Detection of obstructive sleep apnea in young patients suffering from coronary artery disease by performing portable polysomnography studies

Abstract

Background

Obstructive sleep apnea (OSA) is known to be an important contributory factor of coronary artery disease (CAD), but the extent of contribution of OSA in young patients suffering from CAD is not known. Thus, with an aim to detect OSA in young patients suffering from CAD by performing portable polysomnography (PSG), the present study was carried out at a tertiary care chest center.

Methods

A prospective study was carried out from June 2015 to June 2018, wherein 100 consecutive young (age less than 40 years), non-smoking patients with angiographically confirmed CAD, with no identifiable risk factors for cardiovascular diseases except obesity, were subjected to level 3 portable PSG studies.

Results

Of 100 patients with CAD, 80% had OSA (24% with mild OSA, 28% with moderate OSA, and 28% with severe OSA). Body weight and severity of OSA showed a significant correlation with a P-value of 0.033. SPSS software was used for statistical analysis. The categorical variables were compared using Fischer's exact test.

Conclusion

The study detected a significant number of young patients with angiographically confirmed CAD having OSA. A significant correlation was also observed between weight and severity of OSA, suggesting that overweight patients and patients with obesity have higher grades of OSA.

Introduction

Obstructive sleep apnea (OSA) and coronary artery diseases (CADs) have been found to congregate in various clinical studies of sleep clinic cohorts. OSA is estimated to be present in 30–60% of patients with CAD.^2,3 OSA is a common disorder affecting 2–7% of adults in the general population.³ OSA independently causing CAD is controversial, but the association is strongest in middle-aged men,⁴ a group susceptible to varied lifestyle disorders such as obesity, diabetes mellitus, and so on. OSA is likely to be a contributory factor and not an independent causative factor in CAD. There is scarcity of evidence regarding association of OSA in young patients with CAD. Thus, with an aim to detect OSA in young patients with angiographically confirmed CAD by performing level 3 portable polysomnography (PSG) tests, the present study was carried out at a tertiary care cardiothoracic center.

Materials and methods

A prospective study was carried out at a tertiary care center from June 2015- June 2018. Prior clearance from the institute's ethical committee was obtained, and written informed consent was taken from patients. All the data was kept confidential. The consecutive sampling method was used to enroll patients. Hundred patients with coronary angiography–proven CAD with age less than 40 years (young patients) were included. Patients with CAD and identifiable risk factors for CAD other than obesity and patients with history of smoking were excluded. The included subjects underwent overnight PSG using an OSA screener, a level 3 portable PSG test. Two parameters, namely, the apnea hypopnea index (AHI) and oxygen desaturation index (ODI), were recorded using the portable PSG machine. Patients were identified to have OSA based on their AHI and OSA severity as per international classification, which is graded as follows: normal (no OSA; AHI <5 episodes per hour), mild sleep apnea (AHI ≥5 and <15 episodes per hour), moderate sleep apnea (AHI ≥15 and <30 episodes per hour), and severe sleep apnea (AHI ≥30 episodes per hour).⁴

The patient's body mass index (BMI) was recorded and graded as normal (BMI = 18–24.9 kg/m²), overweight (BMI = 25–29.9 kg/m²) and obese (BMI > 30 kg/m²).

The patients were also evaluated for oxygen desaturation. The ODI, i.e., hourly average number of desaturation episodes, was also calculated.

Results

In our study, 59% (59/100) of the patients were older than 35 years, 32% (32/100) of the patients were aged between 31 and 35 years, and 2% patients (2/100) were younger than 20 years (Fig. 1). The majority of the patients were males, i.e., 71%, owing to a male-dominated sample size. Of the 100 patients, 22% had normal BMI, 44% were overweight, and 34% were found to be obese.

Fig. 1.

Age distribution.

In the study, 20% (20/100) of the patients had a normal AHI, 24% (24/100) had mild OSA, and 28% (28/100) each had moderate and severe OSA with an AHI of 15–30 and >30, respectively (Table 1) (Fig. 2). There was no significant correlation between age-groups and severity of OSA as per Fischer's exact test (Table 2).

Table 1.

AHI group distribution of the patients.

AHI group	Number of patients	Percentage
Normal	20	20.0
Mild	28	28.0
Moderate	28	28.0
Severe	24	24.0
Total	100	100.0

AHI = apnea hypopnea index.

Fig. 2.

AHI group distribution. AHI = apnea hypopnea index.

Table 2.

Age-group vs severity of OSA.

Age-group (years)	AHI group				Total	p-value
	Normal	Mild	Moderate	Severe
≤20	1	1	0	0	2	0.225
21–25	1	0	1	1	3
26–30	0	3	1	0	4
31–35	7	7	6	12	32
36–40	11	17	20	11	59
Total	20	28	28	24	100

AHI = apnea hypopnea index; OSA = obstructive sleep apnea.

No statistically significant correlation between severity of OSA and gender was found (p-value = −0.089; chi-square test) (Table 3).

Table 3.

Gender vs severity of OSA.

Gender	AHI group				Total	p-value
	Normal	Mild	Moderate	Severe
Male	17	15	20	19	71	0.089
Female	3	13	8	5	29
Total	20	28	28	24	100

AHI = apnea hypopnea index; OSA = obstructive sleep apnea.

p-value > 0.05 (not significant); the chi-square test was used.

A significant correlation was observed between weight and severity of OSA (p-value = -0.033). It was observed that overweight patients and patients with obesity had higher grades of OSA (Table 4).

Table 4.

BMI vs AHI.

BMI	AHI group				Total	p-value
	Normal	Mild	Moderate	Severe
Normal	10	5	3	4	22	0.033
Overweight	7	13	16	8	44
Obese	3	10	9	12	34
Total	20	28	28	24	100

BMI = body mass index; AHI = apnea hypopnea index.

p-value < 0.05 (Significant) Fisher's exact test used.

No correlation was observed between age and ODI (p-value = 0.452) (Table 5). A significant correlation was observed between BMI and ODI (p-value = 0.004) (Table 6). Patients with obesity had a mean desaturation of 2.85 with a standard deviation (SD) of 24.62. No significant correlation was observed between gender and ODI (p-value = 0.738) (Table 7). The mean ODI was 19.08 for males, with a SD of 21.62, and was 18.52 for females, with a SD of 19.72.

Table 5.

Oxygen desaturation index (ODI) vs age.

Age-group (years)	Number of patients	ODI		p-value
		Mean	SD
≤20	2	11.50	3.54	0.452
21–25	3	7.66	10.69
26–30	4	7.75	9.53
31–35	32	23.00	23.78
36–40	59	18.29	20.35

SD = standard deviation.

p-value > 0.05 (not significant); the Kruskal–Wallis test was used.

Table 6.

BMI vs oxygen desaturation index (ODI).

BMI	Number of patients	ODI		p-value
		Mean	SD
Normal	22	10.05	14.41	0.004
Overweight	44	16.45	18.39
Obese	34	27.85	24.62

BMI = body mass index; SD = standard deviation.

p-value < 0.05 (significant); the Kruskal–Wallis test was used.

Table 7.

Mean ODI with respect to gender.

Gender	Number of patients	ODI		p-value
		Mean	SD
Male	71	19.08	21.62	0.738
Female	29	18.52	19.72

ODI = oxygen desaturation index; SD = standard deviation.

p-value > 0.05 (not significant); the Mann–Whitney U test was used.

Discussion

Obstructive sleep apnea has been recognized as an important public health problem, predominantly falling in the domain of pulmonologists, neurologists, and psychiatrists. However, multifactorially, OSA causes significant impact on other lifestyle disorders such as hypertension, diabetes, dyslipidemia, and, especially, CAD.¹ Our study was conducted with an aim to detect OSA in young patients suffering from CAD by performing portable PSG.

OSA syndrome (AHI ≥5 events per hour with daytime sleepiness) is now being recognized as a common disorder, with the currently estimated prevalence of 938 million patients, which has grown more than ten times than previous estimates.⁵ The Wisconsin Sleep Cohort Study was the first major community-based assessment of prevalence of OSA. The study reported the prevalence of OSA to be 4% in men and 2% in women. The prevalence of moderate to severe OSA (an AHI of 15 or higher regardless of symptoms) was 9% in men and 4% in women.⁶ The same has been estimated in various population prevalence studies since then, and the mean prevalence of OSA has been reported to be 6% (3–18%) in men and 4% (1–17%) in women.⁵ The Wisconsin Sleep Cohort also reported increase in prevalence of OSA with increasing age. The prevalence of OSA among men increased from 12% for ages 30–49 years to 18% for the age-group 50–70 years. Similarly, for women of the same age-groups, the prevalence increased from 3% to 8%.⁶ But irrespective of gender, the incidence of OSA is more than 50% in individuals older than 65 years.⁷

The prevalence of OSA has been found to be two to three times more common in men than in women in various epidemiologic studies.⁸ Many factors have been attributed to male preponderance of OSA such as differences in body fat distribution, upper airway anatomy (length, cross-sectional area), and collapsibility. A protective effect of female sex hormones has also been implicated for less incidence of OSA among women. Although the precise mechanism by which sex hormones act is not known, a higher incidence of OSA seen among postmenopausal than among premenopausal women lends support to hormone theory. However, hormone replacement therapy has not shown benefits in OSA.⁹ In our study also, males were seen to have a higher prevalence, i.e., 71%, than females, i.e., 29%. Higher incidence seen among male gender is in consistent with preceding studies, which highlight that both OSA and CAD occur more commonly among males.

Obesity is an important contributor of OSA. It causes adipose tissue deposition in the neck, leading to decreased upper airway caliber and restrictive lung disorder owing to adipose tissue deposition in the chest and abdomen. It also causes leptin resistance, oxidative strain, and generalized inflammation. Lam et al¹⁰ reported that 58% of patients with moderate to severe OSA were obese. Our study also showed that majority (88%) of the patients were either overweight or obese.

A significant correlation was observed between weight and severity of OSA, emphasizing that patients with obesity have moderate to severe OSA. A significant correlation was observed between weight and ODI also. Patients with obesity had a mean desaturation of 27.85, with an SD of 24.62, compared with individuals without obesity and with OSA who had a mean desaturation of 10.05, with an SD of 14.41. Obesity is a risk factor for both CAD and OSA, and this finding is in consistent with other studies; our study also showed positive correlation of obesity with OSA.

It has been observed in various studies that OSA and CAD commonly coexist. Clinical studies of sleep clinic cohorts have estimated CAD to be present in 20–25% of patients with OSA, and OSA is estimated to be prevalent in approximately 30% of patients with CAD. OSA and CAD both have multiple common etiologies, thus concluding that OSA being a direct causative factor in CAD is inappropriate.³ OSA has important clinical effects on cardiovascular morbidity and mortality.¹ Repeated hypoxia and reoxygenation in OSA enhance lipid peroxidation.¹¹ Apneas during sleep cause vascular damage owing to oxidative stress. There is increase in transmural gradients across the ventricles as they are subjected to repeated high negative intrathoracic pressure during the episodes of airway obstruction. There is further increase in myocardial afterload, which mandates a rise in myocardial oxygen demand during the events of apnea.¹²

A significant correlation between CAD in young patients and OSA was seen in our study, wherein 80% of patients with CAD had OSA. Similarly, Zhang et al.¹³ had reported 80% of angiographically confirmed CAD cases had OSA in their study. Vasheghani-Farahani et al.¹⁴ revealed a significant correlation between OSA and severity of atherosclerosis assessed by angiography and concluded that OSA is an independent risk factor for CAD. Patients with CAD have higher prevalence of OSA than the normal population. Various researchers have reported 26–66% prevalence of OSA in patients with CAD.^8,15, 16, 17, 18 The diverse value of the AHI used to establish diagnosis of OSA has possibly led to such a wide variation in these studies.

In a community-based Sleep Heart Health Study of 6000 patients, an association between severe OSA and incident CAD was seen. A revised longitudinal study of the same cohort after an 8.7-year follow-up did not reveal any significant association after adjusting for other risk factors. A subgroup analysis of the same cohort revealed slightly increased risk of CAD in patients younger than 70 years with higher grades of OSA.¹⁹ On the contrary, in another observational study of >1000 patients, Shah et al²⁰ found a significant association between OSA and incident coronary events or cardiac death after adjusting for other traditional risk factors. Although most of these observational data suggest a robust association, data are not conclusive. The available evidence is still scarce to imply a causative role of OSA in the development of CAD.

Similarly, in our study, association between OSA and CAD was also seen and that only 20% (20/100) of the patients had a normal AHI, 24% (24/100) had mild OSA, and 28% (28/100) each had moderate and severe OSA, with an AHI of 15–30 and >30, respectively.

Treatment of OSA with continuous positive airway pressure (CPAP) therapy in symptomatic patients without known CAD has been associated with a reduction in cardiovascular events.²¹ The utility of CPAP treatment in non-sleepy patients with OSA, aiming at a decrease in cardiovascular events, still remains uncertain.²² A meta-analysis of randomized controlled trials (RCTs) found minimal benefit of CPAP in non-sleepy patients with OSA on sleepiness, systolic blood pressure, or cardiovascular risk.²³ Poor compliance to CPAP treatment has led to variable results, and the results are mostly derived only from observational studies.²⁴ Owing to the lack of placebo-controlled, randomized treatment trials in patients with OSA and CAD, effect of CPAP therapy is inconclusive. An observational study by Milleron et al.²⁵ on 54 patients with stable CAD and severe OSA reported a reduction in recurrent cardiovascular events. Similarly, Cassar et al²⁶ reported fewer cardiac deaths in CPAP-treated patients with OSA undergoing percutaneous coronary intervention for stable angina. Various other researchers such as Barbe et al²⁷ and Peker et al.²⁸ reported reduction in cardiovascular risk in patients on using CPAP for four or more hours per night. These studies point to beneficial effects of diagnosing OSA in patients with CAD and adequately managing the same with CPAP therapy, thereby preventing morbidity and mortality.

Conclusion

The study detected a significant number of young patients with angiographically confirmed CAD having OSA. A significant correlation was also observed between weight and severity of OSA, suggesting that overweight patients and patients with obesity have higher grades of OSA.

Recommendations

• •Because the correlation between CAD in young patients and OSA is significant in the present study, larger randomized trials are needed before safely recommending evaluation of all young patients with CAD for OSA.
• •Obesity has strong correlation with OSA; thus, all patients with CAD and obesity, young or old, should undergo PSG.

Disclosure of competing interest

The authors have none to declare.