THURSDAY, July 31 (HealthDay News) -- A series of genes linked to acute aortic dissection could lead to a rapid diagnostic test for this often fatal problem, German researchers report.

Acute aortic dissection is a tear in the lining of the aorta, the artery that carries blood from the heart to the rest of the body. About 2,000 people a year in North America suffer an acute aortic dissection, according to the American Heart Association.

"Thirty-three percent of acute aortic dissection patients die within the first 24 hours if they remain untreated because the disease is not diagnosed," lead researcher Salah A. Mohamed, from the Department of Cardiac Surgery at the University of Schleswig-Holstein said in a statement.

The report was presented Wednesday at the American Heart Association's Basic Cardiovascular Sciences Conference, in Keystone, Colo.

In the study, Mohamed's team looked at samples of aorta tissue from 19 patients who had acute dissection. These patients had no known connective tissue disease.

The samples were compared with samples from eight patients who had a mutant gene for Marfan syndrome, a disease that affects connective tissue, which in turn makes blood vessels weak. The researchers also compared tissue from six patients who had undergone heart valve replacement.

In all the patients who had acute aortic dissection, the researchers found 88 genes that were significantly different from the same genes in Marfan patients and in patients who had undergone heart valve replacement.

In addition, Mohamed's group found that a protein called MS FBN1 interacted with the proteins of four of the 88 genes, namely, fibulin 1 (FBLN1), fibulin 2 (FBLN2), Decorin (DCN), and microfibrillar associated protein 5 (MFAPS5).

All of these proteins are involved in building tissue that surround the cells in the aorta. Moreover, one of the four is involved in the development of Marfan syndrome, Mohamed noted.

The researchers found that two of the genes were overexpressed by at least threefold, and two were underexpressed by threefold. The underexpressed genes may explain the cause of acute aortic dissection, the researchers noted.

"We did our study primarily to gain a better understanding of the molecular mechanism underlying acute aortic dissection," Mohamed said.

"The study was also aimed at the future development of a clinical test for monitoring patients with a high risk of acute aortic dissection. Most acute aortic dissection patients do not have a known connective tissue disorder. The identification of the four genes could be a starting point to develop a diagnostic tool," Mohamed said.

Acute aortic dissection is usually accompanied by chest pain that may radiate to the back. Other symptoms include nausea, sweating and difficulty breathing. These symptoms can be easily confused with a heart attack.

Dr. Curtis Rimmerman, the Gus P. Karos Chair of Clinical Cardiovascular Medicine at Cleveland Clinic, noted that aortic dissection is a life-threatening condition with high morbidity and mortality rates, and it is most often an unpredictable event.

"Any genomic advance that may be able to identify those patients with a heightened risk for acute aortic dissection represents a significant positive step forward," Rimmerman said.

With the exception of those patients with Marfan syndrome and those with a family history of aortic dissection, no screening program is in place to identify patients at risk for aortic dissection, Rimmerman said.

"Should those patients predisposed to aortic dissection be reliably identified, this would permit heightened attention to lifestyle modification, blood pressure control, and the preemptive administration of certain medications such as beta blockers," Rimmerman said. "Additionally, in those patients identified as high-risk, this would undoubtedly involve focused efforts at aortic imaging," he said.

Rimmerman cautioned, however, that this was a small study and would need to be replicated in a larger patient group before such testing could be ready for clinical use.

More information

For more on aortic dissection, visit the American Heart Association  .

WEDNESDAY, July 30 (HealthDay News) -- Giving the transplant drug cyclosporine to heart attack patients can prevent the injury that's caused by blood rushing back to the damaged heart, French researchers report.

The trial of cyclosporine involved 58 people whose blocked arteries were reopened after heart attacks. It was spurred by several lines of research, noted study lead author Dr. Michel Ovize, professor of physiology and cardiology at the University of Lyon.

One is the finding that some of the damage in heart attack survivors is caused by what is called reperfusion injury -- the unavoidable damage that comes when blood flow is suddenly restored to cardiac tissue through techniques such as balloon angioplasty.

"Recent studies, including some from our group, showed that tissue damage is due at least partially to the reopening of occluded arteries," Ovize explained. "This was new, because it was believed for a long time by doctors that all the damage was due to ischemia [blockage], not reperfusion."

Another line of research established that on the cellular level, damage was due to the opening of a structure called the "mitochondrial permeability-transition pore." Mitochondria are the energy-producing portions of living cells. "Research showed that the mitochondrial permeability-transition pore is a very important structure involved in cell death after [heart attack]," Ovize said.

And a third line of research showed that one of the unintended side effects of cyclosporine was to keep that pore closed. That activity has nothing to do with cyclosporine's use in organ transplants, the scientists said.

So, armed with those insights, the French tram treated half of the heart attack patients with an injection of cyclosporine just before the coronary arteries were reopened, while the other half got standard treatment.

Detailed studies showed that the amount of heart tissue that died was about a third less in people receiving the cyclosporine versus patients who did not get the drug.

Although the study is small and requires larger trials to confirm the finding, indications are that use of cyclosporine (or another drug with the same pore-blocking action) could reduce overall heart attack damage by 10 percent, said Derek M. Yellon, director of the Hatter Cardiovascular Institute at University College London, who wrote an accompanying editorial.

"People are going to do it when you are rushed to the hospital," he said. "You are in danger while they are reperfusing the muscle."

The reason for using a pore-blocking drug is "straightforward," Yellon said. "After a period of ischemia, when certain pores in the mitochondria open, that is detrimental," he said. "You'd rather keep those pores closed."

The French trial, Yellon acknowledged, is "a very small concept study. This area has not yet been well investigated."

"We are already involved in multicenter studies," Ovize said. Those studies will use not only cyclosporine, but also other pore-blocking agents. Drug companies are busily developing such agents, he said.

"In this study, by acting on the target, we were able to prevent cell death," Ovize said. "Now we need more studies to see whether that translates into improvement of left ventricular function and overall heart function."

More information

Current heart attack treatments are described by the U.S. Heart, Lung and Blood Institute.

TUESDAY, July 29 (HealthDay News) -- Despite high levels of smoking, Japanese men are far less likely to have dangerous plaque build-up in their blood vessels than white or Japanese-American men, a difference that researchers believe stems from a lifelong, near-daily consumption of fish.

"Japanese living in Japan eat fish every day, about 100 grams every day," said study author Dr. Akira Sekikawa, an assistant professor of epidemiology at the Graduate School of Public Health at the University of Pittsburgh in Pennsylvania. "They also have very low rates of coronary heart disease, even with a high rate of smoking and other risk factors."

Results of the study are in the Aug. 5 issue of the Journal of the American College of Cardiology.

Current American Heart Association (AHA) guidelines recommend eating oily fish, such as salmon or albacore tuna, at least twice a week if you don't have heart disease. If you already have heart disease, the AHA suggests getting at least one gram of omega-3 fatty acids daily, preferably from fatty fish. However, the AHA cautions that you shouldn't consume more than two grams of fish oil daily without first consulting your doctor, because of a risk of excessive bleeding.

Sekikawa's study included 281 Japanese men, 306 white American men, and 281 Japanese-American men. Along with giving blood samples, all of the men underwent electron beam computed tomography (EBCT) to measure coronary artery calcification (plaque deposits on the heart's arteries) and ultrasound examinations of the carotid artery in the neck.

Overall, the researchers found that Japanese-American men had the highest number of heart disease risk factors of all three groups. They had the highest average body-mass index, blood pressure, triglycerides and the highest levels of diabetes.

The Japanese men living in Japan had far higher rates of smoking -- 47 percent -- and smoking is one of the most significant heart disease risk factors.

But they had significantly less coronary artery calcifications and less build-up in their carotid arteries.

The levels of omega-3 fatty acids in the blood were 9.2 percent for men living in Japan, 3.9 percent for white men, and 4.8 percent for Japanese-American men. Yet, Japanese-American men had more coronary artery calcifications and more build-up in their carotid arteries than the white men and the men in Japan.

"Fish is an important factor in keeping the Japanese healthy," said the author of an accompanying editorial, William Harris, director of the Metabolism and Nutrition Research Center, Sanford Research/USD, in Sioux Falls, S.D.

"The combination of increased fish oil and a low saturated fat diet is probably the best way to lower heart disease risk. Eskimos have a diet high in omega-3s, but also high in saturated fat, and they don't have the same low levels of heart disease," he added.

Harris said what's important is to consume fish or fish oil on an ongoing basis. "A month of supplements won't get you there," he said. But, if you don't like fish, he said that fish oil supplements can also improve your health, but he suggested that you read the supplement label and make sure that each capsule contains one gram of omega-3s. And, he said, they don't have to be expensive to be effective.

If you don't have heart disease, he said, two grams a day "is more than adequate." And, if you like fish, that's even better.

"Choose oily fish, not fried fish, but fish that naturally contain omega-3s, like salmon, sardines, albacore tuna, herring and mackerel, and you need to eat about two 4-ounce servings a week," Harris added.

More information

To learn more about fish, omega-3s and heart health, visit the American Heart Association  .

MONDAY, July 28 (HealthDay News) -- The number of Americans admitted to hospitals for heart failure has jumped in recent years, and the trend almost certainly will continue, government experts report.

"Our study covers more than two decades, from 1979 to 2004, and the number of hospitalizations almost tripled during that time," said Dr. Jing Fang, an epidemiologist with the U.S. Centers for Disease Control and Prevention, and lead author of the report in the Aug. 5 issue of the Journal of the American College of Cardiology.

A major reason for the increase is the aging of the American population, Fang said. Heart failure, in which the heart progressively loses its ability to pump blood, is more common among older people.

"Another reason is the improvement in technology for treatment of patients with other heart diseases, such as acute myocardial infarction [heart attack]," Fang added. "So, people with diseases of the heart live longer."

Data from the National Heart Discharge Survey showed that the number of admissions to hospitals with any mention of heart failure rose from 1.274 million in 1979 to 3.86 million in 2004, the report said. More than 80 percent of those admitted to hospitals were 65 or older, with Medicare or Medicaid covering the cost.

The report did not cover the cost of the hospitalizations, but the American Heart Association has estimated it to be more than $20 billion annually, Fang said.

There has been a marked increase in the number of hospitalizations for which heart failure was not the primary cause, the report said. Heart failure was listed as the primary cause in no more than 35 percent of cases, with respiratory diseases and other conditions given as the reason for hospital admission in all other cases.

"Most are due to pneumonia or another disease that makes heart failure worse," Fang said. Better control of those other conditions, which include diabetes and kidney disease, could reduce hospitalizations for heart failure, Fang added.

But those people tend to keep coming back to the hospital because "you cannot cure people with heart failure," Fang said. "The best medicine [we] can do is to keep the heart functioning enough for the patient to have good quality of life."

A basic problem is that there is no effective treatment for heart failure severe enough to cause hospitalization, said Dr. Javed Butler, director of the heart failure research program at Emory University, and co-author of an accompanying editorial.

"When you are talking about medications that have been proven, they all are for chronic, stable outpatients," Butler said. "We don't have any proven medications for treatment in the hospital."

What is needed is a major effort to develop in-hospital treatments for severe heart failure, he said. "When you consider the huge cost, it is right up high on the list of conditions we need to study," Butler said. "It is a least-studied, most costly problem. We need to get a better grasp on what we should be doing."

More information

Learn about heart failure and its management from the American Heart Association  .