Previously in these pages we’ve discussed the curious phenomenon called broken heart syndrome, stress cardiomyopathy, or takotsubo syndrome (so called because the apex of the heart balloons out, making the heart look like a Japanese octopus trap, or “tako tsubo”), usually occurring during a stressful event. Patients have the symptoms of a heart attack, but no arterial blockage can be found, and the heart is not damaged.
A research team in Italy developed a procedure called myocardial contrast echography, enabling them to study coronary vessels that are too small to be seen by catheterization. They observed that in broken heart syndrome these vessels, the coronary microcirculation, go into spasm, reducing blood flow enough to keep the heart from contracting normally, but not enough to cause permanent damage.
Plaque in an artery becomes calcified in its advanced stages - bits of hard bone-like material develop in it. Usually the plaque itself remains soft enough so that a stent can push it out, with its calcifications, so as to open the artery. But sometimes the whole plaque becomes so hard that nothing will budge it.
If plaque is heavily calcified, and it’s no longer possible to bypass the bypasses, the only remaining options might appear to be luck and nitroglycerin. But there is an alternative, a drilling technology that has been available, at only a few hospitals, since the 1990’s.
Among others, Dr. Fred Leya, a cardiologist at Loyola University Health System, does the procedure about three times a week, boring through bone-hard blockages with a diamond-tipped drill that spins at 250,000 RPM and looks and sounds like a dentist’s drill.
When human hearts are damaged, the injured muscle is replaced by rigid scar tissue. When zebrafish hearts are damaged, the injured muscle is replaced by new muscle. Several different research teams have been looking into how this is done.
One team labeled zebrafish heart cells with a chemical that fluoresced when a gene called gata4 was activated. When they cut out a nearby bit of heart muscle, fluorescence showed that muscle cells began to show gene activity and divided to form new cells at the injury site. The new muscle was fully functional after a few weeks.
Another team used a different fluorescent labeling technique to show that the new muscle came, not from stem cells as might be expected, but from ordinary heart muscle cells. During the regeneration process the cells went through a state similar to the “hibernation” of injured human heart cells, which the researches hope might somehow be “pushed” into regeneration.
Current implantable pacemakers and defibrillators are implanted at a distance from the heart and connected to the heart by a few wires. The more wires are used, the more information the device can get and the more control it can exert, but the number of wires is limited.
A team at the University of Pennsylvania is testing a device that doesn’t use wires. Using flexible silicon-based electronic circuitry, it is implanted in contact with heart tissue. Experimentally they placed nanoscale ribbons of silicon with hundreds of electrodes and thousands of transistors on the heart of a living pig and mapped the activity of the heart in unprecedented detail.
Further work will be directed at developing devices that are not only flexible but stretchable, so they can be wrapped around large curved surfaces on the heart. The aim is to develop “intelligent” pacemakers and other devices that can more effectively correct cardiac arrhythmias.
Fats containing omega-3 fatty acids are famous for contributing to general heart health by reducing risk factors. Recent studies have shown that they can be beneficial in some specific instances.
One such situation is persistent atrial fibrillation (AF). This uncoordinated activity of the upper chambers of the heart can be corrected by electrical cardioversion, but in some patients AF comes back repeatedly after a few weeks or months. A recent study found that an omega-3 fatty acid supplement, in addition to the usual drug treatment, prolonged the average time to relapse from 139 days (with placebo) to 168 days (with the supplement).
Another instance is clopidogrel (Plavix) resistance. Patients who receive stents, especially drug coated stents, take Plavix, often with aspirin, to lower the risk of clotting in the stent (stent thrombosis). In some patients this treatment doesn’t do enough to prevent clotting. Omega-3 fatty acids are known to have anti-platelet effects, and a recent study suggests that they could be useful in combination with Plavix.
According to a study published last month in the Journal of the American Medical Association, patients experiencing heart attack symptoms are 38 percent more likely to delay going to the hospital for six hours or more if they are uninsured, and 21 percent more likely if they are insured but nevertheless have financial concerns. Regardless of insurance status, 42 percent of patients waited more than six hours.
On a brighter note, progress is being made toward insurer participation in programs to lower treatment costs. UnitedHealth plans to provide employer-insured patients with a free 16-week program, at YMCA locations, focused on lifestyle changes to prevent type 2 diabetes. UnitedHealth will also team with its partner pharmacies to help patients with diabetes and prediabetes stick to their treatment plans.