Editorial articles

The European guidelines on cardiovascular disease (CVD) prevention in clinical practice have focused on prevention through behaviour change by highlighting and promoting lifestyle therapies to better address the needs of individuals with a high-risk profile. Programmes using motivational interviewing are promising in encouraging lifestyle change. While motivational interviewing may support individuals to modify risk, its effectiveness remains uncertain. Here, we offer reflections on the application of motivational interviewing in preventive cardiology, areas of controversy, and glimpses of potential future lifestyle interventions using motivational interviewing to prevent CVD development.

Heart disease remains a major cause of death and disability in Scotland, accounting for around 10,000 deaths each year.¹ Ischaemic heart disease is still Scotland’s single biggest killer, responsible for 11.3% of all deaths in 2018, and accounts for 25,000 hospital admissions each year. While it is true that there have been improvements in survival from heart attacks and other acute events in Scotland over the last half century, it is also the case that significant challenges remain.

The reduction in deaths from heart attacks means that more people are living with heart disease as a long-term condition. On top of this, the population is getting older,² and increasingly people are living with associated comorbidities, many requiring long-term support. The number of people living with cardiovascular risk factors in Scotland continues to increase, health inequalities persist and in some cases, have worsened.³

Beyond ischaemic heart disease, the incidence of conditions like heart failure,⁴ heart valve disease,⁵ and atrial fibrillation are increasing. There is also a need to consider the impact of less common, but no less important conditions, such as congenital heart disease and inherited heart conditions. Around 28,000 people in Scotland have an inherited heart condition, the most common of which is hypertrophic cardiomyopathy. Congenital heart disease is one of the most common birth defects in Scotland, affecting around one in every 150 births. Improved survival rates mean that a growing number of people are living into adulthood with congenital heart disease.

“I will not lose; either I win or I learn” – Marian Ionescu, circa 1971

The pericardial heart valve concept is the remarkable legacy of a man and his genius. His single most defining contribution has changed the course of cardiac surgery over the last half a century and benefitted millions of patients worldwide. Since the initial design by Hufnagel of the ball-cage valve implanted in the descending thoracic aorta (1953) to correct a regurgitant aortic valve, nearly 150 valves have been designed and tested. None has stood the test of time as well as the pericardial valve (figure 1). Since the first successful human implant of the pericardial valve in the mitral position in 1971, 10 million of these have been implanted worldwide. Pericardial valves now constitute 80% of all implanted valves. The invention has driven a multi-billion dollar industry that today forms the backbone of the healthcare technology sector.

Cardiorenal syndrome has attracted an enormous amount of attention, particularly in the last decade. A lot of research has been conducted in pathophysiology, haemodynamic manifestations, therapeutic options, and clinical outcomes.^1,2 In practice, however, cardiorenal syndrome remains clinically challenging for both cardiologists and nephrologists. Cardiorenal syndrome covers a wide range of structural and functional disorders of both the heart and kidneys. Typically, the acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other. The interaction between the two organs may well be in multiple interfaces, such as haemodynamic cross-talk between the failing heart and the response of the kidneys and vice versa, alterations in neurohormonal markers, as well as inflammatory molecular characteristics.² Much of the credit for the initial description of cardiorenal syndrome is attributed to Robert Bright who, in 1836, described the interdependent relationship between the kidney and the heart based on his observations on significant cardiac structural changes seen in patients with advanced kidney disease.³ The formal definition of cardiorenal syndrome and its classifications were established more recently,^1,2,4 although uncertainty remains still. The classification appears to be attractive and easily applicable in clinical practice, but its value in aiding treatment or prevention strategy has yet to be ascertained.⁴

The world is changing or is it? Science is changing or is it?

The concept of race based on skin colour, is an entirely social construct and its harbinger, segregation and slavery, projects itself into our modern day as racism. Perhaps more recently, it is acknowledged that racism remains a clear and present danger in today’s world. It is deeply rooted within the fabric of society and can only be tackled by active and persistent engagement.

In scientific circles, what is whispered but not openly spoken about is the cumulative acts of indifference that contribute to racial disparities in healthcare within our society. This comes in the form of implicit and subconscious biases that affect healthcare allocation and worse, delivery, in the form of differential treatment of patients.¹ This is as deadly as it is silent. As clinicians and academics who contribute to healthcare, we can either pretend this doesn’t exist or we can educate ourselves, and others, to foster health equity for all.

The European Society of Cardiology (ESC) updated their guidelines on stable chest pain in 2019,¹ and recommended the use of either imaging stress tests or computed tomography (CT) coronary angiography (CTCA). They emphasised the importance of imaging stress tests or CT fractional flow reserve (CT-FFR) as a second test, to assess any coronary stenoses found on CTCA. The National Institute for Health and Care Excellence (NICE) 2016 guidelines, on stable chest pain,² recommend CTCA for all patients with new-onset chest pain and, in a separate guideline in 2017,³ recommended CT-FFR to assess coronary stenoses. This need for a second test for the assessment of the significance of coronary stenoses is to reduce the need for invasive coronary angiography (ICA), because CTCA can be associated with false-positive results, as it can overestimate the degree of coronary stenosis, compared with ICA.⁴

The renin–angiotensin system (RAS) has been at the forefront of research aimed at mitigating the infectivity and mortality associated with the coronavirus disease 2019 (COVID-19) pandemic. This stems from the observation that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the pathogen that causes COVID-19, utilises angiotensin-converting enzyme 2 (ACE2) as its receptor to invade host cells. Since emergence of COVID-19, conflicting guidance has been published on the use of medications that may increase ACE2 levels. Specifically, initial reports suggested that ACE inhibitors and angiotensin II type 1 receptor blockers (ARBs) may result in increased virulence of COVID-19 due to elevated ACE2. Thus, discontinuation of these RAS blockers was advised. However, the data on ACE2 expression with use of RAS blockers in humans without COVID-19 are not clear, and for humans with COVID-19 are not yet available. Moreover, discontinuation of these medications may be deleterious in some patients for whom they are prescribed to treat heart failure, hypertension and ischaemic heart disease. For this reason, professional organisations, including the American College of Cardiology, American Heart Association, Heart Failure Society of America and the European Society of Cardiology, have issued statements advising against discontinuation of any RAS-related treatments in patients during the COVID-19 crisis.

The benefit of percutaneous coronary intervention (PCI) in ST-elevation myocardial infarction (STEMI) is undisputed. Clinical trials like DANAMI-2 (DANish Acute Myocardial Infarction 2),^1-3 PRAGUE-2 (Primary Angioplasty in AMI Patients from General Community Hospitals Transported to PTCA Units vs Emergency Thrombolysis),^4,5 STAT (Stenting Versus Thrombolysis in Acute Myocardial Infarction),⁶ AIR PAMI (Air Primary Angioplasty in Myocardial Infarction),⁷ Stent Versus Thrombolysis for Occluded Coronary Arteries in Patients With Acute Myocardial Infarction (STOPAMI)-1,⁸ and STOPAMI-2⁹ have demonstrated better outcomes with primary PCI over fibrinolysis. Other clinical trials^10-14 have demonstrated superiority of PCI over sole medical therapy for non-ST elevation myocardial infarction (NSTEMI) and unstable angina.

In contrast, there is ambiguity surrounding the benefit of elective PCI in stable coronary disease. The available evidence suggests no prognostic advantage over optimum medical therapy but deeper data scrutiny indicates that this remains uncertain. COURAGE (Clinical Outcomes Utilizing Revascularization and Aggressive Drug Evaluation),¹⁵ BARI 2D (Bypass Angioplasty Revascularization Investigation 2 Diabetes),¹⁶ and ISCHEMIA (Initial Invasive or Conservative Strategy for Stable Coronary Disease)¹⁷ are the main trials that examined this issue, all concluding against the prognostic usefulness of elective PCI. We argue that those studies contained inherent flaws that impacted on their results, thereby rendering their final conclusions unreliable. We suggest an alternative design for a new trial so the question can be answered decisively, once and for all.

“Alone we can do so little, together we can do so much.” Helen Keller

The links between kidney disease and cardiovascular disease have been reported as far back as 1827 with Richard Bright describing the changes in the left ventricle associated with kidney disease, and subsequently, Frederick Akbar Mahomed reporting increased arterial stiffness in patients with Bright’s disease.¹ Over the last two to three decades it has become increasingly apparent that kidney disease is the most important predictor of outcomes in all cardiology diseases and that cardiovascular disease is the leading cause of death in patients with chronic kidney disease.² In 2008, a systematic approach to the bi-directional interactions of heart and kidney diseases, or cardiorenal syndromes (table 1), was proposed.³ Cardiorenal syndromes can be broadly defined as disorders of the heart and kidney whereby acute or chronic dysfunction in one organ can induce acute or chronic dysfunction in the other.⁴ This was followed by increasing efforts to develop strategies to manage patients with combined heart and kidney dysfunction, as demonstrated by an increasing number of publications on cardiorenal syndromes.⁵

In 2015 one of my patients in the Fourier PCSK9 inhibitor trial asked me if I would like to attend his ‘bespoke’ total knee replacement operation. I said yes and witnessed an amazing procedure.