Cardiology -unresolved questions | Dr.S.Venkatesan MD

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Break through in Brugada syndrome ! . . . always carry this vital data in FINGER tips !

Posted in cardaic physiology, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged asymptomatic brugada, brugada finger registry, brugada syndrome, ep study for brugada, FINGER trial, how to manage asymptomatic brugada ?, icd for brugada, PRELUDE STUDY JACC, should we do ep study for asymptomatic brugada, sodium channel mutation, tyepe 1 brugada, type 1 brugada on June 10, 2012| 2 Comments »

Brugada syndrome continues to fascinate us for two reasons.

One , it deals with mysterious sudden deaths of young men and women

Two , it is one of the fine examples of how advances in molecular biology , links physical defects in ionic channels to sudden electrical death (Most of them are due to inherited defects sodium channels of myocyte cell membrane )

While high risk subsets of Brugada are easily managed , it is the asymptomatic ones that bother us.

The following are some of the difficult questions , a cardiologist faces when dealing with patients , who exhibit only Brugada pattern in ECG .

Should I go for an EP study Doctor ?
Will I require an ICD Doc ?
Do I carry a significant risk of dying suddenly ?
Do I need a genetic test for sodium channel mutation ?

Fortunately, we can answer all these questions with much courage than before.

(Thanks to the European Finger registry published in 2010 !)

“No” is the clear answer for all of them !

Summary from the FINGER registry.

(France , Italy, Netherlands, GERmany)

The registry included 1029 consecutive individuals

(1) Aborted SCD (6%);

(2) Syncope otherwise unexplained (30%);

(3) Asymptomatic patients (64%).

In the follow-up of 31.9 (14 to 54.4) months . A total of 7 death occurred .

The cardiac event rates per year was

7.7% in patients with Aborted SCD,
1.9% in patients with syncope
0.5% in Asymptomatic patients.

Predictors of cardiac event

Previous syncope
Spontaneous type 1 ECG

Non predictors ( Surprisingly there were more non predictors ! )

Gender has no predictive role
Familial history of SCD,
Inducibility of ventricular tachy-arrhythmias during EP study,
Presence of an SCN5A mutation

Follow up

PRELUDE study almost reaffirms Finger data

(PRogrammed ELectrical stimUlation preDictive valuE)

Just publicized in JACC 2012 from the pioneer of Brugada Silvia Priori of university of Pavia Italy

Reference

http://circ.ahajournals.org/content/121/5/635.full.pdf+html

http://content.onlinejacc.org/cgi/content/abstract/59/1/37

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Tough calls in cardiology : Refractory hypotension in septic shock and the role of Hydrocortisone in Septic shock ?

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged corticus study, hydrocortisone in septic shock, refractory hypotension in septic shock on June 5, 2012| 1 Comment »

Time and again cardiologists are called to opine in critically ill ICU patients with hypotension. The circulatory shock of septic shock is often refractory . Many times it degenerates into multi -organ failure . The mortality remains high in- spite modern treatment .Even in those patients who recover , they require prolonged inotropic support (for days or even weeks)

Here is a recent call I attended to .

A 44 year old febrile , ventilated patient (With a pneumonitic patch , PEEP of 6 , near ARDS ) , precarious renal function and altered sensorium , maintaining a blood pressure of 100/70mmhg with high dose dopamine and nor- adrenaline , monitor showing a heart rate of 125 /mt sinus .This status -quo has continued for more than 72 hours. To my surprise, the ICU physician told me there is in-fact a minor improvement in general condition than before . After blinking at the patient’s file for few minutes , I did a customary bed side echocardiogram .The only positive finding I found was his heart was structurally normal and EF was 64 % , still the right heart chambers were struggling to do it’s job fighting with the PEEP.

The physician had a very specific query from the cardiologist . How to wean the inotropic support and shift him off ICU ?

(The poor patient has no insurance , and has to shell Rs 10000 everyday which is equal to his monthly income ! )

A very valid question indeed ! After all , cardiologists claim to have special knowledge and wisdom about disorders of vascular system .

Heart being normal , the crux of the problem is loss of vascular tone. (Autonomic dysfunction ) .How to improve it ? I discussed the following suggestions.

Early passive muscle exercise (Augmenting muscle tone and transforming it to into arteriolar and venous tone )
Venous support ,stockings etc.
Ensure adequate intra-vascular fluids
Sodium supplements
Corticosteroids.
Fludro-cortisone , the mineralo-corticoid may have a specific advantage as it could retain sodium in vessel wall that can be exchanged with smooth muscle calcium and improve vascular tone .
ECMO is often a pre terminal intervention .
Will power . We know vascular tone is in fact neurogenic in origin .The tone flows from brain stem .Administering will power could be a useful intervention . (parental infusion of fighting spirit !)It can be done through pep talks from close family members in conscious patients .(One controversial advice is to allow near and dear into bedside , ICU phobia may delay recovery of vascular tone !)

Finally I suggested , a vascular consult from the GOD . Organised prayer . There is some evidence , even proxy prayers do exert benefits in unconscious patients .

After a 15 minutes stay in the ICU , for doing nothing I received a significant consultation fee , and I left the place sheepishly with a definite dose of guilt !

Reference for role of Hydrocortisone in septic shock

The CORTICUS study

It has no overall impact but hastens recovery from septic shock . Even though the study appears to denote a negative connotation

it has the role in selected individuals .http://www.nejm.org/doi/full/10.1056/NEJMoa071366

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How relevant is oral magnesium for recurrent ventricular tachycardia ?

Posted in cardiac drugs, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, tagged magnesium as anti arrhytmic drug, oral magnesium, oral magnesium and ventricular tachycardia on May 29, 2012| 1 Comment »

Magnesium is a powerful anti-arrhythmic drug . It has a well established role in controlling VT when administered Intravenously especially in polymorphic VT .

Mechanism of action

It acts at the cell membrane.
It has a unique action of blocking calcium channels that reduces the number of oscillations of both early and late after potentials

Link for more on mechanism of action

https://drsvenkatesan.wordpress.com/2010/01/13/how-does-magnesium-acts-as-an-antiarrhythmic-drug/

How often cardiologists administer oral magnesium for long-term control of VT ?

As for as I know , no one uses it ! but dietary supplements are used for general well being .

Why ? Is it because

Magnesium does not get absorbed in the gut
Magnesium levels are un- predictable in plasma if administered orally

Answer : No one has really tried it as a chronic therapy in VT yet !

Final Message

Tablet Magnesium can give a tough fight to Amiodarone and Flecanaide in refractory VT at a fraction of the cost !

Who has the audacity to compare Magnesium with Amiodarone head on ?

Reference

Magnesium as health supplement .

Magnesium is available in tablet form as Malate , Stearate, Taurate and Aspartate along with calcium and Zinc etc .

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Atrial fibrillation with wide qrs tachycardia : Don’t get obsessed with WPW syndrome

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged amiodarone makes af wide qrs, antidromic atrial fibrillation, orthodromic Atrial fibrillation, svt with aberrancy, wide qrs atrial fibrillation, wpw and wide qrs tachycardia on May 26, 2012| Leave a Comment »

Irregular wide qrs tachycardia is a fairly common clinical entity in any cardiac emergency room. The moment you ask about such tachycardia , 9/10 fellows will come out with a prompt answer ” AF with WPW syndrome” even before you complete the question ! It is not that common as we perceive .The problem is with our traditional teaching methods and the attraction of human brains to rare and exotic disorders.

traditionally SVT with aberrancy is diagnosed mainly in the setting of regular tachycardia .

We often forget “AF with aberrancy” is equally common , and it presents with a irregular wide qrs tachycardia .

I wonder whether this phenomenon can be termed as orthodromic aberrancy .This can directly compete in the differential diagnosis of antidromic AF with WPW !

It should also be mentioned antidromic AF can run into very high rates as accessory pathways do not check the incoming signals while orthodromic aberrancy the ventricular rates can not exceed 220 or so at least theoretically . (This simple clue can clinch the issue in favor of WPW )

There is no proper published data available for the true incidence of AF with orthodromic aberrancy in general population

In fact , there are many electrical environments for AF to become a wide qrs AF

1. AF with Antidromic conduction through accessory WPW pathway.

2. AF with Orthodromic aberrancy ( Non WPW – Similar to any SVT with aberrancy )

3. AF with pre existing LBBB

4. AF with Amiodarone effect. (Especially with DCM and cumulative load of Amiodarone )

5. AF with electrolytic / especially excess intra-cellualr potassium

6. Finally , even Atrial based pacing (DDD) can cause wide qrs irregular tachycardia when mode switching fails .Here the ventricles may track the atrial irregularity and respond with a wide qrs bizarre tachycardia .

Final message

There are many causes for wide qrs tachycardias in Atrial fibrillation . WPW with anti-dromic conduction is just one of them .We need to approach the issue with an open mind .Please be reminded , once contemplated WPW syndrome can be a powerful thought blocker !

Note : *We are not including polymorphic ventricular tachycardia here .It is an important subset of wide qrs irregular tachycardia.

** VT can co-exist with AF .This is not surprising as many of the diffuse cardiomyopathies involve both atria and ventricle with extensive scarring and fibrosis a perfect trigger for both atrial and ventricular arrhythmias .

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Why RR interval is irregular in Atrial fibrillation ?

Posted in cardiac physiology, cardiology -ECG, Cardiology -unresolved questions, Cardiology-Arrhythmias, tagged atrial fibrillation, ECG, junctional fibrillation, mechanim of irregularity in af, rr interval irregular on April 5, 2012| Leave a Comment »

RR interval in Atrial fibrillation is irregular because . . .

The Atria fires irregularly
AV node conducts irregularly
Atria confuses the AV node with its random firing and varying penetration *
The ventricle just reflects irregular response of atria .

The answer is all of the above. Response 3 explains best.

*Please note , the AV nodal property is predominantly responsible for the irregular RR interval in AF . Atria confuses the AV node with its random firing .The varying penetration into different depths of AV nodal structure and the resultant concealed conduction make the the AV nodal refractory period into continuous oscillation .This random delays in AV node is reflected in RR interval as irregularity )

The response we get in ventricles in AF can be summed up as “A filtered atrial rhythm”

Paradoxically, amidst the chaos in atria the rate is fairly constant within the atria (Fibrillatory wave firing at up-to 600/mt ) Of course , the FF interval in the atria will also be varying . At a rate of 450-600 this is difficult to quantitate especially in fine AF.

When does RR interval becomes regular in AF ?

When the patient develops complete heart block.
Digoxin toxicity
Associated Sinus node dysfunction

For advanced readers in EP : A mystery explanation for irregular rhythm in AF in the offing ?

AV node is a physiological and electrical sink .

When atria fires at 600/mt it absorbs about 60-70 % of the atrial response .Whether it releases the original impulse or initiate a new rhythm in the junction is not clear.

There is some evidence to suggest the rhythm that control the ventricle in AF may not be filtered original rhythm from the atria .Instead it could be a fast junctional escape rhythm (Is that a junctional fibrillation ?)

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What will be the PCWP in grade 1 LV diastolic dysfunction ?

Posted in cardiac physiology, Cardiology - Clinical, Cardiology -unresolved questions, echocardiography, Uncategorized, tagged left atrail pressure in diastolic dysfunction, pcwp in grade 1 diastolic dysfunction on March 30, 2012| Leave a Comment »

What will be the pulmonary capillary wedge pressure ( PCWP ) in grade 1 LV diastolic dysfunction ?

Significantly elevated
Marginally elevated
Usually Normal
It depends upon age, LA size and LV function.

Answer is 3 . (Of course it depends on 4 ) Normal PCWP is 4-12mmhg

Are these patients with grade 1 LV diastolic dysfunction are at risk for acute pulmonary congestion at times of stress ?

Probably not ( in most )*

The grade 1 LV diastolic dysfunction or defect is the most used (abused ! ) echo terminology .The diagnostic simplicity of this condition namely a simple documentation of “a”velocity more than “e” , has made it as an epidemic in echo labs world wide. After all , it reflects a simple fact that left ventricle has summoned the atria for assistance (Which is all the more physiological at times of stress !)

When does this physiology becomes pathology ?

As long as the atria is doing its job of assisting the LV without any fuss , the mean pressure of LA(PCWP) is maintained within normal level . Only if the atrial function is stretched beyond the limits , PCWP begins to raise. It can happen in a variety of ways . Most commonly it happens elderly hypertensive /Diabetics especially with LVH .

It can also occur in healthy individuals when they become physically deconditioned. (Left ventricle goes for disuse and find it difficult to relax)

Final message

Isolated grade 1 LV diastolic dysfunction in people > 40 years generally do not indicate a serious abnormality.

Only if they have DM/HT and myocardial disease they need to be evaluated further.

One practical clue is , if LA size is normal one can rule out significant diastolic dysfunction.

Caution

* In elderly population , when they undergo any major surgery , presence of even grade 1 LV diastolic dysfunction can be a marker for peri -operative LVF and lung congestion .

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Some delicate issues in the managment of acute prosthetic valve thrombosis

Posted in cardiology -Therapeutics, Cardiology -unresolved questions, valvular heart disease, tagged management of prothetic valve thrombosis, prosthetic valve thrombosis, streptokinase for prothetic valve thrombosis, thrombolysis for porsthetic valve on March 25, 2012| 2 Comments »

Clinical sense

First and fore most dictum is not every prosthetic valve obstruction is thrombotic (Most cardiologists are tuned to think that way )
Pannus, Mechanical failure and vegetations can increase the gradient across prosthetic valve.
If the clinical presentation is acute (< 48 hours ) it is more likely to be a thrombotic event .
History of recent discontinuation of oral anticoagulants /sub optimal INR will favor thrombosis.

A meticulous Echocardiography is vital (TEE though gives more information in an emergency TEE is suffice )

Thrombolysis is to be considered in all .
For right sided prosthetic obstruction thrombolysis is the initial modality of choice.
For left sided valve thrombosis surgery is the preferred option .However a trial of thrombolysis for 24 hours may be tried .
For a high risk mobile thrombus , thromolysis is contrandicated.

The success rate is less with Mitral than Aortic valve . Success depend upon more on the location / Freshness of thrombus than the type of the lytic agent used.

Is there a time window for prosthetic valve thrombolysis ?

Thrombus organisation takes 2 weeks at- least.Hence , it better not to attempt thrombolysis in documented late prosthetic valve thrombosis.

Thrombolysis of left-sided valves has inherent risk of stroke .

Heparin controversy

Simultaneous usage of heparin along with streptokinase or TPA is perceived as risky (No good evidence for this perception )It is logical to expect even as the thrombus lyses the clot lots of pro-coagulant debri are released . Concomitant usage of heparin will definitely help accelerate thrombus dissolution. (I am glad Joseph S Alpert also feels the same ! )

Assessing successful thrombolysis

Can be a tough task .
Relying purely on gradient is vested with risk of huge error.
In a patient with shock or LV dysfunction gradients are not reliable as low flow status masks the gradient.
A accelerated thrombolytic protocol 15lakhs streptokinsae in 60 minute may be tries in unstable patient .
It is wiser to rapidly asses for clinical improvement in high risk subsets and refer the patient for early surgery .

Surgery

Prohibitive mortality reported in many centres.

It need to be remembered no surgeon will operate on a sick patient in shock exposed to cocktail of heparin and streptokinase.

Valve replacement is required in most case. Simple valve debridement (servicing the valve ) and releasing discs from the sticky thrombus is also possible in an occasional patient.( Do not ask reference for this !)

Reference (Surprisingly most of the good papers in the topic appeared in JACC)

http://content.onlinejacc.org/cgi/reprint/41/4/653.pdf

http://content.onlinejacc.org/cgi/reprint/41/4/659.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1881.pdf

http://content.onlinejacc.org/cgi/reprint/35/7/1874.pdf

After thought

I have not seen a single case of acute prothetic valve thrombosis involving Starr Edwards valve in the last 20 years of of clinical cardiology practice.

Is it true . . . the new age valves with more mechanical stress points are proving more injurious to our patients. Our pursuit towards a perfect artificial valve need some introspection .

Read a related article in my site : Who killed Starr Edwards valve ?

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What are the mechanisms of “Pulmonary Arterial Hypertension” in Dilated cardiomyopathy ?

Posted in cardaic physiology, Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, myocardial disease, tagged diastolic dysfunction in dcm, iscemic vs idiopathic pah, mechanism of pulmonary arterial hypertension in DCM, PAH IN DCM, pulmonary hypertension, restrictive lv filling and pah in dcm on February 18, 2012| 1 Comment »

Pulmonary arterial hypertension (PAH ) is an uncommon manifestation of dilated cardiomyopathy .While pulmonary venous hypertension of some degree is expected in most patients with DCM, it is rare for these patients to go for severe arterial hypertension.

The reason for this may be the natural history of DCM do not allow these patients to live that longer to manifest severe PAH. Still , we encounter this problem atleast in tertiary hospitals. Presence of moderate to severe PAH (> 50mm peak PAP) is a sinister sign in DCM. They not only do badly , they also make the transplant outcome dismal .

What causes this severe PAH in DCM ? The following observations are made in our institute .

Now we know , isolated systolic dysfunction is rarely associated with PAH .It is the presence of LV diastolic dysfunction (Often restrictive ) that raises the pulmonary pressures. PAH of DCM is rarely progressive.

One important suggestion is the DCMs which are associated with severe PAH may indeed represent late stages of RCM , when the LV begin to dilate.

Associated mitral regurgitation contributes to PAH

Atrial fibrillation has a significant impact on elevating pulmonary venous and arterial pressures in DCM.

Hypoxic PAH can occur in any medical situation in susceptible population . DCM is no exception

For some reason idiopathic DCM is more often result in PAH than ischemic DCM . (Is that possibel , some form of idiopathic PAH and DCM are etiologically related ?)

Further , the positive inotropic agents when liberally used will worsen the diastolic properties of LV.

Finally involvement of right ventricle in the cardiomyopathy process can have an ameliorating effect on PAH. A good RV function is essential to lift the PA systolic pressure. If RV failure is causing a low PAP , do not be happy .It simply means RV is going to say good bye . . . for the final time !

How to manage PAH in DCM ?

There is no specific management strategy .

We do not know yet whether Sildenafil , Bosentan, and Epoprostenol have any role in this form of PAH. These are all basically vasodilators. It’s use in DCM is vested with a risk of catastrophic hypotension . Of course , we do have a role for balanced vasodilators in cardiac failure .(As most of these patients would be already on adequate ACEI )

Presence of PAH should be considered as an independent indication for anticoagulants as in situ pulmonary thrombus is common.

The effect of cardiac resynchronisation therapy in reducing the PAH of DCM is not convincing.

Final message

PAH in DCM is an unwelcome development. It makes the situation tough . The mechanisms are diverse .Understanding the mechanism would help us deal this problem better . Conventional anti failure treatment may help ,but it is wiser to try reserve drugs.

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Tough calls in cardiology : How will you manage ventricular tachycardia with a mobile LV clot ?

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Clinical cardiology, tagged how to manage lv clot with vt, management of vt, mobile lv clot and vt, ventricular tachycardia, VT with lv clot on February 16, 2012| Leave a Comment »

Clinical cardiac problems can be very demanding at times. Here is a situation even the toughest will struggle.

A 52 year old man comes with a wide qrs tachycardia with a blood pressure of 90 /70 with class 4 dyspnea .He was restless , trying to sit up because of orthopnea. The ECG showed a definitive ventricular tachycardia with LBBB morphology.The patient was connected the oxygen line , cardiac monitor, oximetery, etc

The consultant on call instructed immediate DC shock and he warned about impending ventricular fibrillation .He casually told the fellow to do a echocardiogram also and rule out any structural heart disease. Even as the staff was arranging the defibrillator , the fellow did a rapid bed side echocardiogram . He was shocked to find a large mobile LV clot with a dilated , severely dysfunctional left ventricle having an EF of 25 % .

Now comes the critical time . Should we shock this man with VT and LV clot?

What will be your option now ?

I will not mind the LV clot , will go ahead with DC Shock . Let him dislodge his LV clot . If It is his fate let it be !
Defer the DC shock . Fall back on medical cardioversion like Bretyllium, Amiodarone or magnesium . After all . . . it is not a pulse less VT. He is not in cardiac arrest . He can afford to wait .We can’t risk a stroke .
Give a low energy shock 25 joules with paddles avoiding the LV apex. .It may not dislodge the apical clot , still VT may be terminated.
Try overdrive pacing instead of DC shock
Refer the patient for emergency surgical removal of LV clot
Suck out the LV clot with a LV suction catheter and plan elective DC version*
Insert a temporary Aortic filter and shock the patient **

* Such catheters are in preliminary stage of development . Is that true ? ( If no I should get the royalty for the idea ! )

(Read the related article in my blog )

** A loud imagination . Such filters do not exist.( If IVC can be filtered why not Aorta ? )

What was finally done ?

After analysing each of the above , we decided option one ( “Prey the God and shock the heart” ) After all if it is a VF , this issue becomes null and void ! . Luckily God was with us. The patient was reverted to sinus rhythm with 50joules and had no untoward events . He was subsequently anti-coagulated . He is being planned for CRT/ICD therapy

Final message

Critical care medicine is all about risk taking .Many times , therapeutic maneuvers confer a significant risk to life comparable to the index problem. But that should not be a deterrent . A careful learned decision is warranted.

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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