Editorial articles

Over the last few decades there has been a steady increase in life-expectancy leading to an increase in the ageing population, placing significant demands on health and social care.¹ Among the several healthcare issues that confront older people, frailty has emerged as an important entity, and tackling frailty has assumed greater significance.² There is currently no single agreed definition of frailty, but it is widely accepted as a condition characterised by reduced response to stressors consequent to decline in multiple physiological systems associated with ageing. Prevalence of frailty in community-dwelling older adults is estimated to be around 10–14%, but figures between 4% and 49% have been quoted in various populations.^3,4 Prevalence also varies with age, with around 7% in adults over 65 years, increasing up to 25% in those aged 80 years and above.⁵ There are a number of tools to detect frailty, and the most commonly used tool is the criteria proposed by Fried and colleagues based on data from the Cardiovascular Health Study, which assesses five domains, namely weight loss (≥5% weight loss in the past year), exhaustion (effort required for activities), slow walking speed (>6–7 s per 15 feet), weakness as measured by grip strength and decreased physical activity (kilocalories/week: male <383, female <270), with the presence of three or more of these fulfilling the criteria for frailty.⁵

The paradigm for glucose control in type 2 diabetes has been based on historic and landmark studies demonstrating the unquestionable microvascular benefits of good glycaemic control.^1-3 However, whether better control improves survival and prevents cardiovascular events has been less consistently shown, with one notable study, ACCORD (Action to Control Cardiovascular Risk in Type 2 Diabetes), showing an increased risk of cardiovascular death with tight control.² Over the past few years, a number of randomised, placebo-controlled, cardiovascular outcome trials (CVOTs) testing novel glucose-lowering agents have demonstrated beneficial effects on mortality and cardiovascular events. This has prompted a change in emphasis away from solely targeting glycaemic control in diabetes, and focusing on reducing cardiovascular events and improving survival.

Twitter is a web-based micro-blogging service in which messages called ‘Tweets’, which may include visual media, are shared with followers of the account. Benefits include continuing education, networking and personal branding. This article examines the current use of Twitter among UK-based cardiologists, and General Medical Council guidance on social media interaction.

UK cardiologists using Twitter were identified by reviewing the Twitter accounts followed by the British Cardiovascular Society using an analysis programme (Twitonomy). An iterative process of tracing accounts followed by UK cardiologists was then undertaken. The last 20 Tweets of the 10 UK cardiologists most followed by other cardiologists were then reviewed for content.

There were 301 UK cardiologists identified. The most common location was London, the sub-specialty intervention, and the majority were consultants. Most had tweeted within the past month, and over 100 times. Content analysis of Tweets revealed 64% were cardiology-related, and 80% related to cardiology/medicine/science.

In conclusion, Twitter has been adopted by a relatively small group of UK cardiologists, but evidence suggests that those who have find it useful. While professionalism and patient confidentiality remain valid concerns, Twitter should be promoted as a location-independent, time-efficient way to network, and keep pace with current research and practice.

Congenital heart disease (CHD) is the most common congenital anomaly, with an estimated prevalence of eight per 1,000 births.¹ However, reliable data on long-term survival for this heterogeneous group of patients are still lacking. Previous population-based studies from the US reported age-standardised mortality rates secondary to CHD of 1.2 per 100,000.² Mortality was highest during infancy (48.1% of all deaths occurred under the age of one year), however, the majority of the remaining deaths occurred outside of childhood, following transition to adult care. Yet, while it is accepted that individuals with CHD may have a higher mortality compared with the general population, the wide spectrum of disease means interpretation of population-based mortality rates for individual lesions is difficult. Additionally, a significant number of studies report only on short-term follow-up, meaning that long-term outcomes are unknown. A previous systematic review reported pooled survival estimates for common CHD lesions, however, it only included studies from hospital-based cohorts with survival estimates calculated from the time of surgical repair.³ It, therefore, does not account for those patients who do not need surgical intervention and may not be representative of all patients with CHD. Knowing the expected mortality rates for CHD is not only important for family counselling, but also in service planning.

On 23 June 2016, the UK public took to the polls and voted to leave the European Union (EU). Since that vote, everyone – from the farming community to the financial sector – has been trying to digest the result and understand what it might mean for them. The science community has been no exception, and with good reason. Scientific research is widely acknowledged as an international endeavour and, until now, EU membership has played a role in this. Science is also a real UK strength – UK institutions, when compared internationally, are ranked second in the world for the quality of their research,¹ and the UK has one of the largest drug development pipelines globally – making it all the more important that we secure a positive future for UK science post-Brexit.

In September last year, the Scottish Cardiac Society (SCS) celebrated its 25th anniversary with a two-day symposium held in Crieff – the same venue where the inaugural meeting took place in 1992.

Physicians use tests to inform decision-making. Whether this is a bedside test using a stethoscope, the seemingly ancient technology of recording an electrocardiogram (ECG), or the most advanced imaging modalities and biochemical panels available – all pursue diagnostic clarity. But, more frequently than we might like to admit, the results do not illuminate a clear path of treatment.

We believe that controlled systemic hypertension should be considered as an important clinical entity (figure 1). We know that cardiovascular risks increase with rising blood pressure, each 2 mmHg increase in systolic blood pressure is associated with a 7% and 10% rise in mortality from ischaemic heart disease and stroke, respectively.¹ However, the converse proposition would also seem to be true. Meta-analyses have found significant reductions in stroke and coronary events associated with blood pressure control,² even in grade 1 hypertension. Furthermore, large studies such as SPRINT (Systolic Blood Pressure Intervention Trial)³ have shown that patients with tighter blood pressure control (mean systolic 121.4 mmHg) have significantly lower rates of major cardiovascular events and heart failure in addition to reduced mortality compared with the standard therapy cohort (mean systolic 136.2 mmHg). With reduction of blood pressure the associated risks are reduced.

Hypertension is a significant problem, both in the general population and among pregnant women, with around one in 10 women experiencing a form of hypertensive disorder during pregnancy.¹ It is the third most common direct cause of maternal mortality worldwide, after haemorrhage and infection,² and is also associated with adverse affects to the baby, including intrauterine growth retardation, premature delivery and respiratory distress syndrome.³

Atrial fibrillation (AF) is known to increase stroke risk and can be stratified clinically by the CHA₂DS₂-VASc scoring system, which then informs recommendations for long-term anticoagulation. Susceptibility to thromboembolism is also increased around the time of catheter ablation of AF. Mechanistically, this is accounted for by endothelial injury, hypercoagulability due to contact of blood with foreign surfaces and altered blood flow after conversion to normal sinus rhythm (figure 1).¹ The risk of stroke persists post-ablation, even in patients with low CHA₂DS₂-VASc scores, as the atria may remain stunned for several weeks post-ablation, and the endothelium takes time to heal. This phenomenon forms the rationale for guidelines currently recommending anticoagulation for two to three months post-ablation.²