Results of electromyostimulation therapy in obstructive sleep apnea

Abstract:  Innovative muscle stimulation techniques have become alternatives for therapy of obstructive sleep apnea syndrome breathing disorders. In group I, an individually shaped mouth floor electrode (IME) and in group II, an individually adaptable multi-point electrode (MPE) on a silicone carrier has been used for electromyostimulation (EMS) therapy in patients with obstructive sleep apnea. The enoral-cutaneous EMS was carried out with the low-frequency stimulation apparatus I-pulse over a period of 8 weeks, two times daily for 30 min during daytime hours only. In group III, the patients used EMS therapy for half a year continuously. Before and after stimulation treatment, three-dimensional volumetric sonographical measurement of the geniohyoid muscle was carried out. All patients ( n  = 14) totally applied the EMS therapy. Under IME and MPE application after 4 weeks of EMS therapy, a median volume increase of 19.6% (minimum 9.7%, maximum 27.9%) was registered, the median after 8 weeks IME was 27.6% and in MPE 24.0%). No significant difference (analysis of variance type: P  > 0.05) between electrodes could be found. In all groups, a reduction of the muscle length of 4.7% was proved. In groups I and II after 26 weeks, the volume was near baseline before stimulation (+4.3%). In the third group, the increase of volume persisted (+29.4%) over the observation period of 12–26 weeks. Opposed to established stimulation techniques, a threefold effectiveness enhancement could be verified by using both individually adaptable electrodes. The EMS therapy should be carried out as continuous long-term therapy or as interval therapy.     

Relation of aspirin failure to clinical outcome and to platelet response to aspirin in patients with acute myocardial infarction

Aspirin failure, defined as occurrence of an acute coronary syndrome despite aspirin use, has been associated with a higher cardiovascular risk profile and worse prognosis. Whether this phenomenon is a manifestation of patient characteristics or failure of adequate platelet inhibition by aspirin has never been studied. We evaluated 174 consecutive patients with acute myocardial infarction. Of them, 118 (68%) were aspirin naive and 56 (32%) were regarded as having aspirin failure. Platelet function was analyzed after ≥72 hours of aspirin therapy in all patients. Platelet reactivity was studied by light-transmitted aggregometry and under flow conditions. Six-month incidence of major adverse coronary events (death, recurrent acute coronary syndrome, and/or stroke) was determined. Those with aspirin failure were older (p = 0.002), more hypertensive (p <0.001), more hyperlipidemic (p <0.001), and more likely to have had a previous cardiovascular event and/or procedure (p <0.001). Cumulative 6-month major adverse coronary events were higher in the aspirin-failure group (14.3% vs 2.5% p <0.01). Patients with aspirin failure had lower arachidonic acid-induced platelet aggregation (32 ± 24 vs 45 ± 30, p = 0.003) after aspirin therapy compared to their aspirin-naive counterparts. However, this was not significant after adjusting for differences in baseline characteristics (p = 0.82). Similarly, there were no significant differences in adenosine diphosphate-induced platelet aggregation and platelet deposition under flow conditions. In conclusion, our results suggest that aspirin failure is merely a marker of higher-risk patient profiles and not a manifestation of inadequate platelet response to aspirin therapy.     

Weight gain and insulin resistance during nicotine replacement therapy.

BACKGROUND: Although the cessation of smoking reduces the increased risk for ischemic heart disease, it is associated with marked weight gain and presumably insulin resistance, both of which heighten the risk of coronary heart disease. HYPOTHESIS: We investigated the isolated effect of nicotine on body weight and insulin resistance during smoking cessation. METHODS: Eleven healthy, middle-aged heavy smokers were studied. Insulin sensitivity was assessed by an insulin-enhanced, frequently sampled intravenous glucose tolerance test with minimal model analysis. The subjects were studied at baseline (last day of smoking) (phase 1), at the end of the 6-week nicotine replacement program (phase 2), and after 8 weeks without smoking or nicotine replacement (phase 3). RESULTS: The subjects started to gain weight during nicotine replacement (phase 2) (0.3 +/- 0.2 kg/week, mean +/- standard deviation) and continued to do so at a steady rate after nicotine replacement was stopped (0.2 +/- 0.2 kg/week) (p = 0.3). Insulin sensitivity decreased by 14 +/- 2.6% during nicotine replacement but increased by 16 +/- 5.1% (compared with phase 2) during phase 3, even though the weight gain continued (p = 0.047; 95% confidence interval: 0.05-5.73). CONCLUSIONS: Smoking cessation is associated with weight gain and improvement in insulin resistance. Nicotine is the main ingredient in cigarette smoke causing insulin resistance, but the withdrawal of another, unknown ingredient in cigarette smoke is responsible for the weight gain associated with smoking cessation.     

CHADS2 and CHA2DS2-VASc scores as predictors of platelet reactivity in acute coronary syndrome

BackgroundPlatelet function testing (PFT) in patients treated with P2Y₁₂ inhibitors has been widely evaluated for the prediction of stent thrombosis, myocardial infarction, and bleeding events following percutaneous coronary intervention (PCI) in acute coronary syndrome (ACS). Thus, PFT-guided treatment could positively affect patient outcomes. Data regarding clinical parameters for predicting platelet reactivity in ACS patients are limited. Therefore, our study aims to evaluate CHADS2 and CHA2DS2-VASc scores as predictors for platelet reactivity in ACS patients.MethodsTwo hundred and ninety-one consecutive patients who underwent PCI and were treated with aspirin and clopidogrel due to ACS were tested for their CHADS2, CHA2DS2-VASc scores and platelet reactivity using adenosine diphosphate (ADP)-induced aggregation (conventional aggregometry). Patients were classified into groups according to their CHADS2 and CHA2DS2-VASc scores. Low-risk group (0–1 score) for CHADS2 and CHA2DS2-VASc scores and high-risk group (2–6, 2–9) for CHADS2 and CHA2DS2-VASc scores, respectively. Furthermore, platelet reactivity in each group were compared (low CHADS2 group vs high CHADS2 group, and low CHA2DS2-VASc vs high CHA2DS2-VASc). Platelet reactivity was defined as low platelet reactivity (<19 U), optimal platelet reactivity [(OPR); 19–46 U], and high on-treatment platelet reactivity [(HPR); >46 U]. Thereafter receiver operating characteristic curve analysis was conducted to verify whether CHADS2 and CHA2DS2-VASc scores could predict platelet reactivity.ResultsLow CHADS2 and CHA2DS2-VASc scores were significantly correlated with lower mean platelet ADP-induced aggregation as compared with high CHADS2 and CHA2DS2-VASc scores [45.5 U (± 16) vs. 54.8 U (±15) and 44.2 U (±16) vs. 51.0 U (±17), respectively, p = 0.01 for both].ConclusionIn ACS patients treated with clopidogrel following PCI, high CHADS2 and CHA2DS2-VASc scores correlated with HPR and lower scores correlated with OPR. Further studies are needed to evaluate our findings’ clinical implications.     

Sex Differences in the Management and 5-Year Outcome of Young Patients (<55 Years) with Acute Coronary Syndromes

Background

Young women are usually protected against coronary artery disease due to hormonal and risk-factor profile. Previous studies have suggested poorer outcome in women hospitalized with acute coronary syndrome as compared with men. However, when adjusted for age and other risk factors, this difference does not remain significant. We compared the risk profile and outcome between young (≤55 years) women and men admitted with acute coronary syndrome.

Chylous ascites as a presenting sign of prostatic adenocarcinoma

Chylous ascites is usually associated with either primary disorders of the lymphatic system or malignancies of the lymph nodes such as Hodgkin and non-Hodgkin lymphoma. We describe, however, a young man in whom chylous ascites was a presenting sign of disseminated adenocarcinoma of the prostate gland. Most likely retroperitoneal lymph nodal replacement and tumor blockade of lymphatic collectors by metastatic adenocarcinoma was responsible for the development of chylous ascites.     

MRI of the nasal cavity, the paranasal sinuses and orbits in Wegener's granulomatosis

The purpose of this study was to evaluate diagnostic MRI criteria in Wegener's granulomatosis of the nasal cavity, the paranasal sinuses and orbits. Between March 1991 and January 1996, 62 patients with biopsy-proven Wegener's granulomatosis were studied with T1- and T2-weighted spin-echo (SE) sequences. In 32 patients coronal postcontrast T1-weighted images were obtained. Mucosal thickening of the nasal cavity and paranasal sinuses was demonstrated as high-intensity lesions on T2-weighted SE sequences in 57 patients (92 %). Of this group, inflammatory granulomatous tissue was found on biopsy in 30 patients (48 %) in the nasal cavity and in 4 patients (6 %) in the paranasal sinuses. In 23 patients (37 %) biopsy revealed unspecific inflammatory changes without evidence of granulomatous tissue. In 14 patients (23 %) granulomas were depicted as low-signal intensity lesions on T1- and T2-weighted SE sequences in the paranasal sinuses and orbits. In 5 patients (8 %) osseous destruction was found. After gadolinium injection, 12 of 14 granulomas showed inhomogeneous signal enhancement. In two granulomas no enhancement was found. The MRI technique is helpful in the diagnosis of patients with Wegener's granulomatosis. In the initial inflammatory process of Wegener's granulomatosis, it is not possible to differentiate between mucosal inflammation and granulomatous tissue in MRI. In the later stage of granulomatous transformation, granulomas can be depicted as low-signal-intensity lesions. Therefore, Wegener's granulomatosis should be included in the differential diagnosis of patients with low-signal-intensity lesions on T1- and T2-weighted SE sequences of the nasal cavity, paranasal sinuses and orbits. Received 10 June 1996; Revision received 26 August 1996; Accepted 24 September 1996