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There are several markers of poor prognosis in heart failure (HF). The most established markers of poor prognosis in HF include neurohormonal (NH) imbalance, low ejection fraction (EF), ventricular arrhythmias, intraventricular conduction delays, low functional capacity, low SBP, and renal failure. The relative importance of these factors is unknown, as they have never been studied together. We present a 74-year-old female with nonischemic cardiomyopathy and an EF<20% who over 24 years since diagnosis, never developed clinical or hemodynamic congestion, was never hospitalized for HF, and never required a loop diuretic. She had all of the clinical indicators of poor prognosis in HF except for severe NH imbalance and renal failure, illustrating their importance in HF prognosis. While NH activation in HF is initially an adaptive mechanism, an imbalance of NH effectors causes congestion leading to a vicious cycle of congestion, renal dysfunction, and worsening of HF. The combination of NH activation and renal failure in HF is a vasomotor nephropathy known as the cardiorenal syndrome (CRS) and portends a poor prognosis. Pharmacological disruption of NH pathways early in HF may prevent CRS and, therefore, improve outcomes.

(1) Cardiology input using ACC/ECC guidelines and a brief interview at admission safely reduced total admissions primarily by identifying low risk chest pain admissions inappropriate for inpatient telemetry monitoring. (2) Life threatening arrhythmias occurring in patients admitted to telemetry are rare.

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Background Azathioprine (AZA) is a recognised treatment option for maintaining remission in IBD patients. Myelotoxicity and abnormal liver function tests may present at any stage of therapy, therefore ECCO advises practitioners to check full blood count, liver and kidney function tests at 3-monthly intervals for patients established on therapy. During the COVID-19 pandemic, UK guidance suggested reducing blood test monitoring to a minimum safe frequency to facilitate ‘shielding’ of vulnerable patient groups. Patients established on treatment at St Mark’s Hospital for more than 12 months, on stable doses were deemed eligible for extended blood monitoring intervals of 6-monthly. The aim of this audit was to assess the impact of this extension on patient safety, by measuring outcomes against locally agreed standards. Methods All patients on AZA were identified using the pharmacy dispensing system and patient information software for blood test results, clinic letters and notes. Outcomes for patients who had extended blood monitoring were collected retrospectively including monitoring calls to the IBD advice line and any hospital admissions associated with therapy. Subsequent blood test results were also captured. Results A total of 92 patient records were identified and analysed. Table 1 shows the achieved compliance (%) to the audit standards compared to the target compliance (%). 54% of patients (n=50) received medication that lasted beyond the standard 12-week validity of a blood test, i.e. had extended blood monitoring. Of those 50 patients, 43 were eligible for extended blood monitoring (86%). From 50 patients with extended blood monitoring, one patient had elevated alanine aminotransferase levels which improved after a one-week treatment break. Another patient called the IBD advice line reporting nausea and abdominal cramps due to treatment and was advised to split the dose and monitor for side effects. No patients were admitted to emergency care or hospital due to deranged blood test results or adverse effects from their medication. Conclusion Overall the findings suggest that the temporary relaxation of blood monitoring did not adversely affect patient safety. For more comprehensive results, it would be prudent to repeat the audit using a larger sample size; however the audit has established a baseline at a time of unprecedented changes in the workplace, which will be useful in guiding future practice.

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