Among diseases, cancer may get most of the attention from researchers since it can be a swift killer, but heart disease is still the leading cause of death in the United States. The latest update from the Centers for Disease Control and Prevention utilizing data from 2013 shows that 611,105 deaths were attributed to heart disease, followed by nearly 585,000 attributed to cancer. Put another way, heart disease killed more people in 2013 than chronic respiratory diseases, Alzheimer's disease, diabetes, influenza and pneumonia, nephritis and nephrotic syndromes, stroke, and suicide combined!
Now, this isn't to say researchers don't have a pretty good grasp on the science behind why people get heart disease in the first place. Many of the risk factors, including smoking and obesity, have been known for some time.
However, the underlying mechanisms of how the heart functions have long been a mystery. Researchers understand that calcium helps trigger contraction of the fibrous proteins that make up a person's heart muscle cells, called sarcomeres. Until recently, researchers couldn't explain what made that contraction so synchronous, but the answer to this long-standing question may finally have been solved.
Getting to the possible root cause of heart disease
According to a recently released study conducted by researchers at the University of Maryland School of Medicine, and published in the journal Science Advances, myosin-binding protein C (known as MyBP-C) is the secret agent responsible for keeping our heartbeat in perfect harmony.
During the study, Dr. W. Jonathan Lederer discovered that calcium molecules, which trigger the aforementioned contraction of sarcomeres, aren't distributed evenly across the length of each sarcomere as expected. Instead, they're released at each end of the sarcomere, leaving researchers with a big question mark concerning how the entire sarcomere contracted in unison if there wasn't much calcium near the center of the sarcomere.
Utilizing animal models, researchers were able to uncover the answer. According to the ten authors participating in the study, MyBP-C sensitizes portions of the sarcomere to calcium, allowing the middle of the sarcomere to contract just as much as the ends despite having less calcium to trigger a synchronous contraction.
"Why's this important?" you wonder? With the new understanding of the role MyBP-C plays, researchers also understand that defects in MyBP-C can led to heart arrhythmias, or an irregular heartbeat, which in turn could lead to serious complications or death. Researchers believe this finding could be critical in that drug developers could target MyBP-C to develop drugs to prevent arrhythmias and other potentially dangerous heart diseases.
As usual, though, it's worth pointing out that this test was conducted on animal models, and additional testing will need to proceed in humans before anything can be written in stone. Nonetheless, it's a potentially exciting discovery that could lead to an improvement in the way drug developers attack the root causes of heart disease.
New applications take shape
Realistically, we're probably years away from observing any preclinical activity surrounding MyBP-C, but this doesn't mean there aren't potentially game-changing drugs currently in development to treat dangerous heart problems.
Would it surprise you to learn that one such treatment is currently being developed by Gilead Sciences (NASDAQ:GILD)? Yes, the same company that brought the world an effective cure for hepatitis C may also have the next standard of care for paroxysmal (or occasional) atrial fibrillation.
Last year, Gilead presented its phase 2 study findings from its HARMONY trial at the Heart Rhythm Society's annual meeting. The study tested Gilead's chronic angina drug Ranexa in combination with a low dose of Sanofi's (NYSE:SNY) dronedarone (known by its brand-name, Multaq) for atrial fibrillaton. Both drugs were tested separately to see if they produced a statistically significant reduction in atrial fibrillation burden from baseline relative to the placebo, and both drugs individually failed to do so -- but the combination of both drugs certainly did.
The control group that received a 750 mg dose of Ranexa and 150 mg dose of dronedarone experienced a 45% reduction in atrial fibrillation burden (AFB) over 12 weeks, while the group receiving a 750 mg dose of Ranexa and 225 mg dose of dronedarone showed a 59% reduction in AFB over 12 weeks. The promising combo will be moving to late-stage trials next.
In even later-stage studies, we have Novartis' (NYSE:NVS) experimental heart failure drug LCZ696, which has been granted a priority review by the Food and Drug Administration and could find its way onto pharmacy shelves sometime soon in 2015.
In the enormous PARADIGM-HF study, which spanned 8,842 patients across 47 countries over the course of 27 months, LCZ696 was shown to reduce the risk of sudden death related to heart failure by 20%, lower the risk of hospitalization for heart failure by 21%, and lessen the need for more intense treatments by 16% compared to the control group taking enalapril, the current standard of care. Patients taking LCZ696 also had a 31% lower likelihood of needing intravenous drugs to help their heart pump when they did require hospitalization. In other words, LCZ696 appears as if it's about to completely transform how we treat the millions of patients globally who suffer from heart failure.
Pumping up hopes
Obviously, there's still a lot to be done when it comes to improving quality of life for patients suffering from heart arrhythmias and heart failure. These two clinical-stage therapies are certainly a starting point, and they could become the next standards-of-care for years to come.
But it's also worth noting that just because these two therapies have shown promise, we won't see drug developers sitting on their hands and not exploring new pathways. MyBP-C could be something we're talking about a few years from now, as well as a number of innovative pathways. As long as heart disease remains the leading killer in the U.S., look for this to be a primary focus for drug developers moving forward.
Sean Williams has no material interest in any companies mentioned in this article. You can follow him on CAPS under the screen name TMFUltraLong, track every pick he makes under the screen name TrackUltraLong, and check him out on Twitter, where he goes by the handle @TMFUltraLong.
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