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Dysphagia, defined as a dysfunction in any stage or process of eating, is common in patients with acute exacerbation of heart failure (HF). In some diseases, dysphagia worsens in-hospital mortality, length of hospital stay, and discharge disposition. However, it remains unclear whether dysphagia is associated with poor short-term outcomes in HF patients. The objective of the present study was to determine whether dysphagia affects short-term outcomes in patients with acute exacerbation of HF. A total of 327 patients hospitalized with acute exacerbation of HF were eligible for the study. Patients were divided into a dysphagia group (DG) or a non-dysphagia group (NDG) based on results of the functional oral intake scale (FOIS), which evaluates a patient's ability of eating and swallowing. FOIS is a 7-point scale, with a level of ≤ 5 indicating dysphagia. Following the withdrawal of 16 patients, short-term outcomes such as in-hospital mortality, length of hospital stay, and discharge disposition, of 311 patients were analyzed. All indexes of short-term outcomes were significantly worse in the DG than in the NDG. After propensity score matching, which was performed to adjust for baseline characteristics such as age, sex, height, weight, body mass index, medical history, complications, HF severity, ejection fraction, and biochemical data excluding nutritional status, all short-term outcomes remained significantly worse in the DG than in the NDG. Multivariate analysis showed that FOIS was an independent predictor of in-hospital survival, length of hospital stay, and discharge to home. The present study suggested that dysphagia affected short-term outcomes in patients with acute exacerbation of HF. Therefore, early detection and intervention of dysphagia in HF patients are important.

In isolated cardiac muscle, spontaneous Ca2+ release from the sarcoplasmic reticulum (SR) occurs and is propagated as a wave by a regenerative Ca2+-induced Ca2+ release mechanism. We have already reported that this wave is followed by a refractory period. The aim of this study is to investigate whether such a refractory period could also inactivate Ca2+ release from the SR triggered by an action potential. Myocytes were enzymatically isolated from guinea pig ventricles and loaded with acetoxymethylester form of fura-2 (fura-2 AM). The membrane potential was recorded with a conventional microelectrode technique, and spatio-temporal changes in fura-2 fluorescence were recorded using a digital TV system. After perfusion with potassium-free Tyrode solution, interactions between fluorescence transients due to propagating waves and action potential-induced fluorescence transients were observed. In this study, the action potentialinduced fluorescence transients could be detected in the next video frame after the propagation of the waves and showed gradual restitution of the transients. In addition, the sum of the fluorescence transients triggered by an action potential and the fluorescence transients due to the waves did not show significant change whenever the preceding waves were propagating. These results show that the interaction between the action potential-induced Ca2+ release and the calcium wave-induced Ca2+ release from the SR have the following characteristics: (1) For the action potentialinduced Ca2+ release, no absolute refractory period was observed 33 msec after the calcium wave. This suggests that the calcium waves can be reset by the action potential. (2) Regardless of whether the two release mechanisms are different, both share a common compartment of Ca2+ storage.

The purpose of this study is to clarify the kinds of cells that fluoresce in isolated perfused heart intracoronarily loaded with fura 2-AM or indo 1-AM. The hearts from hamsters perfused by the Langendorff method were loaded with fura 2-AM or indo 1-AM intracoronarily. The epicardium was excited by ultraviolet light at a wavelength of 340 or 380 nm (fura 2) or 360 nm (indo 1). Epifluorescent images from arrested hearts prepared with St Thomas' cardioplegic solution were observed through an inverted microscope and taken by a still camera. Endothelial cells and pericytes of the capillaries showed intense fluorescence. In the intercapillary spaces, a less intense but still apparent fluorescence emitted by myocytes could also be detected. On the other hand, fluorescence from smooth muscle cells and fibroblasts could not be identified. Therefore, epifluorescence in the isolated perfused heart loaded with fura 2-AM or indo 1-AM was mainly generated within endothelial cells, pericytes, and myocytes. To evaluate calcium fluorescence in isolated hearts quantitatively, the fluorescence of endothelial cells and pericytes of the capillaries must be taken into consideration.