The Faces of Cardiovascular Disease: Part 1

This article is part of a mini-series we are calling The Faces of Cardiovascular Disease, looking at the different presentations, symptoms, and root causes of a disease that affects millions of men and women around the world.

Through this series we hope to explore the human side of the problem, to develop a deeper and more companionate understanding of the stories behind the figures, and ultimately to better inform the products we develop.


We have all heard the statistic; you’re more likely to die from cardiovascular disease than from any other cause.

In fact, between 1980 and 2014, 4 in 10 deaths in the United States – 31.9 million people – were a direct result of cardiovascular disease. A sobering figure, but what’s equally alarming is the acceptance of this sad reality rather than asking fundamental questions that may lead to real solutions.

To start, what’s behind these numbers? Am I at risk of suffering a heart attack? A stroke?  What could cause my disease? Is it genetic? Did lifestyle choices contribute? Can I prevent this from happening?

Statistics only tell part of the story.

By digging deeper into the personal stories of those affected we can uncover the root causes of cardiovascular disease and look towards more effective preventions and therapies.

As a research-based biotechnology company, Resverlogix first and foremost tries to understand the biology underlying cardiovascular disease. However, through this series we hope to explore the human side of the problem, to develop a deeper and more companionate understanding of the stories behind the figures, and ultimately to better inform the products we develop.

Let’s get into it, starting with some terminology. When we’re referring to cardiovascular disease what exactly are we talking about?

Cardiovascular disease isn’t a single disease at all.

It’s a general term used to describe a diverse array of disorders and dysfunctions that affect the heart or blood vessels. However, the shared anatomy is not the only commonality of these diseases; despite variability in presentations, cardiovascular diseases often share a few broad underlying processes.

Atherosclerosis – the formation of lipid-filled plaque in the walls of blood vessels – is one of the most common and important processes contributing to cardiovascular disease. In its most severe form, atherosclerosis can result in complete blockages of blood vessels. When this occurs in the coronary arteries – the vessels that feed the heart muscle – it causes a heart attack; if the blockage occurs in the arteries providing oxygen to the brain, a stroke can result. Together, heart attacks and strokes account for nearly 80% of cardiovascular disease-related deaths.

Another common process, Hypertension, or high blood pressure in the arteries, causes the heart muscle to work harder than normal. As wear accumulates, these tissues may not be able to keep up with the extra stress leading to heart failure, aneurysms, and strokes. Hypertension is often called the “silent killer” as symptoms may not be apparent until it has already caused significant damage.

The deposition of calcium-rich minerals, a process normally reserved for bone growth and remodeling, occurring inside arterial walls is characteristic of cardiovascular disease. This calcification can occur in the valves of the heart reducing flow, while calcification of major arteries causes them to stiffen, both of which cause the heart to work harder to maintain sufficient blood flow.

Chronic inflammation – the persistent activation of the immune system – is strongly associated with the multitude of factors and dysfunctions that contribute to cardiovascular disease. Molecular mechanisms designed to protect the body against foreign invaders become a real danger instead, as small tissue damage accumulates over years or decades.

These processes are not isolated from one another.

Inside arteries, chronic inflammation kicks off the development of atherosclerosis; reduced filtration capacity in the kidneys, caused by calcification, raises blood pressure.

When we go one step deeper, into the basic functioning of the body at a cellular and molecular level we find that each of these processes is dependent on genetic and epigenetic factors.

Some examples of genetic contributions to cardiovascular disease are obvious – such as congenital defects of the heart, present at birth. However, genetic factors can also have a more subtle, cumulative impact, causing a slow but critical decline in cardiovascular health. They may also predispose a patient to the development of hypertension, high cholesterol, obesity, diabetes, or chronic inflammation.

But genetics alone don’t tell the whole story, with epigenetics – the process by which genes get turned “on” or “off” – playing a crucial role. Epigenetics is the mechanism by which environmental and lifestyle factors are translated into health outcomes.

Our research group has published a number of papers showcasing the epigenetic basis underpinning lipid metabolism, calcification, and inflammation.

In our series, we will examine the lives of different people with cardiovascular disease and try to understand how genetic and environmental risk factors, translated through epigenetics and the intertwined processes of lipid transport, hypertension, inflammation and calcification, ultimately combine to impact their lives.

Thankfully, much of the harm associated with cardiovascular disease is preventable.

Multiple studies have shown changes in lifestyle can prevent serious cardiovascular events in predisposed populations. In the last 30 years, new advances in treatment and management have cut the deaths associated with cardiovascular disease in half.  

This is reason to be optimistic. In the final installment of this series we will look at some of the things science tells us you can do to reduce your risk of cardiovascular disease, as well as taking a peek at what’s on the horizon in terms of new treatment options.

Check back here towards the end of February for the next installment in our series.