Can T-type calcium channels make a change of heart after myocardial infarction? Fiction or fact, and for better or for worse?

Abstract

This editorial refers to ‘Role of T-type calcium channel subunits in post-myocardial infarction remodelling probed with genetically engineered mice’ by K. Le Quang et al. , pp. 420–428, this issue. The outcome of patients with myocardial infarction has improved dramatically over the last few decades. Evidence-based therapy comprises rapid recanalization with full restitution of flow by acute percutaneous coronary intervention, local and systemic antithrombotic treatment, the use of statins, β-adrenoceptor blockers, angiotensin-converting enzyme inhibitors, and aldosterone receptor antagonists to protect the heart from subsequent adverse remodelling.1 The term ‘cardiac remodelling’ refers to a process involving changes in morphology and mechanical and electrical function that occur after injury such as myocardial infarction and pressure or volume overload. Remodelling allows for the maintenance of haemodynamic function but also results in cardiac hypertrophy, reactivation of a foetal gene programme, and arrhythmias, all relevant for prevention and treatment of heart failure and sudden death.2 Voltage-gated calcium channels play a fundamental role in nano-environmental networks of calcium-dependent effector systems, affecting mechanical and electrical function as well as gene expression of the heart. They appear to be involved in the cardiac remodelling process. Although the classical L (‘long-lasting’, ‘large’)-type calcium channel is essential for cardiac contraction, its ‘little brother’, the T (‘transient’, ‘tiny’)-type calcium channel, was proposed to be involved in cardiac pathophysiology3 soon after its discovery.4 Although known to be regulated by hormones,5 hypoxia,6 and development,7 its pathophysiological role in the ventricular myocardium is far from being clear ( Table 1 ). Its subunits Cav3.1, 3.2, and 3.3 are also called α1G, α1H, and …