Clinical articles

Physiological adaptation to exercise results in a series of electrical, structural, and functional cardiac changes, broadly named ‘athlete’s heart’. Symmetrical enlargement of all cardiac chambers and mild increase in wall thickness are common findings in highly trained athletes. Typical electrocardiogram (ECG) features include sinus bradycardia, first-degree atrioventricular (AV) block, isolated voltage criteria for right and left ventricular hypertrophy and early repolarisation. Cardiac remodelling may be marked in some athletes, and it may be challenging to distinguish physiological adaptation from cardiac conditions at risk of sudden cardiac death (SCD), such as cardiomyopathies. Differential diagnosis often requires a comprehensive assessment starting from a detailed personal and family history to baseline tests, such as ECG and echocardiogram. In some cases, second-line tests, such as prolonged ambulatory ECG monitoring, exercise tolerance test and cardiovascular magnetic resonance are required.

In this narrative review, we will explore the key features of physiological cardiac adaptation to exercise, and we will focus on differential diagnosis between ‘athlete’s heart’ and cardiomyopathies.

Sickle cell disease (SCD) is an inherited haematologic disorder with cardiac-related complications. Cardiac magnetic resonance (CMR) imaging allows us to assess the cardiac morphology and function of this population. Our aim was to better characterise phenotypic variations among SCD patients utilising CMR data.

This retrospective study included 72 patients with SCD who underwent CMR between May 2013 and July 2023. We recorded baseline characteristics, medical history, and indication and setting of CMR. CMR parameters relating to morphology and function were collected. Patients were placed into the following groups based on cardiac parameters on CMR: high output, pulmonary hypertension (PH; defined by mean pulmonary artery pressure >20 mmHg on right heart catheterisation or elevated tricuspid regurgitation velocity >3.4 m/s on echocardiogram), left ventricular (LV) dysfunction, or normal size and function. Between- and within-group comparisons were performed.

Demographic data were similar among groups. The PH group was more likely to have a history of smoking, chronic hypoxia, lower baseline haemoglobin, and need for blood transfusion (p<0.05 for all). There were significant between-group differences in CMR structural and function parameters.

In conclusion, sickle cell patients present with different cardiac phenotypes. Patients with PH are associated with significantly higher morbidities.

Low-density lipoprotein-cholesterol (LDL-C) is accepted as a causal risk factor for development of atherosclerotic cardiovascular disease (CVD) and acute coronary syndromes (ACS). In individuals aged 40–75 years, reducing LDL-C constitutes a main treatment target for prevention of atherosclerotic CVD in all international guidelines. Furthermore, diabetes mellitus (DM) confers a two-fold excess risk of vascular outcomes (coronary heart disease, ischaemic stroke, and vascular deaths), independent of other risk factors. Our audit project identified a deficit in current standards following an audit of adherence to lipid profile and glycated haemoglobin (HbA1c) testing in the high-risk chest pain population in our city hospital setting. We found only 49% of patients had LDL-C checked during their inpatient stay, and only 45% had HbA1c checked, of our targeted 100% of patients. This allowed the introduction of a planned intervention to improve admission testing and re-auditing demonstrated an improvement in testing, mainly driven by improved LDL-C testing. Despite this, a deficit still exists and more work is needed to meet our target of 100% compliance.

A 32-year-old man presented to the emergency department with shortness of breath and altered mental status. He reported a two-day history of epigastric pain, nausea, and vomiting. His past medical and family history were unremarkable. He was haemodynamically unstable, and his initial electrocardiogram (ECG) revealed a Brugada type 1 ECG pattern. The initial diagnostic assessment revealed significant metabolic derangements consistent with diabetic ketoacidosis, accompanied by hyperkalaemia. Notably, the prompt and effective management of hyperkalaemia resolved the Brugada type 1 ECG pattern, confirming the diagnosis of Brugada phenocopy.

Cardiac rehabilitation (ExCR) is an essential, evidence-based part of the management of people with chronic heart failure (CHF), but research indicates it is underused. This retrospective audit explores the eligibility of heart failure inpatients for ExCR, according to the European Society of Cardiology (ESC) consensus statement, and the impact of frailty on referral rates.

The first 100 patients admitted with a diagnosis of CHF from 1 February 2020 within one hospital trust were included in the audit. Only 54% of patients were eligible for ExCR at discharge and, of them, 43% were referred. Most patients (69%) admitted to cardiology wards were eligible for ExCR compared with 14% of those admitted to non-specialist care. Frail patients were less likely to be admitted to cardiology wards (43%) than their non-frail counterparts (93%).

Not all patients admitted to hospital with heart failure are eligible for ExCR, and assessing eligibility is important in identifying the true referral rate to allow national benchmarking. Interventions to improve referral are still important, but focus also needs to be directed to developing interventions for those individuals currently not eligible for standard ExCR programmes.

Myocardial fibrosis is a common pathological process associated with various cardiovascular diseases, contributing to adverse cardiac remodelling and increased morbidity. Angiotensin-converting enzyme inhibitors (ACEi) have been widely used for myocardial protection in high-risk patients. However, there are no clear recommendations for their use for the prevention of fibrosis after myocardial injury. On the other hand, procollagen type III amino-terminal propeptide (PIIIP) and procollagen type I propeptide (PIP) have been identified as effective biomarkers for predicting fibrotic change in the myocardium. It is important to evaluate the effects of ACEi by PIIIP and PIP levels to provide insights into the potential antifibrotic effects of ACEi.

We assessed the effects of ACEi on the process of fibrosis in the myocardium through serum levels of PIIIP and PIP. Four databases were searched to identify relevant studies investigating the association between the use of ACEi and myocardial fibrosis marked by PIIIP and PIP levels. Animal and non-original research articles were excluded.

Six studies with a total of 706 participants met the inclusion criteria. Three studies assessed the change of PIIIP and PIP levels in patients with hypertension, while the other three were in patients with heart failure, myocardial infarction and congenital heart diseases. The included studies demonstrated a significant reduction in PIIIP and PIP serum levels with ACEi therapy (p<0.05), except in patients with post-myocardial infarction. The mean reduction in serum PIIIP levels in all patients treated by ACEi was 20.8%.

These results suggest that ACEi can effectively inhibit collagen synthesis and deposition in the myocardium, potentially preventing, or even reversing, the progression of myocardial fibrosis. This supports the idea that ACEi have potent antifibrotic effects and can contribute to improved clinical outcomes in cardiac conditions that are not currently indicated, including myocarditis.

This case report describes a young man in his early thirties with insulin-dependent diabetes mellitus and ulcerative colitis, who developed acute myocardial infarction (AMI) during an acute flare-up of ulcerative colitis. The case highlights the diagnostic and therapeutic challenges involved in managing AMI in patients with systemic inflammatory diseases and metabolic conditions. The patient was successfully treated with a combination of thrombectomy and a drug-eluting balloon procedure for coronary occlusion, along with pharmacotherapy consisting of intravenous steroids, intravenous glycoprotein IIb/IIIa inhibitor and the involvement of a multi-disciplinary team of cardiologists and gastroenterology specialists. This case underscores the need for an integrated care approach, aggressive cardiovascular risk management, and interdisciplinary collaboration to optimise outcomes in complex clinical scenarios where systemic inflammation intersects with cardiovascular events.

Severe mitral regurgitation (MR), when complicated by a co-existing lung abscess, is a management challenge, as both conventional cardiac and thoracic surgical interventions may be contraindicated. In the case described below, transcatheter edge-to-edge mitral valve repair (TEER) was utilised to achieve haemodynamic stability, permitting subsequent thoracic surgical lung abscess resection.

We report the case of a 60-year-old man with torrential MR secondary to chordal rupture presenting with recurrent pulmonary oedema, complicated by lung sepsis and abscess formation resistant to antibiotic therapy and precluding open valvular repair. The presence of a lung abscess contraindicated open mitral valve repair, and the severity of MR precluded thoracic surgical treatment of the lung abscess, precluding any form of surgical intervention.

A successful TEER procedure resulted in a reduction of MR from severe to no more than mild-to-moderate, enabling haemodynamic stabilisation and permitting subsequent thoracic surgical treatment of the lung abscess.

Our case demonstrates the possibility of treating severe MR with TEER in the presence of a lung sepsis and abscess, when both conventional cardiac and thoracic surgical interventions were considered contraindicated. This later enabled thoracic surgery and treatment of the lung abscess.

A 79-year-old woman presents to the hospital with dyspnoea, fever, and hypotension, and is diagnosed with community-acquired pneumonia and septic shock. Resuscitation is initiated with fluids and vasopressors, and a central venous catheter is placed. However, during the procedure, the guide experiences resistance and cannot be removed, becoming trapped. This is confirmed with tomography and reconstruction, demonstrating intravascular position. The patient is then sent to interventional cardiology for extraction, which is successfully performed using the EN Snare (Merit Medical). The significance of this case lies in the complications of not guiding procedures with ultrasound and how to resolve them, such as the guide being trapped in this patient.

Sudden cardiac death (SCD) is a devastating and tragic occurrence that may affect individuals of all ages. It is defined as an unexpected death occurring within one hour of the onset of symptoms, if witnessed, or within 24 hours of last being seen alive and well, if unwitnessed. Athletes are considered to be the healthiest of all the population, and exercise is known to reduce the risk of atherosclerotic coronary artery disease. However, both amateur and highly trained athletes do die suddenly and unexpectedly, and this gets widespread media attention as it is so shocking and unexpected. This brings SCD, its frequency and causes into the spotlight. This review focuses on the epidemiology and aetiology of SCD in athletes from a pathological perspective.