The work of George Abela, a professor in MSU's Department of Medicine and chief of the department's cardiology section, finds that cholesterol that has built up along the wall of an artery and crystallized from a liquid to a solid state can expand and then burst, sending material into the bloodstream.
It is this chain of events – the expansion of the liquid cholesterol as it crystallizes into a solid – that kick-starts the body's natural clotting process which, unfortunately in this case, works against the body, essentially shutting down the artery.
"As the cholesterol crystallizes, two things can happen," Abela said. "If it's a big pool of cholesterol, it will expand and just tear the cap off the deposit in the arterial wall. Or the crystals, which are sharp, needle-like structures, poke their way through the membrane covering the cholesterol deposit, like nails through wood."
It is the presence of the cholesterol crystals and other debris material released by the plaque rupture into the bloodstream that activates the clotting mechanism.
"What the clotting system is doing is reacting to an injury in the artery," he said. "Once a rupture or erosion of the surface of the artery occurs, then the clotting system is activated to do its job."
Abela compared the crystallization of the cholesterol to putting a plastic bottle of water into a freezer. Over time the water freezes and expands, pushing its way out of the bottle or breaking the bottle altogether.
What this work also means is that physicians and other health care providers now have another weapon in their arsenal against cardiovascular disease.
"So far, treatments have not been focused on this process," Abela said. "Now we have a target to attack with the various approaches we have. In the past, we've treated the various stages that lead to this final stage, rather than preventing or treating this final stage of the condition."
Abela stressed that it remains imperative that people use diet and exercise to keep cholesterol levels low.
"This really drives the point home how important cholesterol control can be," he said.
Until now, scientists had thought that inflammation of the wall had caused the breakdown of the cap that kept the cholesterol in the arterial plaque from rupturing. Abela said his findings don't necessarily discount the inflammation theory, but rather add another dimension to it.
"As the crystals form, they dig their way through the wall of the artery, and that may be a trigger for the inflammation," he said. "Inflammation is a normal mechanism, one that kicks in to repair the damage. That is why it is common to see inflammation at the site of these events."
The research was conducted in Abela's lab, research that he said was "as simple as science can get."
Essentially, Abela and colleagues took varying amounts of cholesterol, reduced it to a liquid form, and then watched it expand as it solidified. In doing so, it tore through thin biological membranes.
"After the cholesterol crystallized, its volume was about 45 percent larger than what we started with," he said. "And the entire process took all of about three minutes."
Journal
Clinical Cardiology