Congestive Heart Disease Reversed

This is an extraordinaryfinding.  High blood pressure leadsinevitably to an enlarge heart and eventual failure.  There has been no cure except a hearttransplant.  Much of post heart attacktreatment is aimed at preventing the development of an enlarged heart, as isthe reduction of blood pressure in the hypertensive.

Now it appears we are on the wayto having a drug able to literally reverse the whole process.  This is obviously great news.

If heart disease could be managedand largely eliminated, the natural lifespan would easily crawl up into thenineties.  This therapy in conjunctionwith the pending ability to replace damaged muscle will do it.  It is perhaps possible to live a perfect lifeand thus to avoid the ravages of heart disease. The point is that almost no one is able to do that.  Thus actual repair is how we presently makeit and this is an important new tool.

I am seeing a range of problemsbeen solved that were death sentences in the recent past.  This was the big one, little discussedbecause no one actually thought it could be.

Drug can reverse overgrown hearts to help prevent heart failure, UTSouthwestern researchers find

Using mice, Drs. Joseph Hill and Dian Cao found that anHDAC inhibitor caused enlarged hearts to regress back to near-normal size.

DALLAS – May 31, 2011 – A promising cancer treatment drug can restorefunction of a heart en route to failure from high blood pressure, researchersat UT Southwestern Medical Centerhave found.

The drug, a type of histone deacetylase (HDAC) inhibitor being evaluated innumerous ongoing clinical trials, has been shown to reverse the harmful effectsof autophagy in heart muscle cells of mice. Autophagy is a natural process bywhich cells eat their own proteins to provide needed resources in times ofstress. The new study appears in Proceedings of the National Academyof Sciences.

 “This opens the way for a newtherapeutic strategy in hypertensive heart disease, one we can test forpotential to promote regression of heart disease,” said Dr.Joseph Hill, chief of cardiology and director of the Harry S. MossHeart Center at UT Southwestern.

Dr. Hill, senior author of the study, and other researchers have shownpreviously that all forms of heart disease involve either too much or toolittle autophagy, normally an adaptive process. For example, in the presence ofhigh blood pressure, the heart enlarges, or hypertrophies, and autophagy isturned on. Ultimately, the hypertension-stressed heart can go into failure.

Prior research from Dr. Hill’s laboratory has shown that HDAC inhibitors bluntdisease-associated heart growth, so researchers designed this study todetermine what impact a particular type of HDAC inhibitor had on autophagy.

The researchers engineered mice with overactive autophagy and inducedhypertrophy leading to heart failure. Scientists then gave the mice an HDACinhibitor known to limit autophagy.

“The heart decreased back to near its normal size, and heart function that hadpreviously been declining went back to normal,” Dr. Hill said. “That is apowerful observation where disease regression, not just disease prevention, wasseen.”

Dr. Hill noted that the research that led to this finding started decades agoand included studies led by Dr.Kern Wildenthal, former president of UT Southwestern and now presidentof Southwestern Medical Foundation.

“This is one of those exciting, but rare, examples where an importantfinding made originally in yeast moved into mouse models and is soon moving tohumans,” Dr. Hill said. “That’s the Holy Grail for a physician-scientist – totranslate those sorts of fundamental molecular discoveries through preclinicalstudies and ultimately in humans.”

Other UT Southwestern researchers involved in the study were Dr. DianCao, postdoctoral trainee in internal medicine; Dr. Zhao Wang, postdoctoralresearcher in internal medicine; Dr. Pavan Battiprolu, postdoctoral researcherin internal medicine; Nan Jiang, research associate in internal medicine; CyndiMorales, student research assistant in internal medicine; Yongli Kong, researchscientist in internal medicine; and Drs. BeverlyRothermeland ThomasGillette, both assistant professors of internal medicine.

The study was funded by the National Institutes of Health, American HeartAssociation, American Diabetes Association and the AHA-Jon Holden DeHaanFoundation.

Visit http://www.utsouthwestern.edu/heartlungvascular tolearn more about UT Southwestern’s heart, lung and vascular clinical services.

http://www.utsouthwestern.edu/utsw/cda/dept353744/files/640789.html