Sleep and the Heart

Sleep and the Heart

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Prof. Dr. Shahira Loza

Director of the Cairo Center for sleep Disorders

President of the Egyptian Scientific Society of Sleep Medicine & Research Board Member of the World Association of Sleep Medicine

One of the most significant advances in clinical medicine has been our understanding that sleep disorders may either be a cause, or may contribute to the progressive morbidity and mortality of various cardiovascular diseases. This accentuates the need to increase awareness of the importance of sleep physiology and pathophysiology among cardiologists .

The importance of this issue to public health is increased by the annual toll of nocturnal sleep related cardiac events which are estimated at 20% of Myocardial infarctions and 15% of sudden cardiac deaths in the US.

During night sleep a broad spectrum of autonomic patterns provide both restitute, and stress to the cardiovascular system . These effects are the consequences of changes in the central nervous system physiology; as the brain periodically re excites during Rem sleep from relative tranquility of Non Rem sleep.

There is a strong neuro humoral coupling between central structures and cardiorespiratory functions, and thus a dynamic fluctuation in the heart rhythm, arterial blood pressure, coronary blood flow and ventilation. Autonomic control of circulation ensures cardiac output to the vital organs through adjustment of heart rate, arterial blood pressure and redistribution of blood flow. Neural circulatory control is coupled with circadian rhythm ( Sleep wake cycle) and ultradian rhythm ( Rem & Non Rem process ) .

As Non Rem sleep progresses from N1 to N3, Muscle Nerve Sympathetic Activity decreases compared to wakefulness. There is an increase in cardiovascular drive and reduction in cardiac and peripheral sympathetic activity. In contrast REM sleep is a state of autonomic instability dominated by fluctuation between parasympathetic and sympathetic influences which produce sudden abrupt changes in the heart rate and blood pressure. The average heart rate and blood pressure are higher during REM sleep compared to Non REM sleep.

Effects of disordered sleep & primary autonomic dysfunction on day / night autonomic changes

Heart rate and blood pressure physiologically decrease during night time compared to daytime. Normal 24 hours blood pressure pattern shows a systolic blood pressure reduction of 10 mmHg during sleep compared to daytime values , a reduction commonly referred to as “dipping”.

The persistence of high night time systolic blood pressure and lack of blood pressure dipping are clinically important and have been linked as precursors of atherosclerotic inflammation and endothelial dysfunction. Lack of systolic dipping and lack of heart rate dipping have been associated with increased cardiovascular mortality, after correction of several confounding variables including daytime values.

Sleep loss and sleep disturbances have been invoked as some of the potential factors underlying these abnormalities.

Controlled studies show that with partial sleep restriction or sleep deprivation blood pressure and catecholamine levels remain high while night time wakefulness is maintained, then decrease normally with subsequent sleep. Morning surge in blood pressure and catecholamine appear more pronounced after sleep deprivation particularly in hypertensive subjects.

Sleep-related breathing disorders are common in patients with cardiovascular disorders and may either play a causative role or contribute to the progression of the cardiovascular pathologic process.

Observational studies suggest that obstructive sleep apnea is a cause of mortality, and that treatment with CPAP improves survival. Similarly, both central and obstructive sleep apnea may contribute to mortality of patients with systolic heart failure, and effective treatment with CPAP may improve survival.

Effect of Sleep Disorders on Cardiovascular Physiology:

It has been established that the most common sleep disorder affecting the cardiovascular system is Obstructive Sleep Apnea, it may be a cause of or may contribute to the progression, morbidity and mortality of various cardiovascular diseases.

OSA is characterized by repetitive

There is a strong neuro humoral coupling between central structures and cardiorespiratory functions, and thus a dynamic fluctuation in the heart rhythm, arterial blood pressure, coronary blood flow and ventilation

episodes of complete (apnea) or partial (hypopnea) upper airway obstruction occurring during sleep. These events result in drop of blood oxygen saturation and drop in heart rate and are terminated by brief arousals. Apneic and hypopneic events last a minimum of 10 seconds and they can occur in any stage of sleep Non Rem N1, N2 , N3 and Rem Sleep. Events are usually longer with more severe decrease in oxygen saturation when they occur during Rem sleep and when the individual is sleeping supine. Oxygen saturation usually returns to baseline values following resumption of normal breathing provided there is no underlying pulmonary pathology. These repeated events of airway narrowing / obstruction result in decrease airflow, intrathoracic pressure and bradycardia. there is increased effort, blood pressure and natriuretic peptide. it also causes disrupted sleep and oxygen saturation swings ( hypoxia, hypo, hypercapnia)

The prevalence of clinically significant OSA in developed countries is about 5%. The Wisconsin Sleep Cohort Study of 3513 subjects aged 3060- years found that 4% of men and 2 % of women had OSA defined as apnea hypopnea index ( AHI) of greater than 5, associated with daytime sleepiness. There is higher prevalence in Obese , hypertensive, diabetics and persons with craniofacial dysmorphism. Higher risk with Obesity ( neck size&waist circumference ), inflammation of upper airway , alcoholism, hypothyroidism, acromegaly and amyloidosis.

Night symptoms of OSA include snoring, respiratory pauses, choking or dyspnea, restless sleep, dry mouth, drooling, reflux, bruxism, parasomnia and nocturia; 28% of cases would need to urinate 47- times during the night .

As for the daytime symptoms they include excessive daytime sleepiness, fatigue, morning headache, cognitive disfunction, memory loss, decrease libido- impotence .

Diagnosing OSA

This patient comes to see you not knowing at all that he even stops breathing!

The only clue apparent symptoms is his loud snoring and his respiratory pauses during sleep.

Both can only be reported by a bed partner.

Diagnosing entails a good history, clinical examination and an overnight Polysomnography recording for confirming the diagnosis.

Association between OSA & CVD

• There is a clear association between OSA and CVD seen as:

• A higher incidence of adverse CV events in untreated OSA

• and better outcome in treated OSA

Recurrent Apneas

The consequences of recurrent apneas and hypopneas include hypoxemia/ reoxigenation in association with hypercapnia and hypocapnia, other consequences are arousals and negative flows in pleural pressure. these consequences result in significant cardiac disfunction, endothelial dysfunction, rise in BP and Arrhythmia

Pathophysiologic consequence elicit acute and chronic cardiovascular changes.

 Systemic Hypertension

In the 7th Report of the Joint Committee on Prevention, Detection, Evaluation and Treatment of High Blood Pressure OSA is recognized as an identifiable cause of hypertension.50% of patients with hypertension have OSA , evidence supports that OSA represents the most prevalent secondary contributor to elevated blood pressure in resistant hypertension.The strongest epidemiological evidence comes from the on going Wisconsin Sleep Cohort Study ( middle aged state employees) 4 year hypertension incidence increases from 10% with no SDB to 32% with OSA. Both adequate control of OSA and adherence to CPAP therapy are required to improve OSA induced hypertension.

Fig 3 Hypertension & OSA

Pulmonary Hypertension

OSA is a cause of secondary pulmonary hypertension, recognized by WHO as an identifiable cause usually mild but maybe severe. Alveolar hypoxia and hypercapnia cause pulmonary arteriolar vasoconstriction and hypertension.

Coronary Artery Disease and OSA

Through the mechanism of endothelial disfunction ,Obstructive Sleep Apnea may be a cause or may contribute to Coronary Artery Disease also being a comorbidity in obese, hypertensive, smoking, hyperlipidimic subjects provides high risk for the development of CAD

Studies focused on snoring habits , the Finnish cohort 4388 men aged 4069- years , snoring provided 1.9 fold increased risk of CAD during 3 years follow up

Spanish study showed that the risk for acute MI tripled in snorers compared to non snorers

Evidence suggests that CPAP decreases the number of ischemic events.

Arrhythmias & OSA

OSA induced arrhythmias including tachycardia- bradycardia oscillation can occur in absence of any major structural cardiac abnormality. Ventricular arrhythmias :( mostly seen in pt with premorbid cardiorespiratory disease or with severe desaturations. There is an increased risk of developing AF , specially in patients with with severe hypoxemia. Untreated obstructive sleep apnea may increase the risk of recurrence of atrial fibrillation after cardioversion and that 50% of patients presenting for cardioversion have a high risk of sleep apnea compared with 30% in a general cardiology clinic.

Heart Failure

• Heart failure has been known for more than two centuries to be associated with abnormal breathing pattern HUNTER CHEYNE STOKES described as crescendo and decrescendo changes in tidal volume with intervening central apnea.

• The pathophysiologic consequences of Sleep Related Breathing disorders and their effects on the cardiovascular system are more pronounced in the patients with HF and CAD.

• PSG studies of ambulatory stable HF patients showed high prevalence it is a worse prognosis if they occur during wake.

• There is high prevalence of both conditions in the older population and because of common symptoms it is some times difficult to detect OSA in the elderly HF patient.

• Treatment of obstructive sleep apnea with CPAP in patients with congestive heart failure has been found to improve ejection fraction.

• In pt with SHF the presence of increased sympathetic activity and decreased LV ejection fraction reversed with CPAP treatment

Insomnia & CVS

An attenuation of blood pressure nocturnal dipping has been noted in normotensive subjects with primary insomnia. the absence of blood pressure dipping was associated with indices of poor and fragmented sleep including longer wake after sleep onset and higher arousal frequency . In these subjects higher night time blood pressure and blunted dipping was associated with increase EEG activity in the beta frequency , a common feature in insomniac.

Sleep disrupting effects of cardiac medications

Several important medications that are widely prescribed for patients with cardiac diseases including antihypertensive agents and beta blockers that cross the blood brain barriers have the potential to disrupt sleep , increase awakenings and total wakefulness , some increase Rem latency and decrease total Rem sleep time. It was postulated that the mechanism of sleep disruption is the depletion of endogenous melatonin. Additionally beta blockers may provoke nightmares.

Conclusion

The importance of recognition of the association of Sleep Disorders and Cardiovascular diseases is due to the burden to patients and society and the improvement of the CV

morbidity and mortality by treatment