The impact of obesity on cardiac dysfunction in patients with sleep-disordered breathing.

INTRODUCTION: Obesity and heart failure are strongly associated with sleep-disordered breathing (SDB). However, the determinants of cardiac dysfunction in patients with SDB are not known. METHODS: We studied 90 patients suspected of having SDB (66 % women and 67 % black), age 50.4 ± 13.4 years and body mass index (BMI) 38.6 ± 9.8 kg/m(2). Apnea-hypopnea index (AHI) and nadir pulse oximetry (SpO2) were determined by polysomnography recordings. Left atrial (LA) diameter and left ventricular posterior wall (LVPW) thickness were determined by echocardiography. Patients who had EF<50 %, estimated right ventricular systolic pressure >45 mmHg or valvular heart disease were excluded. RESULTS: Univariate analysis revealed a positive correlation between LA diameter and each of BMI, neck circumference (NC), and AHI (coefficients, 0.28, 0.34, and 0.36, respectively; p<0.05). Multivariable linear regression analysis revealed that BMI was the only independent predictor of LA enlargement (coefficient 0.02, p<0.05). LVPW thickness correlated with BMI, NC, and AHI (correlation coefficients were 0.43, 0.47, and 0.33, respectively; p<0.05). Multivariable linear regression analysis revealed a significant relationship between LVPW thickness and each of BMI and NC (coefficients 0.016 and 0.007, respectively; p<0.05) but not AHI. BMI and LVPW associated with nadir SpO2 (r=-0.60, p<0.01 and r=-0.21, p=0.05; respectively), and BMI was a predictor of nadir SpO2 during sleep (B=-0.59; CI: -0.84, -0.33; p=0.01). CONCLUSIONS: Obesity can predict cardiovascular morbidity and nocturnal hypoxemia independent of the severity of the SDB. Our findings suggest the independent contribution of excess body weight on cardiac dysfunction and hypoxia in SDB patients.

Expiratory pharyngeal narrowing during central hypocapnic hypopnea.

RATIONALE: Ventilatory motor output is an important determinant of upper airway patency during sleep. OBJECTIVES: We hypothesized that central hypocapnic hypopnea would lead to increased expiratory upper airway resistance and pharyngeal narrowing during non-REM sleep. METHODS: Noninvasive positive pressure ventilation was used to induce hypocapnic hypopnea in 20 healthy subjects. Expiratory pressure was set at the lowest pressure (2 cm H(2)O), and inspiratory pressure was increased gradually during each 3-minute noninvasive positive pressure ventilation trial by increments of 2 cm H(2)O. Analysis 1 (n = 9) included measured retropalatal cross-sectional area (CSA) using nasopharyngoscope to compare CSA at five points of the respiratory cycle between control (eupneic) and hypopneic breaths. The pharyngeal pressure (P(ph)) was measured using a catheter positioned at the palatal rim. Analysis 2 (n = 11) included measured supraglottic pressure and airflow to compare inspiratory and expiratory upper airway resistance (R(UA)) at peak flow between eupneic and hypopneic breaths. MEASUREMENTS AND MAIN RESULTS: Expiratory CSA during hypopneic breaths was decreased relative to eupnea (CSA at beginning of expiration [BI]: 101.5 +/- 6.3 vs. 121.6 +/- 8.9%; P < 0.05); P(ph)-BI was lower than that generated during eupnea (1.5 +/- 0.3 vs. 3.3 +/- 0.9 cm H(2)O; P < 0.05). Body mass index was an independent predictor of retropalatal narrowing during hypopnea. Hypopnea-R(UA) increased during expiration relative to eupnea (14.0 +/- 5.7 vs. 10.6 +/- 2.5 cm H(2)O/L/s; P = 0.01), with no change in inspiratory resistance. CONCLUSIONS: Expiratory pharyngeal narrowing occurs during central hypocapnic hypopnea. Reduced ventilatory drive leads to increased expiratory, but not inspiratory, upper airway resistance. Central hypopneas are obstructive events because they cause pharyngeal narrowing.

Stress-related cardiomyopathy.

Stress-related cardiomyopathy is underdiagnosed in the white population. Recently, an increasing awareness of this syndrome was noted in the United States. Stress-related cardiomyopathy was found mostly in women after an immediate stress. The available literature has indicated excellent short-term prognosis and full recovery. We report the case of a 56-year-old white woman with acute pancreatitis, whose condition necessitated an endoscopic retrograde cholangiopancreatography procedure. Shortly after she received counseling for this procedure, acute retrosternal chest pain and shortness of breath developed. She had ischemic abnormalities on electrocardiography and mild cardiac biomarkers elevation. Subsequent cardiac catheterization revealed normal coronary arteries but reduced ejection fraction (25%), and typical apical ballooning was noted. Ten days later, the left ventricular function completely normalized (ejection fraction of 55%).

Effects of clonidine on breathing during sleep and susceptibility to central apnoea.

UNLABELLED: We hypothesized that administration of clonidine would decrease the hypocapnic apnoeic threshold (HAT) and widen the CO(2) reserve during non-REM sleep. METHODS: Ten healthy subjects (4 females) (age 22.3 ± 3.0 years; BMI 25.5 ± 3.4 kg/m(2)) were randomized to receive placebo or 0.1 mg/45 kg of clonidine on 2 separate nights. Ventilation and upper airway resistance were monitored during wakefulness and sleep. Two separate experiments were performed: Protocol 1 (n=8), CO(2) reserve, HAT and HcVR were determined using non-invasive hyperventilation (NIV) to induce hypocapnia for at least 3 min; Protocol 2 (n=6), peripheral hypocapnic ventilatory response (HcVR) was determined by NIV using short (3 breaths) hyperventilation. RESULTS: Clonidine decreased the systolic blood pressure by 12 ± 10 mmHg but did not affect baseline ventilation or upper airway resistance during wakefulness or sleep. Protocol (1), clonidine was associated with decreased HAT relative to placebo (37.3 ± 3.3 mmHg vs. 39.7 ± 3.4 mmHg, P<0.05), increased CO(2) reserve (-3.8 ± 1.3 mmHg vs. -2.8 ± 1.2 mmHg, P<0.05), and decreased HcVR (1.6 ± 0.6 L/min/mmHg vs. 2.5 ± 1.3 L/min/mmHg, P<0.05). Protocol (2), administration of clonidine did not decrease peripheral HcVR compared to placebo (0.5 ± 0.3 L/min/mmHg vs. 0.7 ± 0.3 L/min/mmHg, P=NS). CONCLUSION: Clonidine is associated with diminished susceptibility to hypocapnic central apnoea without significant effect on ventilation or upper airway mechanics. Reduced susceptibility to hypocapnic central apnoea is not explained by the peripheral chemoreceptor pathway. This suggests a central rather than a peripheral effect of clonidine on the susceptibility to hypocapnic central apnoea.

Obstructive sleep apnea-hypopnea syndrome: Etiology and diagnosis.

Sleep disordered breathing is a common chronic condition in the general population. This review will highlight the prevalence of different types of sleep apnea in general and obstructive type in particular in the United States and Middle East. Despite the extensive research studies on the sleep apnea pathogenesis, the exact mechanism is not well known. Obesity, however, is the leading risk factor to upper airway narrowing and obstruction and main contributor to the escalating prevalence of morbidity worldwide including the Arab countries. Due to the serious consequences of the untreated sleep disordered breathing, this article will emphasize on the importance of early recognition, key clinical manifestations, and how to treat and prevent the disease.

Inhibition of ventilatory motor output increases expiratory retro palatal compliance during sleep.

UNLABELLED: We hypothesized that inhibition of ventilatory motor output leads to increased pharyngeal compliance during NREM sleep, independent of lung volume. METHODS: Eighteen subjects were studied using noninvasive positive pressure ventilation (NPPV) to inhibit ventilatory motor output during stable NREM sleep. Nasopharyngoscopy was used to measure the retro palatal cross-sectional area/pressure relationship (CSA/Pph) in 8 subjects. The effect of NPPV on neck circumference (NC) and end-expiratory lung volumes (EELV) was studied in 10 additional subjects using strain gauge plethysmography and respitrace, respectively. RESULTS: (1) The CSA/Pph was increased during expiration under passive compared to active breathing (11.7 ± 7.1 vs. 8.5 ± 5.6mm(2)/cmH(2)O, respectively; p < 0.05) but not during inspiration. (2) NC correlated with the CSA/Pph during passive expiration (R(2) = 0.77, p < 0.05). (3) NC and EELV did not change between active and passive breaths (p = NS). CONCLUSIONS: (1) Inhibiting the ventilatory motor output increases the pharyngeal compliance. (2) Increased passive expiratory pharyngeal compliance was not associated with changes in NC or EELV.

Hypocapnia is associated with increased upper airway expiratory resistance during sleep.

We hypothesized that hypocapnia is responsible for increased expiratory resistance during NREM sleep. Hypocapnia was induced by hypoxic hyperventilation in 21 subjects (aged 29.4 ± 7.8 yrs, 10 women, BMI 24.4 ± 4.3 kg/m(2)). Isocapnic hypoxia was induced in 12 subjects of whom, 6 underwent hypocapnic hypoxia in the same night. Upper airway resistance (R(UA)) was measured at the linear pressure-flow relationship during inspiration and expiration. Inspiratory flow limitation (IFL) was defined as the dissociation in pressure-flow relationship. (1) Expiratory R(UA) increased during hypocapnic but not isocapnic hypoxia relative to control (11.0 ± 5.6 vs. 8.2 ± 3.6 cm H(2)O/L/s; p < 0.05, and 11.45.0 vs. 10.94.4 cm H(2)O/L/s; p = NS, respectively). (2) No gender difference was found in R(UA) (p = NS). (3) Increased expiratory R(UA) correlated with the IFL change during hypocapnic but not isocapnic hypoxia. (4) No changes were noted in inspiratory R(UA) or IFL. Expiratory R(UA) increased during hypocapnia and was associated with IFL, indicating upper airway narrowing. Gender does not influence the upper airway response to hypocapnic hypoxia.

Methicillin-resistant Staphylococcus aureus infection with intermediate sensitivity to vancomycin: a case report and literature review.

Staphylococcus aureus is a major cause of bacteremia and endocarditis in adults. Vancomycin is the standard therapy for methicillin-resistant Staphylococcus aureus (MRSA) bacteremia. Although clinical failure associated with the development of reduced susceptibility to vancomycin during the course of treatment for MRSA bacteremia has been reported infrequently, such an occurrence is very serious. We report a case of 43-year-old woman with of MRSA bacteremia, who relapsed after initial, apparently successful vancomycin treatment and developed left-sided endocarditis and vertebral osteomyelitis. Two weeks into her second admission, the vancomycin minimal inhibitory concentration rose from