Background: Sepsis survivors are at risk of developing myocardial infarction and heart failure. It remains unclear whether coronary artery disease (CAD) is a major contributor to the development of these complications. This study sought to characterize the burden and distribution of significant CAD in sepsis survivors. Methods: Sepsis survivors who underwent computed tomography coronary angiography (CTCA) or invasive coronary angiography (ICA) in a UK tertiary cardiac center for suspected ischemic heart disease were retrospectively studied. Results: Of the 30 sepsis survivors (age 57 ± 12 years; 50% males), 21 patients underwent CTCA and 9 patients underwent ICA a median 39 days [IQR 12–152] from the sepsis episode. Eight patients (~27%) had angiographically significant CAD (n = 6 severe [>70%] stenosis; n = 2 moderate [50–70%] stenosis). The CT coronary calcium score was higher in patients with significant CAD compared to patients without significant CAD (638 [368–1015] vs. 4 [1–72]; p < 0.001). Of the 8 patients with significant CAD, 3 patients had LV systolic dysfunction (38%) on echocardiography and 8/21 (38%) patients without significant CAD had LV systolic dysfunction (p = 1.00). Long-term adverse complications (all-cause mortality and/or heart failure hospitalization) occurred 3/8 (38%) patients with significant CAD and 4/22 (18%) patients without significant CAD (p = 0.345). Conclusions: A minority of sepsis survivors have significant CAD. The presence of significant CAD cannot fully explain the occurrence of post-sepsis LV systolic dysfunction and adverse outcomes. The ischemic and non-ischemic mechanisms underlying post-sepsis cardiovascular disease require further investigation.

Background: Post-sepsis cardiomyopathy is associated with an increased risk of adverse cardiovascular outcomes. It remains poorly understood, which limits therapeutic development. This study characterised post-sepsis cardiomyopathy using cardiovascular magnetic resonance (CMR) imaging. Methods: Patients admitted with acute sepsis and suspected cardiac injury or heart failure who subsequently (47 days [IQR: 22–122]) underwent CMR at a UK tertiary cardiac centre were included. Age- and gender-matched controls (n = 16) were also included. Subjects underwent CMR at 1.5 Tesla with cines, native T1- and T2-mapping, and late gadolinium enhancement (LGE) imaging. Results: Of the 22 post-sepsis patients (age 50 ± 13 years; 64% males), 13 patients (59%) had left ventricular (LV) dilatation. Patients had significantly elevated left ventricular (LV) end-diastolic and end-systolic volume indices compared to controls (p = 0.011 and p = 0.013, respectively). Eleven patients (50%) had LV systolic dysfunction (ejection fraction < 50%), most of whom (8/11) had non-ischaemic patterns of LGE (n = 7 mid-wall; n = 1 mid-wall/patchy). In the eleven patients with preserved LV systolic function (ejection fraction ≥ 50%), three patients (27%) had significant LGE (n = 1 mid-wall; n = 1 subepicardial/mid-wall; n = 1 patchy). Compared to controls, patients had elevated septal native myocardial T1 values (p < 0.001) but similar septal native myocardial T2 values (p = 0.090), suggesting the presence of myocardial fibrosis without significant oedema. Conclusions: Post-sepsis cardiomyopathy is characterised by LV dilatation, systolic dysfunction, and myocardial fibrosis in a non-ischaemic distribution. Significant myocardial oedema is not prominent several weeks post-recovery. Further work is needed to test these findings on a multi-centre basis and to develop novel therapies for post-sepsis cardiomyopathy.

Cardiac sarcoidosis (CS) and inherited cardiomyopathies (inherited CM) are associated with advanced heart failure, cardiac conduction defects, ventricular arrhythmias and sudden cardiac death. Both conditions can have similar clinical presentations. Differentiating between the two disease cohorts is important in delivering specific management to patients, such as immunosuppressive therapy for CS patients and genetic screening for inherited CM. In this review, we examined the existing evidence on the overlap between CS and common inherited CM, such as hypertrophic cardiomyopathy, arrhythmogenic cardiomyopathy, restrictive cardiomyopathy and dilated cardiomyopathy. In patients where both CS and inherited CM were implicated, CS tended to be diagnosed much later, often when patients presented with complications warranting a workup or cardiac histological confirmation. CS can masquerade as an inherited CM, leading to delays in the instigation of CS therapy. Confirmed dual pathology overlap between inherited CM and CS is rarer. Advanced cardiac imaging, such as cardiovascular magnetic resonance, plays an important role in the clinical workup of both CS and inherited CM. However, findings on cardiac imaging alone often cannot differentiate between the two conditions. Definitive differentiation between CS and inherited CM requires both clinical experience and, at times, a myocardial biopsy.

Background: Over the last two decades, inherited cardiac conditions (ICC) centres have emerged with the aim of improving outcomes for patients and their families, through early diagnosis, genetic testing, risk assessment and specialist treatment. Sources of data: A literature search was performed using PubMed (https://pubmed.ncbi.nlm.nih.gov/). Commissioned ICC service reviews from NHS England, NHS Improvement and PHG Foundation were evaluated. Areas of agreement: ICC patient management requires a multi-disciplinary approach. ICC services are predominantly based within tertiary centres. Despite expansion, provision of care remains inadequate to meet rising demands. Access to services is inconsistent, partly due to geographic variation and lack of standardized pathways. Areas of controversy: The optimal ICC care model remains undecided, although there is growing interest in ‘hub-and-spoke’ networks, which could aid secondary and tertiary service integration and repatriation of care. Growing points: Genetic mainstreaming is a priority for the Genomic Medicine Service Alliance. The benefits of telehealth and virtual clinics have been validated by their use during the COVID-19 pandemic. Other innovations to improve resource efficiency, such as clinical scientist–led and nurse-led clinics, show promise. Areas timely for developing research: An update for the NHS ICC service specifications is planned that appears well timed given the rapid evolution of the ICC landscape in the decade since last review. This has the potential to address needs including national audit, standardized pathways and ICC networks to improve governance and equity of care. Delegation of commissioning for specialist services to integrated care systems may also provide opportunity for increased regional direction.

Background: Sepsis survivors can develop left ventricular systolic dysfunction (LVSD) and heart failure. These patients are often treated with guideline-directed medical therapy (GDMT) known to be effective in patients with non-sepsis-related heart failure. This study sought to assess the use of GDMT on sepsis survivors with LVSD. Methods: Sepsis survivors with suspected myocardial injury and/or heart failure diagnosed with LVSD in a UK cardiac centre were retrospectively studied. Clinical and transthoracic echocardiography (TTE) data were recorded and analysed. Results: Of the 25 sepsis survivors (age 56 ± 11 years; 52% males), 11 (44%) had LVSD (LVEF < 50%). LV end-diastolic internal diameter (LVIDd) was similar between patients with vs. without LVSD (5.2 ± 0.8 cm vs. 4.7 ± 0.8 cm; p = 0.214). Patients with LVSD had significantly greater LV end-systolic internal diameter (LVIDs) than those without LVSD (4.0 ± 1.2 cm vs. 2.8 ± 0.6 cm; p = 0.027). Tricuspid annular plane systolic excursion (TAPSE) was similar between the two groups (2.1 ± 0.5 cm vs. 2.2 ± 0.6 cm; p = 0.910). Of the 11 patients with LVSD, nine patients underwent repeat TTE scans after 6 months [IQR 3–9], most of whom were taking GDMT. The majority (8/9) of these patients demonstrated LV systolic functional recovery (>5% LVEF increase; mean LVEF improvement 16 ± 11%) after GDMT. Reductions were seen in LVIDd (5.3 ± 0.8 cm to 5.0 ± 0.7 cm) and LVIDs (4.1 ± 1.2 cm to 3.7 ± 0.8 cm) after GDMT, though these changes did not reach statistical significance (both p > 0.05). Conclusions: GDMT appears beneficial in sepsis survivors with LV dysfunction. This finding should be validated on a larger and multi-centre basis to further affirm the value of medical therapy in post-sepsis heart failure.