Did you know that 90% of heart attack events occur in men who had conventional diagnostics—testing that couldn’t/didn’t detect significantly diseased blood vessels at arterial sites?

In other words, those men didn’t know what hit them.

And here’s the tricky part: Your heart arteries are small (nearly invisible), hidden within the chest cavity and constantly on the move, especially in asymptomatic individuals.

A stress test only identifies vascular disease with blockage in the inside space of an artery (called an arterial

lumen).

But you would have to have a blockage as much as 70% to actually “fail” the stress test—and almost 90% of heart attacks happen with less than that 70% blockage benchmark. In fact, some stats suggest within a 30% - 60% blockage range.

Why? Because 99% of plaque occurs in the blood vessel wall and does not block blood flow. It’s the inflammation in plaque that causes heart attacks and strokes.

Listen, atherosclerotic vascular disease starts in childhood and progresses over decades, per research.

And, as we all know, it’s a real killer: 65% of men will die from it and 50% of women.

There’s no time like now to get moving on a proactive approach for better heart health. And it’s never to late to work on reducing your risk factors for cardiovascular disease—it may very well extend your life. Here are some things you need to know to do that.

Soft vs. calcified plaque. Blood clots occur when soft plaque in the inflamed artery wall ruptures or erodes through the lining of the blood vessel, causing heart attack or stroke.

Inflammation is the operable word: It thickens arteries and promotes plaque formation—not the calcified kind, but soft or “vulnerable” plaque that is filled with blood-clotting, inflammatory cells.

How it works. The artery absorbs fat droplets, which releases inflammatory cytokines (proteins). These proteins cause the artery wall to become sticky and attract monocytes (immune-system cells) that work their way into the artery wall and transform into macrophages, drinking up fat droplets.

Then these newly transformed fatdroplet cells generate a thin plaque (vulnerable/soft), which can crack and spill into your bloodstream. That’s when the cytokines storm the site, bunching together to form a large clot in an attempt to fix the “crack”—but wind up blocking off the artery in the process.

That’s why testing for subclinical atherosclerosis is critical. Not everyone with underlying atherosclerosis plaque will have a clinical cardiovascular event. However, the Society for Vascular Medicine published a 2008 consensus statement that said “the greater the degree of subclinical atherosclerosis, the greater the risk for cardiovascular events.”

Add to that, most physicians determine heart attack/stroke prevention treatments on a traditional standard of care:

• blood pressure monitoring
• cholesterol levels
• smoking
• diabetes

As important as those risk factors are, they’re simply not going to help you detect hidden disease.

What you need now: CIMT imaging.

The first order of heart-care business is to determine if you have vascular disease.

Many nontraditional blood tests have shown to be excellent for identifying vascular inflammation—that insidious intruder that incites plaque to erode or rupture—and alerting you not only of the presence of blood vessel disease, but also the span of its progression or regression.

The focus is finding an imaging test that fits ideal diagnostic parameters . . . safe, sensitive, affordable and a doorway to proactive interventions. In other words, a Carotid Intima-Media Thickness (CIMT) test with a high-resolution B-mode ultrasound. (More on the B-mode vs. the M-mode in my next issue.)

A CIMT ultrasound measures the thickness of your carotid artery wall in micrometers. The “intima” consists of endothelial cells lining the artery as well as the soft plaque stockpiling in and behind it; the “media” refers to the vessel’s smooth muscle layer. So the “intima-media” is a vessel segment that becomes an interface between anatomy (its structure) and physiology (way it functions) and is a marker for atherosclerosis and risk for heart attack/ stroke.

The ultrasound detects accelerated disease processes and subclinical disease and is called a “valid, reliable independent predictor of heart attack and stroke,” per the American Heart Association. Others agree.

• At the 2000 American Heart Association Prevention Conference, the CIMT was regarded for “further clarification of coronary heart disease risk assessment.”

• The following year, the National Cholesterol Educational Program stated that a CIMT “could be used as an adjunct in coronary heart disease risk assessment . . . and that an elevated CIMT score could elevate a person with multiple risk factors to a higher risk category.”

Research-based. Eight prospective studies done on CIMT and cardiovascular disease risk assessed 1,000 participants and showed a significant association between CIMT and myocardial infarction, stroke, cardiovascular disease death or a combination of these risks. Another study of 10,000 participants showed similar findings.

Here is what research says:

• CIMT increases with age—nearly 3-fold between ages 20-90.

• CIMT is linked with cardiovascular risk factors, prevalent coronary risk factors and the degree of atherosclerosis in many different arterial beds.

• Increased CIMT is related to intimal or medial hypertrophy and is an adaptive response to changes in wall tension, lumen diameter and flow.

• Carotoid wall thickening represents subclinical vascular disease, but is not synonymous with atherosclerosis.

• Risk factor interventions can stop/ reverse CIMT progression.

Look for my next issue to learn who are the best candidates for CIMT testing, why B-mode is best and much more.