Using an ultrasensitive blood test to detect the presence of a protein that heralds heart muscle injury, researchers from Johns Hopkins and elsewhere have found that obese people without overt heart disease experience silent cardiac damage that fuels their risk for heart failure down the road.
For years, a multidisciplinary team of Johns Hopkins researchers has tracked an elusive creature, a complex of proteins thought to be at fault in some cases of sudden cardiac death. As they report Nov. 5 in the online edition of Nature Communications, they have finally captured images of the complex. Those images reveal the connection between some genetic mutations and electrical abnormalities of the heart and provide a starting point for designing therapies.
Heart attack survivors often experience dangerous heart rhythm disturbances during treatment designed to restore blood flow to the injured heart muscle, a common and confounding complication of an otherwise lifesaving intervention
Bruce A. Perler, M.D., M.B.A., was named president-elect of the Society for Vascular Surgery, an international medical society with 5,000 members, at the society’s recent annual meeting in Boston.
A new Johns Hopkins review of 20 years’ worth of published research suggests that risks linked to long-term use of statins, including muscle toxicity, diabetes and dementia, are very low and that the potential benefit is very high. And although some experts say statins may be overprescribed, the new analysis could provide reassurance of the relative safety of the cholesterol-lowering drugs for the more than 200 million people worldwide who take them.
Studies by vascular biologists at The Johns Hopkins Hospital could lead to new treatments for vascular disease. This work was led by Dan Berkowitz, M.B.B.Ch., and Lewis Romer, M.D., both professors of anesthesiology and critical care medicine at the Johns Hopkins University School of Medicine. The studies focus on the balance between (good) nitric oxide, and (bad) oxidants—both important regulators of the inner lining of blood vessels, called the endothelium.
Researchers at Johns Hopkins have spotted a strong family trait in two distant relatives: The channels that permit entry of sodium and calcium ions into cells turn out to share similar means for regulating ion intake, they say. Both types of channels are critical to life. Having the right concentrations of sodium and calcium ions in cells enables healthy brain communication, heart contraction and many other processes. The new evidence is likely to aid development of drugs for channel-linked diseases ranging from epilepsy to heart ailments to muscle weakness.
By analyzing the number of times scientists were cited in others’ papers, the company Thomson Reuters has created a new list of the top 3,215 most highly cited—and therefore most influential— researchers in the world. Seventeen are from the Johns Hopkins University School of Medicine.
New animal studies by Johns Hopkins cardiovascular researchers strongly suggest that sildenafil, the erectile dysfunction drug sold as Viagra and now under consideration as a treatment for heart failure, affects males and females very differently.
Traditional first-line checks of such heart disease risk factors as cholesterol, blood pressure and smoking habits aren’t nearly good enough to identify cardiovascular disease in otherwise healthy, young firefighters, according to results of a small Johns Hopkins study.
A type of cell that builds mouse hearts can renew itself, Johns Hopkins researchers report. They say the discovery, which likely applies to such cells in humans as well, may pave the way to using them to repair hearts damaged by disease — or even grow new heart tissue for transplantation.
Men with long-term HIV infections are at higher risk than uninfected men of developing plaque in their coronary arteries, regardless of their other risk factors for coronary artery disease, according to results of a study led by Johns Hopkins researchers. A report on the research appears in the April 1 issue of Annals of Internal Medicine.
In a study that began in a pair of infant siblings with a rare heart defect, Johns Hopkins researchers say they have identified a key molecular switch that regulates heart cell division and normally turns the process off around the time of birth. Their research, they report, could advance efforts to turn the process back on and regenerate heart tissue damaged by heart attacks or disease.