Reporting in a recent issue of Mayo Clinic Proceedings, researchers at the Mayo Clinic (Rochester, New York) determine that it is safe, more convenient and less costly for many patients to undergo coronary angiography and elective valve surgery on the same day. Mayo cardiologist David Holmes Jr, one of the study authors, said, "We have developed a protocol to allow patients to safely have coronary angiography on the same day as their elective surgery. For patients, we are providing quality care and saving them the time and money it takes to make two trips to the hospital for the test and then surgery."

The researchers underlined the significance of the finding by pointing out that nearly 48,000 heart valve replacement or repair surgeries were registered with the National Database of the Society of Thoracic Surgeons (Chicago) in 2005.

Coronary angiography, recommended preoperatively for all patients who are considered at risk for coronary artery disease, is frequently done several days or even weeks before surgery; the patient goes home and then returns for surgery. However, one of the primary concerns of performing coronary angiography the same day as surgery is the risk of acute kidney failure, an independent predictor of death following cardiac surgery. Mortality rates have been reported as high as 44.4%-63.7%, according to researchers, with the dye used in angiography associated with radiocontrast-induced nephropathy which can cause kidney failure.

When worsening kidney function occurs, serum creatinine levels begin to increase after 24 to 72 hours, peak within three to five days and return to normal within another three to five days, thus the reason for the delay between the angiography and surgery, Holmes says.

To make it possible to do angiography and surgery on the same day and diminish the possibility of renal failure, Mayo physicians minimize the total amount of contrast agents and screen patients at risk for kidney disease, choosing different agents based on the patient kidney function, according to Holmes. "In addition, deciding which patients may benefit from this streamlined approach is dependent on careful patient assessment and collaboration between the cardiologist and cardiovascular surgeon," he says.

The researchers evaluated the medical records of 226 consecutive patients who had undergone cardiac catheterization on the day of elective valve repair or replacement between August 2000 and August 2004. Of the 226, angiography showed that 28.3% had severe enough coronary artery disease to also require bypass surgery, in addition to valve surgery. One patient died within 30 days following surgery, and four of the patients had transient renal failure.

Inflammatory illnesses linked to high rate of death from heart disease

Rheumatoid arthritis, lupus, and other inflammatory rheumatic diseases are associated with a high rate of death from heart disease, according to a study by a team of researchers in Norway and the U.S., affiliated with the Cleveland Clinic Foundation (Cleveland, Ohio) and Brigham and Women's Hospital (Boston). One explanation is a greater susceptibility to atherosclerosis.

Although atherosclerosis is linked to inflammation in healthy individuals as well, the mechanism of inflammation and the reason for accelerated atherosclerosis in patients with inflammatory rheumatic disease remain unclear.

Does atherosclerosis result from systemic inflammation, a hallmark of these rheumatic diseases, or from local inflammation of vessels?

To analyze the link between chronic inflammation and atherosclerosis, the researchers focused on the aortas of recent recipients of coronary artery bypass graft (CABG) surgery, comparing biopsy specimens from patients with inflammatory rheumatic disease to those from patients without it.

Their study, presented in the June 2007 issue of Arthritis & Rheumatism affirms inflammatory rheumatic disease and smoking as independent predictors of vessel wall inflammation, with the possibility that vascular inflammation might be a factor that promotes atherosclerosis and the formation of aneurysms.

Aortic samples were obtained during CABG surgery, performed at two cardiac centers in Norway, from 66 patients with inflammatory rheumatic disease and 51 control patients. The inflammatory rheumatic disease group included patients with rheumatoid arthritis, psoriatic arthritis, lupus, ankylosing spondylitis, polymyalgia and other diseases. Age, body mass index, family history of heart disease and other traditional cardiovascular risk factors were similar in both groups. All specimens were evaluated, by light microscope, for evidence of chronic inflammatory cell infiltration in the aortic wall. This was achieved by counting and measuring the mononuclear cell infiltrates (MCI) in the aorta, with particular attention to the adventitia, the deepest layer of vascular tissue.

Using statistical analysis, the relationship between these inflammatory infiltrates and established lifestyle risk factors for heart disease was also assessed.

In the adventitia, MCIs occurred more frequently in patients with inflammatory rheumatic disease - 47% of this group, compared with 20% of the control group. Along with greater prevalence, these inflammatory cells were larger in size. In the middle layer of the vessel wall (the media), MCIs were detected only in patients with inflammatory rheumatic disease. What's more, MCIs were observed in six of seven patients with a history of aortic aneurysm. In addition to inflammatory rheumatic disease, current smoking was independently associated with more pronounced chronic inflammatory infiltration in the inner adventitia.

"The opportunities for detecting aortic inflammation are limited," acknowledges Ivana Hollan, MD. "Our method of tissue examination allows the condition to be diagnosed in patients undergoing CABG surgery without increasing the preoperative risk."

Despite the limitations of the small enrollment acknowledged by the researchers, they said the study suggests the need for further investigation into an inflammatory process that may increase the risk of dying from a heart attack or aneurysm.

Gene therapy reverses heart disease in rats

The experiments — and successes — with gene therapy continue. Researchers at the Center for Translational Medicine at Jefferson Medical College (Philadelphia) report that they have used gene therapy to reverse heart failure in animals. In addition, they found that the gene therapy strategy had "unique and additive effects" to currently used, standard beta-blockers.

Reporting in the journal Circulation, the journal of the American Heart Association (Chicago), researchers led by Walter Koch, PhD, director of the Center for Translational Medicine and the George Zallie and Family Laboratory for Cardiovascular Gene Therapy in the Department of Medicine at Jefferson Medical College of Thomas Jefferson University, used a virus to carry the gene for a protein, S100A1, into the heart cells of rats with heart failure. The virus expressed the S100A1 gene only in heart cells and not in other organs, essentially making it a tailored therapy. After 18 weeks, those animals that received the gene therapy had significantly improved heart function compared to animals that did not receive the treatment.

The Koch team experimentally produced heart failure in the animals, characterized by a dramatic reduction in the heart's pumping ability. The scientists then delivered a modified adeno-associated virus (AAV) that contained the S100A1 gene to the heart's coronary arteries with the help of a novel heart-specific "gene promoter" that enabled the gene to be present only in heart cells.

The rats with heart failure were then followed for another two months. The animals that received the gene therapy had significantly better heart-pumping abilities compared to the pre-gene therapy level, and overall, the S100A1-treated rats had improved heart health. The researchers found this in both individual heart cells and in the whole animal as well.

The researchers also discovered that the S100A1 gene therapy changed the geometry of the heart. In heart failure, the heart tends to increase in size. The added S100A1 slowed down this process and actually reversed it.

Framingham study links blood inflammation to Alzheimer's

People whose blood shows signs of inflammation are more likely to later develop Alzheimer's disease than people with no signs of inflammation, according to a study published in the May 29, 2007, issue of Neurology, the scientific journal of the American Academy of Neurology.

The study, part of the larger Framingham Heart Study, involved 691 healthy people with an average age of 79. Blood tests determined whether the participants had signs of inflammation. Then the participants were followed for an average of seven years. During that time, 44 of the participants developed Alzheimer's disease.

The participants' blood was tested for levels of cytokines, which are protein messengers that trigger inflammation. Those with the highest amount of cytokines in their blood were more than twice as likely to develop Alzheimer's disease as those with the lowest amount of cytokines. A total of 28% of the women and 30% of the men had high levels of cytokines, yet they made up 42% of the cases of Alzheimer's disease.

"These results provide further evidence that inflammation plays a role in the development of Alzheimer's disease," said study author Zaldy Tan, MD, MPH, of Harvard Medical School (Boston). "The production of these cytokines may be a marker of future risk of Alzheimer's disease."

No Comments