Public Health Rep

19704988672PMCnull688

[Cardiovascular biomarkers in clinical practice of sleep apnea].

Obstructive sleep apnea syndrome (OSAS) leads to cardiovascular complications such as coronary artery disease, left/right ventricular hypertrophy and dysfunction, heart failure, systemic and pulmonary hypertension, arrhythmias and stroke; and these all cardiovascular complications increase morbidity and mortality of OSAS. However, Cheyne-Stokes respiration, central and obstructive apneas may occur in the patient with heart failure. Increased sympathetic activity by hypoxemia and endothelial dysfunction play a role in cardiovascular complications. Some cardiovascular biomarkers have a role in early diagnosis, treatment and prognosis. In the present review, some cardiovascular biomarkers such as serum C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukins, adiponectin, heart-type fatty acid binding protein (hFABP) and brain (B-type) natriuretic peptide (BNP), and their clinical importance were reviewed

[The effects of obstructive sleep apnea hypopnea syndrome on cardiovascular system].

Obstructive sleep apnea hypopnea syndrome (OSAHS) is characterized by repetitive upper airway obstruction during sleep and it is commonly seen in the adult population, 4% in the men, 2% in the women. The most common nocturnal symptom is snoring while the most common daytime symptom is excessive daytime sleepiness. The gold standard in the diagnosis is polysomnography. Nasal continuous positive airway pressure is the most efficient therapy in the treatment and prevention of the disease. The OSAHS may cause cardiovascular complications in long-term, including systemic hypertension, pulmonary hypertension, congestive heart failure, arrhythmias, stroke and myocardial infarction. All these complications increase the morbidity and mortality of OSAHS. In this paper, effects of OSAHS on cardiovascular system were reviewed

[Obstructive sleep apnea syndrome, endothelial dysfunction and coronary atherosclerosis].

In obstructive sleep apnea syndrome (OSAS), repetitive episodes of apnea cause increased sympathetic nerve activity, increased surges in arterial blood pressure, swings in intrathoracic pressure, oxidative stres, hypoxia and hypercapnia. The association of OSAS with some diseases, having endothelial dysfunction in their physiopathology, such as hypertension, diabetes mellitus, obesity, coronary artery diseases, stroke and heart failure is common. Increased sympathetic nerve activity and also endothelial dysfunction which are the results of hypoxia, have important roles in vascular complications of OSAS. When compared with healthy population, an important endothelial dysfunction in OSAS patients and relationship between OSAS severity and endothelial dysfunction have been shown. In this review, the relationship between OSAS and endothelial dysfunction was overviewed

[Heart failure and sleep apnea].

Sleep-disordered breathing is one of the important factors contributing to the development and/or progression of heart failure (HF). This condition is related to recurring attacks of apnea, hypopnea, and hyperpnea, sleep disruptions, arousals, intermittent hypoxemia, hypocapnia, and hypercapnia, and intrathoracic pressure changes. Obstructive sleep apnea (OSA) is characterized by recurrent upper airway obstruction (apnea and hypopnea), increased breathing effort against totally or partially occluded upper airway, and sleep disruptions. Cardiovascular consequences are the most serious complications of OSA and include acute myocardial infarction, heart failure, left/right ventricular dysfunction, arrhythmias, stroke, and systemic and pulmonary hypertension. Cheyne-Stokes respiration and central apneas may also occur in patients with HF. This article reviews the most recent information on the physiopathology, diagnosis, and treatment modalities of obstructive and central apneas in patients with HF

Impact of obstructive sleep apnea on right ventricular global function: sleep apnea and myocardial performance index.

BACKGROUND: Obstructive sleep apnea (OSA) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as heart failure, arrhythmias, myocardial infarction, systemic and pulmonary hypertension. OBJECTIVES: To determine right ventricular diameters and myocardial performance index (MPI) reflecting ventricular global function in uncomplicated OSA patients. METHODS: 49 subjects without hypertension, diabetes mellitus, or any cardiac or pulmonary disease referred for evaluation of OSA had overnight polysomnography and complete echocardiographic assessment. According to the apnea-hypopnea index (AHI), subjects were divided into three groups: group 1: control subjects (AHI or = 15, n = 18). Right ventricular free wall diameter was measured by M mode, and right ventricular MPI was calculated as (isovolumic contraction time + isovolumic relaxation time)/pulmonary ejection time. RESULTS: There were no differences of age, body mass index, heart rates, systolic and diastolic blood pressures among the groups (p > 0.05). Right ventricular end-diastolic and end-systolic diameters were not statistically different between the groups, and were within normal limits. Also, right ventricular free wall diameter was not significantly different between the groups of control, mild OSA and moderate-severe OSA (6.7 +/- 0.9, 6.9 +/- 1.0, 7.1 +/- 1.1 mm, p > 0.05). Right ventricular diastolic dysfunction was shown only in group 3 patients. Right ventricular MPI was statistically higher in group 3 (0.62 +/- 0.18) than in group 2 patients (0.50 +/- 0.10), and group 1 patients (0.48 +/- 0.08, p < 0.001). CONCLUSIONS: It was suggested that patients with moderate-severe OSA had a right ventricular global dysfunction, in addition to the presence of a diastolic dysfunction

Acute improvement of pulmonary artery pressure by non-invasive positive pressure ventilation in the patients with hypercapnic respiratory failure.

It is very important to decrease pulmonary artery pressure (PAP) in patients with chronic obstructive pulmonary disease (COPD) in order to prevent progression to right heart failure. We showed an acute improvement of PAP by non-invasive positive pressure ventilation (NPPV) treatment in patients with hypercapnic respiratory failure. In 26 patients with COPD (18 males and 8 females), physical examination, Doppler echocardiographic evaluation and arterial blood gases analysis were performed on admission and at discharge. PAP was measured by Doppler echocardiography. NPPV was used when 2 of the following were present without contraindications: 1. Respiratory distress with moderate to severe dyspnea, 2. Arterial pH less than 7.35 with PaCO(2) above 45 mmHg, 3. Respiratory rate of 25/minute or greater. Mean age of the patients was 62.6 ± 10.8 year, and mean usage of the NPPV was 12.6 ± 5.5 day. Mean and systolic PAPs of the patients (43.8 ± 16.9 mmHg and 66.7 ± 23.3 mmHg) were significantly decreased with NPPV treatment (26.6 ± 8.4 mmHg, p< 0.0001 and 41.8 ± 14.6 mmHg, p< 0.0001). Also, each parameter of the arterial blood gases was improved significantly with NPPV usage. An echocardiographic assessment in the COPD patients having NPPV treatment due to acute respiratory failure, might be a useful and easy method to show an improvement of PAP as a supportive measure in the management of those patients, in addition to beneficial effects of that treatment on respiratory acidosis, hypercapnia and hypoxemia

Acute effects of automated continuous positive airway pressure on blood pressure in patients with sleep apnea and hypertension.

BACKGROUND: The obstructive sleep apnea-hypopnea syndrome (OSAHS) is characterized by repetitive upper airway obstructions during sleep, and it might cause cardiovascular complications such as myocardial infarction, arrhythmias, and systemic and pulmonary hypertension. OBJECTIVES: We investigated the acute effects of automatic continuous positive airway pressure (automated CPAP) on blood pressure in patients with OSAHS and hypertension. METHODS: Polysomnography was used and ambulatory blood pressure measurements were done in 12 patients with OSAHS. Blood pressure and heart rate were measured at night (10 p.m. to 6 a.m.) and during the day (6 a.m. to 10 p.m.). During these periods systolic, diastolic and mean blood pressure and heart rate of the patients on the diagnostic day were compared with those on the treatment day. RESULTS: Patients had moderate or severe OSAHS; their mean age was 52.8+/-4.2 years. Systolic, diastolic and mean blood pressure and heart rate between the diagnostic and treatment day were not significantly different. Standard deviations of all these parameters during the night of the treatment day (9.1+/-4.5, 7.5+/-3.3, 8.0+/-3.0 mm Hg, and 4.8+/-1.5 beats/min, respectively) were significantly lower than during the night of the diagnostic day (12.6+/-4.9 mm Hg, p=0.023, 10.8+/-3.5 mm Hg, p=0.004, 11.6+/-4.4 mm Hg, p=0.006 and 6.9+/-1.6 beats/min, p=0.003, respectively). We did not find similar results during daytime periods. CONCLUSIONS: Automated CPAP therapy in patients with sleep apnea and hypertension did not decrease systolic and diastolic blood pressures and heart rates acutely. However, it might reduce the variability of these parameters during sleep in patients, but not during the day. It might be suggested that automated CPAP reduces cardiovascular morbidity of OSAHS via stabilizing heart rate and blood pressure during sleep

[Acute effects of adaptive servo-ventilation therapy on neurohormones and Cheyne-Stokes respiration in the patients with heart failure].

OBJECTIVE: Cheyne Stokes respiration (CSR) is frequently seen in the patients with heart failure (HF) and it increases mortality. In the present study, we aimed to evaluate acute effects of adaptive servo ventilation (ASV) on CSR and neurohormones in the patients with HF. METHODS: Nineteen males and 1 female patients with HF in the functional capacity of NYHA II-III were included into the study prospectively. One night polysomnography (PSG) was performed to all patients. In addition to medical treatment, 10 patients having CSR were applied ASV in another night together with PSG.. Arterial blood gases, plasma epinephrine and norepinephrine, serum N-terminal -pro-B type brain natriuretic peptide (NT-pro-BNP) were studied in the first night and after ASV treatment. A Wilcoxon test was used for comparison of parameters before and after treatment;and Mann-Whitney-U test was used for comparison of parameters between the patients with CSR and without CSR. RESULTS: Mean age of 10 patients with CSR was 62.2+/-11.1 years. Their etiologies were ischemic in 9 patients and idiopathic dilated cardiomyopathy in 1 patient. While there were no significant differences in the levels of PaCO2, HCO3, PH, before and after treatment; PaO2 (75.3 mmHg) and SatO2 (94.7%) significantly increased after the therapy (84.7 mmHg, 96.5% and p=0.007 and p=0.008 respectively). While NT-proBNP (3029.6+/-1450.5 pg/ml), norepinephrine (625.4+/-304.7 pg/ml) and epinephrine (65.4+/-24.1 pg/ml) were higher than normal before ASV treatment, all of them showed significant reductions after treatment (1694.0+/-925.9 pg/ml, 333.9+/-165.4 pg/ml and 45.0+/-20.5 pg/ml; p=0.005, p=0.005 and p=0.02, respectively). CONCLUSION: One night ASV treatment improves CSR, partial pressure of oxygen in arterial blood, and oxygen saturation and provides significant reductions in plasma catecholamines and NT-proBNP levels in the patients with HF and CSR. Prospective studies are needed to evaluate long-term effects of ASV treatment on morbidity and mortality in the patients with HF

Evaluation of cardiac biomarkers and right ventricular dysfunction in patients with acute pulmonary embolism.

OBJECTIVE: Right ventricular dysfunction (RVD) with myocardial damage may lead to fatal complications in patients with acute pulmonary embolism (PE). Cytoplasmic heart-type fatty acid-binding protein (HFABP) and the N-terminal fragment of its prohormone (NT-proBNP) are sensitive and specific biomarkers of myocardial damage. We evaluated RVD and cardiac biomarkers for myocardial damage and short-term mortality in patients with acute PE. METHODS: We analyzed 41 patients (24 females, 17 males) with confirmed acute PE prospective. Three groups (massive, submassive, and non-massive) of patients were defined, based on systemic systolic blood pressure measured on admission and RVD by transthoracic echocardiography (TTE). Also, systolic (s) and mean (m) pulmonary artery pressures (PAPs) were recorded by TTE, and plasma concentrations of cardiac troponin T (cTn-T), NT-proBNP, and HFABP were evaluated 6 month follow-up. RESULTS: Seventeen (41.5%) patients experienced a complicated clinical course in the 6-month follow-up for the combined end-point, including at least one of the following: death (n=12, 29.3%; 3 PE-related), chronic PE (n=4, 9.8%), pulmonary hypertension (n=2, 4.9%), and recurrent PE (n=1, 2.4%). Multivariate hazard ratio analysis revealed HFABP, NT-proBNP, and PAPs as the 6-month mortality predictors (HR 1.02, 95% CI 1.01-1.05; HR 1.01, 95% CI 1.01-1.04; and HR 1.02, 95% CI 1.02-1.05, respectively). CONCLUSION: HFABP, NT-proBNP, and PAPs measured on admission may be useful for short-term risk stratification and in the prediction of 6-month PE-related mortality in patients with acute PE