In patients undergoing CTO-PCI, postprocedural hs-TnT elevation is frequent, but is not correlated with higher MACCE and mortality rates after 1-year FU in our small study population, suggestive of the limited long-term impact of troponin elevation.
Introduction: Previous research in the field of cardiovascular diseases suggests a relaxing effect of testosterone (T) on smooth muscle cells. Therefore, it was hypothesized that T could play a significant role in erection development. Aim: To investigate the relaxing effect of T and other molecules of the T signaling pathway on human corpus cavernosum (HCC) tissue. Methods: Samples of the HCC tissue were obtained from men who underwent penile prosthesis implantation (n ¼ 33) for erectile dysfunction. Samples were used for isometric tension measurement in Ex Vivo experiments. Following standardized precontraction with phenylephrine, increasing doses of T or dihydrotestosterone were administered and blocked by NO/H 2 S synthesis inhibitors, a K ATP blocker, and flutamide (androgen receptor inhibitor). Main Outcome Measure: The outcome was relaxation of the HCC tissue, normalized to a maximum precontraction achieved by phenylephrine. Results: A dose-dependent relaxing effect of dihydrotestosterone and T was observed with a relaxation of, respectively, 24.9% ± 23.4% (P < .0001) and 41.7% ± 19.1% (P ¼ .01) compared with 6.8% ± 15.9% for vehicle (dimethylsulfoxide) at 300 mM. The relaxing effect of T was not countered by blocking NO synthesis, H 2 S synthesis, K ATP channels, or the androgen receptor. Clinical Implications: By understanding the underlying mechanisms of T-induced HCC relaxation, potential new therapeutic targets can be identified.
Strengths & Limitations:The strength of the study is the use of fresh HCC tissues with reproducible results. The limitation is the need for supraphysiological T levels to induce the observed effect. Conclusion: Rapid androgen-induced relaxation of HCC is likely to occur via nongenomic mechanisms.
Peyronie's disease (PD) is an idiopathic chronic fibrotic disease that causes a penile curvature (PC), subsequent erectile dysfunction (ED) and impaired sexual intercourse in patients. As of yet, there are no reliable non-surgical treatment options available. Intralesional injection with collagenase Clostridum Histolyticum has been FDA approved since 2013, but post-approval studies have not been unanimously positive. Moreover, it renders a curvature improvement of only 30% on average, usually still requiring surgical intervention to remedy PC. Therefore, there is a need for drugs which could prevent surgery altogether. Development of new drugs can either be through a target-based or phenotypic assay-based approach. The current in vivo model for PD is dependent on treatment of primary PD-derived fibroblasts with transforming growth factor-β1. Moreover, despite the existence of a genetic in vivo PD model, it does not allow for drug screening or testing. While some advances have been made in the past few years, new in vivo and in vivo systems and well-designed studies are urgently needed for the non-surgical treatment of PD.
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