These conclusions were contained in preliminary research presented at the American Heart Association’s Vascular Discovery: From Genes to Medicine Scientific Sessions 2020.

The meeting is a premier global exchange of the latest advances in new and emerging scientific research in arteriosclerosis, thrombosis, vascular biology, peripheral vascular disease, vascular surgery and functional genomics.

“The results of this study advance our understanding of the interconnections among the brain, bone marrow and blood vessels, with activity of the brain emotional center closely linked to heart disease activity and inflammation of blood vessels which are spurred by inflammatory immune cells produced by the bone marrow,” said Dong Oh Kang, M.D., lead study author and clinical instructor in the cardiovascular center of Korea University Guro Hospital in Seoul, Korea.

The researchers obtained simultaneous PET and CT scans to create 3-D images of the brain, major arteries and bone marrow of 62 study participants. The study included 45 people (84% male, average age 60 years) who had a heart attack within the previous 45 days and 17 people with no heart attack history (76% male, average age 59.6 years), the control group. All participants completed widely accepted standard screening questionnaires for depression and perceived stress.

Those who had a recent heart attack had significantly higher activity in the amygdala region of the brain, which is responsible for stress perception and emotional response.

The participants who had a recent heart attack also had increased inflammation in the aorta and carotid artery (neck), which supplies blood to the brain, and increased bone marrow activity, indicating active production of inflammatory cells.

In both groups, those who reported feeling more depressed or stressed on psychological questionnaires showed higher activity in the amygdala.

Butrain emotional activity and inflammation can change over time. After six months, the 10 heart attack patients who underwent follow-up imaging had near-normal PET and CT scans.

“Amygdala activity has previously been reported to be stable over time, however, the changes seen in our study suggest the possibility that stress reduction techniques may lower brain emotional activity and potentially reduce inflammation in arteries and the production of inflammatory cells, thus, potentially modifying the course of heart disease. This could become an additional strategy to prevent a second heart attack,” Kang said.

Although the study found significant links between amygdala activity and artery inflammation, intervention studies are needed to investigate the possible benefits of modifying brain emotional activity on atherosclerosis. Kang also noted more research is needed to identify the most effective stress relief treatments.

Stopping long-term, low-dose aspirin therapy may increase your risk of suffering a cardiovascular event, according to new research in the American Heart Association’s journal Circulation.

Aspirin, taken in low doses, is used to help reduce the risk for recurrent heart attack or stroke. Aspirin inhibits clotting, lowering the risk of cardiovascular events. Nearly 10 to 20 percent of heart attack survivors stop daily aspirin use within the first three years following their event. In broader patient settings, discontinuation rates of up to 30 percent and poor aspirin compliance in up to 50 percent of patients have been reported.

To study the health effects of stopping aspirin therapy, Swedish researchers examined the records of 601,527 people who took low-dose aspirin for heart attack and stroke prevention between 2005 and 2009. Participants were older than 40, cancer-free and had an adherence rate of greater than 80 percent in the first year of treatment.

In three years of follow-up, there were 62,690 cardiovascular events. Researchers also found:

• one out of every 74 patients who stopped taking aspirin had an additional cardiovascular event per year;
• a 37 percent higher rate of cardiovascular events for those who stopped aspirin therapy compared to those who continued; and
• an elevated risk of cardiovascular events that increased shortly after discontinuation of therapy and did not appear to diminish over time.

“Low-dose aspirin therapy is a simple and inexpensive treatment,” said Johan Sundstrom, M.D., Ph.D., lead author and professor of epidemiology at Uppsala University in Sweden. “As long as there’s no bleeding or any major surgery scheduled, our research shows the significant public health benefits that can be gained when patients stay on aspirin therapy.”

Studies have suggested patients experience a “rebound effect” after stopping aspirin treatment; this is possibly due to increased clotting levels from the loss of aspirin’s blood-thinning effects. Because of the large number of patients on aspirin and the high number who stop treatment, the importance of a rebound effect may be significant, Sundstrom said.

“We hope our research may help physicians, healthcare providers and patients make informed decisions on whether or not to stop aspirin use,” Sundstrom said.

The American Heart Association recommends that people at high risk of heart attack should take a daily low-dose of aspirin (if told to by their healthcare provider) and that heart attack survivors also take low-dose aspirin regularly.

Co-authors are Jakob Hedberg, M.D., Ph.D.; Marcus Thuresson, Ph.D.; Pernilla Aarskog, M.Sc.; Kasper Johannesen, M.Sc. and Jonas Oldgren, M.D., Ph.D. Author disclosures are on the manuscript.

The study was funded by Uppsala University, Uppsala County Council and AstraZeneca.

Statements and conclusions of study authors published in American Heart Association scientific journals are solely those of the study authors and do not necessarily reflect the association’s policy or position. The association makes no representation or guarantee as to their accuracy or reliability. The association receives funding primarily from individuals; foundations and corporations (including pharmaceutical, device manufacturers and other companies) also make donations and fund specific association programs and events. The association has strict policies to prevent these relationships from influencing the science content. Revenues from pharmaceutical and device corporations and health insurance providers are available at www.heart.org/corporatefunding.

About the American Heart Association

The American Heart Association is devoted to saving people from heart disease and stroke – the two leading causes of death in the world. We team with millions of volunteers to fund innovative research, fight for stronger public health policies and provide lifesaving tools and information to prevent and treat these diseases. The Dallas-based association is the nation’s oldest and largest voluntary organization dedicated to fighting heart disease and stroke. To learn more or to get involved, call 1-800-AHA-USA1, visit http://www.heart.org/ or call any of our offices around the country. Follow us on Facebook and Twitter.

A release from the publisher explains that three of the most important risk factors for coronary heart disease–lack of exercise, overweight, and stress–are amenable to intervention. While conventional preventive measures concentrate on exercise and advice on nutrition, MBM also embraces relaxation methods and psychological motivation techniques. In the studies analyzed by Cramer et al., coronary events occurred in 68 of 307 patients who received conventional interventions but in only half as many–33/308–of those on MBM prevention programs. The authors point out that despite this positive effect MBM does not decrease mortality in cardiac patients. Nevertheless, the lower incidence of coronary events is beneficial. They therefore endorse MBM or other comparable programs for lifestyle modification.

A release from the university notes that therapeutic hypothermia involves decreasing the body temperature to protect the brain when blood flow is reduced from a cardiac arrest, when the heart stops pumping and the patient has no pulse.

Previous studies have shown the therapy effective on patients with so-called “shockable” heart rhythms like ventricular fibrillation. But Perman’s research demonstrates that it’s also effective on patients with “nonshockable” rhythms when there is no pulse and the patient is in a coma.

The release quotes Perman, an assistant professor of emergency medicine at the University of Colorado School of Medicine, as saying,”Prior to our study, there was minimal data to support the use of this treatment on patients with nonshockable rhythms. As a result, the therapy was not widely used with these patients.”

Every year, 530,000 Americans suffer cardiac arrest and 300,000 of them happen outside of a hospital.

Perman, a clinical expert in cardiac arrest and post-arrest care, and her colleagues looked at data from 519 patients who had nonshockable heart rhythms between 2000 and 2013.

They found those who received therapeutic hypothermia were 2.8 times as likely to survive to be discharged from the hospital and 3.5 times more likely to have better neurological outcomes – returning to their baseline mental state – than those who did not have the treatment.

Physicians who use the technique employ cooling wraps to drop the patients’ temperature from approximately 37 degrees Celsius to 33 degrees Celsius (91.4 degrees F). The therapy has shown to reduce damage to the brain following a cardiac arrest, though scientists continue to investigate why this occurs.

Landmark trials in 2002 studying shockable patients found 49 percent of those who received therapeutic hypothermia had good neurological outcomes as opposed to 26 percent who did not receive the treatment. Another trial showed 55 percent of patients with good neurological outcome against 39 percent who didn’t have the therapy.

“Neurologic injury after cardiac arrest is devastating,” said Perman, who like most physicians at CU Anschutz is both an active researcher and practicing clinician. “We have one chance to give some form of neuroprotection, and that’s immediately after the arrest.”

She said therapeutic hypothermia should be more widely used in comatose patients to protect neurological function.

“We know that patients benefit from this therapy,” said Perman, noting the importance of delivering meaningful research from the laboratory directly to the patient. “Therefore, one of our next challenges is to tailor the hypothermia treatment to the patient’s specific injury in order to improve outcomes further.”

Q. What are non-steroidal anti-inflammatory drugs (NSAIDs)?

A. NSAIDs are a group of drugs used to temporarily relieve pain and inflammation. They work by blocking the production of prostaglandins, or chemicals believed to be associated with pain and inflammation.

Q. What conditions do NSAIDs treat?

A. Prescription NSAIDs are important to help manage many debilitating conditions such as osteoarthritis and rheumatoid arthritis. Some prescription NSAIDs also are used to treat pain. Over-the-counter versions of some NSAIDs are used to treat pain associated with dental problems, tendonitis, strains, sprains and other injuries. NSAIDs are also commonly used to treat fever and to reduce pain associated with menstrual cramps.

Q. What are non-selective NSAIDs and COX-2 selective NSAIDs?

A. Non-selective NSAIDs work by inhibiting two enzymes that are involved with inflammation—cyclooxygenase-1 and cyclooxygenase-2 (COX-1 and COX-2).

There are several non-selective NSAIDs on the market, including diclofenac, ibuprofen, ketoprofen, meloxicam, naproxen, and oxaprozin. Ibuprofen and naproxen are available in both prescription and over-the-counter (OTC) versions. The doses in OTC NSAIDs are lower than the doses of prescription versions and should only be used for up to 10 days without seeing a doctor. So, if you take OTC ibuprofen (Advil and Motrin) or naproxen (Aleve), the doses are about half the doses of prescription versions.

COX-2 selective inhibitors are a newer type of medicine that block the COX-2 enzyme more than the COX-1 enzyme. The only COX-2 selective inhibitor currently on the market in the United States is the prescription drug Celebrex (celecoxib), which is marketed by Pfizer. It was believed that COX-2 inhibitors may be less likely to cause the stomach problems associated with the older NSAIDs, but all NSAIDs carry the risk of stomach problems.

Q. What are the risks of taking NSAIDs?

A. As with all drugs, there is the potential for an allergic reaction to NSAIDs. Symptoms might include hives, facial swelling, wheezing and skin rash.

There is the potential for gastrointestinal bleeding (bleeding in the stomach or elsewhere in the digestive tract) associated with all NSAIDs. The risk of bleeding is low for people who use NSAIDs intermittently. The risk of stomach problems goes up for people who take them every day or regularly, especially for people who are older than 65, people with a history of stomach ulcers, and people who take blood thinners or corticosteroids (prednisone). Alcohol use can also increase the risk of stomach problems.

In addition, using all NSAIDs, except for aspirin, increases the risk of heart attack or stroke. These serious side effects can occur as early as the first few weeks of using an NSAID, and the risk might rise the longer people take non-aspirin NSAIDs.

All NSAIDs also carry the risk of potential skin reactions. Patients should be alert for symptoms such as skin reddening, rash or blisters.

Aspirin is a non-selective NSAID and has been shown in clinical trials to reduce the risks of certain cardiovascular events in patients who have cardiovascular disease or who have already had a heart attack or ischemic stroke. Aspirin is sold in generic forms and under brand names such as Bayer and St. Joseph’s.

Q. Which people are at highest risk for cardiovascular adverse events associated with NSAIDs?

A. People who have cardiovascular disease—particularly those who recently had a heart attack, cardiac bypass surgery or stroke—are at the highest risk for adverse events. According to studies, people who have already had a heart attack are at an increased risk of having another heart attack or dying of heart attack-related causes if they’re treated with NSAIDs, other than aspirin.

Q. Which Cox-2 selective inhibitors have been taken off the market?

A. Merck voluntarily withdrew Vioxx (rofecoxib) in 2004 after finding out the results of a study that showed patients who took Vioxx had a higher risk for heart attacks than patients who took a placebo. FDA asked Pfizer to withdraw Bextra (valdecoxib) from the market in 2005 because the overall risk/benefit profile was unfavorable. The request was based on many factors. Along with the other risks associated with NSAIDs, there was a higher than expected number of reports of serious and potentially life-threatening skin reactions, including death.

An increased risk of cardiovascular adverse events has been shown for all COX-2 inhibitors, including Celebrex, which is still on the market in the United States. Based on available data, FDA determined that the benefits of Celebrex outweigh the potential risks in properly selected and informed patients. FDA asked Pfizer to include a boxed warning on the Celebrex label, and asked manufacturers of all prescription NSAIDs to revise their labeling with a boxed warning too. The boxed warning highlights the potential for increased risk of cardiovascular events as well as serious, potentially life-threatening gastrointestinal bleeding. It is important to know that FDA also determined that the risk for cardiovascular events was most likely present for the non-selective NSAIDs as well, and all of the manufacturers of these drugs were asked to add important warnings to their labels.

Q. What can consumers do to lower their risks with NSAIDs?

A. Tell your doctor about your complete medical history, including any history of cardiovascular disease or stomach ulcers. This will help you and your doctor weigh the risks and benefits. You can also ask your doctor what you can do to lessen the chance for stomach irritation such as taking medication with a meal. Also, ask what steps you can take to lower the risk of cardiovascular disease and report medication side effects to your doctor. Whether you’re taking a prescription NSAID or an OTC NSAID, following directions is important. Available scientific data don’t suggest an increased risk of serious cardiovascular events for short-term, low-dose use of OTC NSAIDs, but it is not known if that is because there is no risk or because there are many challenges when trying to study the use of OTC NSAIDs. Be aware that the OTC labeling states that if you take an NSAID for longer than 10 days, you should see your doctor. The lowest effective dose should be used for the shortest time.

This article appears on FDA’s Consumer Updates page, which features the latest on all FDA-regulated products.

Most important for readers of thirdAGE.com is that “there is not enough available evidence on the benefit and harms of aspirin use in adults younger than age 50 and those 70 and older to recommend for or against its use in preventing CVD [cardiovascular disease] and CRC [colorectal cancer]”. Not only that, but the only definite recommendation given is that “most people between the ages of 50 and 59 who have an increased risk of heart attacks or stroke should take a low-dose aspirin every day.” [Italics mine.]

You can read the recommendations for yourself here. When you get there, click on “Draft: Related Information for Consumers” to download the pdf. Also, you have until October 12th 2015 to leave comments if you want to do that here.

Finally, be sure to consult with your own physician regarding aspirin use no matter what your heath status or your age may be. Don’t “self medicate”. But you knew that!

A release from the publishers explains that osteoarthritis is the most common form of arthritis, affecting 27 million Americans over the age of 25 according to the ACR. As the joint cartilage and bone deteriorates, knee or hip replacement surgery may be the only option to relieve pain and stiffness and restore mobility. Previous studies estimate that 1.8 million arthroplasty procedures are performed each year worldwide, and that number may increase as the population ages.

The release quotes lead study author Yuqing Zhang, D.Sc., Professor of Medicine and Epidemiology at Boston University School of Medicine in Boston, Massachusetts, as saying, “While evidence shows that joint replacement surgery improves pain, function, and quality of life for the osteoarthritis patient, the impact of cardiovascular health has not been confirmed. Our study examines if joint replacement surgery reduces risk of serious cardiovascular events among osteoarthritis patients.”

The present cohort study included 13,849 patients who underwent total knee replacement surgery and 13,849 matched controls who did not have surgery. Patients were 50 years of age or older and diagnosed with knee or hip osteoarthritis between January 2000 and December 2012.

Findings indicate that 306 patients in the arthroplasty group and 286 in the non-surgical group developed myocardial infarction during the follow-up period. Risk of heart attack was significantly higher during the first postoperative month in those who had knee replacement surgery compared to those in the non-surgical group, and gradually declined over time. Venous thromboembolism was a significant risk during the first month and over time for those having total knee or total hip arthroplasty.

“Our findings provide the first general population-based evidence that osteoarthritis patients who have total knee or total hip replacement surgery are at increased risk of heart attack in the immediate postoperative period,” concludes Dr. Zhang. “The long-term risk of heart attack was insignificant, but risk of blood clots in the lung remained for years after surgery to replace a hip or knee damaged by osteoarthritis.”

The findings were published in Science Translational Medicine.

According to a news release from the university, the team found that the loss of the microRNA cluster miR302-367 in mice led to decreased cardiomyocyte cell proliferation during development. In contrast, increased expression of the microRNA cluster in adult hearts led to a reactivation of proliferation in the normally non-reproducing adult cardiomyocytes.

This reactivation occurred, in part, through repression of a pathway called Hippo that governs cell proliferation and organ size. “The Hippo pathway normally represses cell proliferation when it is turned on. The cluster miR302-367 targets three of the major kinase components in the Hippo pathway, reducing pathway activity, which allows cardiomyocytes to re-enter the cell cycle and begin to regrow heart muscle,” explains Morrisey. “This is a case of repressing a repressor.”

In adult mice, re-expression of the microRNA cluster reactivated the cell cycle in cardiomyocytes, resulting in reduced scar formation after an experimental myocardial infarction injury was induced in the mice. There was also an increase in the number of heart muscle cells in these same mice.

However, long-term expression of more than several months of the microRNA cluster caused heart muscle cells to de-differentiation and become less functional. “This suggested to us that persistent reactivation of the cell cycle in adult cardiomyocytes could be harmful and causes the heart to fail,” says Morrisey. The investigators surmised that cardiomyocytes likely need to de-differentiate to divide, but they may lose their ability to contract over time.

“We overcame this limitation by injecting synthetic microRNAs with a short half-life called mimics into the mice,” says Morrisey. Mimic treatment for seven days after cardiac infarction led to the desired increase in cardiomyocyte proliferation and regrowth of new heart muscle, which resulted in decreased fibrosis and improved heart function after injury.

Importantly, the team found that the transient seven-day treatment did not lead to the progressive loss of cardiac function as seen in the genetic models of increased microRNA expression. Overall, these results suggested that any treatment that promotes cardiomyocyte proliferation to improve cardiac regeneration will likely need to be transient to avoid the deleterious effects of maintaining a high level of proliferation and de-differentiation in a tissue that is normally non-proliferative.

“The next stage in this study is to determine whether miRNA mimics will work in a larger animal model and to collaborate with bioengineers to create a local delivery system for the heart, rather than giving it systemically,” notes Morrisey.