myocardial disease | Dr.S.Venkatesan MD

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Right ventricle . . . more intelligent than Left ?

Posted in acute pulmonary embolism, Cardiac MRI, cardiac physiology, cardiac volume, Cardiology -Hemodynamics, Cardiology -unresolved questions, echocardiography, myocardial disease, pulmonary hypertension, Right ventricle, tagged every thing about right ventricle, fontan principle, mechansim of rv clot formation, right ventrcular dysfunction, right ventricle, right ventricle hemodynamics, right ventricle hypertrophy vs dilatation, right ventricle physiology, right vs left ventricle, rv clot in rv apex, rv failure, rv infarction, rv inflow vs outflow, rv outflow body inflow apex, shape size and funcion of right ventricle on July 20, 2014| Leave a Comment »

The right ventricle is considered as a docile cardiac chamber with passive filling and emptying properties .

This belief was reinforced when Fontan in early 1970s suggested a principle in the management of cyanotic heart disease when the right side of the heart is underdeveloped. He proved RV can be by-passed safely , with great veins (IVC/SVC) by themselves take care of filling the pulmonary circulation without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading concept. In clinical cardiology practice ,sudden or non sudden RV deaths happen every day in the form of . . .

RV Infarction
Acute RV dysfunction in massive pulmonary embolism
COPD with RV dysfunction
Most cases dilated cardiomypathy the terminal event is due to RV failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and hemodynamics . We are getting more insights from modern blood pool imaging by MRI , about how the RV handles the blood volume .

I stumbled upon this excellent work by Alexandru G. Fredriksson published in APS (American physiology society ) This MRI study have documented RV fucntion in a dramatic fashion.

We know RV has a unique shape triangular ( partially pyramidal ) . It can be inferred the RV cavity is formed by fusion of many eccentric spacial planes. We have always believed RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.

It is curious to know RV inflow is connected to the outflow by an invisible physiologic Bridge . About 44% of blood traverse the RV in this fashion.

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/

Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical function of RVOT could be most vital. If it fails to handle the first increment which comes directly from RV inflow, stasis is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

Differential dilatation RV chambers to pressure or volume overload is observed .
We need to analyse why RV dilates in some but goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
RV apical clot in restrictive cardiomyopathy is a direct consequence of stasis of blood in RV apical zone .
RVOT pacing may have a hemodynamic advantage over RV apical pacing . However , for anatomical reasons RV apical pacing is far safer than RVOT pacing where the lead is subjected to constant life long strain due to this busy RV inflow to outflow express high way !

Final message

Traditionally we have labeled RV as a passive venous chamber .It is clearly a misnomer.It has to handle both the venous and pumping function beat to beat with precision without back log .Obviously , RV has to think and work more than it’s big brother !

Reference

I wonder , if there is any other site other than APS . . . to find crucial answers in cardiac physiology !

After thought

There is huge gap between physiologists who work in research labs and the physicians at bed side .
I appeal all young cardiologists to visit APS once in a while ,between your busy cath lab schedule and help narrow this gap.
Without understanding the physiology properly how are we going to intervene the pathology ?

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What are the patterns of RV enlargement in various clinical entities ?

Posted in cardiology congenital heart disese, Clinical cardiology, myocardial disease, Right ventricle, tagged arvd, ebstein anomaly, epigastric pulsation with rvh, how is rv in various heart disease, infundibular dilatation, para sternal lift, parts of right ventricle, right ventricle, right ventricle in tof, rv in tricuspid atresia, rv inflow body out flow, rv morphology in various congenital heart disease, rvot dilatation on September 30, 2013| Leave a Comment »

Right ventricle is a passive venous component of the heart .It simply acts a transit pump for blood to reach the lungs.

It is true , RV is dispensable in many complex congenital heart disease as we can connect the great veins directly into the pulmonary artery by Fontan , Glean and it’s clones bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated. RV dysfunction and failure is the key to survival many disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has three different parts connected by three different angle .There is no true apex for RV , it is connected to Inflow and outflow in peculiar fashion .

In the following table I have tired to describe of how different parts of RV behave in various disorders.

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How to diagnose DCM with confidence by myocardial scar photography ?

Posted in Cardiac MRI, Cardiology -unresolved questions, myocardial disease, tagged cardiac mri, demri, epicardial scars, how to differentiate ischemic from non ischemic dcm, late gadolinium enhancement, lge gadolinium, mid myocardial scar, myocardial scar Imaging, scar location within myocardium, subendocardial scars on September 30, 2013| Leave a Comment »

While many of us are preoccupied with wires and balloons ,( coronary myopia ! ) , our radiology colleagues are making rapid strides . Let us spend some time to understand how the myocardial segments are inflicted the final insult . We need to realize , there is a pattern to this myocardial end game of scarring and fibrosis.

MRI is the gold standard to assess the myocardial architecture . It has a role in both assessing the anatomy , function , perfusion and viability .

LV function is assessed by cine MRI
Viability stud by delayed enhancement MRI (DEMRI , also called as LGE- Late Gadolinum enhancement )
Myocardial scar best assessed by DEMRI*

* Why do you require DEMRI to identify scar ?

One can detect scars in plain MRI but contrasts make it better .Hence delayed enhancement in by DEMRI is used to detect scars.

Is it ischemic DCM or Non ischemic DCM ? ( That is the question we commonly ask

We rely too much on CAG anatomy for this. It can be misleading. Cine MRI with DEMRI gives the answer straightway with high degree of accuracy . CAG is required in all , but if it is normal , or has insignificant lesions , the dilemma of ischemic DCM would continue !)

**Note ,there is one simple algorithm proposed by the author to differentiate Ischemic DCM from Idiopathic DCM without MRI – Click here to Link

Following scar patterns in DEMRI help us to arrive a diagnosis.

Favors Non ischemic DCM

Mid myocardial scar
Epicardial scars
Global sub-endocardial scars
No scar(Ironically if no delayed hyper-enhancement is noted it is likely to be non Ischemic DCM )

Favors ischemic DCM

Regional transmural scars
Localised sub-endocardial scars

* Ischemic DCM will always involve subendocardium as ischemic wave front goes from sub-endo to epicardium.

examples for Non Ischemic DCM

Amyloidosis (Can be restrictive as well )
Chagas
Fabrys

Why is scar localisation and Quantification important ?

Apart from differentiating various cardiomyopathies it has few clinical implication .

Since scar indicates irreversible damage , if extensive it will argue against any re-vascularisation .
Scar location becomes vital if we plan CRT .It will be futile to place a CRT lead over a scar.
Scars are often form a macro re-entrant circuits for VT .Help us localize or zeroing in VT focus.
Scar quantification is helpful risk stratification of patients with HOCM .and their family.

Final message

Myocardial scar location and quantification is the new mantra in a patient with dilated heart with cardiac failure.

It may be more important than even a coronary angiogram .MRI will prevail over any of the available echocardiogram modalities to assess the scar pattern.

Reference

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What is the mechanism of Apical Ballooning in Takotsubo cardiomyopathy ?

Posted in myocardial disease, tagged takotsubo cardiomyopathy, What is the mechanism of apical ballooning syndrome on August 31, 2013| Leave a Comment »

Takotsubo cardiomyopathy is an unusual response of the left ventricle to extreme emotional stress .The catecholamine surge has a profound stunning effect of LV apex and a paradoxical hypercontractility of basal LV.

The exact mechanism is not clear , Following factors may contribute.

Multi-vessel coronary artery spasm,
Cardiac microvascular dysfunction.
Abnormal myocardial fatty acid metabolism,
Reperfusion injury after an ACS *

However , the most accepted mechanism is Endogenous catecholamine-induced myocardial stunning and microinfarction

Why is LV apex alone affected ?

Image Source- http://www.radiologyassistant.nl

The adrenergic receptor distribution is high in LV apex .They are exposed to high concentration and gets stunned easily . Basal LV has less adrenergic innervation , so it shows less of catecholamine toxicity , instead it exhibits. hyper-contractile mode. However, this rule is not absolute.

One more suggestion was apical balloons correlated with wrap around LAD.(Báñez B et all 2004)

what is the mechanism of apical ballooning syndrome 2 takotsubo cardiomyopathy

Image courtesy Circulation December 16/23, 2008 vol. 118 no. 25 2754-2762

*Some consider ACS should never be linked to Takotsubo.But it is not easy to differentiate.(Carrillo JACC 2009) (Kosuge JACC 2010)

Reference from this site

https://drsvenkatesan.wordpress.com/2012/05/27/in-extreme-mental-stress-left-ventricle-becomes-a-banana/

Reference from other journals

what is the mechanism of apical ballooning syndrome takotsubo cardiomyopathy

1.Báñez B, Navarro F, Farré J et al. (2004). Tako-tsubo syndrome associated with a long course of the left anterior descending coronary artery along the apical diaphragmatic surface of the left ventricle.]”. Revista española de cardiología (in Spanish; Castilian) 57 (3): 209–16

2.Carrillo A, Fiol M, Garcia-Niebla J, Bayes de Luna A. Electrocardiographic differential diagnosis between Takotsubo syndrome and distal occlusion of LAD is not easy. J Am Coll Cardiol. Nov 2 2010;56(19

3.Dorfman TA, Iskandrian AE. Takotsubo cardiomyopathy: State-of-the-art review. J Nucl Cardiol. Jan-Feb 2009;16(1):122-34

4.Kosuge M, Ebina T, Hibi K, Morita S, Okuda J, Iwahashi N. Simple and accurate electrocardiographic criteria to differentiate takotsubo cardiomyopathy from anterior acute myocardial infarction. J Am Coll Cardiol. 2010;55(22):2514–6. doi: 10.1016/j.jacc.2009.12.059.

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Emergency cardiology consult for Acute abdomen !

Posted in cardiology -ECG, Clinical cardiology, myocardial disease, tagged Ascites, Gross obesity, inferior mi differential diagnosis, pancreatitis and q waves in ecg, q waves in inferior leads on July 18, 2013| Leave a Comment »

The other day my fellow got a call from surgical ward for emergency ECG opinion for a suspected Inferior MI .It later turned out to be an acute cholecystitis.

One of the important anatomical mis-perception among physicians , is to consider inferior, posterior and diaphragmatic surface of heart as separate entities .They are all closely linked.In fact, they more often mean the same anatomical zones !

Heart is a dynamic suspended organ within the middle mediastinum .It can assume a vertical or horizontal position due to number of surrounding anatomical and physiological factors. (Diaphragm, Lung , being important ).The ratio of intra thoracic vs Intra abdominal volume & pressure determine whether the posterior surface of the heart is going to face the back of chest or simply sit and rest on the diaphragm .We know a horizontal heart is likely to inscribe q waves in inferior leads .

acute abdomen diaphragm inferior wall mi cholecystitis pacreatitis

Courtesy : Basic image source from digitallab3d

The diaphragm can be termed as an anatomical causeway , that isolates thorax from the abdominal cavity .Close encounters between the organs separated by this delicate biological membrane is always possible .This is especially true for electrical signals which show little respect for anatomical barriers .

This is the reason there are too many abdominal conditions that mimic inferior MI during a painful emergency (and vice versa when inferior MI mimics acute abdomen .) In our department , we have witnessed the following conditions mimicking Infero-posterior ACS.

Acute ascites with polyserositis
Gross obesity with APD
Posterior fat pad ( Necrosis ?)
Thickened pericardium
Minimal posterior pericardial effusion
Diaphragmatic pleurits
Esophageal spasm
Fundal air trapping and ballooning after a heavy meal !
Acute duodenal ulcer perforation ( With gas under diapharam causing q waves)
Acute cholecystits
Diphragmatic hernia
Achalasia cardia
Pancreatitis

Final message

Do not rush to make a diagnosis of inferior wall MI when you encounter inferior q waves with or without ST /T changes , especially when the symptoms are atypical .

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Ignorance at it’s best :The Adrenal connection of dilated cardiomyopathy ?

Posted in cardiology -Therapeutics, myocardial disease, tagged ignorant dilated cardiomyopathy, irreversible dilated cardiomyopathy, pheochromocytoma and dilated cardiomyopathy, reversible cardiomyopathy on December 25, 2012| Leave a Comment »

The popular clinical entity Idiopathic dilated cardiomyopathy is often a “dust-bin diagnosis” . The fact is the word idiopathic simply reflects our ignorance.

For God nothing is idiopathic . . . he knows how each and every cell would behave .

so , when a patient presents with progressive dilatation and heart failure refractory to all medical therapy he is termed as idiopathic and posted for heart transplantation. And only later , we realize the whole thing is due a terrible form of reversible DCM . That is pheochromocytoma induced DCM , which recurred again in the transplanted heart. What a costly Ignorance ?

pheochromocytoma and dilated cardiomyopathy reversible dcm tachycardic

Image courtesy and source http://www.dreamstime.com.

Is sub- clinical pheo like situations rampant ?

We know that high levels of both epi and nor- epinephrine circulate in cardiac failure . We presume it to be a secondary effect .

How can we so sure about it ? There is a distinct possibility of adrenal gland hyperfunction and hyperplasia in all DCMs (Idiopathic or ischemic ! ) The dramatic beneficial effects of beta blockers in cardiac failure will vouch for it .

So , It remains a fertile filed for the youngsters to explore . . . the hyper adrenergic mediated reversible component of any cardiomyopathy and cardiac failure .

Final message

The default approach in any patient with progressive / refractory cardiac failure should be , to consider whether they fit into any form of reversible myocardial disease . What is idiopathic in remote clinic of your distant country side may be well recognized secondary cardiomyopathy . The irony is , even sophisticated university hospitals many times miss the true etiology as in the above case report .

So, the term Idiopathic dilated cardiomyopathy (iDCM ) may aptly be named as Ignorant forms of DCM , with an attractive abbreviation . . . iDCM

Reference

1.J Surg Educ. 2009 Mar-Apr;66(2):96-101. doi: 10.1016/j.jsurg.2008.11.004. Pheochromocytoma presenting as acute severe congestive heart failure, dilated cardiomyopathy, and severe mitral valvular regurgitation: a case report and review of the literature.

2.Kelley SR, Goel TK, Smith JM.Prog Cardiovasc Nurs. 2005 Summer;20(3):117-9. Pheochromocytoma presenting as heart failure.

3.Pheochromocytoma masquerading as a cardiomyopathy. Garcia R, Jennings JM. Am J Cardiol. 1972 Apr;29(4):568-71.

4. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1894695/pdf/20070600s00025p244.pdf

5. http://downloads.hindawi.com/crim/medicine/2011/596354.pdf

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How do you assess LV diastolic function in the presence of Atrial fibrillation ?

Posted in Cardiology -unresolved questions, echocardiography, Hemodynamics, myocardial disease, valvular heart disease, tagged atrail fib as a marker of diastolic dysfunction, atrial fibrillation and diastolic dysfunction, e a ratio, grading of diastolic dysfunction, LV diastolic dysfunction on July 31, 2012| Leave a Comment »

Doppler Mitral Inflow velocity profile is the key to assess LV diastolic function . The ratio between E and A has become most popular parameter .

In the absence of atrial contraction what shall we do ?

The answer is simple . We have 2 D parameters of LV diastolic function.

LA dimension ( > 30 % basal dimension which is usually > 4 cm ) is a most specific marker of diastolic dysfunction in the absence of mitral regurgitation or stenosis.

The only available velocity E wave profile can help .A short E deceleration time in a short cycle would suggest significant diastolic dysfunction.High amplitude E wave > 2 M/sec in the absence of MR will suggest diastolic dysfunction .

Curiously , it can be assumed an episode of lone AF per-se , be an indicator of diastolic stress for the left atrium .

After all , why should a person all of a sudden develop an episode of AF .(Hypoxia, Ischemia , excluded )

Other parameters.

Mitral annular velocities / E propagation velocity / E/E’ are other tissue Doppler parameters can be used.

Pulmonary venous flow velocity is largely not useful (Since A reversal does not occur )

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Tips in clinical cardiology : Differential diagnosis for constrictive pericarditis .

Posted in Cardiology - Clinical, cardiology -Therapeutics, myocardial disease, pericardial disease, tagged constrictive pericarditis, deep y desend, differential diagnosis of constrictive pericarditis, pericardial knock, restrictive cardiomyopahty, square root sign on June 14, 2012| 3 Comments »

A patient who presents with predominantly right heart failure is an interesting clinical challenge . Constrictive pericarditis (CP) remains a popular diagnosis in this setting. However in the bed side clinical examination (and in cardiology Board exams ) the following differential diagnoses are to be considered .( And ruled out one by one)

Restrictive cardiomyopathy* especially Right sided .In India endo myocardial fibrosis tops the list
Primary Tricuspid valve disease( Tricuspid stenosis / Carcinoid etc)
Chronic cor-pulmonale in terminal RV failure
Silent Mitral stenosis with right heart failure
Ebstein anomaly
Severe forms of valvular pulmonary stenosis with RV dysfunction
SVC obstruction
Cirrhosis of liver
Porto pulmonary hypertension

( The list is not complete , readers may contribute )

Bed side clues

Remember a deep “y” descent is the bed side counter part of Square root sign recorded by invasive RV pressure study
Similarly , pericardial knock is the auditory equivalent (You hear the square root ! . . .yes )as the ventricle thuds the rigid thickened pericardial shell in very early diastole !)
Pulsus paradoxus and kussmal sign can occur in both CP and RCM.
If a good LV apex , is palpated it goes against CP .
Please be reminded , even restrictive cardiomyopathy will ultimately dilate their chamber pre-terminal and clinical features may be confounded with that of DCM.
Silent heart would suggest CP.
AV valve regurgitation would favor RCM
Features of Pulmonary hypertension will help confirm Mitral valve disease , Cor pulmonale,
Deep “y”descents are against any form of Tricuspid stenosis.
Opening snap of mitral valve is to be distinguished from pericardial knock.( Opening snap high pitched and occur later than pericardial knock in diastole , best heard in expiration )
Cirrhosis liver with hypo- proteinimic fluid retention is a traditionally close mimicker .It may be ruled out by the careful history taking as exertional dyspnea is an exception , if at all , it is a very late event in cirrhosis.
The issue gets further weird as chronic constriction can lead on to chronic congestive liver and cardiac cirrhosis .
Severe forms of constriction can invade the myocardium and result in features of myocardial dysfunction .It is more common than we recognise.

How to confirm ?

Following should be performed in that order

ECG
X -Ray
Echocardiogram
CT scan
MRI

*Cath study is no longer done (Only for academic purpose )

Final message

Even in this era of sophisticated medical imaging , clinical examination remains the key . One should realise the importance of meticulous clinical history , sequential examination and interpretation .It will “rule out or rule in” majority of cardiac disorders .

The hi tech imaging modalities should be used only to confirm , risk stratify and plan management . If you skip the clinical part , one may still arrive at a correct diagnosis but there is high chances of erring in management.

(Cardiac pearls lie in the bed side not in cath labs ! Here is one such pearl . Not every constriction require surgery !

Please note about 20 % of constrictive pericarditis are transient !)

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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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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