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                 The pathogenesis  of OSAS-related  consequences    in patients with OSAS.
                 is  assumed to be chronic  intermittent  hypoxia  (IH)   Pusuroglu  et  al  [26]  have shown that  Galectin-3  is
                 inducing alterations at the molecular level, oxidative   associated with coronary plaque burden & OSAS se-
                 stress,  persistent  systemic inflammation,  oxygen   verity. Galectin-3 is a chemical that plays an import-
                 sensor  activation and increase  sympathetic activity   ant role in the regulation  of inflammation,  develop-
                 [19].
                                                                    ment of  cardiac fibrosis  and  remodeling.  The  mean
                 New  research  is  coming to fore  about the mecha-  Galectin-3  level was significantly higher  with  OSAS
                 nisms and effects of OSAS:                         patients compared to controls.
                                                                    There has been a meta-analysis of OSAS on cardio-
                 Pathophysiology                                    vascular events after  percutaneous coronary  inter-
                 May et al [20] looked at the mechanistic insights at   vention  [27],  which  revealed that  OSAS  could  inde-
                 the production of cardiac arrhythmogenesis in OSAS.   pendently increase the risk of cardiovascular events.
                 Abnormal  sympathetic and parasympathetic fluctu-  There have been many other studies on OSAS and its
                 ations, intermittent  hypoxia and hypercapnia  and   association with the  cardiovascular system:
                 structural changes  such as  ventricular hypertrophy
                 and fibrosis  all  play  a part  in the generation  of  car-    - OSAS  was common  in peripheral  arterial  disease
                 diac arrhythmia.                                     (PAD ) and the OSAS severity correlated with PAD
                                                                      severity  [28]
                 An et al [21]    has  strong evidence that  microR-
                 NA-130a (miR-130A) may be involved in the progres-    - OSAS is associated  with  increased readmission
                 sion of OSAS-associated pulmonary hypertension by    in heart failure [29].  Sommerfield et al looked at
                 down-regulating the GAX gene.                        344  patient encounters  and  found  that  heart fail-
                                                                      ure  patients with OSAS  have an elevated  rate  of
                 Chen et al [22] concluded that the Oestrogen/ERR-al-
                 phaa signaling  axis  is  associated with fiber-type   readmission  compare  to the general  heart  failure
                 conversion of upper airway muscles in patients with   population.
                 OSAS. This finding may represent an interesting ther-    - Effects of OSAS on the response to hypertension
                 apeutic target , especially in postmenopausal women.  therapy  [30]  . Because of the sympathetic over-
                                                                      activity  in OSAS,  Beta1 blocker  therapy  may be
                 According to Chen et.al [23] there  is   an apparent   required in these patients with resistant hyperten-
                 correlation between systemic inflammation and cere-  sion.
                 bral perfusion in OSAS because of  haemodynamic
                 alterations. [23]                                    - Stroke  and other  cardiovascular events  are  more
                                                                      common in patients with OSAS  [31]. In this study,
                 Cardio Metabolic Complications                       1100 individuals were  studied and it was found
                 Epidemiological  studies  have  documented  the host   that cardiovascular events were significantly high-
                 of cardiometabolic effects of OSAS including arterial   er  with increasing  OSAS  severity  and  untreated
                 and/or  pulmonary hypertension,  arrhythmias, isch-  OSAS patients had more cardiac events
                 aemic heart disease, diabetes mellitus and metabolic     - Occurrence  of OSAS  in patients with TIA   [32].
                 syndrome. Over the past few years  there have been   It was found  that  there was a significant  higher
                 many new findings about the effects of OSAS on the   occurrence  of OSAS  in TIA  patients compared to
                 cardiometabolic system.                              patients without a vascular diagnosis.
                 Ruchala  et al [24]    suggests that  bony and  endo-    - The Pulmonary Artery  Stiffness in patients with
                 crine abnormalities that occur in OSAS lead to seri-  OSAS  was evaluated in 52 patients. [33] . It was
                 ous consequences. The sex hormones, aldosterone,     found that the elastic properties of the pulmonary
                 insulin, prolactin and corticosteroids, are all affected   artery deteriorate with severity of OSAS and may
                 in OSAS.                                             be responsible  for right ventricular dysfunction  in
                 There is also some evidence of haematological mark-  OSAS.
                 ers as predictors of cardiovascular disease in OSAS,     - Sommer field et al  [34]  showed that heart failure
                 according to Saygin et al [25] . In a study containing   patients with OSAS have an elevated rate of read-
                 142 patients,  it was  found that   red  cell  distribution   mission particularly within  the first 90  days after
                 width (RDW), could be used with other markers, espe-  discharge.
                 cially other markers platelet count and platelet distri-
                 bution width, in prediction of cardiovascular disease


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