Sleep Disordered Breathing in Acute Coronary Syndrome
Sleep Disordered Breathing in Acute Coronary Syndrome
To our knowledge, no study has examined the persistence of sleep disordered breathing in acute coronary syndrome (ACS) patients. We examined the time course of SDB in ACS patients by assessing them within days of the acute event and again after 6 months.
Consecutive patients with ACS were asked to voluntarily participate in the study. Patients underwent an overnight polysomnography (PSG) approximately 3 days after the acute event. Patients with an apnea hypopnea index (AHI) > 10/h then underwent another PSG after they were stable (approximately 6 months).
Fifty patients were studied. First PSG showed an AHI was 23.1 ± 3.6/h. A second PSG was performed 6.1 ± 0.3 months later on 21 patients and showed an AHI > 10/h in the first assessment. The AHI and the obstructive apnea index did not change over the 6 months. However, the central apnea index all was lower at the second assessment.
Sleep disordered breathing (SDB) is a relatively common problem, with more than five apneas and/or hypopneas per hour of sleep identified in 24% and 9% of middle-aged men and women, respectively. The association between SDB and ischemic heart disease (IHD), hypertension and congestive heart failure (CHF) is well documented. Patients with SDB may experience a number of potentially adverse physiological events during sleep that may affect the cardiovascular system, including gas exchange abnormalities and increased sympathetic nervous system activity. The latter is probably in response to intermittent hypoxemia and hypercapnia, chemoreflex activation and increased central nervous system arousal that occurs with obstructed breathing. Mechanisms related to increased cardiovascular morbidity in SDB patients include repeated nocturnal hypoxemia, sympathetic activation, disturbed endothelial function, depressed baro-reflex sensitivity, increased platelet aggregability and increased vasoconstrictor sensitivity to angiotensin II. A variety of data suggest that patients with SDB could be at increased risk of IHD.
Most evidence connecting SDB and IHD is based on snoring studies. Myocardial infarction episodes were reported as being more frequent in snorers than non-snorers. Fewer studies are available for measured apneic activity. There is a high prevalence of SDB in acute myocardial infarction (AMI) patients. A cross-sectional analysis of the Sleep Health Heart Study (SHHS) cohort showed obstructive sleep apnea (OSA) was an independent risk factor for IHD, although the association was modest.
Moruzzi et al. found a high prevalence of SDB in patients with acute coronary syndromes (ACS). Moreover, they demonstrated that the prevalence of SDB was significantly higher in patients with ACS compared with patients with stable IHD. This observation raises a very important question: Does the strong association between SDB and acute coronary events, indicate causality or is the high prevalence of SDB in ACS patients, the result of ventilatory instability or other transient conditions that occur following an acute cardiac event, which then improve after medical stabilisation? Although the prevalence of SDB in patients with ACS has been found to be high, to our knowledge, no time-course studies have been undertaken to assess the persistence of SDB in ACS patients months after the acute event.
We sought to determine whether SDB is a consequence of the acute phase in ACS patients. To achieve this aim, we analysed the prevalence, frequency and characteristics of SDB in ACS patients, and examined the same characteristics after the acute cardiac event had stabilised.
To our knowledge, no study has examined the persistence of sleep disordered breathing in acute coronary syndrome (ACS) patients. We examined the time course of SDB in ACS patients by assessing them within days of the acute event and again after 6 months.
Consecutive patients with ACS were asked to voluntarily participate in the study. Patients underwent an overnight polysomnography (PSG) approximately 3 days after the acute event. Patients with an apnea hypopnea index (AHI) > 10/h then underwent another PSG after they were stable (approximately 6 months).
Fifty patients were studied. First PSG showed an AHI was 23.1 ± 3.6/h. A second PSG was performed 6.1 ± 0.3 months later on 21 patients and showed an AHI > 10/h in the first assessment. The AHI and the obstructive apnea index did not change over the 6 months. However, the central apnea index all was lower at the second assessment.
Sleep disordered breathing (SDB) is a relatively common problem, with more than five apneas and/or hypopneas per hour of sleep identified in 24% and 9% of middle-aged men and women, respectively. The association between SDB and ischemic heart disease (IHD), hypertension and congestive heart failure (CHF) is well documented. Patients with SDB may experience a number of potentially adverse physiological events during sleep that may affect the cardiovascular system, including gas exchange abnormalities and increased sympathetic nervous system activity. The latter is probably in response to intermittent hypoxemia and hypercapnia, chemoreflex activation and increased central nervous system arousal that occurs with obstructed breathing. Mechanisms related to increased cardiovascular morbidity in SDB patients include repeated nocturnal hypoxemia, sympathetic activation, disturbed endothelial function, depressed baro-reflex sensitivity, increased platelet aggregability and increased vasoconstrictor sensitivity to angiotensin II. A variety of data suggest that patients with SDB could be at increased risk of IHD.
Most evidence connecting SDB and IHD is based on snoring studies. Myocardial infarction episodes were reported as being more frequent in snorers than non-snorers. Fewer studies are available for measured apneic activity. There is a high prevalence of SDB in acute myocardial infarction (AMI) patients. A cross-sectional analysis of the Sleep Health Heart Study (SHHS) cohort showed obstructive sleep apnea (OSA) was an independent risk factor for IHD, although the association was modest.
Moruzzi et al. found a high prevalence of SDB in patients with acute coronary syndromes (ACS). Moreover, they demonstrated that the prevalence of SDB was significantly higher in patients with ACS compared with patients with stable IHD. This observation raises a very important question: Does the strong association between SDB and acute coronary events, indicate causality or is the high prevalence of SDB in ACS patients, the result of ventilatory instability or other transient conditions that occur following an acute cardiac event, which then improve after medical stabilisation? Although the prevalence of SDB in patients with ACS has been found to be high, to our knowledge, no time-course studies have been undertaken to assess the persistence of SDB in ACS patients months after the acute event.
We sought to determine whether SDB is a consequence of the acute phase in ACS patients. To achieve this aim, we analysed the prevalence, frequency and characteristics of SDB in ACS patients, and examined the same characteristics after the acute cardiac event had stabilised.