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Posts Tagged ‘angina’

Now , some one wanted to know,  Can we diagnose unstable angina without Chest pain ?

Crazy question isn’t , Angina by definition  should have chest pain .There is nothing called silent angina , only silent Ischemia  .

  • We know Ischemia can occur silently .
  • We also know STEMI can occur silently (About 10 % of MI do occur without any symptoms )
  • If STEMI occurs  silently  why not UA/ NSTEMI combo ? (Collectively called as  NSTE-ACS)

The debate goes like this .If stable angina can present with equivalents ? what prevents  “Unstable angina”  to present with  Anginal  equivalents without chest pain ?

If  a diabetic patient who had a silent MI in the past  . . .  subsequently  experience  severe episodes of resting ischemia  , will he feel the pain , that is supposed to occur  with his  “unstable angina”  or not ?

Hmm , difficult to guess right,   So it seems highly plausible  UA/NSTEMI  do  occur silently ! Literature hasn’t looked into this specifically. Chest pain is built integral  into definition of UA , infact it is a symptom  complex rather than an disease entity by itself, while NSTEMI is ECG and enzyme combo ! Making the term  NSTE-ACS  look  perfect.

Any other technical explanation ?

The concept of Ischemic cascade says angina occurs last, well after biochemistry , wall motion defect and ECG , hence its distinctly possible for UA/NSTEMI present to be painless !

Final message

Anginal pain perception is related to intactness of neurogenic circuits and also probably the severity of Ischemia.If full thickness myocardial necrosis can be painless in few, nothing prevents from an episode of UA/NSTEMI  be truely painless .

Clinical implication of this conundrum

Can we admit a patient as UA/NSTEMI with out chest pain ?

Yes, it would seem so .

No, we can’t .

Indeed we can , if ECG changes are there .

No, we can admit even with normal ECG if its real unstable angina.

This is the crux of the problem in ERs all over the globe. Our knowledge base is simply not good enough. Every one of us has seen Troponin positive silent NSTEMIs ! but . . . to me still something is missing in the link .

Modern day approach 

Pain or no pain,any  fresh ECG changes ( Both T and ST shifts*) should be rushed to cath lab.Whenever you are not sure .Always better to err on the side of over investigation.That’s the mantra ! So ,you do an Angiogram , find an Incidental intermediatroy lesion which may not be responsible for the ECG changes but you are compelled to go after it FFR//iFR , OCT, IVUS and so on !

*There is huge list of non Ischemic ST/T shifts in ECG that can be read elsewhere .

Counterpoint

Can’t agree with this article. Foolish to diagnose UA without chest pain. Never  treat ECG  in isolation unless its a convincing  ST elevation or depression with clinical input and thorough scrutiny of  past record . Realise , how important is  the basics principles of medicine taught  by Oslers and Cushings a  century ago.

 

 

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We know cardiac pain is often  referred to Jaw and neck .

What prevents the neck pain of cervical spinal disease to be referred over the  heart ? Can pure spinal lesions mimic angina ?

The answer seems to be “Yes” . The neuronal  circuit is  there .Only , the traffic has to be reversed. Medical logic is always puzzling. There is indeed an entity called cervical angina.

The cardiac pain  can be  referred any where between  dermatomes  C3 to T 10 It is generally  believed cervical radicular pain  can go only one way . . . ie towards the nape of neck and  arms .Dermatomal overlap ,neural cross talks  thalamic inputs and cortical  reflection and perception always make the subject of referred pain too  complex.

Now,It seems possible ,the neck  pain can  spill over into the anterior chest wall ,mimicking  angina .Imagine the  confusion  if the patient  has both  cardiac and cervical entities ! Does the pain signals from the two sites  collide in the local spinal network ? Does one extinguish or amplify the other ?

 

refered pain

This article which was published  in the Spinal Cord .

cervical angina  reverse referral pain

Read also linked angina

http://www.nature.com/sc/journal/v44/n8/pdf/3101888a.pdf

 1.Guler Net al.Acute ECG changes and chest pain induced by neck motion in patients with cervical hernia: a case report. Angiology 2000; 51:861–865.
2.Wells P. Cervical angina.Am Fam Physician1997;55 2262–2264.
3.Jacobs B. Cervical angina. NY State J Med 1990;90: 8–11.
 4.Baba H et al. Late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. spine 1993;18: 2167–2173.

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Stable angina is graded by Canadian cardiovascular society classification ( CCSC ) by 4 grades. Angina at rest  usually  denotes unstable angina. But,  patients with stable angina  may also experience rest angina according to CCSC ,  still this is   not considered as  unstable angina by many . Post prandial angina is one such  example.

Few consider post prandial angina as unstable angina . This sort of reasoning can not be faulted .

In  the logical sense ,  we are dealing with varied  categories of unstable angina.  The importance of diagnosing unstable angina is to intervene early ,  so that we can avoid  major adverse outcome .

The problem in CAD is , often , the plaques and angina do not  obey the conventional  rules  !

.The following permutations and combinations could be  observed in any coronary care unit .

  1. Unstable angina –  stable plaques  – stable ECG – stable patient
  2. Unstable angina – unstable plaques  –  unstable patient
  3. Unstable Angina  – unstable plaque  –  stable patient
  4. Stable Angina –  unstable plaque  –  unstable patient
  5. Stable angina  –  stable plaque  –    stable patient
  6. Stable angina –  unstable  plaque  – stable patient

Among the above 6 categories  2nd  is   probably  the most dangerous group and category 5 is most benign.

Post prandial angina is a serious  form of angina.It implies  , even   diversion of  little blood to GI system immediately after a meal can provoke an episode of  ischemia  .This infers a  very tight  lesion somewhere in the coronary tree,  very often it could be the  left main or proximal LAD.

Of course ,  there is  another mechanism for post prandial angina, namely GI neurotransmitters  like gut peptides acting as a coronary vasoconstrictor.

Snippets on  post prandial angina  .

It is also recognised , post prandial angina occurs more often during dinner, followed by lunch and breakfast. Carbohydrate foods are  more likely to precipitate it .

Does PPA cause ST depression ?

Logically it should .In reality It happens in few .

How to manage it ?

It is very important to recognise , even though this article  argues  for including  PPA  as UA, there is no acute thrombotic process during  an   episode of  post prandial angina . In fact , it is  more of a secondary UA due to altered  blood flow pattern.

So , do not admit these patients  in CCU and administer  heparin or 2a 3b blockers.  (Unless of course ,they have other forms of rest angina )

Link to reference

1 PP angina angiographic correlation

2.Effect of carbohydrate diet on postprandail angina

3.Hemodynamics of eating !

Final message

Post prandial angina has all the characters  of a severe form of angina  .There  is every reason to label it as UA .It is suggested , ACC,ESC, AHA  should consider including  post prandial  angina as  UA or at least  UA equivalent .This would help intervene this entity early.

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Pulmonary embolism is  one of the  important  causes of acute chest pain . It can mimic  acute coronary syndrome . In fact along with aortic dissection  , it forms  a  differential diagnosis for STEMI especailly if the ECG is not typical.

pulmonary embolism chest pain dvt d dimer ventilation perfusion

The Chest pain of acute pulmonary embolism can originate in one of the following structures  with different mechanism

  • Lung parenchyma ( Necrotic pain ?)
  • Pluritic pain in adjacent necrotic segment
  • Main Pulmonary artery and it’s branches
  • Right ventricular mechanical stretch
  • Right ventricular ischemia
  • Hypoxia induced LV ischemia with coexisting CAD.
  • Multiple contribution from any of  the above *

It should also be remembered , medicine never respects logic, as some times  an episode of pulmonary embolism can occur without any chest pain

Localisation of chest pain

One can imagine ,  how difficult for the  nervous system to zero in on the origin of this  pain as  the structures involved in acute pulmonary embolism are in different planes  and in different depths  within the chest cavity . Patients  often complain vaguely  the site of pain but  what is universal is severe resting pain deep within the chest . If the ischemic lung segment  transmit pain signals , the location and radiation depend on the  bronchpulmonary segment involved.This again adds on to the complexity in the  genesis of pain  .It can be virtually any where in the back or front of chest.

But , the central and retrosternal chest  pain are equally common as invariably the central pulmonary arteries go for a acute stretch which can be severely painful .In fact , current thinking is it could contribute maximum  for the intensity of chest pain. Similarly,  acute dilatation of RV result in mechanical pain. RV sub endocardial ischemia may   also contribute .An intact bronchial  circulation( From aorta)  can limit the  ischemic lung pain .

Final message

Analysing  the chest pain of acute pulmonary embolism can be an  interesting academic exercise . It could arise from multiple structures with different mechanisms. It may not be much significant with  reference to management . But it has a diagnostic role.  A pain which is severe , and  atypically located should raise the suspicion of acute PE especially  if the patient has associated dyspnea.

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Coronary arterial spasm is a commonly discussed entity  in clinical cardiology. Originally described by prinzmetal decades ago .It was reported to occur only in coronary care units as variant angina .There is nothing called stable spasm every episode of spasm is considered as unstable angina.

How common is coronary artery spasm ?

This condition thought to be very  common during ACS , but  notoriously difficult to confirm.In fact many of episodes are clinically suspected and never confirmed. There has been lot of provocative tests for confirming coronary spasm like ergonavine etc.None of these tests were  neither useful nor practical.

What are the clinical situations where coronary spasm occur ?

Old concepts die hard.Most of us believe , the most common cause for coronary spasm is prinzmetal’s  angina ie , angina   in normal coronary arteries or  with minimal lesions .Clinical experience ,  has taught us coronary spasm can occur in all spectrum of acute coronary syndrome or even chronic coronary syndromes.

Some believe every episode of STEMI will have a component of coronary spasm.

In NSTEMI/Unstable angina spontaneous coronary spasm is an important pathogenetic mechanism

Now,  we witness transient coronary artery spasm in the cath lab due to catheter and other hard ware.The spasm  here  , is secondary to mechanical stress and this in no way related to the coronary spasm described by prinzmetal in the pre cath era.

What is the link between coronary spasm and electrocardiogram ?

The most common  fallacy among  coronary care physician is , if it is spasm  there must be ST elevation

The classical cardiology teaching all over the world , has been so powerful  this myth continues to prevail over . The fact  of the matter is ,  the  coronary arterial spasm  , can never have any direct impact on the ECG. (Unless , coronary smooth muscle generate ST currents !)  . So , whatever  be  the effect of spasm it  is through it’s effect on the myocardial  blood flow.

Hence ,  it is not the coronary artery spasm that will dictate  the movement of ST segment . It is the impact of myocardial blood flow  to the layers of the myocadium  namely , endocardium, epicardium  , epicardium (  or a combination of  the above )  that will dictate ST segment dynamics.

What are the  the ECG features of coronary artery spasm ?

It can be

  1. ST depression
  2. ST elevation
  3. Only with T wave changes (Tall or Deep T invrsions)
  4. Flattish ST segment  or  rarely , entirely normal ECG indicating balanced ST forces

Among this , the most common manifestation of coronary spasm is thought to be ,  subendocardial ischemia and resultant ST depression .This classically occur in many cases of NSTEMI/UA .

This makes  ST depression  the dominant manifestation of spasm  ,

How coronary spasm can elevate the ST segment ?

If it  can   induce a transmural ischemia  it  can elevate a ST segment . Does  all episodes coronary spasm result in transmural ischemia ? No,not at all .in fact it happens very rare  as we have already seen .

To result in transmural ischemia , the spasm should be total &  sustained ,   at least for few minutes   to   completely   occlude  the blood flow .

Milder forms of spasm can elicit only  a  sub endocardial ischemia  that  depress the ST segment.

*There is a rare variety of spasm where subepicardium is more affected than endocardium and hence ST elevation may occur.

What is the effect of Nitroglycerine on coronary spasm ?

This is a very powerful coronary spasmolytic agent.We can witness it’s action more vividly in cath lab .

It brings back the ST segment to neutral position , from either a elevated or depressed state  .Many believe , ( may it’s a fact ) much of the early  benefit of angina relief in UA/NSTEMI is  amelioration of coronary spasm

Is coronary spasm a neural event or a biochemical event ?

The exact  answer is not known .It should be chemicals as  neural  signals are also mediated by chemicals.

What are the biochemical mediators of coronary spasm ?

  • Smooth muscle calcium : Calcium flux is the immediate cause for spasm
  • Mediators .Neural :Catecholamine ,
  • Thrombus  secretes  Thromoxane A2  which is a powerful vasoconstrictor

Smooth muscle calcium

Is  coronary vasoconstriction  and  coronary spasm  are synonymous ?

Both terms are synonymous . Vasoconstriction is often used to refer  constriction of  microvasculature

while  spasm  often describes  the event in large  epicardial vessel. Some times the term coronary vasomotion is used to describe  fluctuating coronary arterial tone.

What are the determinants of coronary artery spasm ?

  • Location (RCA>LCA)
  • Lesion characteristics -Eccentric overhanging lesion can trigger a spasm by  the plaque ‘s weight.
  • Thrombus content
  • Acuteness of the event
  • Adrenergic tone and nerve activity
  • Concomitant betablockade  .  Theoretical risk ?

What are the types  of coronary spasm ?

  • Discrete ring or band like  spasm
  • Segmental
  • Diffuse long segment  spasm
  • Multilevel spasm in same coronary artery
  • Pan coronary spasm entire vessel (rare)
  • Remote spasm away from catheter tip

Unanswered questions in coronary spasm

Can a totally normal  coronary artery go for spasm all of a sudden ?

It is thought to be rare. Even in prinxmetal series some amount of atherosclerosis was documented in most patients.

What is the relationship between spasm and adjacent lesion ?

Spasm following PCI :Can spasm crush a stent ?

Can a  coronary collaterals go for spasm ?

Logically  Spasm  can  occur  coronary collaterals .But it is difficult to document .coronary collaterals eventhough  has three layes as that of artery (Intima, media, adventia) th medial smooth muscles are less sparse. Advential lack vasa nervorum and hence neural input is less.So spasm is a rare event in coronary collaterals

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NSTEMI  constitutes a  very heterogeneous population .The cardiac   risk   can vary  between very low to very high .  In contrast ,  STEMI patients  carry  a high risk for  electro mechanical complication including   sudden death .They all need immediate treatment  either with  thrombolysis or PCI to open up the blood vessel  and salvage the myocardium.

The above concept , may  be true in   many situations  ,  but what we fail to recognize   is  that ,   STEMI   also  is  a heterogeneous clinico pathological  with varying risks and outcome !

Let us see briefly ,  why this  is very important  in the management of STEMI

Management of STEMI  has undergone great  change  over the past 50 years and  it is the standing example of evidence based coronary care in the modern era ! The mortality  ,  in the early era was around 30-40% . The advent of coronary care units, defibrillators, reduced the mortality to around 10-15%  in 1960 /70s . Early use of heparin , aspirin   further improved the outcome .The inhospital mortality  was greatly  reduced to a level of  7-8% in the thrombolytic  era. And ,  then  came the interventional approach, namely primary PCI ,  which is now considered the best form of reperfusion when done early by an experienced team.

Inspite of this wealth of evidence   for the   superiority  of PCI  , it is only a fraction of  STEMI patients get  primary PCI   even in some  of the  well equipped centers ( Could be as low as  15 %)

Why ? this paradox

Primary PCI   has   struggled  to establish itself  as a global  therapeutic concept  for STEMI ,   even after   20 years of it’s introduction (PAMI trial)  .  If we  attribute ,  lack of   infrastructure  , expertise are  responsible for this low utility of primary PCI , we are mistaken ! There are so many institutions , at least in developing world ,   reluctant to do primary PCI  for varied reasons.( Affordability , support system , odd hours ,and finally perceived fear of untoward complication !)

Primary PCI may be a great treatment modality , but it comes with a inherent risk related to the procedure.

In fact the early hazard could exceed the potential benefit in many of the low risk STEMI  patients !

All STEMI’s are not  same , so all does not require same treatment !

Common sense and logic would   tell us any medical condition should be risk stratified before applying the management protocol. This will enable  us to avoid applying “high risk  – high benefit”  treatments in low risk patients . It is a great surprise,  the cardiology community has extensively researched to risk stratify NSTEMI/UA   ,  it has  rarely  considered risk stratification of STEMI before  starting the treatment.

In this context , it should  be emphasized  most of the clinical trails on   primary PCI  do not address  the clinical  relevance and the  differential outcomes   in various  subsets of  STEMI .

Consider the following two cases.

Two young men with STEMI  , both present within  3  hours   after  onset of symptoms

  1. ST elevation in V1 -V6 , 1 , AVL   ,  Low blood pressure , with severe  chest pain.
  2. ST elevation in 2 ,3, AVF , hemodynamically stable , with minimal  or no  discomfort .

In the above example,   a  small inferior  MI by a distal RCA occlusion  ,  and a proximal LAD lesion jeopardising entire anterior wall , both  are  categorized as STEMI !

Do you want to advocate same treatment  for both ?  or Will you  risk stratify the STEMI and treat individually ?  (As we do in NSTEMI !)

Current guidelines , would  suggest PCI for both situations. But , logistic ,  and real world experience would clearly favor thrombolysis for the second patient .

Does that mean,  the second patient is getting an inferior modality of treatment ?

Not at all . In fact there is a strong case for PCI being inferior in these patients as the risk of the procedure may far outweigh the benefit especially if it is done on a  random basis  by  not so well experienced cath lab team.

(Note : Streptokinase  or TPA does not  vary it’s action ,  whether given by  an ambulance drive or a staff nurse or even a  cardiologist !  .In contrast ,  the infrastructure and expertise have the  greatest impact on the success and failure  of PCI )

Final message

So , it is argued the world cardiology societies(ACC/ESC etc)  need to risk stratify STEMI (Like we do in NSTEMI ) into low risk, intermediate risk and high risk categories and advice primary PCI only for high risk patients.

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Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While  ,the former generally is considered   innocuous  the  later conveys a sinister  signal to the patient as well as  the physician. 

Why stable angina is  stable ?

In stable angina

  • The patient knows how the pain is going to behave by his past experience.
  • Very predictable .The patient knows at what distance it’s going to come
  • He also knows when  it will disappear.(For some , with rest for others with nitrates)
  • He also knows where the chest pain will radiate.
  • If some thing is unusual it is unlikely to be  stable angina , also any  first episode of angina is considered unstable as one wouldn’t  know how the angina is going to behave !

How is that stable angina has such a learned behaviour ?

The main reason for  the beningn nature of  stable angina is the coronary artery has “stable plaques”

Stable plaques produce stable angina  ,Unstable plaques cause unstable angina

Stable plaque s restrict blood flow only at times of  increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.

Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in  unstable angina, not only the angina is unstable , the plaque is unstable  ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.

Is there a overlap between stable and unstable angina?

Yes. In fact it is more common than we realise.

Read this post https://drsvenkatesan.wordpress.com/wp-admin/post.php?action=edit&post=2177

Related topics

How is a stable palque converts into a unstable plaque ?

How do you identify these vulnerable plaques ?

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