Stories about: heart attack

An FDA-approved drug could prevent valve damage after heart attack

Losartan is shown to prevent thickening of the mitral valve after heart attack, in comparison with an untreated heart
An untreated mitral valve (left) shows much more thickening and fibrosis after heart attack than a mitral valve treated with losartan (right).

On average, one in four people who have a heart attack sustain long-lasting damage to the mitral valve, which has the important job of making sure blood pumps through the heart’s ventricles in the right direction. If the valve is damaged, the heart’s pumping efficiency is reduced and blood can flow backward, which can lead to heart failure and death.

Now, a team of collaborators from Boston Children’s Hospital, Massachusetts General Hospital and Brigham and Women’s Hospital has shown, for the first time, that it’s possible to treat and even prevent mitral valve damage after heart attack with an FDA-approved, anti-hypertension drug called losartan. Their findings are published in the Journal of the American College of Cardiology.

Read Full Story | Leave a Comment

Mitigating blood vessel damage from heart attack, stroke

Mouse hearts showing the impact of a therapeutic protein fusion on blood vessel health
Imaging of mouse hearts reveals widespread tissue damage (light-colored areas) after heart attack. At far right, however, mice that were treated with an engineered, optimized ApoM protein containing S1P have better tissue recovery than untreated mice (left) and mice that were given an inactive “dud” ApoM treatment (center). Credit: Hla lab/Boston Children’s Hospital

The average human has 60,000 miles of blood vessels coursing through their body. There are a number of mechanisms the body uses to keep that vast vascular network healthy, including a tiny fat molecule, a lipid called S1P, that plays a particularly important role.

S1P receptors dot the surface of the endothelium, a layer of cells that line the inside of all the body’s blood cells. Together, these so-called endothelial cells form a barrier between the body’s circulating blood and surrounding tissue. When S1P molecules activate their receptors, it suppresses endothelial inflammation and generally helps regulate cardiovascular health.

Now, researchers led by Timothy Hla, PhD, from the Boston Children’s Hospital Vascular Biology Program, report a novel therapeutic fusion that could trigger increased S1P receptor activity and recover blood vessel health following the onset of hypertension, atherosclerosis, stroke, heart attack and other cardiovascular diseases.

Read Full Story | Leave a Comment

Modified RNA offers drug-like approach to regenerating heart tissue

In mice, VEGF-A modRNA visibly improved blood supply to heart muscle (right image).
In mice, VEGF-A modRNA visibly improved blood supply to heart muscle (right image) as compared with no treatment.

Heart attacks cause the death of billions of the heart’s muscle cells. If these cardiomyocytes could be made to regenerate after an infarct, the heart could potentially be mended and its function restored.

Researchers have struggled to find the right approach to cardiac regeneration. Cell transplants have been tried, but the cells don’t engraft well long term and haven’t shown efficacy. Gene therapy to spur regeneration has been tested in animals, but dosage is hard to control and there’s a risk of genes going where they shouldn’t, causing tumors and other problems. Protein drugs have been tried, but they have short half-lives, being degraded or eliminated by the body before they can do much good. They are also hard to target to the heart.

A more recent approach to cardiac regeneration is to stimulate the body itself—and, specifically, progenitor cells— to repair the heart from within.

Read Full Story | Leave a Comment

Putting the squeeze on blood clots to stop a stroke

Blood should flow through an artery like water through a hose. The stress of a blockage can encourage clots to form, potentially resulting in a heart attack or stroke. Donald Ingber thinks the same forces could be used to help dissolve clots. (Beth Kingery/Flickr)

Grab a garden hose. Put your thumb over the end, but not all the way, and turn the water on. What happens? The water coming out of the hose gets squeezed as it tries to push past your thumb, putting a lot of force on the molecules in the water and making a big spray.

Now do the same thing with an artery: Partially block it with a clot and let blood flow through it. In this case, the force you’ve created in the artery could be lethal—creating fertile ground for blood clots that could lead to a stroke or heart attack.

But what if that combination of force and pressure could be used to stop something like a stroke instead? What if it could release a clot-dissolving drug on the spot? Donald Ingber, MD, PhD, a member of Boston Children’s Hospital’s Vascular Biology Program, had wondered that for many years. To find out, Ingber, who also directs the Wyss Institute for Biologically Inspired Engineering at Harvard, had his team start with a simple question: How do clots form?

Read Full Story | Leave a Comment

Could nanotechnology improve treatment of heart attack and heart failure?

People who have had a heart attack or have coronary artery disease often sustain damage that weakens their heart. Milder forms of heart failure can be treated with medications, but advanced heart dysfunction requires surgery or heart transplant. A team of physicians, engineers and materials scientists at Children’s Hospital Boston and MIT offers two alternative ways to strengthen weakened, scarred heart tissue — both involving nanotechnology.

One approach blends nanotechnology with tissue engineering to create a heart patch laced with gold whose cells all beat in time – as shown in the above video.

The other uses minute nanoparticles that can find their way to dying heart tissue, carrying stem cells, growth factors, drugs and other therapeutic compounds.

Read Full Story | 2 Comments | Leave a Comment

Battling rising hypertension in children: 5 tools

FDR (here signing the Declaration of War against Japan, 1941) died from a stroke caused by years of hypertension. Millions of U.S. children could meet the same fate – unless we act now.

While many of us recall that President Franklin Delano Roosevelt had polio, few remember that he died in 1945 from another cause: stroke. The sentiment of his physician — that it “had come out of the clear sky” — reflected the prevailing view that heart attack and stroke were bolts from the blue that doctors could act on only after the event.

But a few mavericks challenged this “salvage” paradigm, establishing the Framingham Heart Study in 1948 to identify predictors of cardiovascular events. One leading maverick, Dr. William Kannel, who passed away last month, coined the term “risk factors” to describe these predictors. Acting on the insight that controlling risk factors could prevent cardiovascular disease saved the lives of more than 150,000 Americans from heart disease alone between 1980 and 2000.

Judging by the surviving medical records, Roosevelt’s stroke may have been preventable with treatment for one such risk factor, hypertension. How different would the world have been had his persistent high blood pressure been treated?

The world is different now, not all for the better. High blood pressure has been attacking more and more children over the last 30 years,

Read Full Story | Leave a Comment