Scotland is a world-leader. It leads in renewable energy, gender equality and, in 2019, it was even voted the most beautiful country in the world. Unfortunately, it also leads much of Western Europe in the number of heart attacks and cardiovascular-related deaths.

However, there are ways we can improve this. In Scotland we have access to myriad drugs that have been found to reduce risks of heart disease. Improving the management of cardiovascular disease could be an important way of bridging this gap and potentially reducing the burden. In my PhD, I’ve been investigating this through looking at how people take their medications and whether they adhere to prescription guidelines agreed upon with their doctor.

One of the drug classes I’m interested in are ACE inhibitors. Not named for their ‘ace’ abilities in controlling blood pressure (though they are admittedly good at that), they’re in fact named for the protein – angiotensin-converting enzyme – that they interact with in the body. Blocking this enzyme prevents it from its normal function of narrowing the blood-vessels. Wider blood vessels means more physical space for the blood to flow through, reducing pressure on the blood vessels and the heart.

You may have heard of ACE recently if you’ve been closely following news on SARS-CoV-2 – the virus responsible for the COVID-19 pandemic we now find ourselves living through. In fact, ACE even got a mention in the first prime-minister’s questions to be held since the UK lockdown began. ACE2 is a receptor in the lung (and elsewhere in the body), which the novel coronavirus binds to and uses to get into our cells. It attaches to this receptor using spike proteins on the viral surface, which form a halo (or ‘corona’) around the virus. In images these are often coloured but in reality, viruses are too small to have colour – they’re smaller than the visible light spectrum (you may want to take a moment to wrap your head around that one).

One potential treatment for COVID-19 hinges on this interaction between viral spike proteins and ACE2 by creating ‘decoy’ ACE2 proteins. In theory, the virus binds to these decoy-proteins instead of the cell receptor, meaning the spike proteins are ‘blocked’ and the virus is no longer able to attach to human cells, stopping the infection in its tracks. So far this has been found to work in cell-culture but it is yet to be seen if it will be safe and effective in human studies.

ACE inhibitors and related cardiovascular drugs are thought to upregulate ACE2, increasing the number of these receptors present on our cells. If you’ve been following the news of the pandemic, you may also be aware that people with cardiovascular disease are at an increased risk from COVID-19; and you could be forgiven for linking these together. It would make sense that an increase in the number of ACE2 receptors mean more opportunities for the virus to enter our cells and make us sick.  

However, evidence so far suggests that is indeed safe to continue taking these drugs, and that they may in fact have a protective effect at later stages in the disease progression. If anything, it is ever more pertinent to keep taking any heart medications you may be on. Respiratory viruses, such as flu and coronavirus, are known to put the body and the cardiovascular system under increased strain, and it is this that puts people at an increased risk of becoming much more severely affected.

Of course, COVID-19 is caused by a brand new virus, so we are still learning about how it affects us and what risk factors could make the disease more dangerous. The jury is still out on the exact role that ACE inhibitors may play. For now, the safest thing to do is to stick with your meds and do not make any changes to this without contacting your GP first.