New Test May Predict the Possibility of a Heart Attack

New findings from a landmark research study led by Scripps Translational Science Institute (STSI) -- a collaborative program between Scripps Health and The Scripps Research Institute (TSRI) -- shows a promising new blood test may be useful in helping doctors predict who is at risk for an imminent heart attack.

Results of the study, titled "Characterization of Circulating Endothelial Cells in Acute Myocardial Infarction," were published this week in Science Translational Medicine. The study concludes that circulating endothelial cells (CEC) from heart attack patients were abnormally large and misshapen and often appeared with multiple nuclei, which indicates that CECs are promising biomarkers for the prediction of acute ongoing arterial plaque rupture.

"The ability to diagnose an imminent heart attack has long been considered the holy grail of cardiovascular medicine," said Dr. Eric Topol, the study's principal investigator and director of STSI. "This has been a tremendous collaboration of two institutions on the research side, three health care systems in San Diego, and a life science industry leader, which has resulted in an important discovery that may help to change the future of cardiovascular medicine."

The study involved 50 patients who presented to emergency rooms with heart attacks at four acute care hospitals in San Diego. Using different cell isolation platforms, including the Veridex CellSearch System, the researchers found that CEC counts and the cell structural features were dramatically altered in the heart attack population when compared to the healthy control group.

"We are pleased to have collaborated on this important investigational study, said Mark Connelly, PhD, Director, Cellular Research, Veridex. "CellSearch has proven to be a powerful tool for oncology research and the care of metastatic cancer patients. This study highlights the value of accurate rare cell capture and..."

Note though that “Veridex” is the sponsor of the study, not that I know a darned thing about them, mind you.
Just pisses me off that all of science is corrupted by “studies” for which these companies pay.
I do know sh*t from shinola though.

I don’t believe anything anymore, I am the ultimate science cynic.

I don’t believe anything anymore, I am the ultimate science cynic.

I don't know about Veridex, but Eric Topol is no run of the mill shlep going for the bucks. He has a serious reputation to protect. And other folks complain about NIH funding.

You want an easy test?

93% of heart attack patients have had a root canal. The bacteria found in their hearts is bacteria that normally lives in the mouth. When the person’s immune system gets older, less efficient, or compromised by another illness, and/or the person suffers a mouth injury bacteria from the mouth can travel fro, the mouth to the heart and cause infection there.

Vitamin K2 holds promise as an agent that reduces the calcification of arterial walls and subsequent rupture:

K2: Your Arteries’ Best Friend? Animal studies have shown that K2, but not K1, can inhibit the calcification of arterial plaque. As a recent review notes: “Calcification of the vessel walls is one of the features of atherosclerosis and is by itself considered to be a risk factor for plaque rupture.”38 And plaque rupture in a heart artery is often the final trigger for a (possibly fatal) myocardial infarction (heart attack). A 1996 study found that high-dose K2 inhibited the increase in aortic or kidney calcium induced by megadose synthetic vitamin D2. The authors noted that “a pharmacological dose of vitamin K2 might have a usefulness for the prevention and treatment of arteriosclerosis with calcification.”39 A 1999 study found that high-dose K2 could inhibit the increase in aortic calcium in rats made arteriosclerotic by high-dose D2 and an atherogenic diet.40 A 1997 rabbit study found that high dose K2 “prevents both the progression of atherosclerosis and the coagulative tendency by reducing the total-cholesterol, lipid peroxidation and factor X activity in plasma, and the ester cholesterol deposition in the aorta of hypercholersterolemic rabbits.”41 In 2003 Spronk and colleagues reported “that MK-4 [K2] and not K1 inhibits warfarin-induced arterial calcification.”42 Most importantly, a study published in 2001 examined more than 4,000 humans followed from 1990 to 1996. Subjects were examined for their dietary K2 intake. Those with a “high” K2 intake (greater than 33 mcg per day) had only 43 percent of the risk of suffering a heart attack compared to the low K2 group (less than 22 mcg per day). The risk of dying from a heart attack was only 37 percent as high in the high-K2 group compared to the low-K2 group. “The dietary intake of vitamin K1 showed no consistent relation with cardiac events or aortic atherosclerosis.”43

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