cardiology -Therapeutics | Dr.S.Venkatesan MD

Archive for the ‘cardiology -Therapeutics’ Category

A funny Arrhythmia called Acclerated Idioventricular rhythm

Posted in cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Arrhythmias, Uncategorized, tagged accelerated idioventricular rhythm, aivr, reperfusion arrhythmias, slow vt on March 31, 2012| 1 Comment »

Cardiac arrhythmias by nature connote a serious implication ,especially so with ventricular ones. Here is an arrhythmia which arise from the ventricle by excessive automaticity , fires independently , still very benign compared to others ventricular arrhythmias.

Why AIVR is a stable arrhytmia ?

Primarily due to its low rate.

Since it is a reperfusion arrhythmia the outcome is good.

Mechanism

It is not due to reentry , it is thought to be due to enhanced automaticity without pathological intra-myocytic calcium spikes (Like true VT )

Absence in surface ECG does not mean it is not existent. In-fact there is some evidence to call this arrhythmia as a form of ventricular parasystole.

Focus of arrhythmia

Since it is a reperfusion arrhythmia it has to arise somewhere from re-perfused myocardium.

The fact that it can occur in both RCA and LCA reperfusion indicate the focus can be in any of the ventricle .

Usually it follows the reciprocal rule of bundle branch block pattern (RBBB in LV focus LBBB in RV focus.)

Septal AIVR can have either RBBB or LBB morphology. Usually left axis is noted .

How to differentiate it from non sustained VT ?

Ventricular rate in AIVR should be between 60 -110 .(Note -The inherent ventricular rate is 35/mt .There is three fold acceleration )
Basic idoventricular rhythm is about 35. Three times accelerated
Characteristically AIVR starts with an escape beat rather than an ectopic beat .

AIVR is common in RCA or LCA reperfusion ?

It is supposed to be more common in infero-posterior MI as sinus slowing is an important predisposing factor for releasing the idio ventricular rhythm.

AIVR after primary PCI

Is not reported much as current interventional cardiologists do not bother much to watch about this arrhytmias

Other causes for AIVR

Myocarditis.
Digoxin toxicity

Management

(The commonest issue with AIVR could be . . . Nurses /Fresh interns may mistake it as VT and pressing the false alarm ! )

Rarely requires treatment .
Atropine ,Isoprenaline to increase sinus rate.

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Cardiology quotes : Failed thrombolysis and rescue PCI !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology quotes, cardiology- coronary care, Cardiology-Coronary artery disese, Quotes, tagged failed thrombolysis, rescue pci, stemi management on March 25, 2012| Leave a Comment »

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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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Well known secrets about post Infarct angina !

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, critical care ccu, tagged chest pian following stemi, ira angian, non ira angina, post infarct angina on March 22, 2012| 1 Comment »

Up to 24 hours

Failed thrombolysis and persistent infarct related chest pain
Prolonged Infarct pain in spite of successful thrombolysis (Rare)
Dual STEMI and Dual ACS ( Combination of STEMI/NSTEMI) *

* Generally until after 24 hours one should not make a second coronary syndrome though logically it is possible ( Dual acute coronary syndrome)

After 24 hours -up to 2 weeks

Post MI angina – IRA related (Re-occlusion, Threatened reocclusion)
Post MI angina -Non IRA related ( Critical non -IRA lesion)
Thrombus migration /Side branch occlusion
Re infarction -Same territory
Re-infarction-Remote territory
Infarct extension, Infarct expansion , Dyskinetic segments ( Acute ventricular remodeling has a potential to generate pain )
Combinations of the above

Caution

24 hour is arbitrary cut off .There can be spill overs and over laps

*Refractory non ischemic chest pain often atypical not relieved by anti anginal medication – Pericardits, Coronary dissections , myocardial /Pap muscle tears .

After thought

Do we need to break our brain to find the source of angina following STEMI ?

Principles of scientific medicine would demand it . However in this era of hyper active interventional cardiologists there is little purpose as they tend to open up all occluded arteries guided by the their ignorance about the source of chest pain.

Reference

Video on Dual coronary syndrome

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Fine art of thrombus suction in STEMI !

Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, tagged export catheter, primary pci, thrombo suction, thrombus aspiration, tornus catheter on February 29, 2012| Leave a Comment »

The key word for successful primary PCI is

Suction & Aspiration of thrombus with micro catheters like export catheters
One can do away with a stent during primary PCI but can never do away aspiration
Distal protection as concept is rapidly dying out as we aim to remove all the thrombus .

Tips for effective thrombus aspiration

Apply continuous negative pressure once catheter reaches the thrombus do not release it till you enter back into the guide.
Make sure you are sucking only blood products not the endothelium
Watch out for side branch spill over.
7F sheath 7F catheter ideal for aspirating with a micro catheter
Please be informed some thrombus require more negative pressure especially in the late presenters of STEMI

* During dire emergency when you do not have a specialized suction catheter do not hesitate to push even a diagnostic catheter into the coronary .We have saved few lives !

Crazy questions in primary PCI ( or Is it futuristic )

Can we connect the suction apparatus into LAD micro catheter ?

Do we have camera guided suction catheter ?

Can you flush the thrombus if you are not succeeding in aspiration ?

Is ultrasonic desiccation of thrombus possible ?

Acknowledgement

Some of the tips were gathered from the recently concluded India Live 2012 conference in New Delhi .

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Unusual arrhythmias during Excercise stress testing

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Clinical cardiology, tagged excercise induced vt, polymorphic vt during stress testing, prinzmetal angina, ventricular arrhythmias during stress testing on February 29, 2012| 4 Comments »

A young man fell off the tread mill soon after complaining of chest pain in the immediate recovery phase.

He had just completed 8 minutes of standard Bruce without any difficulty .

Even as the defibrillator was being moved near him , he was successfully shocked with hands of a hefty nurse ! ( 25 joules ? ) . He got into this rhythm !

Note the ECG shows diffuse ST elevation . The ECG soon settled and a diagnosis of variant angina was presumed.

He was shifted to CCU. There was no elevation of enzymes , though he showed a transient wall motion defect lasting up to 48 hours.

The subsequent elective angiogram did not reveal any critical CAD favoring Prinzmetal angina.

Provocative tests for vaso spasm is not practiced in our part of the world (I wonder whether it is still in vogue at all !)

* The classical angina of prinzmetal is not related to exertion . Can we call this as a variant of the variant angina ?

Final message

VTs are rare arrhythmias during EST. However , there are important link between exertion , VPDs and VT .
Exercise induced RVOT VTs are supposed to more common. However , ischemic VT during exercise has to be ruled out in every patient.
Non sustained VTs in patients who have baseline VPDs are usually benign .
Paradoxically VPDs disappear in many during exertion indicating overdrive suppression by sinus rate .This again can be ignored.
Mono morphic VTs would suggest structural defects.
Polymorphic VTs during exercise indicate either ischemia or electrolytic origin

Also read

Wrong concepts in coronary spasm

Acknowledgement

ECG Courtesy: Dr G.Gnanvelu MD,DM Professor of cardiology . Madras medical college

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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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Basic lessons in STEMI :Does dying myocytes release potassium into the circulation ?

Posted in cardaic physiology, cardiac physiology, cardiology -ECG, cardiology -Therapeutics, cardiology- coronary care, Cardiology-Coronary artery disese, tagged beta blockers and hyperkalemia, betablockers in stemi and hyperkalemia, ecg tall t waves hyperacute mi, electrolytes in stemi, hyperacute stemi, nernst equation animation, potassium levels in acute stemi, pottasium and stemi, resting membrane potential, why tall waves in stemi on February 10, 2012| Leave a Comment »

Human life is a bundle of energy orchestrated by ions coming in and going out of every cell . Potassium is the life sustaining ion which determines the resting membrane potential of our cells.

When the heart suffers a massive necrotic attack what would happen to the potassium dynamics inside the myocytes ?

K + is the dominant intracellular cation , when about 100 million myocytes die suddenly , a chaos in the potassium metabolism is expected is it not ? .

When skeletal muscles dies it releases potassium . We know this from typical crush injuries and rabdomyolyis.

It is more of a common sense to expect this . . . from myocardium as well .

Source : http://nernstgoldman.physiology.arizona.edu

Which ion is responsible for the current of injury ?

We know a strong and continuous negative current that emanates from the necrotic zone after STEMI . (It is so powerful it shifts the baseline itself !), We do not know yet what exactly is causing this current of injury . It goes without saying sodium should sustain the depolarisation wave but potassium will also have a major role in the propagation of this injury current.

Do dying myocytes excrete the potassium into the circulation   ?

Is    k+ a marker of extent of MI ?

What is the mechanism of hyper acute tall T waves in MI ?

Questions galore . . . Answers struggle !

When a large area of cardiac muscle goes for necrosis it leads to leaking   of K +    . If it is true , it is expected to be a marker for extent of infarct. In reality it is not . Why ? This is because cardiac potassium pool is much small . A leak from an organ which weighs 400 grams do not elevate the ECF potassium . Still , there is ample evidence for   K + to accumulate in the local intracellular milieu. (Myocardial hyper-kalemia ) In fact , one of the mechanisms suggested for tall T waves in hyper-acute MI phase   potassium excess .

Image courtesey hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

http://hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html

Potassium levels and incidence of ventricular tachycardia.

Many of the primary ventricular arrhythmias are due to acute ischemia . We have conflicting evidence for the effect of ischemia on QT interval. How does ischemia trigger VT ?
The answer to this question remain as a missing link ! . Grossly simplifying , one could suggest it is due to ischemic cell membrane damage that alters the ion channel function , resulting in intracellular accumulation of calcium and triggered activity .

What is the effect of potassium on cardiac contractility ?

Myocardial paralysis. (Please note it is the hypokalemia that primarily causes paralysis in skeletal muscles !)

It causes myocardial stunning a manifestation of local potassium leak ! A temporary myocardial paralysis.

What does the current guidelines of ACC/AHA state about potassium hemostasis in STEMI ?

It suggests a fairly aggressive maintenance of potassium levels to upper normal levels. Traditionally we are worried more about hypokalemia than the hyper. It is surprising we had the facts wrong . . . for so long !

What is new in the regulation of potassium level during STEMI ?

This landmark paper from JAMA seeks to set right the misconceptions about potassium during STEMI. It suggests K + levels has a U shaped morbidity curve in STEMI . One need to be cautious in correcting borderline hypokalemia . Serum K + is absolutely useless surrogate marker for myocardial K + . We do not know how K + behaves in the vicinity of MI zone . So extreme caution is required when giving IV K + supplements in coronary care units .

Watch out : Beta blockers /ACEI may worsen hyperkalemia

Early introduction of ACEI and ARBs is a strong risk factor for systemic as well as myocardial hyperkalemia . This is especially true in diabetic individuals who have low rennin levels due to diabetic micro circulation defect in kidneys .(Hypo-reninic hypo-aldosternosim )

Beta blockers are also known to raise potassium by two mechanism

1.Blocking rennin

2.Reduced uptake of K + in to the cells.

http://medicineforresidents.blogspot.in/2010/09/hyperkalemia-with-beta-blockers.html

Final message

In the management of STEMI , revascularization of the myocardium is considered as the only therapeutic aim . We need to realise it is much more than that . There are some subtle but important ways of resuscitating and protecting myocardium . Over indulgence in electrolytic management in coronary care is to be avoided.

Reference

Importance of sympathetic drive and potassium levels

http://www.nejm.org/doi/full/10.1056/NEJM198002213020803

http://ccn.aacnjournals.org/content/23/6/14.full.pdf+html

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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