Pharmaceutical Market Europe • January 2022 • 18-19
CVD
Cardiovascular disease:
Europe’s hidden crisis
The growing crisis: why we need a new CVD strategy
By Sephy Philip
Over the past year, the global pandemic has dominated the healthcare landscape, but beneath the headlines, vaccine roll-outs and emerging new variants, there is a hidden health crisis that has been intensified by COVID-19.
Cardiovascular disease (CVD) is one of the biggest health crises facing Europe today; it is the continent’s number one killer, accounting for 3.9 million deaths and costing the European Union €210bn.
Such is the scale of the challenge that the European Society of Cardiology (ESC) recently branded CVD ‘the biggest epidemic in human history. It has affected the greatest numbers, it has had the greatest cost and it is not over yet’.
COVID-19 has amplified the already existing healthcare challenges of CVD. There is clear evidence to suggest that CVD patients are at heightened risk from the virus in terms of experiencing more serious complications and potentially fatal outcomes.
The statistics tell a stark story; a recent paper in the European Journal of Preventive Cardiology (EJPC) has suggested that there could be 31,000-62,000 excess deaths in people with CVD caused directly by COVID-19 infections in England alone. There could also be an additional 50,000-100,000 indirect deaths, possibly resulting from strains to the healthcare system and patients who are increasingly reluctant to seek help.
Moreover, the reprioritisation of clinical resources during the pandemic has created a serious critical care backlog that has left CVD patients without much-needed medical help. The British Heart Foundation found a 150-fold increase across England in patients waiting more than a year for cardiac surgery or intervention – 4,273 in January 2021, compared to just 28 in February 2020.
In the UK, general practitioner referrals to cardiology clinics for diagnostic testing plummeted by 75% between April 2019 and April 2020. This diagnosis deficit is partly driven by behaviour change and the ‘stay away’ mentality adopted during the disruption. This toxic combination of factors risks laying the foundations for a future crisis.
‘Cardiovascular disease (CVD) is one
of the biggest health crises facing Europe today; it is the continent’s
number one killer, accounting for
3.9 million deaths and costing the European Union €210bn’
There have been growing calls in the industry to tackle CVD differently post-COVID-19. For example, the ESC has called for national CVD strategies spanning all dimensions of cardiovascular health, including primary and secondary prevention, detection, treatment, rehabilitation and follow-up. Similarly, the EJPC study concluded that ‘excess CVD deaths can be reduced with a more integrated approach, focused on reducing COVID-19 infection rates and managing comorbidities’.
A more integrated approach is needed for countries to bounce back from COVID-19 and safeguard their health services. However, any future strategy must also recognise that COVID-19 is a potential form of vascular disease.
COVID-19 as a vascular disease?
COVID-19 is often thought of as a lung or respiratory condition. However, there is a growing body of evidence to suggest that some of the most severe complications associated with the virus go far beyond the lungs.
It has become increasingly apparent that the virus has a detrimental effect on the body’s blood vessels. This can increase the risk of deep vein thrombosis, potentially fatal strokes, heart attacks and neurological issues.
COVID-19 may cause these serious complications by attacking the lining of the blood vessels known as the endothelium. The endothelium plays a vital role in ensuring that the body’s blood vessels function effectively; it acts as a biological gatekeeper allowing and blocking certain substances to pass through the bloodstream. Thus, it makes sure blood flows effectively around the body and releases targeted measures to prevent inflammation and the formation of harmful blood clots.
The vascular endothelium provides a crucial interface between the blood compartment, tissues and host defences, forming
the front-line barrier of encounters with pathogens such as COVID-19.
One of the effects of the virus is that it damages the lining of the vessels and their ability to operate effectively, creating what is known as endothelial dysfunction. Through its harmful effects on the endothelium, the SARS-CoV-2 virus has the potential to cause disruptions across the entire body, including blood clotting, fluid in the lungs and brain inflammation.
A paper in Nature Reviews published by the Nature Publishing Group in April 2021 indicates a potential link, demonstrating the virus’s ability to infect endothelium. This report suggested endothelial dysfunction to be a key pathophysiological event. The novel coronavirus may directly infect vascular endothelial cells and lead to cellular damage and cell death which can decrease the antithrombotic actions of the endothelium. This was developed further by a study in the New England Journal of Medicine (NEJM), which showed that COVID-19 caused the formation of tiny blood clots in the lungs’ capillaries. One of the study’s most striking findings is that there were nine times as many of these clots in COVID-19 patients compared with those with flu.
Emerging evidence indicates SARS-CoV-2 impacts platelet aggregation by binding to endothelial cells, where cell fragments stick together and form clots, which may have the potential to lead to stroke or heart attack.
These scientific insights have helped piece together the puzzle of why people with cardiovascular conditions may be more susceptible to developing serious aftereffects of COVID-19. The growing scientific understanding of this issue has created the need for the development of a new treatment paradigm to tackle these issues in COVID-19 patients.
The need for a new treatment paradigm
The growing evidence of COVID-19 as a vascular disease suggests that one consideration, among others, of treating COVID-19 is limiting the formation of blood clots. The figures show that up to 30% of people with acute COVID-19 could develop serious life-threatening blood clots. However, it has been predicted that clinical outcomes may be improved with the administration of blood-thinning agents. There are several other potential treatment options being tested, such as statins and other blood pressure drugs like angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARBs).
‘A recent paper in the European Journal of
Preventive Cardiology has suggested that there
could be 31,000-62,000 excess deaths in people
with CVD caused directly by COVID-19 infections
in England alone’
A healthy functioning endothelium releases several substances to help to limit the formation of blood clots, including:
Another important feature of healthy blood vessels related to nitric oxide production is a hormone called angiotensin II, which narrows the blood vessels and increases blood pressure. Angiotensin II can cause inflammation resulting in endothelial dysfunction and reduced nitric oxide production. In COVID-19 patients, it is thought that it is important to restore the balance between angiotensin II and angiotensin 1-7, which would normally be regulated by ACE2.
Whilst research is at an early stage and requires further clinical data, there is a clear challenge for the health service to address the vascular effects of COVID-19 through targeted interventions.
In the wake of the COVID-19 crisis, we need a new treatment paradigm informed by the emerging science for CVD patients across Europe. This is vital to minimise at-risk CVD patients against the potential scarring long-term after-effects of the virus and help tackle potentially one of the most important predictors of clinical vulnerability to COVID-19.
References are available on request.
Sephy Philip is
Executive Director of Global Medical Affairs
at Amarin Corporation
Pharmaceutical Market Europe (PME)
Pharmaceutical industry news, articles, jobs, reports, advice and services