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Kiran Musunuru, a clinical and research fellow at Massachusetts General Hospital and research affiliate at the ӳ����ý, has received the ӳ����ý’s Lawrence H. Summers Fellowship for research for 2010-2011.

The year-long fellowship, named after former Harvard president Lawrence Summers, gives scientists an opportunity to advance their research at the ӳ����ý. Kiran intends to deepen his research into the causes of heart attacks, as well as the role that genetics plays in regulating levels of cholesterol and triglycerides in the blood.

Despite the widespread use of drugs like statins and aspirin, and high-tech devices like implantable cardioverter-defibrillators, heart attacks remain the leading cause of death in the developed world. Doctors have a good understanding of what causes heart attacks at a basic level: atherosclerotic plaques form in the coronary arteries that nourish the heart muscle, and when these plaques suddenly rupture, they cause clots to form that can block off arteries and starve heart muscle, causing it to die.

But far less is understood on a molecular level. What causes the plaques to form? What causes them to rupture?

Kiran began exploring these questions when he was a clinical cardiology fellow at Johns Hopkins Hospital from 2006 to 2008. “We’re leveraging an enormous amount of technology, an enormous amount of healthcare resources – billions of dollars – to help patients after their heart attacks, and yet we’re able to do relatively little to prevent the heart attacks from happening,” he says.

Three years ago, three different genome-wide association studies (GWAS) – in which the human genome is scanned at high resolution to find common variants – pointed to an association between heart attacks and a single location on chromosome 9p21. Those findings seemed imbued with a degree of mystery that intrigued Kiran – and marked a watershed of sorts. He decided to transfer to Boston to work at the ӳ����ý and at MGH with ӳ����ý associate member Sek Kathiresan, who at the time was leading some of the first GWAS on cholesterol and heart attack.

“I really felt that GWAS was going to give us new insights into new mechanisms. At the same time, I think everyone appreciates that it is just the beginning. GWAS is really the first step of several steps in the process of discovery,” Kiran says.

Kiran hopes the coming year will help him “close the circle” and deepen his understanding of how genotype connects to phenotype, or the disease state, and to explore new molecular pathways.

“If you’re a dreamer,” Kiran says, “you hope that way down the road we become so good at doing this that we can actually eradicate heart attacks and remove a major cause of human suffering.”