HUB's LIST of medical fun facts

“ Dead heart muscle tissue after a heart attack is replaced by non-contractile fibrosis or scar tissue and the heart can not generate new muscle fibers.”
                  -K.B. Margulies, MD, NEJM, 349:20, May 28, 2026

When you have a heart attack a part of your heart muscle dies. Placing coronary artery stents or creating coronary vessel bypasses along with intensive medical treatment with a variety of medications seek to maintain the heart’s usual function as the “blood pumper, chest thumper” (as one of my favorite anatomy professors called it.) If surgical intervention and intensive medical treatment does not improve or maintain heart function, congestive heart failure often develops. Fifty percent (50%) of patients with congestive heart failure die within 5 years of that diagnosis.

The amount of blood each heart beat pushes out into your aorta is called the “ejection fraction” (my professor would have called it “good blood”, the “stuff with oxygen in it”). Without enough “enuff stuff” being pumped out with each beat, aka a “low ejection fraction” (less than 35% of normal), you will suffer from congestive heart failure. Artificial hearts (mechanical pumps) can assist the failing heart. They are getting smaller and smaller in size, but are still cumbersome, complex and costly.  Unsuccessful efforts to regenerate new heart tissue by injecting stem cells into hearts have been under study for years.  A heart transplant is the final option for a failing heart.  Recently a new technique of placing lab-grown heart muscle cells attached to a piece of a special gauze , a “bandaid”, to the damaged outside wall of the heart has been tested in 20 patients. (NEJM 349:20, May 28, 2026)

All 20 patients had severe congestive heart failure (very low ejection fractions; not “enuff good stuff” with each heart beat) despite maximal medical and surgical interventions, including implanted pacemakers and defibrillators. And, all had an area of dead heart cells on the outside wall of the left ventricle (the strongest “pump” part) of the heart. Single units of heart-engineered-muscle of 34 million contractile heart muscle cells and 6 million connective tissue cells, all derived from stem cells, were grown in the lab. These units were then assembled into 5, 10, or 20 unit arrays on a thin membrane. Each array,  called a BioVat (Biologic Ventricular Assist Tissue), was about the size and shape of the usual bandaid. The BioVat array was then minimal-invasively sutured, muscle units against the heart, to the outside wall of the damaged area of the left ventricle, like a bandaid over a scrape.

Since the new heart tissue was a “foreign” graft  to the host, all patients were treated with immunosuppression.  Three patients died of non-coronary causes, and one left the study due to a graft-host reaction. Two years after application the 16 patients who received the maximum dose of 20 BioVat arrays had improvement in the thickness of the ventricle wall (less danger of lethal rupture and a reduced stress on the ventricle), improvement of the ejection fraction from 24% to 31% (more “good stuff” to the brain and body, but still low), and “modest” improvement of quality-of-life measures.

Two editorials made it clear that this procedure was no way “ready for prime time”, but both agreed that it opened up a whole new avenue of research in an innovative treatment of severe congestive heart failure.

“This one study extends the ‘transactional arc’ of two decades of basic and clinical research into effective treatment for patients with advanced heart failure. . . . The scientific importance of this work lies in its demonstration of feasibility. This notable feat sets the stage for further study of treatment efficacy of this product. The ultimate impact of BioVat transplantation is uncertain, but it is clear that the science underlying this effort has matured from aspiration to clinical experimentation.” (D. Srivastava, MD, NEJM349:20, May 28, 2026)