rem sleep associated angina | Dr.S.Venkatesan MD

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What are the mechanisms of “Nocturnal” Angina ?

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease, tagged angina during sleep, aortic regurgitation and nocturnal angina, nocurtnal angina, rem sleep associated angina on February 2, 2012| Leave a Comment »

Angina occurring at night is relatively uncommon . It is still more rare for angina to occur exclusively at night (With a possible exclusion of syphilitic aortits with AR !) The underlying conditions and mechanism of nocturnal angina are largely unexplored. In most clinical situations nocturnal angina is associated with day time angina as well .

Various mechanisms are proposed

It is primarily due to increased demand (Holter monitoring has documented brief bursts of HR acceleration just before nocturnal angina with manifest ST depression )
Increased demand during REM sleep .
Dreams related adrenergic surge has been implicated.
Rarely it is due to supply side defect .
Coronary vaso-spasm ( Mostly in a pre-exisiting lesion )
It could simply represent paroxysmal nocturnal dyspnea (pnd)
Sleep apnea can precipitate angina ( Ironically angina occur during re-breathing phase )
Altered hemo-rheology
Nocturnal gap in anti anginal medication *

* May be more common than we realise.

Cardio vascular hemo-dynamics at night

If we believe , sleep is the great relaxation , and the heart would enjoy the “night time” we are absolutely wrong . Even in sleep , heart has to pump the same 250 ml of blood every minute. Of course , the sleeping heart rate slows down considerably , still it is interspersed with spikes of activity. When the heart rate slows down , diastole is prolonged , coronary blood flow is expected to be copious unless there is critical CAD.

We know , sleep is not a passive process , even as the autonomic nervous system takes complete control over the somatic system .The true colors of our delicate autonomic system will come to light only during sleep.The muscle tone , the sympathetic drive fluctuates according a pre-set degree . Dreams and REM sleep disturbance can have considerable impact on the sympathetic nerve terminals which ooze catecholanines .

Sudden awakening from early sleep is vested with a risk of dangerous spikes of adrenaline release .This becomes especially important in compromised coronary circulation .In fact , this is commonest sleep -awake sequence in patients with nocturnal angina.

Silent ischemia at night

It is curious to note 24 hour Holter monitoring reveals most episodes of ST depression at night are silent. There must be a specific pain threshold above which a patient awakens with angina. The available studies do not answer this issue and are not perfect . We have no way to find true silent ischemia during sleep.(PET scan in thalamus ?)

Nocturnal angina in Aortic regurgitation

Aortic regurgitation has special relationship with dusk .For angina to occur AR must be severe and usually isolated .

Prolonged diastole at night -Regurgitation time is prolonged .
Dilated LV . Increased LV mass .Increased demand.
Raised LVEDP due high wall stress.
Diastolic coronary stealing . Venturi effect of AR jet

Nocturnal Angina : Is it stable or unstable ?

Most consider it as a type of stable angina .Now ,we have reasons to suspect it could a marker of unstable angina as it is an expression of rest angina .

Nocturnal angina vs nocturnal STEMI

How often an episode of nocturnal angina end up in STEMI ?

STEMI is more common in the early hours of the day and is more related to the hemo-rheological factors . Please note , STEMI is a supply side defect while most episodes of nocturnal angina is due to demand ischemia . However it is possible nocturnal angina episode can precipitate STEMI if vasospasm is the underlying mechanism and if it is prolonged can trigger thrombosis.

We do not know the answer as yet.

Nocturnal Angina : Can it be PND equivalent ?

Paroxysmal nocturnal dyspnea (PND) is a classic manifestation of episodic LVF. We know dyspnea can be an anginal equivalent. What prevents angina to become a dyspnea equivalent ! ( Especially the nocturnal ones , since the mechanism of generation of PND are very similar to the genesis of angina ). It is distinctly possible one may be mistaken for the other . Both occur when sudden hyper-adrenergic state is evoked which demands high MVO2 . An ischemic heart has every reason to respond with angina .

It is well known ischemia can result in transient diastolic dysfunction and elevate the PCWP simultaneously and PND would be the sequel . When we analysed the nocturnal calls ( Our fellows , do get lots of such calls from general wards at night ), many patients with LV dysfunction who complained of classic chest pain had some degree of dyspnea and few crackles over lung base as well .

Nocturnal angina and obstructive sleep apnea

The incidence of nocturnal angina is more common in obese population with obstructive sleep apnea.

The reason is two-fold

1 .Hypoxia mediated

2. Inappropriate tachycardia during recovery phase

Is there any specific management strategies to control nocturnal angina ?

General principles apply .
The timing of anti anginal medication can be adjusted . Long acting preparations taken in morning hours to be avoided as they do not cover night time.
A calcium channel blocker (with optional beta blocker ) at night may be the best bet to prevent nocturnal ischemia.
Dinner to sleep time to be widened.
Heavy diet at night to be avoided.
Sedatives role is not clear. (Can Diazepam suppress nocturnal angina ? If so . . . we can call it as anti anginal drug . . . is isn’t )

References