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Sleep apnea, snoring & the heart

Clive Layton, MD London Bridge Hospital

Editor's note: Dr. Layton is a cardiologist at London Bridge Hospital, London, England. He is involved in using the Internet to help educate people about heart disease and its treatment. He has kindly responded to our request for a discussion on the relationship between sleep apnea and snoring and heart disease. Sleep disordered breathing (SDB) is a term often used to cover sleep apnea (spelled apnoea in England), snoring, and other irregularities of breathing that take place during sleep. Dr. Layton's precise and cautious scientific analysis underscores the possibly dangerous effects of sleep disordered breathing. It seems to strengthen the importance for persons with snoring or apnea to have their condition evaluated, and if treatment is prescribed, to maintain it. To contact Dr. Layton: [email protected]

Readers should discuss their concerns and all treatment issues with their physicians.

How does a cardiologist view the relationship between snoring or sleep apnea and the heart?

The question you raise is a fascinating one to try and answer and the literature on the subject is vast---we have located several thousand papers on sleep apnoea and snoring in the last few years alone. As far as the relationship between sleep disordered breathing (SDB) and cardiovascular disease is concerned there are two aspects to the problem which are really quite separate. First the prevalence and effects of SDB on patients who already have coronary artery disease and secondly the relationship between the incidence and prevalence of coronary disease and SDB. Bear in mind the important point that just because there is an association between the prevalence of two conditions that does not mean that one causes the other. There may be a third factor causing both! This is very important when it comes to considering the effects of treatment.

SDB in people with coronary artery disease

It has been established, and I believe fairly conclusively, that SDB is commoner in patients with coronary disease than in a control population without. That may be because SDB is a cause of coronary disease, is a risk factor for its development, or may merely be a marker for the disease. Either way it is important as several studies have shown that SDB, and in particular sleep apnoea, are associated with drastic reductions in arterial oxygen tension (hypoxia) and in patients with coronary disease this is likely to cause arrhythmias which can be very serious and potentially fatal. Ischaemia of the heart will be potentiated by any drop in arterial oxygen tension and if coronary blood flow is borderline the change in oxygen availability may tip the balance in a highly unfavourable direction. This may cause asymptomatic episodes of ischaemia at one end of the scale or nocturnal sudden death at the other extreme.

It is reasonable to assume (though it is not proven) that treatment with continuous positive airway pressure (CPAP) would minimise the episodes of hypoxia and therefore the potential for ischaemia. In that case routine use of CPAP should largely abolish the danger of ventricular arrhythmias and nocturnal sudden death.

Incidence of coronary artery disease, hypertension and other vascular disease in patients with SDB

It again seems quite clear that patients with SDB are more likely to develop any of the above disorders. One of the difficulties in analysing this is that some factors which predispose to SDB (for example obesity) also predispose to the various cardiovascular disorders but there nevertheless is adequate evidence to suggest that SDB may be an independent predictor of the development of vascular disease even in when these confounding factors are excluded.

What is not known is whether prophylactic treatment of SDB will avert the development of the cardiovascular problems. This is obviously an important point to establish as it will help to decide whether all patients with SDB should be advised to be treated on a preventive basis. Bearing in mind the frequency of the problem, which is almost certainly underestimated anyway, this could pose a major logistic problem. What all patients with SDB should be advised is to ensure that all other risk factors are avoided (smoking, obesity, hypertension, hyperlipidaemia, diabetes etc) so that the chances of developing coronary disease are minimised.

See below for selected abstracts from the professional literature.

Selected abstracts from the professional literature

Attached below are a few references in the literature over the past 5 years which give an insight into the problem.

A community study of snoring and sleep-disordered breathing.

Olson LG. King MT. Hensley MJ. Saunders NA. Institution Discipline of Medicine, University of Newcastle, New South Wales, Australia. Title Source American Journal of Respiratory & Critical Care Medicine. 152(2):717-20, 1995 Aug.

Abstract Four hundred forty-one subjects 34 to 69 yr of age were recruited from a random sample of the community. They answered a questionnaire and were monitored in their homes for sleep-disordered breathing (SDB). This report concerns the association between observed SDB and arterial hypertension and vascular disease. Hypertension was defined as self-report of a diagnosis of hypertension made by a physician, current treatment for hypertension, or a systolic pressure greater than 150 mm Hg or a diastolic pressure greater than 90 mm Hg. Coronary artery disease was defined by self-report of angina or myocardial infarction of "heart attack." There were few cases of stroke or claudication, and a category of "occlusive vascular disease" was defined by self-report of coronary artery disease or of "blocked arteries" or stroke. Subjects were classified as snorers (n = 289) or nonsnorers (n = 73) by self-report of regular snoring, and as having SDB (n = 79) if more than 15 abnormal respiratory events were recorded per hour of recording. There were significant increases in the prevalence of hypertension, coronary artery disease, and occlusive vascular disease from nonsnorers (26, 7, and 10%, respectively) through snorers (39, 12, and 17%) to subjects with SDB (57, 20, and 28%). The crude odds ratio for SDB versus nonsnorers was 3.8 (95% CI, 1.9 to 7.5)for hypertension, 3.5 (1.2 to 10.0) for coronary artery disease, and 3.7 (1.5 to 9.1) for occlusive vascular disease.

Title [Prevalence of sleep apnea syndrome with primary arterial hypertension in a cardiologic rehabilitation clinic].

Authors Engel S. Karoff, M. Raschke, F. Fischer J. Institution Klinik Konigsfeld, Ennepetal und Klinik Norderney, LVA Westfalen. [German] Source Pneumologie. 49 Suppl 1:145-7, 1995 Mar.

Abstract In a group of 132 randomly selected male patients with the admission diagnosis arterial hypertension in a cardiological rehabilitation clinic, nightly monitoring was performed with Mesam 4 with records of the metabolism laboratory values and sleep disturbances longitudinally. Desaturation indexes of > or = 10/h after manual correction for plausibility revealed a total prevalence of 27.3% in the case of breathing disturbances.

The prevalence increased to 52% in the over 55 year-old patients with a Broca index of > or = 120% in comparison to merely 15.4% in standard weighted, comparable age group. No differences were found in the laboratory values. These results again show the frequent occurrence of the combination adiposity, hypertension, and sleep apnea syndrome which has often been missed previously in specialist rehabilitation clinics.

[Should patients with asymptomatic sleep apnea syndrome be treated with CPAP ].

Authors Gugger M. Rochat T. Institution Departement Medizin, Universitatskliniken, Inselspital Bern. Title [German] Source Schweizerische Medizinische Wochenschrift. Journal Suisse de Medecine. 125(10):496-501, 1995 Mar 11.

Abstract Treatment of sleep apnea patients may be justified even when symptoms are absent. On the one hand, hypersomnia or daytime sleepiness are subjective symptoms and only reflect one aspect of the clinical syndrome of sleep apnea. On the other hand, an apnea index in excess of 5, e.g. the "laboratory diagnosis" of sleep apnea, has been reported as an independent risk factor for myocardial infarction. The main problem is scientific definition of cut-off points for treatment. There is no controversy about whether patients with symptoms should be treated or not. A CPAP trial seems to be justified in asymptomatic patients with an apnea/hypopnea index in excess of 20-30 and in patients with cardiovascular risk factors when the apnea/hypopnea index is in excess of 5. These laboratory cut-off values are not absolute values but represent flexible guidelines for initiating a CPAP trial in asymptomatic patients with apnea. The reasons for uncertainty whether or not to treat patients with asymptomatic sleep apnea are discussed.

Observation of sleep-related breathing disorders in patients with coronary artery disease by ambulatory electrocardiogram-respiration monitoring system. Authors Tateishi O. Okamura T. Itou T. Murakami M. Suda T. Nishimuta I. Obata S. Nagata T. Institution Department of Internal Medicine (IV), Jikei University School of Medicine, Tokyo, Japan. Title Source Japanese Circulation Journal. 58(11):831-5, 1994 Nov.

Abstract Eighty-five coronary artery patients examined using an ambulatory electrocardiogram-respiration monitoring system (AERMS) in which a respiratory sensor was strapped to the right upper abdominal wall. Apnea was defined as a cessation of abdominal wall movement lasting at least 10 sec. Sleep-related breathing disorder (SRBD) was diagnosed if at least 30 apneic episodes were observed during sleep. The cardiac events evaluated during follow-up included occurrence of sudden death, myocardial infarction and ventricular tachycardia. SRBD was detected in 9 of 85 patients (11%). There were more patients with low EF (EF < 50%) in the SRBD group than in the non-SRBD group (p < 0.01). During follow-up for a mean period of 18.4 +/- 7.6 months after ambulatory recording, four of nine (44%) patients in the SRBD group had cardiac events, compared with only four of 79 (6%) patients in the non-SRBD group (p < 0.001). Thus, coronary artery patients who were complicated with SRBD showed poor cardiac function and had a high incidence of cardiac events.

Snoring and the severity of coronary artery disease in men.Authors Ketterer MW. Brymer J. Rhoads K. Kraft P. Kenyon L. Institution Department of Psychiatry, Henry Ford Hospital, Case Western Reserve University, Detroit, MI. Title Source Psychosomatic Medicine. 56(3):232-6, 1994 May-Jun.

Abstract Previous studies have found associations between snoring, or polysomnographic documented sleep apnea, and hypertension, cerebral vascular disease, and myocardial infarction. The present study examined the relationship of coronary artery disease (CAD) and snoring. One hundred and twenty-two males with positive angiographic studies were compared with fifty-six men, matched in age and socioeconomic status, who had no known history of coronary heart, or other atherosclerotic, disease. The percentage of subjects reporting that they snore "usually" or "always/loudly" increased across the four CAD severity groupings (nonpatient controls = 19.6%, 1 vessel = 44.4%, 2 vessel = 41.9%, 3 vessel = 56.0%) with a p value of .005. Hypertension, body mass index, and pack years of smoking were found to be associated with both coronary artery disease severity and snoring. When these variables were controlled in a multiple regression analysis, the relationship of snoring and CAD severity remained significant at p = .050.

Title [Nocturnal ventricular arrhythmia in patients with sleep apnea and suspected coronary heart disease]. Authors Koehler U. Glaremin T. Cassel W. Feuring M. Pomykaj T. Schafer H. Stellwaag M. Institution Zentrum Innere Medizin, Medizinische Poliklinik, Philipps-Universitat, Marburg. [German] Source Medizinische Klinik. 88(12):684-90, 1993 Dec 15.

Abstract BACKGROUND: Patients with sleep apnea and nocturnal brady- and tachyarrhythmia are considered to be patients at especially high risk within the group of all apnea patients. PATIENTS AND METHODS: 13 patients with sleep apnea (apnea-index > 10 events/h), suspected coronary heart disease and known increased frequency of nocturnal premature ventricular contractions (PVC) were studied. Polysomnography, long-term ECG and six-lead ECG were performed. RESULTS: Within the period studied (1.00 to 6.00 o'clock), an average of 47 PVC per hour was recorded (range 4 to 337/h). In two patients 24 episodes of nocturnal myocardial ischemia were observed, but were not accompanied by PVC. Interestingly only 387 of 1371 premature ventricular contractions (28.2%) were associated to apnea/hyperventilation episodes. Arrhythmia occurred mainly during sleep stages I/II and REM (n.s.). There was a tendency towards more frequent PVC with more pronounced oxygen desaturations. CONCLUSION: Patients with coronary heart disease, obstructive sleep apnea and severe hyoxemia are at higher risk of developing nocturnal PVC because reduced hypoxic tolerance of the heart may lead to electrical instability.

Authors Koehler U. Dubler H. Glaremin T. Lubbers C. Peter JH. von Wichert

Title [Nocturnal hypoxia--its relevance with reference to sleep structure in patients with coronary heart disease]. P. Institution Medizinische Poliklinik, Phillips-Universitat Marburg. [German] Source Pneumologie. 47 Suppl 1:162-5, 1993 Mar.

Abstract A disorder in the physiological structure of the sleep cycles (macrostructure) is known to occur both in patients with sleep apnoea (SA) and coronary heart disease (CHD). The study presented here was concerned with the problem whether the sleep structure in patients suffering from CHD and apnoea-conditioned hypoxia is greatly disturbed e.g. by myocardial ischaemia. Polysomnographic recordings including EEG, EOG, EMG and 6-channel ECG were performed for 6 nights in 30 patients suffering from sleep apnoea (AI > 10/h) and/without CHD. The average age of the patients was 57.9 years (range 47-68 yrs). The 2nd, 4th and 6th nights were subjected to fine analysis. In 6 patients it was possible to detect a total of 144 episodes with nocturnal myocardial ischaemia, 123 of these during cumulative apnoea and oxygen desaturation. The 30 patients spent on the average 67.1% in sleep stages I and II, 14.9% in deep sleep (stages III and IV) and 18% in REM sleep. 77.8% of the ischemie, episodes occurred during REM sleep and only 1.4% during the deep sleep stages. Sleep during myocardial ischaemia showed significantly more arousals than to control periods without ischaemia. There was furthermore a dependence of the degree of arousal on the degree of oxygen desakivations during apnoea. I. Patients suffering from CHD and sleep apnoea are endangered by nocturnal hypoxia-conditioned myocardial ischaemia which in turn can lead to increased electrical instability. II. The macrostructure of the sleep of patients suffering from CHD and sleep apnoea is comparatively as disturbed as that of patients with apnoea without CHD.

Title Snoring and risk of cardiovascular disease. Authors Zaninelli A. Fariello R. Boni E. Corda L. Alicandri C. Grassi V. Institution Department of Internal Medicine, University of Brescia, Italy. Source International Journal of Cardiology. 32(3):347-51, 1991 Sep. Abstract In order to evaluate the possible role played by snoring as a risk factor for cardiovascular disease, we studied 400 patients aged 30-80 years, divided into 4 groups matched for age, sex and body mass index. The first group consisted of 100 patients who snored, having risk factors (hypertension, diabetes, obesity, smoking, high serum cholesterol level) for cardiovascular disease. The second group consisted of 100 non-snoring patients with risk factors. The third and fourth groups were formed by 100 snoring and 100 non-snoring patients without risk factors. We investigated the morbidity and the mortality from cardiovascular disease over a period of five years (1982-1987). An increase in morbidity and mortality was found for snorers with risk factors (36 and 17 respectively) compared to non-snorers with risk factors (10 and 4, P less than 0.001), and also to both snorers and non-snorers without risk factors (7 and 3, P less than 0.001; 3 and 1, P less than 0.001 respectively). No difference was noted between snorers and non-snorers without risk factors. A higher morbidity and mortality for cardiovascular disease was found in snorers with risk factors as compared with non-snorers having risk factors. Furthermore, the morbidity and mortality in patients without risk factors was found to be lower compared with that found in snorers with risk factors. In conclusion, snoring worsened the prognosis of patients with risk factors for cardiovascular disease, but did not represent an independent or predictive risk factor in itself.

Title Nocturnal myocardial ischemia and cardiac arrhythmia in patients with sleep apnea with and without coronary heart disease. Authors Koehler U. Dubler H. Glaremin T. Junkermann H. Lubbers C. Ploch T. Peter JH. Pomykaj T. von Wichert P. Institution Zentrum Innere Medizin, Medizinische Poliklinik, Philipps-Universitat Marburg. Source Klinische Wochenschrift. 69(11):474-82, 1991 Aug 1.

Abstract To study the effect of apnea and hypoventilation-induced hypoxemia on the heart, we carried out polysomnographic recordings over 4 nights with electrocardiographic tracings in 30 patients with and without coronary heart disease. Evaluations of the data were based on the 2nd and 4th nights. In six subjects, five with coronary heart disease, we found 85 episodes of nocturnal ischemia, mainly during REM sleep (83.5%), high apnea activity, and sustained and progressive hypoxemia. Complex ventricular ectopy was observed in 14/13 patients (nights 2/4) and repetitive ventricular ectopy in 5/3. There was no significant difference in the quality and quantity of ventricular ectopy during wake and sleep states between the CHD group and the control group. In one patient ventricular bigeminy was observed only at a threshold of SaO2 below 60%. Bradyarrhythmia was made evident in four subjects from the CHD group and correlated mainly with apnea activity. We suppose that patients with sleep apnea and CHD are at cardiac risk because coronary heart disease can be aggravated by insufficient arterial oxygen supply due to cumulative phase of apnea and hypoventilation. The reduced hypoxic tolerance of the heart may lead to myocardial ischemia and increased electrical instability.

Title [Sleep-related respiratory disorders and coronary heart disease]. Authors Koehler U. Pomykaj T. Dubler H. Hamann B. Junkermann H. Grieger E. Lubbers C. Ploch T. Peter JH. Weber K. et al. Institution Zentrum Innere Medizin, Medizinische Poliklinik, Philipps-Universitat Marburg. [Review] [German] Source Pneumologie. 45 Suppl 1:253-8, 1991 May.

Abstract A review of the literature shows that more than 50% of examined patients suffering from coronary heart disease were also suffering from sleep-related apnea. We were able to diagnose a pathological sleep apnea in 9 out of 25 patients (36%) suffering from an angiographically confirmed coronary 2-vessel and 3-vessel disorder. Patients with this combination--this is the hypothesis derived from our study--are at risk due to nocturnal apnea-induced myocardial ischaemia and rhythmic disorders. In 15 patients with sleep apnea and coronary heart disease or small vessel disease, nocturnal polysomnography was conducted, in parallel a 6-channel ECG was recorded. The apnea index (second night) was on the average 33 phases/h, the maximal duration of an apnea phases being 120 seconds. The minimal blood gas saturation recorded during sleep was between 46 and 89% (median 76.0%). In 4 of the 15 patients it was possible to confirm myocardial ischaemia (correlated via REM and also via NREM) with a maximum duration of 60 seconds, mainly during the phases of maximal apnea activity and blood gas desaturation. On comparing the ventricular arrhythmias waking/sleep, the Lown class did not change in 12 patients; there was deterioration in 2 patients and in one patient a qualitative improvement during the sleep phase. Patients suffering from sleep-related respiratory disorders and coronary heart disease are at cardiac risk, the more so since long-lasting apneas can lead to conditions of hypoxia at the heart in pre-existing changes in the coronary arteries, restricted coronary reserves and reduced tolerance to hypoxia. Such hypoxia can in turn induce enhanced electrical instability and a disturbance of the contractile function.

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