Transradial artery access for percutaneous coronary intervention is associated with lower bleeding and vascular complications than transfemoral artery access, especially in patients with acute coronary syndromes. A growing body of evidence supports adoption of transradial artery access to improve acute coronary syndrome–related outcomes, to improve healthcare quality, and to reduce cost. The purpose of this scientific statement is to propose and support a “radial-first” strategy in the United States for patients with acute coronary syndromes. This document also provides an update to previously published statements on transradial artery access technique and best practices, particularly as they relate to the management of patients with acute coronary syndromes.

BACKGROUND Peripartum cardiomyopathy shares some clinical features with idiopathic dilated cardiomyopathy, a disorder caused by mutations in more than 40 genes, including TTN, which encodes the sarcomere protein titin. METHODS In 172 women with peripartum cardiomyopathy, we sequenced 43 genes with variants that have been associated with dilated cardiomyopathy. We compared the prevalence of different variant types (nonsense, frameshift, and splicing) in these women with the prevalence of such variants in persons with dilated cardiomyopathy and with population controls. RESULTS We identified 26 distinct, rare truncating variants in eight genes among women with peripartum cardiomyopathy. The prevalence of truncating variants (26 in 172 [15%]) was significantly higher than that in a reference population of 60,706 persons (4.7%, P = 1.3×10−7) but was similar to that in a cohort of patients with dilated cardiomyopathy (55 of 332 patients [17%], P = 0.81). Two thirds of identified truncating variants were in TTN, as seen in 10% of the patients and in 1.4% of the reference population (P = 2.7×10−10); almost all TTN variants were located in the titin A-band. Seven of the TTN truncating variants were previously reported in patients with idiopathic dilated cardiomyopathy. In a clinically well-characterized cohort of 83 women with peripartum cardiomyopathy, the presence of TTN truncating variants was significantly correlated with a lower ejection fraction at 1-year follow-up (P = 0.005). CONCLUSIONS The distribution of truncating variants in a large series of women with peripartum cardiomyopathy was remarkably similar to that found in patients with idiopathic dilated cardiomyopathy. TTN truncating variants were the most prevalent genetic predisposition in each disorder.

(N Engl J Med. 2016;374:233–241) It is possible that peripartum cardiomyopathy is influenced by genetic factors, though this remains unclear. Similar to idiopathic dilated cardiomyopathy, this disease is associated with decreased systolic function, enlarged cardiac dimensions, and nonspecific histologic findings. These similarities are significant in that idiopathic dilated cardiomyopathy has been shown to be caused by a number of gene mutations. The authors of this study sequenced the DNA of 172 women suffering from peripartum cardiomyopathy to investigate whether there was a contribution from variants in the 43 genes known to be associated with dilated cardiomyopathy.

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