SummaryThe importance of fibrosis in organ pathology and dysfunction appears to be increasingly relevant to a variety of distinct diseases. In particular, a number of different cardiac pathologies seem to be caused by a common fibrotic process. Within the heart, this fibrosis is thought to be partially mediated by transforming growth factor-b 1 (TGF-b 1 ), a potent stimulator of collagen-producing cardiac fibroblasts. Previously, TGF-b 1 had been implicated solely as a modulator of the myocardial remodelling seen after infarction. However, recent studies indicate that dilated, ischaemic and hypertrophic cardiomyopathies are all associated with raised levels of TGF-b 1 . In fact, the pathogenic effects of TGF-b 1 have now been suggested to play a major role in valvular disease and arrhythmia, particularly atrial fibrillation. Thus far, medical therapy targeting TGF-b 1 has shown promise in a multitude of heart diseases. These therapies provide great hope, not only for treatment of symptoms but also for prevention of cardiac pathology as well. As is stated in the introduction, most reviews have focused on the effects of cytokines in remodelling after myocardial infarction. This article attempts to underline the significance of TGF-b 1 not only in the post-ischaemic setting, but also in dilated and hypertrophic cardiomyopathies, valvular diseases and arrhythmias (focusing on atrial fibrillation). It also aims to show that TGF-b 1 is an appropriate target for therapy in a variety of cardiovascular diseases.

Intimal thickening is the most important cause of in-stent restenosis. The pathology of intimal thickening is attributable to a local inflammatory response after vascular injury which results in the production of cytokines. Transforming growth factor-beta1 (TGF-beta1) is a profibrotic cytokine that is involved in the induction of intimal thickening. Up-regulation of TGF-beta1 after arterial injury results in the activation of various downstream pathways which stimulate the proliferation and migration of vascular smooth muscle cells, as well as the production of local extracellular matrix proteins. Recent evidence suggests that antagonizing TGF-beta1 activity with direct or indirect inhibitors may attenuate or prevent intimal thickening. Additionally, TGF-beta1 synthesis, activation and downstream regulation may also serve as significant sources of treatment. This review attempts to show the role of TGF-beta1 in the pathology of intimal thickening and underlines the importance of TGF-beta1 as a target for therapy.

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Residual CAD, as assessed by the rSS, confers a worsened prognosis in patients undergoing PPCI. Diabetes, previous MI and multi-vessel disease were independent predictors of a high rSS. © 2016 Wiley Periodicals, Inc.