[A clinical case of hemangioma of the face and tongue concurrent with severe obstructive sleep apnea syndrome complicated by cardiac arrhythmias and conduction disturbances]. / Klinicheskii sluchai gemangiomy litsa i yazyka v sochetanii s sindromom obstruktivnogo apnoe vo sne tyazheloi stepeni, oslozhnivshimsya narusheniyami ritma i provodimosti serdtsa.

The paper describes a clinical case of a female patient with severe obstructive sleep apnea syndrome in the presence of congenital hemangioma of the face, soft palate, and tongue concurrent with paroxysmal atrial fibrillation and atrial flutter, paroxysmal supraventricular tachycardia, and sinoatrial block (maximally up to 3.9 sec). Continuous positive airway pressure therapy could reduce the number of paroxysms of atrial fibrillation and atrial flutter, supraventricular tachycardia and eliminate sinoatrial block.

Effects of CPAP on "vascular" risk factors in patients with obstructive sleep apnea and arterial hypertension.

BACKGROUND: The aim of this study was to assess the effects of continuous positive airway pressure (CPAP) on arterial stiffness, central blood pressure, and reflected pulse wave characteristics in patients with severe obstructive sleep apnea (OSA) and stage 2-3 arterial hypertension. METHODS: Forty-four patients with hypertension and severe OSA (apnea/hypopnea index > 30) received stepped dose titration of antihypertensive treatment, consisting of valsartan 160 mg + amlodipine 5-10 mg + hydrochlorothiazide 25 mg. CPAP therapy was added after 3 weeks of continuous antihypertensive treatment with BP < 140/90 mmHg or after adjusting triple treatment in patients with resistant arterial hypertension. The patients were randomized to effective CPAP (4-15 mm H2O) or placebo CPAP (pressure 4 mm H2O) for three weeks, then crossed over to the alternative treatment in a single-blind manner. Office blood pressure (BP), ambulatory BP monitoring, ambulatory arterial stiffness index (AASI), aortic BP, carotid-femoral pulse wave velocity (cfPWV), and systolic wave augmentation index were measured using a Sphygmocor® device at baseline, after antihypertensive treatment, placebo CPAP, and effective CPAP. RESULTS: Baseline cfPWV was above the normal range in 94% of patients. After reaching target BP, the cfPWV decreased by 1.9 ± 1.0 msec (P = 0.007). Effective CPAP achieved a further cfPWV reduction of 0.7 msec (P = 0.03). Increased arterial stiffness (pulse wave velocity > 12 msec) persisted in 35% of patients on antihypertensive treatment and effective CPAP, in 56% of patients on antihypertensive treatment alone, and in 53% of patients on placebo CPAP. Only the combination of antihypertensive treatment with effective CPAP achieved a significant reduction in augmentation index and AASI, along with a further reduction in aortic and brachial BP. CONCLUSION: Effective CPAP for 3 weeks resulted in a significant additional decrease in office BP, ambulatory BP monitoring, central BP, and augmentation index, together with an improvement in arterial stiffness parameters, ie, cfPWV and AASI, in a group of hypertensive patients with OSA.

[Treatment of patients with long nocturnal asystoles and obstructive sleep apnea syndrome by creating continuous positive air pressure in the upper respiratory tract].

AIM: To study prevalence of obstructive sleep apnea syndrome (OSAS) in patients with nocturnal asystoles, and assess therapeutic efficiency of constant positive air pressure (CPAP) applied to upper respiratory tract in this category of patients. METHODS: The study incorporated 37 patients (33 men and 4 women, average age 50+/-11 years) with nocturnal heart beat interruptions of over 3 seconds. Baseline examination revealed grade II-III arterial hypertension in 67.5%, coronary heart disease - in 19%, diabetes mellitus in 8% and no cardiovascular disease - in 5.5% of patients. Sinus rhythm was registered in 30 (81%) of patients, 7 (19%) patients had permanent atrial fibrillation. Causes of deteriorated cardiac conduction were as follows: sinoatrial blocks and sinoatrial arrests (n=18), grade II-III atrio ventricular block (n=10), combination of these forms of bradyarrhythmias (n=2) and block of conduction to ventricles in permanent atrial fibrillation (n=7). According to intra esophageal cardiac pacing, the function of sinus node and atrio ventricular conduction appeared to be undisturbed in all patients with sinus rhythm. All patients have undergone polysomnographic (PSG) examination. For patients with OSAS, an individual selection of therapeutic pressure was carried out using the CPAP apparatuses. CPAP therapy was considered effective against OSAS if normalization of apnea/hypopnea index (AHI) was observed. RESULTS: OSAS was registered in 25 cases (68%) (mean AHI 54.9+/-28.7), 20 patients (80%) had severe grade of the syndrome. CPAP therapy appeared to be effective in all patients. At the background of treatment AHI decreased from 60.7 to 5.5 episodes per hour of sleep, mean oxygen saturation of arterial blood rose from 74 to 90%. Effect of CPAP therapy relative to cardiac conduction abnormalities was attained in all 19 patients with sinus rhythm and only in one patient with permanent atrial fibrillation. CONCLUSION: OSAS was revealed in 68% of patients with nocturnal bradyarrhythmias. Individually selected therapy with constant positive pressure in patients with nocturnal asystoles and OSAS efficiently eliminated in sleep asystoles and made it possible to avoid pacemaker implantation in some patients.

[Obstructive sleep apnea and a cardiovascular risk in patients with arterial hypertension].

OBJECTIVE: To study an independent role of the obstructive sleep apnea syndrome (OSAS) in patients with arterial hypertension (AH) according to the data of a retrospective observation. SUBJECTS AND METHODS: all patients underwent polysomnographic test (EMBLA Flaga, Iceland) and the frequency of unfavorable events (stroke, myocardial infarction, chronic heart failure, atrial fibrillation, intermittent claudication, or death) was determined during the case-control observational longitudinal retrospective study. The diagnosis of OSAS was made when the apnea-hypopnea index (AHI) of more than 15 events per hour of sleep; the patients with an AHI of less than 15 formed a control group. RESULTS: Among 120 enrolled patients, 64 (53%) had OSAS. In the patients with OSAS, the baseline AHI was 50.9 +/- 23 events per hour whereas in the control group it was 8.9 +/- 5.2 per hours. Both groups were comparable in age, height, weight, body mass index, snore duration, drowsiness, and respiratory standstill during sleep, blood pressure, total cholesterol, and creatine. While analyzing OSAS, there was no change in the risk for a combined end point (all-cause death, stroke, myocardial infarction, chronic heart failure, atrial fibrillation, or intermittent claudication). Our study was retrospective, the patients were few and AH is itself an important cardiovascular risk factor which should be borne in interpreting the results of our study. We consider that the study of the independent role of OSAS should be continued within a well-designed prospective observation.