Association of sleep apnea with coronary slow-flow phenomenon.

BACKGROUND: Both obstructive sleep apnea (OSA) and coronary slow-flow phenomenon (CSFP) are known to share similar etiopathogenic mechanisms, such as chronic sympathetic activation, upregulation of inflammatory pathways, oxidative stress and, finally, endothelial dysfunction. OBJECTIVE: We evaluated whether there is an association between OSA and coronary flow rates. METHOD: We retrospectively reviewed medical records of all patients who underwent diagnostic nocturnal polysomnography for suspected OSA. Those who had coronary angiography performed within the same year of polysomnography were divided into two main groups: those with (group 1) and without (group 2) OSA; also, angiographic coronary TIMI (thrombolysis in myocardial infarction) frame counts (TFC) were compared between the groups. Patients with coronary arterial stenosis and angiograms with inadequate filling of the coronary arteries or visualization of the distal landmarks for frame counting were excluded from the study. RESULTS: There was a statistically significant difference between the groups regarding TFCs. We found a significant positive correlation between mean TFC and apnea-hypopnea index (r=0.611, P<0.001). CONCLUSION: The current study demonstrated that sleep apnea impairs coronary flow rates and is associated with CSFP.

Influence of the right- versus left-sided sleeping position on the apnea-hypopnea index in patients with sleep apnea.

PURPOSE: Sleep and sleep position have a significant impact on physical, cardiac and mental health, and have been evaluated in numerous studies particularly in terms of lateral sleeping positions and their association with diseases. We retrospectively examined the relationship between the sleeping position and position-specific apnea-hypopnea index (AHI) in obstructive sleep apnea-hypopnea (OSA) patients. METHODS: We assessed the sleeping body position and the body position-specific AHI score in patients who were referred for suspected OSA and underwent diagnostic nocturnal polysomnography. In order to eliminate inter-individual differences, only those who had a similar percentage of time spent in the LSSP and RSSP for each patient were enrolled. To provide this validity, only subjects that had a similar percentage of left and right lateral sleep time (±10%) were included in the analysis. RESULTS: A total of 864 patients had nocturnal diagnostic PSG. Of them, 131 patients met the inclusion criteria. The percent rate spent in the supine sleeping position (SSP) was 31.3 ± 18.7%, in the LSSP was 31.8 ± 10% and in the RSSP was 32.6 ± 10.8%. Whereas the SSP-specific AHI score was the highest with 60.4 ± 36.2/h among all the sleeping position-specific AHI scores (p < 0.001), the LSSP-specific AHI score was statistically higher than that for RSSP (30.2 ± 32.6/h vs. 23.6 ± 30.1/h; p < 0.001). When comparing individuals sub-grouped based on OSA severity, there was a statistically significant difference between the LSSP-specific AHI score and RSSP-specific AHI score in patients with severe (p = 0.002) and moderate (p = 0.026), but not mild (p = 0.130) OSA. CONCLUSION: We found that the sleeping position had a significant influence on apneic events and RSSP decreased the frequency of obstructive respiratory events in patients with moderate and severe disease.

Influence of the severity of obstructive sleep apnea on nocturnal heart rate indices and its association with hypertension.

OBJECTIVE: Both heart rate (HR) and blood pressure parameters provide important information on the pathophysiology of the cardiovascular regulatory mechanisms, and are mainly affected by the autonomic nervous system. We sought to clarify whether the severity of obstructive sleep apnea (OSA) affects nocturnal HRs and whether there is a relationship between nocturnal HRs and the presence of hypertension. METHODS: We retrospectively reviewed medical records of all patients who performed nocturnal polysomnography with monitoring of HRs, and examined whether there is a relationship among the nocturnal HRs, the severity of OSA and the presence of hypertension. RESULTS: A total of 540 patients were included in the study. Nocturnal mean and maximal HRs were significantly higher in severe OSA group than in moderate (p=0.002 and p>0.05 in females; p<0.049 and p=0.044, in males, respectively) and mild OSA groups (p<0.001 and p=0.003, respectively in females, p<0.001 and p=0.004, respectively in males); and there was a positive correlation between the nocturnal mean HR and apnea-hypopnea index (Pearson's p=0.504, p<0.001 in female group; Pearson's p=0.254, p<0.001 in male group) and again the nocturnal mean HR and the presence of HT (Spearman's p=0.090, p=0.394 in female group; Spearman's p=0.272, p<0.001 in male group) in both gender groups. CONCLUSION: We found that nocturnal mean and maximal HRs to be associated with severity of OSA and the presence of hypertension. We speculated that increased nocturnal mean and maximal HRs caused by sympathetic nervous system activation in OSA might be one of the mechanisms in explaining the hypertension and OSA association.

Association of anticonvulsant hypersensitivity syndrome with Herpesvirus 6, 7.

BACKGROUND: Anticonvulsant hypersensitivity syndrome (AHS) is one of the most severe forms of drug eruption with potentially lethal, and multiorgan involvement. Recently, it has been suggested that Human Herpesvirus (HHV) infection has been involved in this syndrome, although the pathogenesis of this syndrome remains still unclear. METHODS: The objective of this study was to determine the clinical characteristics of AHS and the possible role of viral infection as a co-factor. We prospectively analyzed clinical, laboratory and virological findings for 23 cases of AHS. A viral study including viral serology and a polymerase chain reaction (PCR) was performed. RESULTS: The most common anticonvulsant was carbamazepine (12) followed by phenytoin (6), phenobarbital (4) and gabapentin (1). All patients met fulfill the clinical criteria of AHS. Even though internal organ involvement such as liver (52%), kidney (34%), and lung (13%) has been observed, involvement of heart, lung, thyroid, muscle, pancreas, spleen, and brain was less frequent. We also noted two patients who died due to multiorgan failure. No association with viral infection including HSV, VZV, HHV-8, CMV, EBV, measles, rubella and parvovirus B19 was detected in the current series. Increased serum anti-HHV-6 IgG and HHV-7 titers and presence of HHV-6 and -7 DNA in serum, revealed by PCR analysis, suggested reactivation of HHV-6. In contrast to the control groups, DNA for HHV-6 was detected in serum in 5 out of the 23 patients while HHV-7 was seen in two patients. We found an evidence to link reactivation of HHV-6 or HHV-7 in the development of only carbamazepine-induced AHS. CONCLUSIONS: We propose that some cases of AHS are accompanied by reactivation of not only HHV-6 but also HHV-7. HHV infection may contribute to the severity, prolongation, or relapse of AHS and may possibly have fatal consequences in some susceptible individuals receiving the anticonvulsants.

Progression in acute ischemic stroke: frequency, risk factors and prognosis.

BACKGROUND AND PURPOSE: The aim of this study was to investigate the frequency, possible predictive factors and the prognosis of deteriorating ischemic stroke. METHODS: A total of 266 stroke patients who presented within 24h of onset were enrolled. Clinical deterioration was defined as a decrease of > or =1 points in the Canadian Neurological Scale (CNS). Rankin Score (RS) was performed at discharge and at six months. RESULTS: Of the 266 patients studied, 26 (9.8%) worsened. Involvement of posterior circulation (odds ratio (OR) 3.16) and noncardioembolic infarction (OR 4.5) were found to be independently associated with neurological worsening. Death occurred in 19.2% of progressive (P) and in 4.16% of nonprogressive (NP) groups. Functional outcome was worse in the P than in NP patients at discharge and at sixth months. CONCLUSIONS: Involvement of posterior circulation and noncardioembolic subtypes of infarct independently affect neurological progression in acute ischemic stroke. Clinical deterioration significantly worsens the prognosis.