7 Heart Disease Risk Factors That Go Unseen

7 Heart Disease Risk Factors That Go Unseen

The majority of early heart disease is preventable.

Yet, we do a bad job of preventing it.


Most people know that they are at risk of heart disease or may already have heart disease, and they are concerned about it worsening.

The steps required to reduce the future risk of heart disease have been well described, but we consistently do not evaluate or manage them.

Because of this, people are left with unmanaged risk and go on to have events that could have been avoided.

Sometimes, that risk is partially managed, but so much of it lurks beneath the surface as what is called ‘residual risk’.

In truth, most ‘residual risk’ is just our failure to identify and manage it properly.

What is worse is that many patients believe that their ‘risk’ has been appropriately managed when, in reality, they have substantial risks for future events that are not being addressed.

When they inevitably have a heart attack, the physician and the patient are often surprised, but if they had looked, they might have seen where that risk was coming from and what to have done about it.

Whether we like to admit it or not, we could do a better job reducing even the most fundamental aspects of risk.

Even in those with documented coronary artery disease, less than half were on statin therapy, which has been repeatedly proven to decrease risk in this high-risk group1.

To address this issue of residual risk, we must know where to look, and then we can put in place strategies to decrease that risk.

Here are seven things you can assess to see if you have excess risk lurking underneath the surface.

Lipoprotein (a)

Approximately 1 in 5 people have the Lp(a) variant of cholesterol particle that significantly increases the risk of early heart disease and stroke.

It is genetically mediated, so if you have an early family history of heart disease, this is something to consider2.

While there is no approved therapy to directly lower Lp(a) levels, that does not mean overall cardiovascular risk cannot be reduced.

Do not be blind to this obvious risk amplifier.


The fundamental basis of coronary artery disease is when a cholesterol particle is retained in the artery wall, and an inflammatory cascade occurs, resulting in the formation of atherosclerosis.

The greater the number of particles, the higher the risk.

The number of APOB particles is the best measure of that risk.

LDL cholesterol can be a reasonable measure of that risk, but in the settings of insulin resistance, metabolic syndrome and diabetes, the level of risk suggested by LDL-C may underestimate the true risk.

For the best assessment of risk, measuring APOB is key.

APOB Particles doi: 10.1161/JAHA.122.025858.

Insulin Resistance

Everyone exists along a continuum of insulin sensitive to highly insulin resistant, the later stages being characterised by type 2 diabetes.

The more insulin resistant a person is, the higher their risk of coronary artery disease.

The very late stages of insulin resistance are characterised by elevations in blood glucose, but serum insulin levels rise for many years previous to this. With this rise in serum insulin comes a higher risk of heart disease.

While markers of diabetes are routinely checked, measures of insulin resistance are rarely formally evaluated.

Because of this, significant elevations in risk often go unnoticed and unmanaged.

Blood Pressure Control

For every 20 mmHg increase in systolic blood pressure, the risk of dying from heart attack or stroke doubles3.

Blood pressure is rarely measured correctly; elevations are often incorrectly attributed to ‘White Coat’ high blood pressure, and even when recognised, there is often a reluctance to appropriately attempt to reduce it.

In general, we do a bad job of identifying and managing high blood pressure. 

For most adults, the difference between having average systolic blood pressure in the low 120s range versus the mid 130s can mean a 25% difference in the rate of heart attacks and stroke4.

Excess high blood pressure is all too common and frequently goes untreated.

Visceral Adipose Tissue

The real risk of obesity comes from the inflammatory engine of visceral fat found in the abdominal cavity.

Excess subcutaneous fat, which you can pinch on your side, only adds marginally to the risk of future heart disease.

Most people in the obese category have excess visceral fat, but some don’t.

However, many people who do not fall into the obese or overweight category have excess visceral fat and, consequently, have significantly higher rates of heart disease.

For these ‘normal weight’ individuals, the real risk of excess fat is often missed. This is why measuring metrics such as waist circumference and visceral adipose tissue (VAT) mass on a DEXA scan are incredibly useful but rarely done.

All fat is not created equal; it is the search for visceral fat that will yield the greatest results.

Subcutaneous Versus Visceral Adipose Tissue. doi: 10.2147/NSS.S327341.

V02 Max

V02 max is a measure of aerobic fitness. Some of it is genetically determined, but in large part, it can be trained and is a reflection of the years of activity levels prior.

If activity levels have been low, V02 max will be low.

If activity levels have been high, V02 max will be high.

V02 max does not lie.

You can tell your doctor you have been ‘active’, but your V02 max will tell the truth. A truth you cannot hide from.

The higher your V02 max, the greater the likelihood you will live a longer life.

We cannot rely on subjective questions of “Are you active or do you exercise regularly?” we need to move to more objective assessments of aerobic fitness capacity with the greatest predictive power.

For those in the highest fitness categories, the risk of dying from ANY cause is five times less than someone in the bottom 25% of fitness levels5.

This is huge. And rarely formally tested.


The evidence that poor sleep increases the risk of future heart disease has grown considerably.

Shortened sleep is classified as sleeping less than 7 hours per night.

35% of US adults sleep less than 7 hours per night6.

Shortened sleep is associated with higher rates of:

  • Coronary artery disease

  • Early death

  • High blood pressure

  • Weight gain

And many other adverse outcomes.

However, it is rarely considered an important risk factor for heart disease, and because of this, considerable risk goes unmanaged.

Sleep Duration and Hypertension: Analysis of > 700,000 Adults by Age and Sex. J Clin Sleep Med. 2018 Jun 15;14(6):1031-1039

Many other factors contribute to the concept of ‘residual risk’, which frequently goes unseen and unmanaged.

But as the Ayn Rand quotation goes:

“You can avoid reality, but you cannot avoid the consequences of avoiding reality.”

These risks are lurking underneath the surface, resulting in a much higher risk of future heart disease than you may or may not be aware of.

Regardless of whether you are aware of them or not, they will increase your risk.

It is up to you and your doctor to identify and manage them as best you can.

In summary, even if you ‘think’ you and your doctor have things under control, ask yourself this:

Do you know your:

  1. Lp(a)

  2. APOB

  3. Insulin Resistance Status

  4. Blood Pressure target

  5. Visceral Fat Level

  6. V02 Max

  7. Sleep Status

Because if you don’t, there is likely substantial risk that you are not evaluating and, therefore, managing.

Always remember, it is YOU who has the most to gain and the most to LOSE by understanding these factors.

While it would be reasonable to think that this is solely your doctor's responsibility, it is not.

This is a team sport, but in the end, only one of the members of that team is playing with their life on the line.


High-Intensity Statin Use Among Patients With Atherosclerosis in the U.S. J Am Coll Cardiol. 2022 May 10;79(18):1802-1813.


Duarte Lau F, Giugliano RP. Lipoprotein(a) and its Significance in Cardiovascular Disease: A Review. JAMA Cardiol. 2022 Jul 1;7(7):760-769.


Prospective Studies Collaboration. Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies. Lancet. 2002 Dec 14;360(9349):1903-13


A Randomized Trial of Intensive versus Standard Blood-Pressure Control. N Engl J Med. 2015 Nov 26;373(22):2103-16. doi: 10.1056/NEJMoa1511939.


Association of Cardiorespiratory Fitness With Long-term Mortality Among Adults Undergoing Exercise Treadmill Testing. JAMA Netw Open. 2018 Oct 5;1(6):e183605.



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