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Sixty years ago, hypertrophic cardiomyopathy (HCM) was considered a rare lethal disease that affected predominantly young adults and for which there were few treatment options. Today, it is recognised to be a relatively common disorder that presents throughout the life course with a heterogeneous clinical phenotype that can be managed effectively in the majority of individuals. A greater awareness of the condition and less reluctance from healthcare practitioners to make the diagnosis, coupled with improvements in cardiac imaging, including greater use of artificial intelligence and improved yields from screening efforts, have all helped facilitate a more precise and timely diagnosis. This enhanced ability to diagnose HCM early is being paired with innovations in treatment, which means that the majority of patients receiving a contemporary diagnosis of HCM can anticipate a normal life expectancy and expect to maintain a good functional status and quality of life. Indeed, with increasing translation of molecular genetics from bench to bedside associated with a growing number of randomised clinical trials of novel therapies aimed at ameliorating or perhaps even preventing the disease, the next chapter in the story for HCM will provide much excitement and more importantly, offer much anticipated reward for our patients. [ABSTRACT FROM AUTHOR]

End stage renal disease is associated with a very high risk of premature cardiovascular death and morbidity. Early stage chronic kidney disease (CKD) is also associated with an increased frequency of cardiovascular events and is a common but poorly recognised and undertreated risk factor. Cardiovascular disease in CKD can be attributed to two distinct but overlapping pathological processes, namely atherosclerosis and arteriosclerosis. While the risk of athero-thrombotic events such as myocardial infarction is elevated, arteriosclerosis is the predominant pathophysiological process involving fibrosis and thickening of the medial arterial layer. This results in increased arterial stiffness causing left ventricular hypertrophy and fibrosis and the exposure of vulnerable vascular beds such as the brain and kidney to high pressure fluctuations causing small vessel disease. These pathophysiological features are manifest by a high risk of lethal arrhythmia, congestive heart failure, myocardial infarction and stroke. Recent work has highlighted the importance of aldosterone and disordered bone mineral metabolism. [ABSTRACT FROM AUTHOR]

Objective To explore the relationship between serum phosphate, arterial stiffness and left ventricular mass (LVM) in patients with early-stage chronic kidney disease (CKD). Design A cross-sectional observational study. Setting Single centre. Patients 208 patients with stage 2 to stage 4 non-diabetic CKD. Interventions Arterial stiffness was determined through measurement of aortic pulse wave velocity (PWV). Cardiac magnetic resonance was used to determine LVM. Main outcome measure Relationship between serum phosphate, aortic PWV and LVM. Results Mean age was 54±13 years, mean glomerular filtration rate was 50±15 ml/min/1.73 m², mean serum phosphate was 1.11±0.21 mmol/l and mean PWV was 8.6±2.1 m/s. When the cohort was divided into quartiles according to serum phosphate, LVM increased across quartiles (p=0.04), with no significant differences in age, kidney function, blood pressure or PWV. Serum phosphate correlated with LVM (r=0.173; p=0.01), but PWV did not (p=0.2). In a regression model containing gender, serum phosphate, office systolic blood pressure, albumin/creatinine ratio and haemoglobin, 30% of the variation in LVM was explained (p<0.0005), with serum phosphate accounting for 5% of the variance. Conclusion Serum phosphate is independently associated with LVM in patients with CKD. Interventional studies are required to determine whether this association is causative and whether reducing phosphate exposure reduces LVM in this population. [ABSTRACT FROM AUTHOR]

Several letters to the editor are presented in response to articles in previous issues such as the understanding of the long term consequences of living kidney donation and the increased risk of cardiovascular disease compared with matched non-donors in the general population.