Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_4538_Библиотеки_им_академика_М_И_Перельмана

AHT is diagnosed when the ofce systolic blood pressure is ≥140mmHg and/or the diastolic blood pressure is ≥90mmHg [3]. Untreated AHT results in left ventricular hypertrophy and atherosclerotic processes and is a potent cardiovascular risk factor [4]. It is well established that AHT is very prevalent (50%–60%) among patients with OSA and that the risk of AHT increases with OSA severity [5–7]. In a large cross-sectional study (n=2677), Lavie etal. [6] found that for every apneic event per hour of sleep, the odds of AHT increased by about 1%. In contrast, every 10% decrease in nocturnal oxygen saturation increased the odds by 13%. Moreover, OSA is regarded as one of the most important causes of secondary AHT and resis­tant AHT (uncontrolled AHT despite the use of ≥3 different antihypertensive drugs). Consequently, it is recommended to screen for underlying OSA in patients with resistant AHT [8].

The diagnosis of AHT cannot be made by a single ofce visit. Still, it should be conrmed by repeated measurements at the ofce or, preferably, at home using a 24-h ambulatory blood pressure monitor to rule out white-coat hypertension (the phenomenon of blood pressures that are only elevated at the ofce) [3].

(AHI≥15), the prevalence ranges from 10% to 35%. However, in clinical practice, OSA is often underdiagnosed and undertreated [20–24]. Importantly, the presence of OSA is similar in heart failure with reduced ejection fraction (HFrEF), dened as systolic dysfunction with left ventricular ejection fraction (LVEF) ≤40%, and heart failure with preserved ejection fraction (HFpEF), dened as diastolic dysfunction with LVEF ≥50% [19, 25].

30]. Finally, it is important to determine the etiology, such as coronary artery dis-

Patients with heart failure have high mortality rates and frequently require hospital­ization for acute decompensation. Heart failure management is largely based on optimal medical treatment and differs between HFrEF and HFpEF.In patients with HFrEF, most recent guidelines recommend the simultaneous use of beta-blockers, angiotensin-converting enzyme inhibitors (ACE-I)/angiotensin receptor-neprilysin inhibitors (ARNI), mineralocorticoid receptor antagonists, and sodium-glucose

(reentry). Rapid ring from a focus (such as the pulmonary veins) initiates propa­gating reentrant waves in a vulnerable atrial substrate. The perpetuation of AF relies more on the substrate than on triggers [49]. Slowing of conduction velocity (e.g., through brosis) and shortening of the effective refractory period increase the excitable gap and promote the ability of the atrium to harbor sustainable cir­cuits [50]. Episodes of OSA can cause episodes of hypercapnia, hypoxemia, intra­thoracic pressure oscillations, sympathovagal imbalance, and structural remodeling. Animal models have shown that chronically repeated OSA episodes caused an increase in AF inducibility, conduction slowing and cardiac remodeling with an increase of brosis [51, 52], while the application of negative tracheal pressure during obstructive respiratory events can shorten the effective refractory period and increased AF inducibility through vagal activation [53]. In humans, alleviation of airway obstruction through uvulo-palato-pharyngoplasty signi­cantly reduced the risk of AF, suggesting a role of obstruction in arrhythmogene­sis [54]. Right and left atrial voltages and conduction velocities were lower in patients with AF and OSA than those without OSA [55]. Low voltage areas are thought to correlate with zones of increased brosis. Thus, the ndings of lower voltage in OSA patients might suggest a more diffuse substrate. The presence of inammation, a condition shared by both AF and OSA, could worsen the substrate [26, 56]. The severity of OSA varies from night to night. Recently, it has been demonstrated that the risk of having a period of AF during a certain night was higher if the severity of OSA during that night was higher [57]. Similarly, atrial ectopic beats were higher during episodes of obstructive respiratory events right after cardioversion than during normal, nonobstructed breathing [58]. This sug­gests a dynamic factor on top of the more static, insidiously changing substrate (such as changes in refractory periods on return to eucapnia or sympathovagal balance alterations) [59].

• Drugs and Cardioversion: The oldest approach to rhythm control is the use of