Cardiovascular disease: the impact of COVID-19 on patient outcomes

have also proven beneficial in preventing the first CV event (aka primary prevention) in patients who are at high risk for ASCVD. While statins have proven themselves to be of great benefit to patients, challenges with statin intolerance, an inability to reach LDL-C goals and an evidence-based push for even lower LDL-C goals established the need for new therapeutic options to add to existing statin treatment or to serve as an alternative where use of a statin is not possible.

PME: How significant are the improvements in patient outcomes that statins offer?

JF: The rapid rise in lipid-lowering drugs, at least in England, has been driven almost entirely by the increased use of statins; in 2019, 95.8% of all community-prescribed lipid-lowering strategies were statins, an increase from 93.1% in 2009. The drop in the prevalence (2009: 3.5-4.4% versus 2019: 3.1-3.9% based on country in UK) of CVD is likely to be directly attributable to some extent to this significant increase in lipid control strategies.

PME: How have positive results from clinical trials impacted CVD care?

JF: Clinical trials have had a significant impact on the way we treat patients with ASCVD. As the treatments and trials evolved over time, so has our understanding of the role of LDL-C lowering on clinical outcomes relative to the level of LDL-C achieved. When investigators evaluated multiple large clinical trials involving all types of lipid-lowering therapies, there was a linear relationship showing that lower LDL-C levels correspond to a lower risk of a vascular event. To that end, I would anticipate that a multimodal approach to achieve lower LDL-C levels earlier during a patient’s treatment to become the standard.

PME: How has research into drug treatments for CVD improved in the last decade?

JF: CVD drug treatment research has evolved from ‘treating a number’, such as a quantitative amount of blood pressure lowering or LDL-C lowering, to also including an emphasis on ‘hard outcomes to treat the patient’. The endpoints used in CVD trials have migrated towards disease specific endpoints (eg, non-fatal stroke, non-fatal myocardial infarction, heart failure hospitalisation) rather than broad endpoints (eg, all-cause mortality). This change in focus for primary endpoints of trials translates nicely into understanding the cost-effectiveness of therapies and can also demonstrate the efficacy and safety results for CVD drug candidates without the extremely large patient populations needed to power all-cause mortality primary endpoint trials.

PME: What steps can people take to minimise their risk of developing CVD?

JF: In 2019, 79.2% of all UK CVD deaths were attributable to factors, including high blood pressure, smoking and dietary risks. These are known in medicine as treatable or modifiable risk factors, in other words, something can be done to remove (modify) these risks from the equation. Additional risks include high or abnormal cholesterol levels, irregular heartbeat, high blood glucose levels, diabetes, chronic kidney disease, inadequate physical activity, obesity and excess alcohol consumption. In the UK, a sustained decline in cigarette smoking, improvements in hypertension treatment and control, and treatment interventions, such as widespread use of statins to lower circulating cholesterol levels, will all have contributed to preventing the development of CVD. While people cannot change their biological gender, age or genetic make-up, they should be encouraged to maintain a healthy lifestyle and use treatments as instructed by their medical providers to minimise those risks we have control over.
References are available on request.