explained the most variance in the penalty (R(2) range 0.21-0.44).HF ERR, not the number of cases, was related to penalty magnitude. These findings have implications for the design of hospital-based quality initiatives regarding readmissions.

Precision medicine, or personalized medicine, refers to the tailoring of therapy to the individual characteristics of patients. It can be applicable to patients with advanced disease and to preventative interventions as well. The impetus for this approach came from sequencing of the human genome and the anticipation that an individual’s sequence would inform treatment, aided perhaps by Big Data algorithms. In heart failure, advances in omics have occurred alongside other disciplines but from a practical standpoint, our ability to provide precision medicine remains more or less in the neutral position. In this article, we maintain that despite significant limitations on our ability to use genotyping or Big Data to impact real-world heart failure care in real time, we are in fact practicing a significant degree of precision medicine and can continue to do more of the same with relatively modest changes in approach to practice. The advent of angiotensin-converting enzyme inhibitors and β-blockers impacted heart failure therapeutics1,2 in a truly revolutionary way. They are recommended across all New York Heart Association classes for the management of patients with heart failure with reduced ejection fraction (EF).3 Although β-blockers have not been critically examined in patients with class I symptoms, we accept the notion that for these 2 classes of drugs, one size truly does fit all. We argue about dose, not whether we should use the drugs.4,5 We can also debate the duration of treatment in patients who have normalized their EF and the likelihood of recurrence of heart failure if those medications are stopped. Fundamentally, the importance of blockade of the renin–angiotensin system and adrenergic stimulation are fully accepted concepts that apply in young and old, symptomatic and asymptomatic, borderline low and very low EF, left ventricular failure and biventricular failure, in the …