Diseased Carotid Arteries - Credit: David Davies, University of Binghamton
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A couple of months ago, in Post-Disaster Stress Cardiomyopathy: A Broken-Hearted Malady, we looked at a study that found a significant increase in a very rare type of heart problem called Takotsubo cardiomyopathy – also known as broken heart syndrome – following high impact natural disasters.
This stress related syndrome causes acute ballooning of the heart ventricles, and is a well-recognized cause of acute heart failure and dangerous cardiac arrhythmias.
Johns Hopkins Medicine has a Frequently Asked Questions about Broken Heart Syndrome, that describes the condition:
1. What is “stress cardiomyopathy?”
Stress cardiomyopathy, also referred to as the “broken heart syndrome,” is a condition in which intense emotional or physical stress can cause rapid and severe heart muscle weakness (cardiomyopathy). This condition can occur following a variety of emotional stressors such as grief (e.g. death of a loved one), fear, extreme anger, and surprise. It can also occur following numerous physical stressors to the body such as stroke, seizure, difficulty breathing (such as a flare of asthma or emphysema), or significant bleeding.
We’ve looked at other post-disaster (likely stress related) cardiac problems, including earlier last March in Tulane University: Post-Katrina Heart Attack Rates – Revisited, where an ongoing study finds that heart attack rates remain elevated by 300% in New Orleans six years after that hurricane struck.
While there is plenty of anecdotal evidence showing that stress, fear, grief, or other emotional stressors can cause sudden heart attacks thus far we haven’t had a good model as to how that might happen.
Yesterday the open access journal mBio published a fascinating bit of work that attempts to show how a sudden release of the right stress hormone (norepinephrine) can dissolve bacteria laden biofilm deposits in the carotid artery, potentially initiating a heart attack or stroke.
Bernard B. Lanter, Karin Sauer, David G. Davies
IMPORTANCE The association of bacteria with atherosclerosis has been only superficially studied, with little attention focused on the potential of bacteria to form biofilms within arterial plaques.
In the current work, we show that bacteria form biofilm deposits within carotid arterial plaques, and we demonstrate that one species we have identified in plaques can be stimulated in vitro to undergo a biofilm dispersion response when challenged with physiologically relevant levels of norepinephrine in the presence of transferrin. Biofilm dispersion is characterized by the release of bacterial enzymes into the surroundings of biofilm microcolonies, allowing bacteria to escape the biofilm matrix.
We believe these enzymes may have the potential to damage surrounding tissues and facilitate plaque rupture if norepinephrine is able to stimulate biofilm dispersion in vivo. This research, therefore, suggests a potential mechanistic link between hormonal state and the potential for heart attack and stroke.
(Continue . . . )
The American Society for Microbiology has a press release that explains in layman’s terms the mechanism this study believes it has discovered.
Bacteria help explain why stress, fear trigger heart attacks
WASHINGTON, DC – June 10, 2014 - Scientists believe they have an explanation for the axiom that stress, emotional shock, or overexertion may trigger heart attacks in vulnerable people. Hormones released during these events appear to cause bacterial biofilms on arterial walls to disperse, allowing plaque deposits to rupture into the bloodstream, according to research published in published today in mBio®, the online open-access journal of the American Society for Microbiology.
"Our hypothesis fitted with the observation that heart attack and stroke often occur following an event where elevated levels of catecholamine hormones are released into the blood and tissues, such as occurs during sudden emotional shock or stress, sudden exertion or over-exertion" said David Davies of Binghamton University, Binghamton, New York, an author on the study.
Davies and his colleagues isolated and cultured different species of bacteria from diseased carotid arteries that had been removed from patients with atherosclerosis. Their results showed multiple bacterial species living as biofilms in the walls of every atherosclerotic (plaque-covered) carotid artery tested.
In normal conditions, biofilms are adherent microbial communities that are resistant to antibiotic treatment and clearance by the immune system. However, upon receiving a molecular signal, biofilms undergo dispersion, releasing enzymes to digest the scaffolding that maintains the bacteria within the biofilm. These enzymes have the potential to digest the nearby tissues that prevent the arterial plaque deposit from rupturing into the bloodstream.
According to Davies, this could provide a scientific explanation for the long-held belief that heart attacks can be triggered by a stress, a sudden shock, or overexertion
All of this is a very simplistic summation of a complex, and fascinating paper, one that many will want to read in its entirety. While far from settled science, it proffers a very interesting avenue for further investigation.
Of note, while some heart attacks and Takotsubo cardiomyopathy are thought to be induced by similar cascades of stress-related hormones, their actual physical effects appears to be quite different. Johns Hopkins describes the theories behind the cause of stress-cardiomyopathy below:
The precise way in which adrenaline affects the heart is unknown. It may cause narrowing of the arteries that supply the heart with blood, causing a temporary decrease in blood flow to the heart. Alternatively, the adrenaline may bind to the heart cells directly causing large amounts of calcium to enter the cells which renders them temporarily dysfunctional.
The bottom line, I suppose, is that by whatever mechanism, overwhelming stress can take a heavy toll on our physical and mental health.
And in ways that we are only just now beginning to unravel.
