Ivabradine reduces myocardial stunning in patients with exercise-inducible ischaemia.

Ivabradine is an effective treatment for angina in patients with stable coronary artery disease (CAD) and for heart failure. Experiments in a canine model have shown that ivabradine reduces both acute left ventricular (LV) dysfunction and post-ischaemic stunning. Aim of this study was to investigate the effect of ivabradine on LV dysfunction and stunning in patients with CAD and exercise-inducible ischaemia. Fifteen patients with ejection fraction >40 % and heart rate >70 bpm were enrolled. After pharmacologic washout, echocardiography was performed at rest, at peak treadmill exercise and during recovery until return to baseline. After 2 weeks of ivabradine (7.5 mg bid) stress echocardiography was repeated at the same workload achieved during washout. Peak global and segmental (ischaemic vs. remote normal segments) LV longitudinal strain (LS) was assessed by 2D speckle tracking analysis. At washout, LS was significantly impaired in ischaemic compared to remote segments at peak stress and for several minutes during recovery. After ivabradine a smaller, albeit still significant, impairment of LS in ischaemic segments was observed at peak whilst no difference with remote segments was present during recovery. Furthermore, the average global LS value improved significantly after treatment. In conclusion, ivabradine reduces both acute LV dysfunction and stunning in patients with CAD and exercise-inducible ischaemia. We hypothesise that this mechanism might contribute to reduce chronic LV dysfunction in patients with CAD. In this setting the drug might limit the development of hibernating myocardium which is believed to result from repeated episodes of ischaemia and stunning.

Erectile dysfunction in heart failure patients: a critical reappraisal.

Heart failure (HF) is a complex clinical syndrome with a constantly increasing incidence and prevalence in western countries. Total absence of sexual activity is registered in 30% of HF patients. Moreover, HF-induced reduction in exercise tolerance, side effects of HF medications and the coexistence of shared risk factors between HF and sexual dysfunction may further aggravate the sexual health of HF patients. The purpose of this review is to examine the pathophysiological mechanisms behind the association of erectile dysfunction (ED) and HF, the potential therapeutic approaches and the eventual indications for sexual activity in HF patients. Medline and Cochrane Library search was performed from January 1970 through October 2012 to retrieve relevant papers outlining the association between ED and HF. Many evidences have outlined a tight association between ED and HF pathophysiological standpoint. Shared risk factors, common pathogenic traits and epidemiologic association represent some of the links between these conditions. Erectile dysfunction has been recognized as an earlier predictor of cardiovascular events; moreover, HF itself may cause and/or worsen ED because of its particular feature and co-morbidities. Furthermore, some cardiovascular drugs may contribute to impaired erectile function. In stable patients with stable HF, sexual activity is generally not contraindicated but it should be encouraged, as a form of moderate-intensity physical exertion. An effective treatment of ED in HF patients should be founded on the correction of reversible risk factors, on the choice of cardiovascular drugs with the lowest effect upon patient's erectile function, and on the use of phosphodiesterase-5-inhibitors. Physicians should be aware of the close relation between HF and ED and of the related clinical and therapeutic implications, in order to improve patients quality of life and clinical outcome.