Editorial articles

I first started using the V scan myself over four years ago, and I have found this hand-held mobile device extremely useful for providing rapid and important diagnostic information at the bedside. The quality of the images of the V scan are usually of sufficiently high quality to make a useful clinical assessment. It is usually possible to make a fair assessment of systolic function of the left ventricle. I have also found that the identification of a dilated right heart has often been very useful for diagnosing massive pulmonary emboli – quite frequently when this diagnosis would not otherwise have been suspected. Valve lesions of significance are invariably pretty obvious and the images are usually adequate to identify vegetations as well. Pericardial effusion is readily detected.

Cardiac implantable electronic devices (CIEDs) have an unquestionable evidence base in patients with reduced left ventricular ejection fraction (LVEF), already on optimal medical therapy. Implantable cardioverter defibrillators (ICDs) effectively treat ventricular arrhythmias, which account for up to 50% of mortality in patients with reduced LVEF.¹ Likewise in appropriately selected patients, cardiac resynchronisation therapy (CRT) reduces hospitalisation rates, improves symptoms and prolongs life-expectancy.²

The Government is soon to publicly disclose a league table for cardiac surgical units within National Health Service (NHS) England. While this information may be useful and raise questions as to why one unit may be better or worse than another, we are also to be made aware of surgeons who are performing significantly better or worse than expected in terms of risk-adjusted mortality. But are patient deaths following surgery caused exclusively by the surgeon, as surgeon-specific mortality data (SSMD) would imply? And is the surgeon with the lowest operative mortality the best doctor? In my opinion the answer to both these questions is a resounding no.

Life-expectancy is now approaching 90 years, and it won’t stop there. Healthy life-expectancy is also extending, so that the average 60 year old can expect a further 11 years of healthy life. Currently, 35% of the UK population is over 50 years, and growing – and on the whole they are healthier, more skilled, better educated and more dynamic than ever before.

Contemporary guidelines have lowered the threshold for statin use in primary prevention (7.5% risk of a cardiovascular event over 10 years in the USA,¹ 10% risk according to National Institute for Health and Care Excellence [NICE] guidelines in the UK).² Applying these thresholds, the majority of men over 50 years and more than half of women over 60 years will qualify for statin use. Countering the more widespread uptake of statin use in primary prevention advocated by these guidelines are claims, popularised by the lay press and uncritically published in some medical journals,^3,4 that statin use is accompanied by an unacceptable incidence of side effects that adversely compromise lifestyle and which challenge whether the small absolute benefits in some lower risk groups are worth the intolerance of the statin.

When the National Institute for Health and Care Excellence (NICE) clinical guideline 180 on atrial fibrillation (AF) was published in June 2014, out if its many recommendations, two points seemed paramount. First, it is the patient, and not the clinician, who should make the decision as regards the nature of the treatment they are to receive, whether this be for stroke prevention or for symptom management, and that all those with AF should be offered stroke preventive therapy, with the exception of those without risk factors (CHA₂DS₂-VASc 0 or 1 in females).

A non-fatal myocardial infarction (MI) is an inconvenience; a non-fatal stroke is a catastrophe. While this is a simplification, it draws attention to the fact that most patients with a non-ST-segment elevation MI (NSTEMI) do quite well. Conversely, most patients who suffer a non-fatal stroke suffer a massive change to their lives and their families’ lives, and experience a devastating change in their quality of life.

We share Professor Brady et al.’s opinion¹ that stroke prevention is the single greatest priority in the management of patients with atrial fibrillation (AF). It is reasonable to say that highlighting the inappropriately low levels of anticoagulant uptake as a major public health issue and seeking to improve anticoagulant uptake nationwide was uppermost in the minds of the Guideline Development Group (GDG) members.

The heart beats 120,000 times a day pumping 7,000 litres. Ischaemia or inflammation decimate this workload causing end organ dysfunction. New National Institute for Health and Care Excellence (NICE) guidelines for acute heart failure (AHF) acknowledge very high early mortality. Of 67,000 acute admissions, 11% die in hospital, 50% are readmitted and 33% are dead within 12 months.^1,2 When cardiogenic shock ensues, prognosis is poor.^3-5 Most patients are elderly but several thousand deaths occur in those under 65 years. Many are salvageable using advanced resuscitation techniques. When the prospectively randomised-controlled trial (RCT) IABP-SHOCK II trial (Intra-Aortic Balloon Pump in Cardiogenic Shock II) revealed the intra-aortic balloon pump (IABP) as ineffective, a New England Journal of Medicine (2012) editorial stated “we must move forward understanding that a condition with 40% mortality at 30 days remains unacceptable”.^3,4 So do the guidelines help with this? 

Cannabis has been employed medicinally and recreationally for thousands of years,^1,2 but it was not until the 1960s that the structure and pharmacology of its primary phytocannabinoid components, cannabidiol (CBD)³ and tetrahydrocannabinol (THC)⁴ were identified, and another generation before the nature and function of the endocannabinoid system (ECS) were elucidated (see reference 5 for a comprehensive review). The ECS consists of endogenous cannabinoids, anandamide (AEA) and 2-arachidonoylglycerol (2-AG), their biosynthetic and catabolic enzymes, and their receptors: CB₁, which is psychoactive, analgesic, neuromodulatory and the most abundant G-protein coupled receptor in the brain, and CB₂, which is non-psychoactive, immunomodulatory and anti-inflammatory. The ECS may be thought of as a grand homeostatic regulator of chordate physiological functions, whose roles have been summarised as: “relax, eat, sleep, forget and protect”.⁶ Those actions closely describe the effects of THC and AEA, which are both weak partial agonists at CB₁ and CB₂.