Monday, May 05, 2008

Ever heard of cardiac bridging?

Have you every heard of cardiac bridging? It is a anatomical phenomenon where one of the major arteries that supply the heart with oxygenated blood traverses through cardiac muscle and becomes compressed during the contracted pumping stage (systole), a transient problem that reverses when the heart returns to its resting phase (diastole). You may be surprised to learn that odds are your coronary arteries exhibit “cardiac bridging.”

An excellent online visual display of myocardial bridging can be found here: http://indianheartjournal.com/2001-5/NovDec2002/Myocardial%20Infarction%20due/myocar16.gif

Recognized more than 200 years ago, and first reported in depth in 1951, cardiac bridging is generally thought to be of little significance. But with so many cases of sudden cardiac death, hundreds of thousands of unexplained cases a year, and evidence cardiac bridging may be a triggering factor, a re-investigation of this largely unknown phenomenon is in order.

The left anterior descending coronary artery is usually the location of cardiac bridging. Cardiologists generally estimate the prevalence of cardiac bridging ranges from 1.5% to 16% when assessed by coronary angiography, but in some autopsy series, it is as high as 80%. Yes, that’s 8 in 10 people.

The inner wall thickness of the tunneled artery is significantly thinner (66.3 µm) than that of the nearby segment (406.6 µm) of the artery.

Researchers have found that cardiac bridging (tunneling of coronary arteries under heart muscle) impairs widening (dilatation) of the left descending artery and arterial plaque is not found within the bridged area of the artery itself, but in the area in close proximity to the bridge (75% of cases). [Echocardiography 2006 Aug; 23(7):577-81]

When acetycholine, a nerve messenger chemical, was infused into the left coronary artery among middle aged men (57-58 years, mean age), arterial spasm was more likely to occur among men with cardiac bridging (62 of 81, or 76%) than men with no cardiac bridging (31 of 195, or 16%). [American Journal Cardiology 2007 Oct 1; 100(7):1083-6]

The question is what to do about cardiac bridging. Strategies to strengthen coronary artery would be in order. Humans are known to exhibit weak arteries with the lack of vitamin C in the diet. There are many vitamin C human studies involving carotid (neck), radial (outside the heart) and peripheral (leg) arteries, but none available on the effect of vitamin C upon the four coronary arteries.

A study that may have application to cardiac bridging is a published study involving vitamin C among cigarette-smoke exposed hamsters. White blood cells tend to accumulate and adhere to damaged areas inside arteries, meaning they are attempting to heal a wound there. Adherence of white blood cells to the arterial wall occurs more frequently among smokers. Dietary vitamin C supplementation prevents this occurrence. Smoking depletes vitamin C and weakens arteries. [Journal Clinical Investigation 99: 2358-64, 1997]

In another study, the provision of supplemental vitamin C and E to swine showed that these antioxidant vitamins inhibited damage to coronary arteries caused by inflation of a balloon. [Arteriosclerosis Thrombosis Vascular Biology1995 Jan; 15(1):156-65] This would be similar to the damage caused in proximity to the cardiac bridging.

While there is no study involving vitamin C and cardiac bridging per se, it would seem prudent to take vitamin C supplements throughout the day to maintain high blood levels, and thus minimize arterial damage in proximity to the bridge that provokes plaque formation. The transient but repeated compression of a coronary artery due to cardiac bridging is an overlooked cause of coronary artery disease and most likely, sudden cardiac death. - Copyright 2008 Bill Sardi, Knowledge of Health, Inc.

Labels: myocardial bridging, sudden cardiac death, Vitamin C