cardiovascular-agents and Sleep-Apnea--Obstructive

This article briefly reviews the diagnosis and initial evaluation of the patient with suspected heart failure and then describes how newer treatments fit within heart failure management priorities and strategies.

Topics: Adrenergic beta-Antagonists; Aminobutyrates; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Biomarkers; Biphenyl Compounds; Cardiac Rehabilitation; Cardiac Resynchronization Therapy; Cardiovascular Agents; Defibrillators, Implantable; Diuretics; Drug Combinations; Echocardiography; Heart Failure; Heart-Assist Devices; Humans; Ivabradine; Obesity; Physician's Role; Physicians, Family; Sleep Apnea, Obstructive; Stroke Volume; Tetrazoles; Valsartan

Leukotrienes are biologically active lipid mediators of inflammation involved in atherogenesis. Obstructive sleep apnoea (OSA) patients exhibit early atherosclerosis and activation of the leukotriene pathway. In OSA patients, the production of leukotrienes is increased in relation to OSA severity and in vitro exposure of immune cells to intermittent hypoxia increases leukotriene pathway transcription. Moreover, the leukotriene transcriptional pathway is associated with early vascular remodelling. Lastly, obesity is a major confounding factor for leukotriene activation in OSA. The aim of this review was to focus on the intricate network of leukotrienes, chronic intermittent hypoxia, and atherosclerosis, with an emphasis on the role of leukotrienes in the early atherosclerosis observed in OSA patients.

Topics: Animals; Atherosclerosis; Cardiovascular Agents; Confounding Factors, Epidemiologic; Gene Expression Regulation; Humans; Hypoxia; Inflammation Mediators; Leukotrienes; Obesity; Risk Factors; Signal Transduction; Sleep Apnea, Obstructive; Transcription, Genetic

The obstructive sleep apnoea syndrome (OSAS) had become a major public health concern in modern society due to its high prevalence but, above all, to its associated morbidity, especially cardiovascular.. Untreated OSAS is associated with an increased incidence of fatal (myocardial infarction and stroke) (odds ratio: 2.87) and non-fatal cardiovascular events (myocardial infarction, stroke, coronary artery bypass surgery and coronary angiography) (odds ratio: 3.17). Moreover, the prevalence of hypertension in patients with OSAS is high, between 35 and 80%. The pathophysiological mechanisms leading to these complications are mainly due to intermittent hypoxia secondary to repeated episodes of apnoea/hypopnoea during sleep. These mechanisms include sympathetic hyperactivation, impairment of vasomotor reactivity, vascular inflammation, oxidative stress and metabolic disorders. In patients with OSAS, the impact of continuous positive pressure is proven in terms of prevention of cardiovascular events although blood pressure reduction is limited. Obviously these effects are proportional to observance.. OSAS does increase the cardiovascular risk, independently of other risk factors. Although the impact of treatment is relatively low in decreasing blood pressure, it seems essentially effective in preventing cardiovascular morbidity. Therefore, OSAS screening, and the association of specific treatments in cardio-metabolic patients and OSAS patients respectively, should be included in clinical strategies.

Topics: Cardiovascular Agents; Cardiovascular Diseases; Cerebrovascular Disorders; Comorbidity; Continuous Positive Airway Pressure; Endothelium, Vascular; Glucose Intolerance; Humans; Hypertension; Hypoxia; Metabolic Syndrome; Nitric Oxide; Obesity; Oxidative Stress; Prevalence; Sleep Apnea, Obstructive; Sympathetic Nervous System; Vasculitis

Most patients with comorbid sleep apnea (OSA), cardiovascular (CV) disease, and/or cerebrovascular (CeV) disease simultaneously take medications. Whether OSA and continuous positive airway pressure (CPAP) interact with CV/CeV medications remains unknown. This study aimed to determine the interaction among OSA, CPAP, and CV/CeV medications; the effects of medications on major adverse cardiac and cerebrovascular events, and survival in patients with comorbid OSA and CV/CeV.. This was a post hoc analysis of the data from one center of the Sleep Apnea Cardiovascular Endpoints Study. Participants (aged 45-75 years) with comorbid OSA and CV/CeV were randomized to receive usual care with or without CPAP from December 2008 to November 2013. The primary endpoint was death and the secondary endpoint was a composite of death, myocardial infarction, stroke, hospitalization for unstable angina, heart failure, and transient ischemic attack.. In total, 131 patients were analyzed. Sixty-three were in the CPAP group and 68 were in the usual care group, 41 had good adherence to CPAP (65.1%), and the median follow-up time was 43.0 (35.0, 54.0) months. In Cox regression analysis, ACE inhibitors and nitrates were independent factors for decreased survival in patients with comorbid OSA and CV/CeV (chi-square = 22.932, P = 0.003; ACE inhibitors: OR 7.241, P = 0.048, 95% CI 1.016-51.628; nitrates: OR 18.012, P = 0.011, 95% CI 1.923-168.750). ACE inhibitors increased mortality and secondary endpoints in the CPAP group (chi-square = 4.134, P = 0.042) but not in patients with good CPAP adherence. Clopidogrel and nitrates decreased survival in usual care group (clopidogrel: chi-square = 5.312, P = 0.021; nitrates: chi-square = 6.417, P = 0.011), but not in CPAP group.. OSA may predispose patients with CV/CeV and CV/CeV medications to a negative effect. CPAP treatment may neutralize the negative effects of OSA by relieving chronic intermittent hypoxia. Trial registration ClinicalTrials.gov (NCT00738179, first registration date: 20/08/2008).

Topics: Adrenergic beta-Antagonists; Aged; Cardiovascular Agents; Cardiovascular Diseases; Cerebrovascular Disorders; Comorbidity; Continuous Positive Airway Pressure; Female; Humans; Hydroxymethylglutaryl-CoA Reductase Inhibitors; Hypoglycemic Agents; Male; Middle Aged; Nitrates; Proportional Hazards Models; Risk Factors; Sleep Apnea, Obstructive; Survival Analysis

The aim of this study was to investigate the effects of a noninvasive positive pressure ventilation therapy on cardiac structure and function in patients with coronary heart disease combined with obstructive sleep apnea/hypopnea syndrome (OSAHS).. Eighty patients with coronary heart disease OSAHS were divided randomly into treatment (n=40) and control (n=40) groups. Both groups received standard medications. The treatment group received additional noninvasive mechanical ventilation support for at least 3 h (3-6 h) every night. On the first day after selection and 3 months afterwards, participants were examined with echocardiograms, 24-h ambulatory blood pressure monitoring, and blood analyses. Primary endpoints were left ventricular end-diastolic diameter, left ventricular end-systolic diameter, left ventricular ejection fraction, left atrial diameter as well as serum concentrations of N-terminal prohormone of brain natriuretic peptide, and high-sensitive C-reactive protein. Secondary endpoints included cardiac death, nonfatal myocardial infarction, and hospitalization.. After the 3-month study period, patients in the treatment group showed significantly improved left ventricular end-diastolic diameter (P=0.02), left ventricular end-systolic diameter (P=0.035), left ventricular ejection fraction (P=0.05), and left atrial diameter (P=0.02) values, and their serum N-terminal prohormone of brain natriuretic peptide (P=0.01) and high-sensitive C-reactive protein (P=0.04) concentrations were significantly improved compared with the control group. During the 3 months, three cardiovascular complications occurred in the treatment group versus nine in the control group (P<0.05).. For patients with coronary heart disease combined with OSAHS, noninvasive mechanical ventilation therapy can significantly improve heart functions and reduce the occurrence of cardiovascular complications.

Topics: Aged; Atrial Remodeling; Biomarkers; C-Reactive Protein; Cardiovascular Agents; China; Combined Modality Therapy; Coronary Artery Disease; Female; Humans; Male; Middle Aged; Natriuretic Peptide, Brain; Noninvasive Ventilation; Peptide Fragments; Positive-Pressure Respiration; Prospective Studies; Recovery of Function; Sleep Apnea, Obstructive; Stroke Volume; Time Factors; Treatment Outcome; Ventricular Function, Left

We tested whether breath hold divers (BHD) and obstructive sleep apnea (OSA) subjects had similar middle cerebral artery velocity (MCAV) responses to hypercapnea and hypocapnea. We analyzed changes in MCAV (cm/s) in response to hypocapnea and hyperoxic hypercapnea during placebo or after 90 min of oral indomethacin (100 mg) in BHD (N=7) and OSA (N=7). During control hypercapnea MCAV increased for 54.4% in BHD and 48.4% in OSA. Indomethacin blunted the MCAV increase in response to hypercapnea in BHD (P=0.02), but not in OSA. Indomethacin attenuated the mean arterial pressure response in BHD, but not in OSA. The blunted MCAV responses to hypercapnea with indomethacin in BHD, but not in OSA patients suggests that (a) the normal contribution of local vasodilating mechanisms to the cerebrovascular responses to hypercapnea is absent in OSA patients and (b) exposure to chronic/repeated apneas is not causal per se in limiting the contribution of vasodilating mechanisms to the cerebrovascular responses to hypercapnea in OSA.

Topics: Adult; Blood Flow Velocity; Blood Pressure; Cardiovascular Agents; Cerebrovascular Circulation; Cross-Over Studies; Diving; Double-Blind Method; Heart Rate; Humans; Hypercapnia; Hypocapnia; Indomethacin; Male; Middle Aged; Oxygen Consumption; Respiratory Mechanics; Sleep Apnea, Obstructive

Emerging evidence suggested that obstructive sleep apnea (OSA) was independently associated with the development of heart failure. In this study, we explored the influence of chronic OSA on left ventricular structural remodeling in canines, and the potential therapeutical role of metoprolol.. Chronic OSA model was established by stopping the ventilator and closing the airway for 4 h/day apnea-ventilation cycles every other day for 12 weeks while metoprolol (5 mg· kg(-1)· day(-1)) were administered continuously. Norepinephrine concentration was measured by Enzyme Linked Immunosorbent Assay. Transmission electron microscopy, Hematoxylin and eosin, TUNEL and Masson trichrome staining were employed to detect the morphology, apoptosis and fibrosis of cardiomyocytes. Protein expression of apoptosis and fibrosis-related factors including apoptosis-inducing factor (AIF), caspase 3, Bcl-2, Bax, α-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), and p38 mitogen-activated protein kinase (MAPK) were examined by Western blotting.. Norepinephrine concentration was markedly increased in chronic OSA dogs and reduced by metoprolol. Both the apoptotic ratio and collagen volume fraction were significantly increased in left ventricular myocytes of chronic OSA dogs, and was reversed by metoprolol. Moreover, chronic OSA-induced upregulation of AIF, cleaved caspase 3, Bax, α-SMA, and TGF-β1 as well as downregulation of Bcl-2 was markedly recovered by metoprolol, which was mediated by p38 MAPK.. Metoprolol protects against chronic OSA-induced cardiac apoptosis and fibrosis in left ventricular myocytes of canines, which may provide new potential strategy for drug therapy of OSA.

Topics: Actins; Animals; Apoptosis; Apoptosis Inducing Factor; bcl-2-Associated X Protein; bcl-Associated Death Protein; Cardiovascular Agents; Caspase 3; Disease Models, Animal; Dogs; Fibrosis; Gene Expression Regulation; Heart Ventricles; Humans; Male; Metoprolol; Myocytes, Cardiac; Norepinephrine; p38 Mitogen-Activated Protein Kinases; Sleep Apnea, Obstructive; Transforming Growth Factor beta1; Ventricular Remodeling