Acquired thrombocytopenia was common after TAVR and was mostly resolved at patient discharge. The severity of thrombocytopenia after TAVR could be used as an excellent, easily obtainable, marker for worse short- and long-term outcomes after the procedure.

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Recently, a growing body of clinical data has shown that the first generation of drug-eluting stents (1st-gen DES) implantation could elicit coronary conduit artery vasomotor dysfunction at nonstented reference segments as late as 12 months after implantation compared with that seen with bare-metal stents. The mechanism of this phenomenon is still not fully understood. Pathological studies have implicated delayed arterial healing and poor re-endothelialization after the 1st-gen DES implantation. Given the vast use of DES globally, a thorough understanding of the early and long-term safety of these devices is paramount. Therefore, this article systematically reviews the current clinical, pathophysiological, and histopathological available data regarding 1st-gen DES-associated vascular endothelial dysfunction. Meanwhile, we will also review the newer generation of DES and emerging endothelial-friendly technology.

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Ghrelin, a newly discovered bioactive peptide, is a natural endogenous ligand of the growth hormone (GH) secretagogue receptor and initially identified as a strong stimulant for the release of GH. Subsequent research has shown that ghrelin and its various receptors are ubiquitous in many other organs and tissues. Moreover, they participate in the regulation of appetite, energy, bodyweight, metabolism of glucose and fat, as well as modulation of gastrointestinal, cardiovascular, pulmonary, immune functions and cell proliferation/apoptosis. Increasing evidence has demonstrated that ghrelin has a close relationship with cardiovascular system. Ghrelin and its receptors are widely distributed in cardiovascular tissues, and there is no doubt that the effects of ghrelin in the cardiovascular system are mediated not only via its growth-hormone-releasing effect but also by its direct effects on the heart. Exogenous administration of ghrelin can dilate peripheral blood vessels, constrict coronary artery, improve endothelial function, as well as inhibit myocardial cell apoptosis. So, ghrelin may have cardiovascular protective effect, including lowering of blood pressure, regulation of atherosclerosis, and protection from ischemia/reperfusion injury as well as improving the prognosis of myocardial infarction and heart failure. Some of these new functions of ghrelin may provide new potential therapeutic opportunities for ghrelin in cardiovascular medicine. In this paper, we will review the existing evidence for cardiovascular effects of ghrelin, including the cardiovascular function, the variations in ghrelin plasma levels in pathophysiologicalogical conditions, the possible protective mechanisms of ghrelin, as well as its future potential therapeutic roles.