Titin, an important protein in the sarcomere, is the largest human protein. This study identified mutations in the titin gene that result in a truncated protein as important causes of dilated cardiomyopathy.

The authors report on a U.S. registry of cardiac arrests during marathons and half-marathons. The rate of arrest was equal to or lower than rates for other strenuous physical activities. The most common cause was hypertrophic cardiomyopathy or coronary artery disease.

A mutation that abrogates the function of ADAM17, an enzyme that cleaves cell-surface proteins such as tumor necrosis factor α, was found to be associated with inflammatory skin and bowel disease in a pair of siblings.

Patients with CAD and LV dysfunction were assigned to receive either medical therapy alone or medical therapy plus CABG. There was no evidence of significant interaction between myocardial viability and treatment assignment.

Patients with CAD and LV dysfunction were assigned to either medical therapy alone or medical therapy plus CABG. At 5 years, there was no significant difference between the two study groups in the rate of death from any cause.

This study shows that myocardial fibrosis is an early characteristic of hypertrophic cardiomyopathy caused by sarcomere mutations. The C-terminal propeptide of procollagen type I was shown to be a serum biomarker of early myocardial fibrosis.