Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0037315 (sleep apnea)
 8,000 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Obesity produces an increase in total blood volume and cardiac output because of the high metabolic activity of excessive fat. In moderate to severe cases of obesity, this may lead to left ventricular dilation, increased left ventricular wall stress, compensatory (eccentric) left ventricular hypertrophy, and left ventricular diastolic dysfunction. Left ventricular systolic dysfunction may occur if wall stress remains high because of inadequate hypertrophy. Right ventricular structure and function may be similarly affected by the aforementioned morphologic and hemodynamic alterations and by pulmonary hypertension related to the sleep apnea/ obesity hypoventilation syndrome. The term obesity cardiomyopathy is applied when these cardiac structural and hemodynamic changes result in congestive heart failure. Obesity cardiomyopathy typically occurs in persons with severe and long-standing obesity. The predominant causes of death in those with obesity cardiomyopathy are progressive congestive heart failure and sudden cardiac death.
 ...
PMID:Obesity cardiomyopathy: pathophysiology and evolution of the clinical syndrome. 1130 64

Its is well established that sleep apnea (SA) is a health problem of paramount importance because it disrupts sleep and quality of life and may induce serious neuroendocrine and cardiovascular complications. There is little doubt that chronic renal failure is an independent cause of SA. The hypothesis that SA may depend on the accumulation of endogenous opioids still remains to be tested. Cytokines, particularly TNF-alpha and IL-6 which are much elevated in end-stage renal disease (ESRD), may also be implicated in the pathogenesis of SA. Nocturnal hypoxemia is an independent predictor of cardiovascular events in ESRD and the prediction power of this parameter remains strong and substantially unmodified after statistical adjustment for established cardiovascular risk factors in the dialysis population. Left ventricular hypertrophy and dysautonomia appear to be most likely intermediate mechanisms mediating the adverse cardiovascular effects of SA in ESRD.
 ...
PMID:Nocturnal hypoxemia: a neglected cardiovascular risk factor in end-stage renal disease? 1180 69

Obesity, as defined by bodily weight (body weight) and by bodily conformation-derived variables, accompanies hypertension in many patients. Both conditions are independent cardiovascular risk factors. In a formal survey carried out in the adult general population of Uruguay (LATIR Study, 575 adult and elderly subjects of whom 41.6% were males), we found the prevalence of hypertension to be 28.5% (95% CI: 24.9-32.4%) and that 74.4% of hypertensive individuals had a body mass index (BMI) higher than 25 kg/m(2) (95% CI: 67.0-80.8%). This association between obesity and hypertension forms part of a broader relationship between body weight and blood pressure (BP). In the general population, BP bears a positive linear correlation with BMI and waist-to-hip ratio over the continuous ranges of normal and unfavourable values of these three variables (r = 0.42, P < 0.001 for the correlation between BMI and mean BP, LATIR Study). Patients who present hypertension and obesity usually present other unfavourable conditions for cardiovascular prognosis, including changes in carbohydrate and lipid metabolism, hyperuricaemia, left ventricular hypertrophy, and/or the obstructive sleep apnoea syndrome. On average, hypertension is salt-sensitive in obese patients, and plasma volume and cardiac index are increased. Adequate control of body weight results in substantial reductions in total blood volume, cardiac output, BP and left ventricular mass, and in an amelioration or the disappearance of sleep apnoea. Adequate sodium intake restriction must form part of any diet prescribed to obese hypertensive patients. Various drug classes may be used to treat hypertension efficaciously in patients who also present obesity.
 ...
PMID:Hypertension and obesity. 1198 87

The usual model of intermittent hypoxia (sleep apnoea) corresponds to repeated episodes of hypoxia from a few seconds to a few hours interspersed with episodes of normoxia. The aim of this study was to evaluate in rats the effect of two periods of intermittent exposure for 2 months to hypoxia (IHX1, 24 h in hypoxia (428 Torr), 24 h in normoxia; IHX2, 48 h in hypoxia (428 Torr), 24 h in normoxia) as a new model of hypoxia simulating intermittent exposure to high altitude experienced by Andean miners. We assessed the haematological parameters, time course of resting heart rate and systolic blood pressure. We also evaluated the expression of adrenergic and muscarinic receptors. IHX1 and IHX2 produced an increase in haematocrit, haemoglobin concentration and mean corpuscular volume as previously seen in most hypoxic models. IHX1 and IHX2 induced a similar sustained elevation of systolic blood pressure (132 +/- 2 and 135 +/- 3 mmHg, respectively, vs. the control level of 121 +/- 16 mmHg) after 10 days of exposure without change in heart rate. Right ventricular (RV) hypertrophy (225 +/- 13 and 268 +/- 15 mg g(-1), vs. 178 +/- 7 mg g(-1) and downregulation of alpha1-adrenoceptor (RV: 127 +/- 21 and 94 +/- 16 fmol mg(-1) vs. 157 +/- 8 fmol mg(-1); left ventricle (LV): 141 +/- 5 and 126 +/- 9 fmol mg(-1) vs. 152 +/- 5 fmol mg(-1)) have been found in both groups, with right ventricular hypertrophy being greater and alpha1-adrenoceptor density being lower in IHX2 than in HX1 groups. These data indicate that both parameters are related to the time of exposure to hypoxia. IHX1 and IHX2 produced the same magnitude of upregulation of muscarinic receptors (LV, 60%; RV, 40%), and no change in beta-adrenoceptors. In conclusion, exposure to intermittent hypoxia led to polycythaemia and RV hypertrophy as observed in other types of hypoxia. A specific cardiovascular response was seen, that is an increase in blood pressure without change in heart rate, which was different from the one observed in episodic and chronic hypoxia. Furthermore, this model involved specific modifications of alpha1-adrenergic and muscarinic expression.
 ...
PMID:Effect of intermittent hypoxia on cardiovascular function, adrenoceptors and muscarinic receptors in Wistar rats. 1239 9

The high incidence of association between sleep apnea syndrome and cardiac disturbance was widely descripted during the last decade and has been the target of intensive investigation. Our retrospective study included 12 patients with sleep apnea syndrome diagnosed by polysomnography. 7 patients had HTA with left ventricular hypertrophy (5 cases). The CPAP stabilise blood pressure in 6 of them, 3 patients had ventricular or atrial arrhythmia. CPAP resolved 2 of them. 3 other patients had coronaropathy. Another one presented stoke. The sleep apnea syndrome has been descripted in association with heart failure or unstable HTA.
 ...
PMID:[Cardiovascular complications of sleep apnea syndromes]. 1266 5

Sleep apnoea (SA) is common, especially in elderly people. In severe cases, arterial P(O2) may be lowered for a third or more in a night of sleep. To simulate the degree and duration of severe SA we exposed rats in a normobaric environmental chamber to 10% O(2) for 4h daily for 56 days (intermittent hypoxia: IH group) and compared them with rats continuously exposed for 8 weeks (continuous hypoxia: CH group) and control rats breathing room air (normoxic: N group). We found significant cardiopulmonary and cerebral changes. Right ventricular hypertrophy developed in IH and to a greater extent in CH. Small peripheral lung vessels developed thicker walls (assessed by a new method), which reduced their lumen, more in CH than IH. Coronal brain sections were immunostained for the glucose-transporter 1 (GLUT1) and the vascular endothelial growth factor (VEGF). The percentages of immunoreactivity in the frontal and temporal cortex, hippocampus, accumbens and putamen were determined by image-capture analysis. We noted GLUT1 immunoreactivity of the capillaries was similarly increased in all regions after CH but less so after IH. However, there was a significant linear trend in GLUT1 reactivity from N to IH to CH (R(2) = 0.73, P = 0.007) that was also confirmed by analysis of variance. The extent of VEGF-stained neurones and glial cells was significantly increased in all regions after IH but not after CH. This suggests that the signals for angiogenesis were complete or arrested after CH. Our findings have implications for the elderly subjected to hypoxic episodes during sleep apnoea.
 ...
PMID:Hypoxia of sleep apnoea: cardiopulmonary and cerebral changes after intermittent hypoxia in rats. 1510 28

Obesity, now an epidemic in the USA, northern Europe, and Italy, is associated with several co-morbidities that shorten life expectancy, in particular type 2 diabetes mellitus (T2DM), arterial hypertension, and hyperlipidemia. The impact of obesity on mortality is evident in all ages, and is especially strong in young persons. Obesity, especially visceral obesity, associated with a sedentary lifestyle, is among the strongest risk factors for T2DM, and a diagnosis of T2DM seems to increase linearly as a function of duration of obesity. The pathogenesis of T2DM is based on a dual defect, i.e. increased insulin resistance coupled with defective insulin release. The main abnormality in obesity is increased insulin resistance, while insulin release, even though defective compared with body needs, is usually abundant. The incidence of obesity among children aged 6-16 years is now even greater than that among adults: in Italy, figures up to 30% have been reported. As in adults, obesity is a cause, among children, of arterial hypertension, left ventricular hypertrophy, hyperlipidemia, non-alcoholic-steato hepatitis, sleep apnea syndrome (SAS), and orthopedic, psychological, and social problems. Together with an increase in body weight, there is an increase of visceral fat. Obesity in children has also led to a tremendous increase in the prevalence of impaired glucose tolerance (IGT); the percentages span from 25% in a multiethnic cohort in the USA, to 4% in Italian Caucasians. Management of obesity and of T2DM in children has to face the issue of poor compliance; there is consensus that dietary treatment of obese T2DM children is a failure, so that drugs are required; the only drug evaluated in a formal trial is metformin, that behaves in terms of efficacy and of minor side effects as in adults. In conclusion, obesity in children is not pure obesity, but is accompanied by co-morbidities that cluster to form the "metabolic syndrome" just like in the adults. If this epidemics continues and is not properly challenged, in the next decades we will face an epidemic of early cardiovascular morbidity and mortality.
 ...
PMID:Type 2 diabetes mellitus is becoming the most common type of diabetes in school children. 1566 74

Ischemic or hemorrhagic cerebrovascular disease (CVD) produces injury of brain regions important for executive function, behavior, and memory leading to decline in cognitive functions and vascular dementia (VaD). Cardiovascular disease may cause VaD from hypoperfusion of susceptible brain areas. CVD may worsen degenerative dementias such as Alzheimer disease (AD). Currently, the global diagnostic category for cognitive impairment of vascular origin is vascular cognitive disorder (VCD). VCD ranges from vascular cognitive impairment (VCI) to VaD. The term VCI is limited to cases of cognitive impairment of vascular etiology, without dementia; VCI is equivalent to vascular mild cognitive impairment (MCI). Risk factors for VaD include age, hypertension, diabetes, smoking, cardiovascular disease (coronary heart disease, congestive heart failure, peripheral vascular disease), atrial fibrillation, left ventricular hypertrophy, hyperhomocysteinemia, orthostatic hypotension, cardiac arrhythmias, hyperfibrinogenemia, sleep apnea, infection, and high C-reactive protein. Research on biomarkers revealed increased CSF-NFL levels in VaD, whereas CSF-tau was normal. CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. VaD shows low CSF acetylcholinesterase levels. This condition responds to acetylcholinesterase inhibitors, confirming the central role of cholinergic deficit in its pathogenesis. Evidence strongly suggests that control of vascular risk factors, in particular hypertension, could prevent VaD.
 ...
PMID:Vascular dementia. Advances in nosology, diagnosis, treatment and prevention. 1587 77

Chronic constant hypoxia (CCH), such as in pulmonary diseases or high altitude, and chronic intermittent hypoxia (CIH), such as in sleep apnea, can lead to major changes in the heart. Molecular mechanisms underlying these cardiac alterations are not well understood. We hypothesized that changes in gene expression could help to delineate such mechanisms. The current study used a neonatal mouse model in CCH or CIH combined with cDNA microarrays to determine changes in gene expression in the CCH or CIH mouse heart. Both CCH and CIH induced substantial alterations in gene expression. In addition, a robust right ventricular hypertrophy and cardiac enlargement was found in CCH- but not in CIH-treated mouse heart. On one hand, upregulation in RNA and protein levels of eukaryotic translation initiation factor-2alpha and -4E (eIF-2alpha and eIF-4E) was found in CCH, whereas eIF-4E was downregulated in 1- and 2-wk CIH, suggesting that eIF-4E is likely to play an important role in the cardiac hypertrophy observed in CCH-treated mice. On the other hand, the specific downregulation of heart development-related genes (e.g., notch gene homolog-1, MAD homolog-4) and the upregulation of proteolysis genes (e.g., calpain-5) in the CIH heart can explain the lack of hypertrophy in CIH. Interestingly, apoptosis was enhanced in CCH but not CIH, and this was correlated with an upregulation of proapoptotic genes and downregulation of anti-apoptotic genes in CCH. In summary, our results indicate that 1) the pattern of gene response to CCH is different from that of CIH in mouse heart, and 2) the identified expression differences in certain gene groups are helpful in dissecting mechanisms responsible for phenotypes observed.
 ...
PMID:Gene expression and phenotypic characterization of mouse heart after chronic constant or intermittent hypoxia. 1592 8

The activation of adrenergic and renin-angiotensin-aldosterone (RAA) systems observed in patients with obstructive sleep apnoea syndrome (OSA) strongly affects functional status of the cardiovascular system. In this paper we discuss the link between obstructive sleep apnoea syndrome and common cardiovascular diseases such as systemic and pulmonary hypertension, ischaemic heart disease, stroke, arrhythmia and ventricular hypertrophy. We also present the importance of early pharmacologic treatment in preventing cardiac hypertrophy and ventricular dysfunction in patients with obstructive sleep apnoea syndrome.
 ...
PMID:[Cardiovascular abnormalities in patients with obstructive sleep apnoea syndrome]. 1599 58


<< Previous 1 2 3 4 5 Next >>