In systolic HF patients, CAs occurred throughout a 24-h period and were associated with a neurohormonal activation, ventricular arrhythmic burden, and worse prognosis.

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Background The contribution of the lung or the plant gain ( PG ; ie, change in blood gases per unit change in ventilation) to Cheyne‐Stokes respiration ( CSR ) in heart failure has only been hypothesized by mathematical models, but never been directly evaluated. Methods and Results Twenty patients with systolic heart failure (age, 72.4±6.4 years; left ventricular ejection fraction, 31.5±5.8%), 10 with relevant CSR (24‐hour apnea‐hypopnea index [ AHI ] ≥10 events/h) and 10 without ( AHI <10 events/h) at 24‐hour cardiorespiratory monitoring underwent evaluation of chemoreflex gain (CG) to hypoxia ( ) and hypercapnia ( ) by rebreathing technique, lung‐to‐finger circulation time, and PG assessment through a visual system. PG test was feasible and reproducible (intraclass correlation coefficient, 0.98; 95% CI , 0.91–0.99); the best‐fitting curve to express the PG was a hyperbola ( R 2 ≥0.98). Patients with CSR showed increased PG , (but not ), and lung‐to‐finger circulation time, compared with patients without CSR (all P <0.05). PG was the only predictor of the daytime AHI ( R =0.56, P =0.01) and together with the also predicted the nighttime AHI ( R =0.81, P =0.0003) and the 24‐hour AHI ( R =0.71, P =0.001). Lung‐to‐finger circulation time was the only predictor of CSR cycle length ( R =0.82, P =0.00006). Conclusions PG is a powerful contributor of CSR and should be evaluated together with the CG and circulation time to individualize treatments aimed at stabilizing breathing in heart failure.

In remote ischemic conditioning (RIC), several cycles of ischemia and reperfusion render distant organ and tissues more resistant to the ischemia-reperfusion injury. The intermittent ischemia can be applied before the ischemic insult in the target site (remote ischemic preconditioning), during the ischemic insult (remote ischemic perconditioning) or at the onset of reperfusion (remote ischemic postconditioning). The mechanisms of RIC have not been completely defined yet; however, these mechanisms must be represented by the release of humoral mediators and/or the activation of a neural reflex. RIC has been discovered in the heart, and has been arising great enthusiasm in the cardiovascular field. Its efficacy has been evaluated in many clinical trials, which provided controversial results. Our incomplete comprehension of the mechanisms underlying the RIC could be impairing the design of clinical trials and the interpretation of their results. In the present review we summarize current knowledge about RIC pathophysiology and the data about its cardioprotective efficacy.