Left ventricular function and exercise capacity in patients with slow coronary flow

Background: Endothelial and microvascular dysfunction have been implicated in slow coronary flow (SCF). How and to what extent do these etiological factors affect left ventricular (LV) function and exercise capacity? Aim: The aim of the study was to evaluate LV systolic and diastolic function by pulsed tissue Doppler imaging (TDI) in SCF patients and their effects on exercise capacity. Subjects and methods: Sixty SCF patients and 20 control subjects were included in the study. Echocardiographic examination, treadmill exercise test, and TDI were performed. Isovolumic myocardial acceleration (IVA) and myocardial performance index (MPI) were measured. Results: TDI mean parameters for systolic and diastolic LV function were significantly impaired in SCF group with decreased Sa, IVA, Ea/Aa, and increased MPI (0.31 ± 0.06 vs. 0.26 ± 0.04, P < 0.01) compared to control. There was significant correlation between thrombolysis in myocardial infarction (TIMI) frame count and TDI mean parameters for LV systolic function (Sa & IVA, r =?0.53, P < 0.01 & r =?0.36, P < 0.05, respectively). Mean TIMI frame count was correlated with MPI and E/Ea. SCF patients had poorer peak exercise capacity than the controls (9.9 ± 1.9 METs vs. 12.7 ± 2.3, P < 0.01) with significant negative correlation with mean TIMI frame count (r =?0.46, P < 0.01). Conclusion: There is impairment of LV systolic and diastolic function in SCF patients with clinical impact on exercise capacity which emphasizes the importance of close follow‐up of these patients for risk stratification. (Echocardiography 2012;29:158‐164)     

Gastrointestinal hypomotility with loss of enteric nicotinic acetylcholine receptors: active immunization model in mice

Background Autoimmune gastrointestinal dysmotility (AGID) is a limited form of dysautonomia. The only proven effector to date is IgG specific for ganglionic nicotinic‐acetylcholine receptors containing α3 subunits [α3*‐ nicotinic acetylcholine receptor (nAChR)]. Rabbits immunized with recombinant α3‐polypeptide produce α3*‐nAChR autoantibodies, and profound AGID ensues. Human and rabbit α3*‐nAChR‐specific‐IgGs induce transient hypomotility when injected into mice. Here, we describe success and problems encountered inducing gastrointestinal hypomotility in mice by active immunization. Methods We repeatedly injected young adult mice of seven different strains susceptible to autoimmunity (spontaneous diabetes or neural antigen immunization‐induced myasthenia gravis or encephalomyelitis) with: (i) α3‐polypeptide, intradermally or (ii) live α3*‐nAChR‐expressing xenogeneic cells, intraperitoneally. We measured serum α3*‐nAChR‐IgG twice monthly, and terminally assessed blue dye gastrointestinal transit, total small intestinal α3*‐nAChR content (radiochemically) and myenteric plexus neuron numbers (immunohistochemically, ileal–jejunal whole‐mount preparations). Key Results Standard cutaneous inoculation with α3‐polypeptide was minimally immunogenic, regardless of dose. Intraperitoneally injected live cells were potently immunogenic. Self‐reactive α3*‐nAChR‐IgG was induced only by rodent immunogen; small intestinal transit slowing and enteric α3*‐nAChR loss required high serum levels. Ganglionic neurons were not lost. Conclusions & Inferences Autoimmune gastrointestinal dysmotility is inducible in mice by active immunization. Accompanying enteric α3*‐nAChR reduction without neuronal death is consistent with an IgG‐mediated rather than T cell‐mediated pathogenesis, as is improvement of symptoms in patients receiving antibody‐depleting therapies.     

Discovery of Lacosamide Affinity Bait Agents That Exhibit Potent Voltage-Gated Sodium Channel Blocking Properties

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冠状动脉慢血流现象患者内皮功能的研究

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