The incidence and prevalence of atrial fibrillation (AF) are projected to increase significantly worldwide, imposing a significant burden on healthcare resources. The disease itself is extremely heterogeneous in its epidemiology, pathophysiology, and treatment options based on individual patient characteristics. Whilst ageing is well recognised to be an independent risk factor for the development of AF, this condition also affects the young in whom the condition is frequently symptomatic and troublesome. Traditional thinking suggests that the causal factors and pathogenesis of the condition in the young with structurally normal atria but electrophysiological “triggers” in the form of pulmonary vein ectopics leading to lone AF are in stark contrast to that in the elderly who have AF primarily due to an abnormal substrate consisting of fibrosed and dilated atria acting in concert with the pulmonary vein triggers. However, there can be exceptions to this rule as there is increasing evidence of structural and electrophysiological abnormalities in the atrial substrate in young patients with “lone AF,” as well as elderly patients who present with idiopathic AF. These reports seem to be blurring the distinction in the pathophysiology of so-called idiopathic lone AF in the young versus that in the elderly. Moreover with availability of improved and modern investigational and diagnostic techniques, novel causes of AF are being reported thereby seemingly consigning the diagnosis of “lone AF” to a rather mythical existence. We shall also elucidate in this paper the differences seen in the epidemiology, causes, pathogenesis, and clinical features of AF in the young versus that seen in the elderly, thereby requiring clearly defined management strategies to tackle this arrhythmia and its associated consequences.

Atrial fibrillation (AF) continues to impose a significant burden upon healthcare resources. A sustained increase in the ageing population and better survival from conditions such as ischaemic heart disease have ensured that both the incidence and prevalence of AF continue to increase significantly. AF can lead to complications such as embolism and heart failure and these acting in concert with its associated co-morbidities portend increased mortality risk. Whilst some studies suggest that the mortality risk from AF is due to the “bad company it keeps” i.e. the associated co-morbidities rather than AF itself; undoubtedly some of the mortality is also due to the side-effects of various therapeutic strategies (anti-arrhythmic drugs, bleeding side-effects due to anti-coagulants or invasive procedures). Despite several treatment advances including newer anti-arrhythmic drugs and developments in catheter ablation, anti-coagulation remains the only effective means to reduce the mortality due to AF. Warfarin has been used as the oral anticoagulant in the treatment of AF for many years but suffers from disadvantages such as unpredictable INR levels, bleeding risks and need for haematological monitoring. This has therefore spurred a renewed interest in research and clinical studies directed towards developing safer and more efficacious anti-coagulants. We shall review in this article the epidemiological features of AF-related mortality from several studies as well as the cardiovascular and non-cardiac mortality mechanisms. We shall also elucidate why a rhythm control strategy has appeared to be counter-productive and attempt to predict the likely future impact of novel anti-coagulants upon mortality reduction in AF.

Hypertrophic cardiomyopathy (HCM) is the most common genetic cause of cardiomyopathy worldwide. Significant advances and widespread availability of genetic testing have improved detection of the sarcomeric mutations that cause HCM, but have also highlighted the significance of inborn errors of metabolism (IEM) or metabolic storage disorders that can mimic HCM (‘HCM phenocopies’). These conditions cannot always be reliably differentiated on the basis of imaging alone. Whilst HCM phenocopies are relatively rare, it is crucial to distinguish these conditions at an early stage as their natural history, management and prognosis vary significantly from that of HCM with sarcomeric mutations. This review illustrates the salient features of HCM phenocopies and stresses the need for a high level of suspicion for these conditions in the assessment of cardiac hypertrophy.

The purpose of this review is to describe the present evidence for exercise and nutritional interventions as potential contributors in the treatment of sarcopenia and frailty (i.e. muscle mass and physical function decline) and the risk of cardiorenal metabolic comorbidity in people with heart failure (HF). Evidence primarily from cross-sectional studies suggests that the prevalence of sarcopenia in people with HF is 37% for men and 33% for women, which contributes to cardiac cachexia, frailty, lower quality of life, and increased mortality rate. We explored the impact of resistance and aerobic exercise, and nutrition on measures of sarcopenia and frailty, and quality of life following the assessment of 35 systematic reviews and meta-analyses. The majority of clinical trials have focused on resistance, aerobic, and concurrent exercise to counteract the progressive loss of muscle mass and strength in people with HF, while promising effects have also been shown via utilization of vitamin D and iron supplementation by reducing tumour necrosis factor-alpha (TNF-a), c-reactive protein (CRP), and interleukin-6 (IL-6) levels. Experimental studies combining the concomitant effect of exercise and nutrition on measures of sarcopenia and frailty in people with HF are scarce. There is a pressing need for further research and well-designed clinical trials incorporating the anabolic and anti-catabolic effects of concurrent exercise and nutrition strategies in people with HF.

Aims The coronavirus disease 2019 (COVID‐19) pandemic has created significant challenges to healthcare globally, necessitating rapid restructuring of service provision. This questionnaire survey was conducted amongst adult heart failure (HF) patients in the United Kingdom (UK), to understand the impact of COVID‐19 upon HF services. Methods and results The survey was conducted by the Pumping Marvellous Foundation, a UK HF patient charity. ‘Survey Monkey’ was used to disseminate the questionnaire in the Pumping Marvellous Foundation 's online patient group and in 10 UK hospitals (outpatient hospital and community HF clinics). There were 1050 responses collected (693/1050—66% women); 55% (579/1050) were aged over 60 years. Anxiety level was significantly higher regarding COVID‐19 (mean 7 ± 2.5 on anxiety scale of 0 to 10) compared with anxiety regarding HF (6.1 ± 2.4; P < 0.001). Anxiety was higher amongst patients aged ≤60 years about HF (6.3 ± 2.2 vs. 5.9 ± 2.5 in those aged >60 years; P = 0.005) and COVID‐19 (7.3 ± 2.3 vs. 6.7 ± 2.6 those aged >60 years; P < 0.001). Sixty‐five per cent of respondents (686/1050) reported disruption to HF appointments (cancellation or postponement) during the lockdown period. Thirty‐seven per cent reported disruption to medication prescription services, and Thirty‐four per cent reported inability to access their HF teams promptly. Thirty‐two per cent expressed reluctance to attend hospital (25% stated they would only attend hospital if there was no alternative, and 7% stated that they would not attend hospital at all). Conclusions The COVID‐19 pandemic has caused significant anxiety amongst HF patients regarding COVID‐19 and HF. Cancellation or postponement of scheduled clinic appointments, investigations, procedures, prescription, and monitoring services were implicated as sources of anxiety.

Key points: For the heart to function as a pump, intracellular calcium concentration ([Ca²⁺]_i) must increase during systole to activate contraction and then fall, during diastole, to allow the myofilaments to relax and the heart to refill with blood. The present study investigates the control of diastolic [Ca²⁺]_i in rat ventricular myocytes. We show that diastolic [Ca²⁺]_i is increased by manoeuvres that decrease sarcoplasmic reticulum function. This is accompanied by a decrease of systolic [Ca²⁺]_i such that the time‐averaged [Ca²⁺]_i remains constant. We report that diastolic [Ca²⁺]_i is controlled by the balance between Ca²⁺ entry and Ca²⁺ efflux during systole. The results of the present study identify a novel mechanism by which changes of the amplitude of the systolic Ca transient control diastolic [Ca²⁺]_i. The intracellular Ca concentration ([Ca²⁺]_i) must be sufficently low in diastole so that the ventricle is relaxed and can refill with blood. Interference with this will impair relaxation. The factors responsible for regulation of diastolic [Ca²⁺]_i, in particular the relative roles of the sarcoplasmic reticulum (SR) and surface membrane, are unclear. We investigated the effects on diastolic [Ca²⁺]_i that result from the changes of Ca cycling known to occur in heart failure. Experiments were performed using Fluo‐3 in voltage clamped rat ventricular myocytes. Increasing stimulation frequency increased diastolic [Ca²⁺]_i. This increase of [Ca²⁺]_i was larger when SR function was impaired either by making the ryanodine receptor leaky (with caffeine or ryanodine) or by decreasing sarco/endoplasmic reticulum Ca‐ATPase activity with thapsigargin. The increase of diastolic [Ca²⁺]_i produced by interfering with the SR was accompanied by a decrease of the amplitude of the systolic Ca transient, such that there was no change of time‐averaged [Ca²⁺]_i. Time‐averaged [Ca²⁺]_i was increased by β‐adrenergic stimulation with isoprenaline and increased in a saturating manner with increased stimulation frequency; average [Ca²⁺]_i was a linear function of Ca entry per unit time. Diastolic and time‐averaged [Ca²⁺]_i were decreased by decreasing the L‐type Ca current (with 50 μm cadmium chloride). We conclude that diastolic [Ca²⁺]_i is controlled by the balance between Ca entry and efflux during systole. Furthermore, manoeuvres that decrease the amplitude of the Ca transient (without decreasing Ca influx) will therefore increase diastolic [Ca²⁺]_i. This identifies a novel mechanism by which changes of the amplitude of the systolic Ca transient control diastolic [Ca²⁺]_i.