|
 
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| REVIEW ARTICLE |
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| Year : 2023 | Volume
: 21
| Issue : 1 | Page : 62-67 |
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Coexistence of obstructive sleep apnea and cardiovascular disease: A narrative review
Natasha Anindhia Harsas1, Rana Zhafira Amanda2, Sidhi Laksono Purwowiyoto3, Hillary Kusharsamita1
1 Department of Emergency Medicine, Pertamina Central Hospital, Jakarta, Indonesia
2 Department of Emergency Medicine, Urip Sumoharjo Hospital, Bandar Lampung, Indonesia
3 Department of Cardiology and Vascular Medicine, Pertamina Central Hospital, Jakarta, Indonesia
| Date of Submission | 08-Sep-2022 |
| Date of Decision | 06-Nov-2022 |
| Date of Acceptance | 07-Nov-2022 |
| Date of Web Publication | 17-Jan-2023 |
Correspondence Address:
Dr. Sidhi Laksono Purwowiyoto
Faculty of Medicine of Universitas Muhammadiyah Prof Dr Hamka, Jl. Raden Patah No. 01, Rt. 002/ RW. 006, Parung Serab, Kec. Ciledug, Kota Tangerang, Banten 13460
Indonesia
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cmi.cmi_101_22
There is substantial evidence that patients with obstructive sleep apnea (OSA) have a higher incidence of cardiovascular disease (CVD). However, the exact mechanism that links OSA with CVD is still insufficiently understood and often underdiagnosed and undertreated. This review aims to summarize the pathomechanisms coexistence of OSA and CVD and a diagnostic evaluation of the treatment options for OSA. The Pubmed was searched using the keywords “OSA;” and “CVD.” Related papers published from 2013 to February 2022 were chosen. OSA has been associated with intermittent hypoxemia, significant intrathoracic pressure changes, and arousal from sleep, all of which have been linked to adverse health effects, particularly in the case of CVD. The need for the early detection of CVD patients and OSA screening is critical. Screening techniques include identifying specific OSA symptoms through medical history, using screening questionnaires or devices, followed by diagnostic testing thorough sleep evaluation that differs depending on the underlying cardiovascular condition. The need to improve the early diagnosis and treatment of OSA, a highly prospective modifiable CVD risk factor, is crucial given the growing body of research on the relationship between OSA and CVD as well as the effectiveness of OSA treatment.
Keywords: Cardiovascular, early diagnosis, outcome assessment, sleep apnea
How to cite this article:
Harsas NA, Amanda RZ, Purwowiyoto SL, Kusharsamita H. Coexistence of obstructive sleep apnea and cardiovascular disease: A narrative review. Curr Med Issues 2023;21:62-7 |
How to cite this URL:
Harsas NA, Amanda RZ, Purwowiyoto SL, Kusharsamita H. Coexistence of obstructive sleep apnea and cardiovascular disease: A narrative review. Curr Med Issues [serial online] 2023 [cited 2023 Jun 6];21:62-7. Available from: https://www.cmijournal.org/text.asp?2023/21/1/62/367854 |
| Introduction | |  |
The depiction of obstructive sleep apnea (OSA) is obstruction of the upper airway, either complete (apneas) or partial (hypopneas), which results in intermittent hypoxemia (IH), autonomic variation, and repetitive short interruption of sleep.[1] OSA is remarkably common, affecting 17% of women and 34% of men worldwide.[2] The prevalence of hypertension, heart failure, pulmonary hypertension, cardiac arrhythmias, coronary artery disease (CAD), and cerebrovascular illness is significantly greater in individuals with OSA. OSA leads to inadequate quality and duration of sleep. A systematic review of prospective studies concluded that abnormal sleep duration was associated with cardiovascular disease (CVD). This study included ten studies with a total of 361.041 participants, which showed that short sleep duration was associated with coronary artery calcification, hypertension, and heart failure. Whereas, atrial fibrillation (AF) and coronary heart disease, on the other hand, were associated with short and long sleep duration.[3] Regardless, OSA has complex and poorly understood pathophysiology. Therefore, in this study, we intend to review the coexistence of OSA and CVD.
| Methods | | |
Using PubMed, a thorough electronic search was carried out. The search was restricted to publications from 2013 until February 2022 using these keywords: OSA and CVD. A direct search of related journals and reference lists from the included studies for potential publications that might be a good fit for inclusion was done. Reviews, original publications, and case reports are all included in searches. Articles written in languages other than English and articles with limited access were the exclusion criteria. Utilizing Mendeley software, the obtained articles were organized and maintained. After sorting the search results by title and abstract, we reviewed the complete texts of the articles and excluded those that met the exclusion criteria [Figure 1].
| Results and Discussion | | |
Classification
IH is characterized by a short duration of oxygen desaturation (15–20 s), followed by reoxygenation. It occurs for 6–8 h during sleep and lasts for many years.[4],[5] According to the American Academy of Sleep Medicine, based on the severity, OSA can be categorized into mild, moderate, or severe [Table 1].
The Apnea-Hypopnea Index (AHI) and respiratory disturbance index (RDI) have been widely utilized to identify OSA severity. AHI serves the average number of apneas and hypopneas that occur each hour during sleep time. Besides apneas and hypopneas, RDI includes respiratory effort-related arousals (RERAs) as an additional factor. With RERAs' incorporation, the RDI may analyze more patients as having OSA than AHI using the same threshold. Nonetheless, there is no consensus yet on the gold-standard index for the severity of OSA between the two.[1],[2]
| Clinical Manifestations | | |
Symptoms of OSA vary and can happen during the day and at night. Snoring is reported as one of the most common symptoms [Table 2]. While excessive daytime sleepiness or fatigue are common daytime symptoms.[6]
| Pathophysiology | | |
The development of OSA is generated from the interaction between upper respiratory tract anatomy and sleep-related changes in airway physiology.[1] Most people with OSA have a smaller diameter of the upper airway. Two factors contributed are pharyngeal muscles and fat deposition in the parapharhyngeal muscles. Morphological abnormalities, such as tonsil hypertrophy and increased neck soft tissue, also play roles in the stage of the development of OSA.[1],[7] Collapses in the upper airway causing the immediate consequences of airflow obstruction. IH, significant alteration in intrathoracic pressure, and awakening from sleep constitute an initial cascade of collaborating mechanisms that worsen health outcomes, especially CVD[7] [Figure 2]. | Figure 2: Pathophysiologic mechanisms of OSA affecting cardiovascular function.[6] OSA: Obstructive sleep apnea
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An increase in breathing effort against an obstructed airway and hypoxemia caused sleep arousals. Thus, patients usually complain of excessive sleepiness in the daytime. The reactive oxygen species are produced by those two factors and then trigger the sympathetic nervous system (SNS) and the hypothalamic-pituitary-adrenal axis, contributing to acute and chronic high blood pressure. Consequently, cardiac preload and afterload are also increased. Sympathetic activity and oxidative stress also induce metabolic disorders, systemic inflammation, and disruption of normal endothelial function. All the processes described above are interrelated and contribute to the development of heart failure and arrhythmia. In addition, patients with OSA also have lower heart rate and blood pressure during sleep. This due to peripheral arteries constriction that caused by increased in aterload and parasympathetic modulation.[5],[7],[8]
| Screening Tools | | |
Several screening questionnaires commonly used to determine the likelihood of OSA include the OSA50, berlin questionnaire, and the STOP-Bang. These screening tools, while sensitivity appears to be in the higher range (between 77% and 89%), they tend to have poor sensitivity (32%–34%), ensuing in more number of false positives that further limit the utility of these as an instrument for the diagnosis of OSA.[1] Therefore, the primary role of any screening questionnaire would be to reduce the number of physiological tests required by ruling out those unlikely to have severe or symptomatic disease.[9]
Among those questionnaires, the STOP-Bang questionnaire delivered the most sensitivity to distinguish high-risk patients for OSA in distinct age, gender, and comorbidities, such as hypertension, diabetes mellitus, CAD, chronic obstructive pulmonary disease, and asthma.[9],[10]
The Epworth Sleepiness Scale (ESS) has a different approach, focusing on the tendency for dozing in the daytime, and is considered an inadequate screening tool due to its superior specificity (67%) but low sensitivity (42%).[1] However, the ESS score does not always parallel with AHI, as not all OSA patients will have symptoms of excessive daytime drowsiness, considering there are multiple explanations beyond OSA (e. g., other sleep disorders and depression). Accordingly, the ESS is not a recommended sole screening tool to determine whether patients are at high risk for OSA.[11]
| Diagnostic Evaluation | | |
Diagnostic tests choice for OSA comprises nighttime clinical examination, multichannel polysomnography (PSG), or at-home sleep apnea testing (HSAT). Patients requisitely have (1) nocturnal respiratory distress, like snoring, snorting, or pauses in breathing during sleep, or excessive sleepiness or exhaustion regardless of adequate rest with no other possible medical conditions caused in the daytime; and (2) respiratory event index (REI) ≥5episodes/h for diagnosing OSA. In a patient without symptoms, we can diagnose OSA if the condition AHI or RDI is 15 or surpassing/h.[1]
Sleep apnea evaluation begins with a thorough assessment of sleep. This evaluation includes a comprehensive medical history of signs and symptoms and a review of the record of relevant risk factors. Suspected sleep apnea patients should go through diagnostic testing. PSG, known as a sleep study, is acknowledged as the gold-standard diagnostic test for OSA. This tool subsists of simultaneously recording multiple parameters associated with sleep and wakefulness, such as EEG activity and cardiac telemetry, to assess sleep stages, arousal, and heart rate. The primary drawback of PSG is its limited supply regardless of increasing need.[12]
HSAT is a viable substitute testing method. Some HSAT utilizes a portable monitor to count heart rate and oxygen saturation, and some measure pressure of nasal, chest-abdomen plethysmography, and peripheral arterial tonometry. The preciseness of HSAT in diagnosing is low, depending on the population and the diagnostic standards, compared to PSG. However, the potential advantage is that HSAT is less costly than PSG.[2]
AHI and RDI are outcome data indices of the PSG in assessing the sleep-related obstructive event. On the other hand, in HSAT, sleep staging channels are usually not included in the measurement, which impacts the usage of recording time as the divisor of the REI (the phrase represents AHI derived from HSAT) in substitute to sleep time in AHI/RDI.[12]
| Obstructive Sleep Apnea and Cardiovascular Disease | | |
OSA is considered as a risk factor for cerebro-CVD. Some associated complications of OSA include hypertension, AF, arrhythmias, heart failure, pulmonary hypertension, and atherosclerotic disease. Several processes involve in its pathomechanism harm through mechanical, chemical, neurohumoral, and inflammatory mechanisms.[1],[13],[14]
| Resistant Hypertension | | |
OSA and hypertension are common conditions that coexist and involve complex mechanisms. Hypertension becomes refractory when blood pressure remains uncontrolled despite maximal therapy; thus, it is called resistant hypertension. Individuals with resistant hypertension may have OSA with a percentage of 80%.[1] A previous systematic review and meta-analysis study discussed the affiliation of OSA with hypertension with 26 studies included. Among them, 6 studies demonstrated that OSA is significantly related with resistant hypertension (pooled odds ratio [OR] = 2.842, 95% confidence interval [CI] = 1.703–3.980, P < 0.05), while another 20 studies revealed that OSA is significantly associated with essential hypertension (pooled ORs of 1.184, 95% CI = 1.093–1.274, P < 0.05 for mild OSA; pooled ORs of 1.316, 95% CI = 1.197–1.433, P < 0.05 for moderate OSA; pooled ORs of 1.561, 95% CI = 1.287–1.835, P < 0.05 for severe OSA).[15] The pathomechanism of hypertension and OSA depends on several factors, such as peripheral vasoconstriction, sympathetic tone activity increment, renin-angiotensin-aldosterone activity increment, and baroreceptor reflexes impairment. At night, fluid is redistributed from the lower extremities to the neck, leading to further blockage and elevation in blood pressure. The recurring event of upper airway obstruction can cause hypoxia and increase renin activation. Renin is produced by the kidney and is known as a hormone that plays role in increasing blood pressure.[16],[17]
| Heart Failure | | |
The prevalence of sleep apnea in HF patients ranges from 50% to 70%, and the obstructive type accounts for one-third of the events.[2] Former studies have indicated a 12%–53% higher prevalence of OSA in HFrEF patients than in the general population. Older age, male gender, higher BMI, and habitual snoring are risk factors for the existence of OSA in HF patients.[18] Coexisting sleep apnea is associated with poor outcomes, including symptom progression, hospitalization, and mortality. During mechanical airflow obstruction sequence, there is a magnified drop in intrathoracic pressure, oxygen desaturation, and arousal. It can cause an increase in left ventricular (LV) transmural pressure, which has the effect of increasing afterload. The venous return also increases and causes distention of the right ventricle and a leftward shift of the interventricular septum. It has the effect of decreasing LV filling. OSA also affects increasing sympathetic nervous system activity (SNA). An increase in LV afterload combined with the augmented SNA results in myocardial oxygen supply-demand imbalance, leading to cardiac ischemia and arrhythmias. Chronically, this can result in LV wall hypertrophy, LV enlargement, and HF. Those mechanisms also lead to the activation of renal-angiotensin-aldosterone and several other metabolites and can trigger inflammatory and hormonal changes.[14],[18] Conversely, the accumulation of fluid in the neck veins and soft tissue edema around the pharynx in HF patients contributes to the obstruction of the neck and might leads to the progression of OSA.[19]
| Pulmonary Hypertension | | |
The prevalence of moderate-to-severe OSA in pulmonary hypertension patients is low, estimated to be 10%–20%. Hypercapnia and hypoxic episodes during sleep trigger pulmonary arteriolar to constrict and result in an acute elevation of pulmonary artery pressures. This mechanism induces inflammatory pathways by releasing nitric oxide (NO), endothelin, serotonin, NADPH-oxidase, and angiopoietin-1. Chronically, those can cause pulmonary vessels remodeling and escalation in pulmonary vascular resistance permanently. Repetitive upper airway obstruction during sleep in OSA can cause increased venous return, leading to increased right ventricular (RV) preload. It leads to RV hypertrophy and eventually raises pulmonary artery pressure.[2],[20] The presence of OSA in severe PH patients is associated with increased mortality. The pathomechanism of pulmonary hypertension in sleep apnea can be divided into postcapillary and precapillary. Postcapillary pulmonary hypertension is caused by high pressure in pulmonary veins. It is usually a secondary effect of LV dysfunction and causes an increase in its filling pressures. Upper airway obstruction causes impaired intrathoracic pressure, which can lead to significant changes to the heart, both structurally and functionally. Systemic vasoconstriction occurs due to an increase in the sympathetic tone caused by repeated apneas and CO2 retention. Those factors result in afterload increase, LV and RV hypertrophy, and even failure. Meanwhile, precapillary pulmonary hypertension is potentially caused by vasoconstriction of the pulmonary arterioles due to Intermittent Hypoxia (IH). There are impairments in endothelial function and its structure. IH has also been implicated in suppressing the potent pulmonary vasodilator, NO.[21]
| Arrhythmias | | |
Arrhythmias and conduction disturbances are of interest among the CVDs associated with OSA. Various anomalies such as sympathovagal imbalance and hypoxia are unfailingly found in OSA and bound with arrhythmia and increased cardiovascular threat in OSA patients.[22]
OSA instigated the advancement of arrhythmia through two mechanisms, direct and indirect. Direct effects are the firsthand aftermath of airway collapse during sleep that is responsible for the development of hypoxemia and hypercapnia, sympathetic and parasympathetic tone change by vagal nerve, and negative effects of intrathoracic pressure on both the free walls of atria and ventricles. In addition, OSA can cause indirect changes in cardiac structure. Structural heart disease is also affected. Indirect effects comprehend the progress of CVDs such as hypertension, heart failure, and CAD, which induce to development of arrhythmias.[23]
Based on previous research studies, several associations between OSA and arrhythmias, especially AF, have been observed. Multiple studies have shown that AF occurs significantly more frequently in patients with OSA.[24] Arrhythmia frequency increases with the severity of OSA. In addition, another study showed that untreated OSA had a high recurrence rate of AF after successful cardioversion.[25]
Besides AF, OSA is akin to various cardiac arrhythmias and sudden cardiac death.[2] Sinus node dysfunction, including bradycardia with chronotropic insufficiency, sinoatrial exit block, and tachycardia-bradycardia syndrome, is expected in OSA patients. However, there is wide variability between studies, indicating incidences ranging from 5% to 50% susceptible to the extent of hypoxemia following sleep apnea.[22],[23]
| Coronary Artery Disease and Cerebrovascular Disease | | |
OSA is a frequent condition in patients with cardiovascular and cerebrovascular events affecting 60% to 70% of this population.[26] The American Sleep Health Research Centre has shown that AHI >5 can significantly escalate the incidence of cardiovascular events and mortality. Various studies have documented a broad range of OSA incidence from 26% to 66%, which is justified by the different values of AHI used to diagnose OSA. A recent report from De Torres-Alba et al. emphasizes the underrecognition of OSA in patients hospitalized for ACS, with 69% prevalence for OSA and 34% for severe OSA (AHI >30).[27],[28] Studies also show that OSA is a substantial element affecting the prognosis of CAD. In a follow-up study, 6-months ensuing PCI, major adverse cardiac and cerebrovascular events (MACCEs) were found in nearly 24% of OSA patients in contrast to 5% without OSA.[29]
Along with CAD, OSA is a well-recognized independent risk factor for stroke. The prevalence of OSA in the general population range from 3% to 7%, whereas in stroke patients ranges from 30% to 70%.[26]
Some pathophysiological processes linking OSA to CAD and cerebrovascular disease include intermittent hypoxia (IH), fragmentation of sleep, fluctuations in intrathoracic pressure leading to shifting in cardiac and pulmonary vascular hemodynamics, and augmented activity of the SNS, oxidative stress, and predisposition to inadequately maintained or resistant hypertension. Other pathological mechanisms including endothelial function impairment, metabolic dysregulation, and promotion of a pro-coagulation state have also been recognized.[2],[30]
| Treatment | | |
Effective treatment for OSA includes lifestyle modification through behavioral therapies, medical devices, and surgery. The initial approach for OSA is usually behavioral therapies that incorporate weight loss, regular aerobic exercise, abstinence from alcohol, and positional therapy. Nevertheless, most patients will require further therapy as only 10%–30% of patients achieve a goal of AHI <5 in either medical or surgical weight loss trials. Exercise may also improve OSA regardless of weight loss. Some systematic review and meta-analysis studies revealed that lifestyle interventions significantly reduce AHI (P < 0.0001) and episodes of OSA.[2],[6],[31]
In the sleep Action for Health in Diabetes study, 264 overweight and obese patients with OSA and type 2 diabetes mellitus were enrolled in a weight loss program through diet, exercise, and diabetes control. After 1-year-follow-up, it showed a greater 10.2-kg weight loss and a 9.7-event/h decrease in AHI.[7]
Positional therapy is an adjunctive therapy that uses a device to retain a position during sleep other than supine. The commonly used definition of positional OSA is at least 50% lower AHI when in the nonsupine sleeping position. Mandibular repositioning devices or mandibular advancement devices (MAD) are suitable for patients with mild to moderate OSA. A review of some studies showed that OSA patients treated with MAD experienced AHI reduction, 45% showing complete responses (AHI <5) and 100% partial responses (>50% reduction in AHI from baseline or AHI >5).[2],[7],[32]
Continuous positive airway pressure (CPAP) considered as the most efficacious noninvasive therapy for sleep apnea, proven by its ability to reduce AHI and improve self-reported sleepiness. Nonetheless, patient nonadherence, which is common and caused by various factors, can limit the effectiveness.[2]
Previously available data on the CPAP effect on cardiovascular in OSA patients have been conflicting. With the development of CPAP, there have been successful RCTs for sleepiness, quality of life, and blood pressure in OSA. These studies demonstrate the apparent advantages of CPAP therapy in relatively short-term endpoints. Meanwhile, Aslan et al. conducted a meta-analysis study and encountered that CPAP treatment remarkably improved LV ejection fraction despite no decrease in all-cause mortality or incidence of cardiovascular events.[33],[34] Recent RCTs on the impacts of OSA treatment on CVD have been unfavorable. However, based on the study by Pack et al., these RCTs have significant challenges and biases, such as sample selection bias and low adherence to therapy, which likely explain the negative result, and still hurried to assume that CPAP treatment does not lower cardiovascular events.[34],[35]
Despite their invasiveness and complexity, surgery of the upper airway is a viable option for symptomatic patients who are unable to tolerate CPAP as therapy. The most popular surgical procedure is modifying the soft tissue of the upper airway, including the palate, tongue base, and lateral pharyngeal walls, such as tonsillectomy and uvulopalatopharyngoplasty.[7],[16]
| Conclusions | | |
OSA has been disclosed as a risk factor for several CVD entities. Therefore, it provides a rationale for OSA screening and early diagnosis for CVD patients. Proceed with diagnostic testing through a comprehensive sleep examination that differs based on the underlying cardiovascular comorbidity. Numerous treatment options are available and should be considered subject to the patient's clinical characteristics, manifestations, comorbidity, and preferences. CPAP is the most effective noninvasive medication for OSA and should be offered for patients with severe OSA. With increasing studies regarding the conjunction between OSA and CVD and the effectiveness of OSA treatment, it is critical to enhancing early detection and treatment of OSA, a highly potential modifiable CVD risk factor.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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[Figure 1], [Figure 2]
[Table 1], [Table 2]
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