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Original Research: SLEEP MEDICINE |

Obstructive Sleep Apnea in Patients Admitted for Acute Myocardial Infarction: Prevalence, Predictors, and Effect on Microvascular Perfusion FREE TO VIEW

Chi-Hang Lee, MBBS; See-Meng Khoo, MBBS; Bee-Choo Tai, PhD; Eric Y. Chong, MBBS; Cindy Lau, BSc; Yemon Than; Dong-Xia Shi; Li-Ching Lee, MBBS; Anand Kailasam, BSc; Adrian F. Low, MBBS; Swee-Guan Teo, MBBS; Huay-Cheem Tan, MBBS
Author and Funding Information

*From the Departments of Medicine (Drs. C.-H. Lee, Low, and Tan, and Ms. Lau, Ms. Than, and Ms. Shi) and Community, Occupational and Family Medicine (Dr. Tai), Yong Loo Lin School of Medicine, National University of Singapore; and The Heart Institute (Drs. C.-H. Lee, Chong, L.-C. Lee, Low, Teo, and Tan, and Mr. Kailasam) and Department of Medicine (Dr. Khoo), National University Hospital, Singapore.

Correspondence to: Chi-Hang Lee, MBBS, Cardiac Department, National University Hospital, 5, Lower Kent Ridge Rd, Singapore 119074; e-mail: mdclchr@nus.edu.sg


The authors have no conflicts of interest to disclose.

Source of funding: Cardiac Department Fund, National University Hospital, Singapore.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (www.chestjournal.org/site/misc/reprints.xhtml).


© 2009 American College of Chest Physicians


Chest. 2009;135(6):1488-1495. doi:10.1378/chest.08-2336
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Background:  We investigated the prevalence and predictors of obstructive sleep apnea (OSA) in patients admitted to the hospital for acute myocardial infarction and whether OSA has any association with microvascular perfusion after primary percutaneous coronary intervention (PCI).

Methods:  Recruited patients were scheduled to undergo an overnight sleep study between 2 and 5 days after primary PCI. An apnea-hypopnea index (AHI) of ≥ 15 was considered diagnostic of OSA. Impaired microvascular perfusion after primary PCI was defined as an ST-segment resolution of ≤ 70%, myocardial blush grade 0 or 1, or a corrected Thrombolysis in Myocardial Infarction (TIMI) [antegrade flow scale] frame count > 28.

Results:  Sleep study was performed in 120 patients and completed in 105 patients (study cohort, mean age 53 ± 10 years, male 98%) with uncomplicated myocardial infarction. An AHI was ≥ 15 in 69 patients (OSA-positive), giving a prevalence of 65.7%. Diabetes mellitus was found to be a significant risk factor for OSA (odds ratio, 2.86; 95% confidence interval, 1.06 to 8.24; p = 0.033). There were no differences between OSA-positive and OSA-negative groups with regard to the percentage of patients with ≤ 70% ST-segment resolution (73% vs 64%, respectively; p = 0.411), myocardial blush grade 0 or 1 (39.1% vs 38.9%, respectively; p = 1.000), or corrected TIMI frame count > 28 (21.7% vs 25.0%, respectively; p = 0.807).

Conclusions:  We found a high prevalence of previously undiagnosed OSA in patients admitted with acute myocardial infarction. Diabetes mellitus was independently associated with OSA. No evidence indicated that OSA is associated with impaired microvascular perfusion after primary PCI.

Figures in this Article

Obstructive sleep apnea (OSA) is a disorder characterized by repetitive throat muscle and soft-tissue collapse during sleep, resulting in intermittent oxygen desaturation. Compelling evidence indicates that the prevalence of OSA is higher in patients with hypertension,1,2 stroke,3,4 heart failure,5,6 and coronary artery disease6,7 than it is in the general population. Yet, there is little epidemiologic data of OSA in patients hospitalized for acute myocardial infarction. Untreated OSA has a significant negative impact on long-term survival,8,9 and it may have contributed to the high mortality and morbidity after acute myocardial infarction. In contrast, treatment with continuous positive airway pressure (CPAP) has the potential to reverse the poor prognosis.8,9 Therefore, it is important to know the prevalence as well as the predictors of OSA in patients with acute myocardial infarction.

Primary percutaneous coronary intervention (PCI) remains the cornerstone of treatment for acute myocardial infarction.10 When done by an experienced team in a timely manner, it is associated with high success rates of opening the occluded epicardial artery. Nonetheless, it has been demonstrated that despite success in achieving epicardial artery patency, impaired microvascular perfusion occurs in approximately a third of patients undergoing primary PCI.11,12 Impaired microvascular perfusion is associated with poor recovery of left ventricular function and adverse clinical outcomes.12In vivo and in vitro studies suggest that OSA is associated with increased platelet aggregation,13,14 blood hypercoagulability,1517 and endothelial dysfunction.18,19 These may adversely affect microvascular integrity in patients with coronary artery disease. We therefore hypothesized that impaired microvascular perfusion after primary PCI occurs more often in patients with OSA, thus explaining the impaired recovery of left ventricular function after acute myocardial infarction in these patients.20

In this prospective study, we sought to investigate the prevalence and predictors of OSA in patients admitted to the hospital for acute myocardial infarction, and whether OSA has any effect on microvascular perfusion after primary PCI.

Study Design and Patient Population

This was a prospective observational study in a tertiary institution in which primary PCI is the recommended revascularization strategy for acute myocardial infarction presenting within 12 h of symptom onset. Patients 21 to 80 years of age who were admitted to the National University Hospital in Singapore with a first acute myocardial infarction and who underwent a primary PCI were eligible. Exclusion criteria were patients with known OSA, those who were intubated and receiving mechanical ventilation, and those with electrical instability with a high risk of malignant ventricular arrhythmia, cardiogenic shock, previous coronary artery bypass surgery, previous PCI to the target vessel, or inability to give informed consent.

Eligible patients were screened during their index hospital stay. Recruited patients were scheduled to undergo an overnight sleep study in either the coronary care unit or the cardiac ward using a portable diagnostic device between day 2 and 5 after the primary PCI. The PCI procedures were done, and hospital discharge medications were given according to the international guidelines for good clinical practice and were not affected by the study protocol. All patients underwent a transthoracic echocardiogram before hospital discharge. The study was approved by the local institutional review board, and all patients provided written informed consent.

Overnight Sleep Study

Sleep studies were performed using a portable diagnostic device (Somte; Compumedics; Melbourne, VIC, Australia). The parameters measured included nasal airflow (nasal cannula), thoracoabdominal movements (inductive respiratory bands), arterial oxygen saturation (pulse oximetry), snoring episodes (derived from the integrated pressure transducer), limb movement, ECG, and body position (continuous actigraphy). This system has been validated against 12-channel in-hospital polysomnography for quantifying sleep-disordered breathing.2123

Outputs from the portable diagnostic device were analyzed by two investigators without knowledge of the clinical characteristics of the patient. Respiratory events were defined according to recommendations of the American Academy of Sleep Medicine.24 An apnea was defined as cessation of airflow of > 10 s, and hypopnea as a > 50% reduction of airflow lasting > 10 s. An event was also considered to be a hypopnea when there was a reduction in airflow that did not reach the 50% criteria but was associated with an arterial oxygen desaturation of > 3%. Apneas are classified as obstructive if there was thoracoabdominal movement and as central if there was no thoracoabdominal movement. The apnea-hypopnea index (AHI) was calculated as the number of apneas and hypopneas per hour of recording time in bed, with the start of recording the point at which respiration settled to a rhythmic, stable pattern. The end of the recording time was either the waking time recorded by the subject or the point at which the thoracoabdominal tracings became disturbed, which was consistent with wakefulness. An AHI of 15 events per hour was considered clinically significant.

Angiographic Assessment of Epicardial and Microvascular Perfusion

All angiographic films were digitally acquired at either 12 or 15 frames per second. Appropriate angiographic images were analyzed offline by an investigator blinded to the results of the sleep study and ST-segment resolution. Using standard techniques, the following variables were assessed before and after PCI of the infarct-related artery: (1) Thrombolysis in Myocardial Infarction (TIMI) antegrade flow scale25 (which reflects epicardial reperfusion); (2) corrected TIMI frame counts26 (using standard landmarks for each vessel as a continuous variable and assigning 100 for vessels with TIMI 0 flow; assessed in a dichotomous fashion using 28 as the upper cutoff point for TIMI 3 flow);27 and (3) myocardial blush grades (assigned as previously described by Van 't Hof and associates28 as follows: 0, no myocardial blush; 1, minimal myocardial blush or contrast density; 2, moderate myocardial blush or contrast density but less than that obtained during angiography of a contralateral or ipsilateral non–infarct-related coronary artery; and 3, normal myocardial blush or contrast density similar to that obtained during angiography of a contralateral or ipsilateral non–infarct-related coronary artery). Persistent myocardial blush suggested leakage of contrast medium into the extravascular space and was given a grade of 0. A corrected TIMI frame count > 28 and myocardial blush grade of 0/1 were considered impaired microvascular perfusion.

ST-Segment Resolution

Baseline and postprocedural 12-lead ECGs were reviewed, and ST-segment resolution was analyzed by an investigator blinded to the results of the sleep study and the angiographic assessment of epicardial and microvascular perfusion. The single lead that subtended the injured myocardium and had the highest ST-segment elevation was identified.29,30 The extent of ST-segment elevation measured at 20 ms from the J-point was compared between the baseline and postprocedural 12-lead ECGs. Complete resolution was defined at > 70%, partial resolution 30 to 70%, and absence of resolution at < 30% ST-segment resolution. ECG resolution ≤ 70% was considered impaired microvascular perfusion.

30-Day Adverse Events

Clinical outcomes at 30 days were collected by dedicated research nurses via telephone calls and/or clinic chart reviews, and all the information was prospectively entered. Relevant adverse events included death, reinfarction, stroke, heart failure requiring hospitalization, and unplanned revascularization.

Statistical Analysis

Univariate association between OSA-positive and impaired microvascular perfusion as well as other patient-related risk factors (eg, diabetes and hypertension), which were recorded as categorical variables, were evaluated using the Fisher exact test. For continuous risk factors, the t test or the Wilcoxon rank sum test was used for evaluating the relationship. We further explored the relation between OSA and impaired microvascular perfusion via logistic regression, adjusting for potential confounders such as diabetes mellitus and body mass index in the analysis. All statistical analyses were carried out using a statistical software package (STATA 10; StataCorp LP; College Station, TX), assuming a two-sided test with a 5% level of significance.

Between January 2007 and April 2008, a total of 290 patients who had undergone primary PCI for a first acute myocardial infarction were screened. An overnight sleep study was done in 120 patients and completed in 105 patients (Fig 1). The sleep study was not tolerated, and therefore discontinued prematurely, in the remaining 15 patients. Among the 105 patients who formed the study cohort, the mean (± SD) age was 53 ± 10 years, and the majority (n = 103, 98%) were men. Table 1 shows the baselinedemographic and clinical characteristics of the patients. None of the patients had received prior fibrinolytic therapy. The infarct-related artery was successfully opened in all patients, each of whom received at least one stent. IV glycoprotein IIb/IIIa inhibitors were used in 31 patients (29.5%). The median symptom-to-balloon time and door-to-balloon time were 213 and 73 min, respectively. After the PCI, final TIMI 3 flow was achieved in all except one patient (TIMI 2). Table 2 shows the angiographic and procedural characteristics of the patients.

Table Graphic Jump Location
Table 1 Patient Demographic and Clinical Characteristics

*Values are given as mean (SD).

†Values are given as No. (%).

Table Graphic Jump Location
Table 2 Patient Angiographic and Procedural Characteristics

*Data are presented as median (range).

The median duration from hospital admission to sleep study was 44 h (range, 7 to 106 h), and the median duration from PCI to sleep study was 43 h (range, 7 to 106 h). The overnight sleep study was done in the coronary care unit with 39 patients (37.1%) and in the cardiac ward with 66 patients (62.9%).

Prevalence of OSA

Among the 105 patients who completed the overnight sleep study, AHI ranged from 2.0 to 78.0 events per hour (Fig 2). AHI was ≥ 15 events per hour in 69 patients, giving a prevalence of OSA of 65.7% (95% confidence interval [CI], 55.8 to 74.7). The median AHIs for the OSA-positive and OSA-negative groups were 38.1 and 8.5 events per hour, respectively (p < 0.001).

Figure Jump LinkFigure 2 Distribution of AHI of the study patients.Grahic Jump Location
Predictors of OSA

Univariate analyses showed diabetes mellitus to be a significant risk factor for OSA (odds ratio, 2.86; 95% CI, 1.06 to 8.24; p = 0.033). The prevalence of OSA in diabetic patients was 79.5% (95% CI, 63.5 to 90.7). Multivariable analysis, including age, hypertension, diabetes mellitus, body mass index, location of myocardial infarction, target vessel, and peak creatine kinase level, did not find any other significant risk factor for OSA, apart from diabetes mellitus.

Effect of OSA on Microvascular Perfusion

The percentages of patients with an interpretable ST-segment resolution, myocardial blush grade, and corrected TIMI frame count were 100%, 97.1%, and 99.0%, respectively. There were no significant differences between the OSA-positive and the OSA-negative groups with regard to percentage of patients with 70% less than ST-segment resolution (73% vs 64%, respectively; p = 0.411), myocardial blush grade 0 or 1 (39.1% vs 38.9%, respectively; p = 1.000), or corrected TIMI frame count > 28 (21.7% vs 25.0%, respectively; p = 0.807).

Hospital Discharge Medication and 30-Day Clinical Outcomes

The hospital discharge medications given to the patients were in accordance with international guidelines and included aspirin (96.2%), clopidogrel (100%), β-blockers (90.5%), angiotensin-converting enzyme inhibitors and angiotensin receptor blockers (85.7%), and lipid-lowering agents (96.2%). Thirty-day clinical follow-up data were available for all patients. There was one case of heart failure hospitalization in the OSA-negative group. Otherwise, there were no other adverse events.

The intimate relation between OSA and cardiovascular diseases has been gradually uncovered over the last decade. In patients with stable coronary artery disease, depending on sex and AHI cutoff, prevalence of OSA ranges from 30 to 54%.31,32 Treatment of OSA with CPAP is associated with a decrease in the occurrence of new cardiovascular events.33 However, the prevalence and predictors of OSA in patients with acute myocardial infarction, as well as whether OSA has any association on microvascular perfusion after primary PCI, are unclear. We conducted a prospective study in an institution in which primary PCI is the standard reperfusion strategy for acute myocardial infarction. We found a high prevalence of previously undiagnosed OSA in patients admitted to the hospital with acute myocardial infarction. Diabetes mellitus was independently associated with OSA. Using multiple quantitative parameters including ST-segment resolution, myocardial blush grade, and corrected TIMI frame count to evaluate microvascular integrity, there was no significant association between OSA and impaired microvascular perfusion after primary PCI.

There are a few published series20,3436 reporting the prevalence of OSA in patients with acute cardiovascular events. However, with the exception of one study,20 all3436 included a heterogeneous patient population such as stable angina, unstable angina, myocardial infarction, and heart failure. Our study focused on a homogeneous group of patients who had experienced a first acute myocardial infarction. Using an AHI of 15 events per hour as a cutoff, we found a relatively high prevalence of OSA (65.7%). Because patients with known OSA were excluded from this study, it is conceivable that we might have underestimated the actual prevalence among all patients admitted to the hospital with acute myocardial infarction. Nonetheless, the prevalence is higher than that reported in previously published series. In a study of Japanese patients admitted to the hospital with acute myocardial infarction, Nakashima and associates20 reported a prevalence of 43%. However, in their study, the sleep study was done 14 to 21 days after hospital admission, whereas in ours, it was done 2 to 5 days after hospital admission. Skinner and associates34 reported an OSA prevalence of 46% in 26 patients admitted with acute coronary syndrome. In another two studies35,36 using a lower AHI cutoff of 10 (instead of 15), the prevalence of OSA in patients with acute coronary syndrome ranged from 57 to 66.4%. There are a number of possible reasons for the difference in the prevalence of OSA between studies. Differences in the timing of sleep studies, diagnostic criteria applied, diagnostic device used, and characteristics of the study population can all affect the measurement prevalence. It was suggested that performing sleep studies during acute cardiovascular events might result in a high rate of false-positive diagnoses due to detection of transient abnormalities.34 However, an alternative explanation to their findings was that these patients were not really “false positives” but demonstrated true sleep-disordered breathing, albeit transient, during an acute cardiac illness.37 Furthermore, it could be argued that identifying and treating OSA, a risk factor known to influence long-term outcomes in patients with cardiovascular disease, should be done as early as possible when patients are in the hospital where facilities for prompt investigation are more likely to be available. The issue on the ideal timing of investigation for OSA after an acute cardiovascular event remains unresolved. Another possible explanation for the higher prevalence observed in our series is selection bias. Patients who suspected they might have OSA might have been more likely to participate in the study. In fact, 45.5% of the male patients screened (117 of 257 patients) underwent the overnight sleep study, whereas only 9.0% of the female patients screened (3 of 33 patients) underwent the test. Besides, acute myocardial infarction represents the highest risk category among patients with unstable coronary syndrome. It is possible that the prevalence of OSA increases along the spectrum of severity of coronary artery disease.

OSA is common but underdiagnosed; the health consequences of underdiagnosing OSA can be substantial. Moreover, treatment with CPAP is effective in reversing the adverse prognosis.8,9 For all these reasons, having a high index of suspicion in susceptible patients is paramount to recognizing this dis ease. We found that among patients admitted to the hospital for acute myocardial infarction, diabetes mellitus was independently associated with OSA. Our findings are in agreement with those of other reported series.38,39 The exact underlying pathophysiological mechanisms that play a role in this link are uncertain. But experimental studies in humans and animals have demonstrated that intermittent hypopnea and reduced sleep duration due to sleep fragmentation exert adverse effects on glucose metabolism.40 Finally, despite the strong epidemiologic relation, the causal relation between diabetes mellitus and OSA remains to be established. Likewise, whether diabetes mellitus predisposes to OSA or the reverse remains a controversy.40

Primary PCI is the preferred reperfusion strategy for acute myocardial infarction.10 Compared with fibrinolytic agent, primary PCI is associated with a higher success rate of opening the epicardial artery. Yet, it has been increasingly recognized that establishing normal (TIMI 3) antegrade flow in epicardial artery does not equate with achieving microvascular perfusion at the cellular level. Clinically, patients with impaired microvascular perfusion often present with persistent chest pain and hemodynamic instability after the PCI. Other surrogate markers include suboptimal resolution or persistent elevation of the ST segment on ECG, absent or low myocardial blush grade, and high corrected TIMI frame count. The underlying mechanisms for impaired microvascular perfusion are complex and not fully understood, but they are at least partly due to distal embolization of thrombi.11 In fact, thrombus aspiration before PCI was recently associated41 with better microvascular perfusion and clinical outcomes, supporting the role of a thrombus in causing microvascular dysfunction.

In this regard, OSA is associated with several factors linked with a prothrombotic state. Patients with OSA have increased platelet activation and platelet aggregation.13,14 Total serum fibrinogen,15 plasminogen activator inhibitor,42 and whole-blood viscosity17,43 levels are elevated in OSA. Besides, OSA leads to endothelial dysfunction by promoting inflammation and oxidative stress while decreasing nitric oxide availability and repair capacity.18,19 However, despite the biological plausibility, no relation between OSA and impaired microvascular perfusion was demonstrated in our study. There are several possible explanations. First, only stable patients considered unlikely to need resuscitation or electrical cardioversion during the sleep study were recruited. We may be unable to demonstrate the impact of OSA on microvascular perfusion in low-risk patients. Second, patients with OSA manifest silent nocturnal ST-segment depression, which indicates recurrent myocardial ischemia.44 This might elicit an ischemic preconditioning effect, in which the myocardium may develop tolerance to more ischemia, thereby counteracting other adverse pathophysiologic effects of OSA. The ischemic preconditioning effect has been demonstrated to be clinically relevant.45 Third, the negative impact of OSA on acute myocardial infarction may be negligible compared with other factors associated with impaired microvascular perfusion, such as total ischemic time.

Limitations

Several limitations in this study must be addressed. This study included a relatively small number of stable patients. Exclusion of hemodynamically unstable patients, although it avoided resuscitation from being hindered by the monitoring devices and cables, might have introduced bias in this study. The subjects in this study were predominantly men, and therefore the results cannot be extrapolated to women. All patients in this study underwent primary PCI as the reperfusion strategy. The effects of OSA on microvascular perfusion after fibrinolytic therapy were not addressed. Other modalities to assess microvascular perfusion, such as myocardial contrast echocardiogram and cardiac MRI, were not performed.

In conclusion, we found a high prevalence of previously undiagnosed OSA in patients admitted to the hospital with acute myocardial infarction. Diabetes mellitus is a significant predictor for OSA. Although we did not find an association between OSA and impaired microvascular perfusion after primary PCI, in view of the high prevalence and negative impact on long-term clinical outcomes, screening for OSA is warranted. We suggest that overnight sleep studies be performed on patients with diabetes admitted to the hospital with acute myocardial infarction.

AHI

apnea-hypopnea index

CI

confidence interval

CPAP

continuous positive airway pressure

OSA

obstructive sleep apnea

PCI

percutaneous coronary intervention

TIMI

Thrombolysis in Myocardial Infarction.

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Tables

Table Graphic Jump Location
Table 1 Patient Demographic and Clinical Characteristics

*Values are given as mean (SD).

†Values are given as No. (%).

Table Graphic Jump Location
Table 2 Patient Angiographic and Procedural Characteristics

*Data are presented as median (range).

References

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