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Posts Tagged ‘chronic stable angina’

Poverty is the number one killer in this world . Malnutrition, infectious diseases  , poor maternal child and health are the leading killers. The life expectancy is short in many underdeveloped countries.

While the scenario  is dismal for most of the poor people in this world.

Can affulence be a risk factor for poor health ?

Yes. This seemingly awkward  answer is  many times true. The disease  acquired by affluence is labeled attractively as life style diseases . They are : Obesity, Diabetes mellitus, cardiovascular diseases, some forms of cancer etc .

coronary angiogram cardiology

How else can affluence affect the health of an individual ?

Apart from affluence being a risk factor ,  it  is a powerful  risk factor for getting  inappropriate  medicines,  procedures  &   surgeries  ,  hence  the resultant  adverse effects.

It is a  non-established fact , in  both  developed  and developing world , the single important  predictor of a given form of treatment  say  revascualrisation or  surgery  for CAD  is affordability to the treatment (Either  by insurance or  self payment) .Financial well being , interferes with applying  valid scientific principles on them . Applying  the  results of  the  land mark trials CAD trials ,   COURAGE  &  BARI 2D  are very difficult  for them , which argues for   simple , less costly , less glamorous medical therapy for CAD.

Example 1

A wealthy adult  male  who  lands  up for master health check up  in a big state of the art  hospital found to have a  borderline stress test , CAG reveals a single vessel distal RCA disease .He was given an  option of PCI , undergoes  it ,  and ends up in a complication and damages his entire  inferior myocardial  territory.

Had he been a poor uninsured  guy , he would have promptly be  labeled as stable CAD and would have been on  good medical therapy*  and his  myocardium could have been saved .

* PCI can never be an option  for him ,  courtesy : His wealth status !

Mind you , this is not an isolated  example, such  affordability  guided treatment modalities  are rampant in the society and has a potential to make  our rich and  affluent a major health risk target !

Final message

Being wealthy and affluent can also be a health risk factor. While the poor suffer from lack of health care the  rich many times suffer because of  too much health care ! (or  Is it care less ,  health care ?)

Coming Soon

How reccession  time  is a  boon  for human health  !

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pci-ptca-ebm-stent

Scientifically ,  the  indication for coronary revascularisation   should be  based on following

  1. Patient’s  symptom ( more specifically angina , dyspnea is less important !)
  2. Prov0kable  ischemia  ( A significantly positive stress test )
  3. Signifcant LV dysfunction with  documented  viable myocardium &  residual ischemia
  4. A revascularisation eligible coronary anatomy * TVD/Left main/Proximal LAD etc ( *Either 1, 2 or 3 should be  present  in addition )
  5. All emergency PCI during STEMI /High risk NSTEMI

Practically ,

A CAD  patient  may fulfill  “Any of the above 5 or  “None of the above 5” ,  but ,  if   a coronary obstruction  was  revealed  by coronary angiogram  and if he  fulfils The 6th criteria , he becomes  eligible for  revascualrisation

6th criteria

If the patient has  enough monetary   resources (by self  ) or by  an  insurance company  to take care of PCI /CABG *

*The sixth  criteria overrides all other criteria in many of the cath labs .Of course , there are few genuine ones still  fighting hard , to keep the commerce out ,  from contaminating cardiology !

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Anginal pain is a type of visceral pain.It is carried by type  C  unmylinated  nerve fibres.The perception of angina is a complex process.It is a combination of visceral and cutaneous referral pain.

How often is angina silent in diabetes mellitus ?

Presence of  diabetes per se does not make an angina silent. In fact,  if  one takes 100 patients with diabetes  , if angina occur in them , it is more often  , manifest than silent. So , only few of  the  diabetic patients who develop diabetic autonomic neuropathy fail to have angina.The exact incidence is not known.It could be around 20%.

If angina can be silent in diabteics , can they have anginal equivalents ?

This again is not answered in literature. Among the anginal equivalents , the most common is  dyspnea , which  can occur in diabetics.But now , we know dyspnea also needs thoracic nerve signals  from the intercostal muscle spindle and colgi organs.This can also be impaired in diabetics.

Can silent and mainfest episodes occur in a same  patient  ?

Yes.

Once silent does not mean always silent, and similarly once angina is felt it  does not mean he is going to feel the next episode as well !

This  strongly reminds us medical science  is  much a complex  subject and what we know is very little in pain perception.

How is silent ischmia different from silent angina ?

There is considerable  overlap  between  silent ischemia and silent angina

The questions to be answered are 

Which is silent  ?  Is it the angina or is it the ischemia or both ?

Silent ischemia can occur in any individual ,  this is also called as silent CAD . When  ischemia occurs  but  fails  to generate pain it is silent ischemia .Undiagnosed  CAD in asymptomatic individuals is also called silent ischemia or CAD.In this population  Exercise stress testing detects  CAD which was otherwise silent and masked.These patients may develop angina during EST.

During exercise stress testing many times patient has significant ST depression  more than 2mm but still chest pain may not occur.These episodes may either be silent ischemia or  ngina. Many times the EST is terminated before angina is manifest .( Chest pain is the last to occur in the chain of events following ischemia- Concept of ischemic cascade )

What are the other situations where angina can be silent ?

  • Pain perception  and threshold  level is  high ,  so patient indeed has anginal  signals but fails to feel it .
  • Patients on  antianginal medication , fail to feel the angina.
  • Chronic betablocker therapy can exactly mimic  autonomic neuropathy

Is it a blessing for the patient  to have painless episodes of angina ? 

When their  ischemic colleagues , suffer a lot with chest pain it is tempting to think these diabetic patients  are blessed!

Scientifically , this could be true in at least in  some  especially in a patients  who’s coronary anatomy is known  and devoid of any critical proximal lesions. For example a small PDA  lesion can produce  severe angina  , but may be silent  in diabetic and be comfortable .This lesion is  insignificant other wise * !

It should  also be recalled , pain relief has been an important goal for treatment  of CAD .In olden days,  thoracic sympathectomy was done for angina . In fact ,  even in  CABG  , one of the the  mechanisms  for  angina  relief  is attributed  to cardiac denervation.

Caution: Even a small  episode of ischemia can trigger an electrical event .But it is rare.

 How common is silent infarct (STEMI) in diabetic patients ?

In a simple questionnaire we asked the diabetic patients in our CCU how they felt their pain during MI.Most felt it normally as do other non diabetic .  Diabetes  does not make  all anginal episodes  silent. Severe episodes of ischemia may be painful while less severe episodes may be painless. Diabetic autonomic neuropathy  is a  least recognized and  poorly understood complication of diabetes.Diabetes , involves  the vasanervorum of the autonomic nerves.

 The other mechanisms postulated in diabetic neuropathy are

  • Reduction in neurotrophic growth factors.
  • deficiency of essential fatty acids .
  • Reduced endoneurial blood flow and
  • Nerve hypoxia .

Is diabetic autonomic neuropathy treatable ?

Very difficult problem indeed.Controlling diabetes may partially correct  the neural dysfunction.Many add on neuro vitamins and aminoacids are having a good market !

If you successfully treat diabetic autonomic neuropathy will my patient  start feeling the  hitherto silent episodes of angina ?

We don’t know.Logic would answer ” YES”

What is the ultimate effect of cardiac autonomic neuropathy.

Cardiac denervation.  The manifestations  are

  • Tachycardia, exercise intolerance
  • Orthostatic hypotension

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                                        Angina pectoris , classically occur on exertion and gets relieved on rest .This is called typical chronic stable angina as described by Heberden (CSA ) .  Unstable angina(UA), the term originally described by Noble O Fowler in early 1970s. ( Also being referred as  intermediate coronary syndrome , preinfarction angina etc).The definition for unstable angina has evolved  over the years  and currently  refers to .

 1.All new onset angina of any degree* Some include severe angina only ! New onset angina of very mild degree on exertion could be the onset of the first episode of  stable  angina. 

 2.Rest angina of more than >30 mts not relieved by taking sublingual nitroglycerine.

 3.All Post MI angina

 4.Any angina in patients who have been stented by PCI.

How to recognise a patient  who is shifting from  stable angina to  UA ? 
UA is  to be suspected when  a patient develops. 
5.More frequent episodes than usual
6.Angina occurring at lesser level of exertion than before 
7.Angina radiating to new site ( Example : Chest pain radiating  to jaw rather than to the usual left arm or vice versa)

Why the first episode of angina is given a special status and often considered critica ?

Angina is the  clinical expression of   myocardial ischemia.The course of  the  first  episode of angina , can not be predicted.It could be a the beginning of a chronic disease process, or it could be a progressive coronary occlusion as in unstable angina /NSTMEI , or the onset of even a STEMI.
In contrast a patient with chronic stable angina  has a predictable chest pain , at a particular level of exertion, radiation to same site, same character, and the patient knows for sure the pain  would promptly dissappear  when he takes rest or nitroglycerine  tablets.

What is the underlying pathology in UA ?  

Generally it is very rare for  a stable plaque to produce a  serious episode of unstable angina .It  requires  an unstable plaque* to  precipitate an unstable angina !
Unstable plaque refers to any plaque which is eroded, fissured, ruptured or  hanging  eccentrically ,  with
an active thrombus.

What is the significance of post PCI angina?

It is an irony, any angina following PCI is to be considered unstable as sudden occlusion of stent is quiet common.This is a paradox of sorts as one would wonder in a patient  with CSA who undergoes PCI with stenting  of left anterior descending coronary artery  (LAD)  all his subsequent episodes of angina  will be labelled as UA  even if a stable angina occur in his other coronary artery.And these patients would go for early invasive approach and potentially inappropriate interventions even if they are at low risk !

Is all angina at rest can be termed as unstable angina ?

No, but many times ,  rather most of the times  cardiologist believe all rest angina to be unstable.

What are the situations where stable angina can occur at rest?

An episode of angina during mental stress, or post prandial* state are very common in patients with CSA. This gets relieved after the stress. Some times  patients with CSA during episodes of fever may get angina at rest .These are considered variants of stable angina.
Post prandial angina , may be considered by some as unstable

How often a diagnostic confusion occur between CSA and UA ?

Generally, this issue is rarely addressed in cardiology literature , for the  simple reason it is never considered an  issue at all !
According to Canadian cardiovascular society grade 4 stable angina  is almost similar to unstable angina , as it denotes angina occurs with minimal effort or even at rest. In fact CCSC grade 4 should be termed as UA.

Can ECG be useful to identify stable angina from unstable angina ?

                                    ECG will some times  come to our rescue when one is confused between stable and unstable angina even though resting ST depression can occur in both stable and unstable angina . Statistically , if ST depression is noted during an episode of angina it is more likely to be UA rather than CSA. . Apart  from ECG , Troponin T or I levels may be elevated in some of the patients with unstable angina. Rarely stable angina can also show elevated troponin.

In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA 

So differentiation between, stable and unstable angina even though appear simple and  straight forward, it requires a diligent appraisal of history , physical examination (Aortic stenosis /HCM  may cause stable angina)  and ECG, enzyme evaluation.

Final message

In any coronary care unit ,  admissions with initial diagnosis of  ACS/UA/NSTEMI , subsequently turn out to be simple stable coronary artery disese . This error happens because the chest pain  or ECG changes  are aggravated by non cardiac factors like a mental stress or a post operative stress  or fever etc.
There could  be another school of thought, that is to err on the side of  safety, and manage all  rest angina as UA  .But the hazards of unwarranted therapy might exceed the risks of leaving these patients alone.
In this context ,there is a need for a new definition for unstable angina .
One ideal version could be . . .
  • Any angina , of any degree  which is caused  mainly by the supply side defect (By a acute thrombotic /disruptive plaque   occluding the  coronary lumen  with a imminent danger of myocardial infarction is to termed as real UA.
  •  All post MI and post PCI angina are unstable angina
  •  Rest angina which occurs due to increased demand situations need not be  labelled  as unstable angina for the simple reason  there is neither an active plaque nor a  fresh thrombus likely  in these patients. They rarely develop  recurrent angina or MI . The mechanism of angina at rest here is most often due to a tachycardia and resultant increase in MVO2 .(myocardial oxygen consumption) .Currently they are called as secondary unstable angina.In fact , anti thrombotic drugs are misused in these situations as they satisfy the criteria of UA/NSTEMI.

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                                Coronary artery  by pass graft surgery has become the most common cardiac surgery done world over ever since it was first introduced by Favalaro in 1969.The common indications  are, triple vessel disease and left main disease in any of the following situationsE.

Elective CABG(Non emergent)

1.Chronic stable angina

Either emergent or elective

1.Unstable angina

Emergency CABG*

1.Acute myocardial infarction.-Cardiogenic shock

2.Failed thrombolysis

3.Failed primary PCI

4.Complications during routine PCI(Cath lab crashes !  etc)

5.As an associate procedure after a  mechanical complication during MI (Septal rupture, Acute MR etc)

*In emergency situations even a single vessel disease would require a  CABG

Hybrid CABG

Combining CABG and PCI in the same patient is followed in very few centres .(Example LAD graft and RCA angioplasty)This is done in patients who have co morbid conditions who can not tolerate prolonged surgical times.Further there can be situations  one lesion is very ideal for PCI  while for other grafting is the only solution.

Controversial CABG

1.CABG as a primary revascularisation  in STEMI*

(Rarely done now , almost obsolete , primary PCI has almost replaced it  . . . but it is still  useful if performed within 6 hours of MI )

2.Incidentally detected CAD*  following routine coronary angiogram.

( *CABG for incidentally detected asymptomatic CAD is  increasing in many parts of world )

Inappropriate CABG

         If it’s triple vessel disese it must be CABG -CASS study (1980s)

                       Coronary artery surgery study (CASS) still has considerable influence among the  cardiology  community in the decision making process  for CABG , even though it is many decades old .There has been a phenomenal development in both medical as well as interventional techniques since  CASS . (Thrombolysis, Statins, ACEI, PCI  DES to name a few) .

                     When CASS study was done many decades ago,it was believed triple vessel disese constitute a  homogeneous population and  carry  the same clinical significance . For example a 90% proximal LAD , 50% RCA and 50% OM technically qualify for a CABG and unfortunately , some of them are  subjected to it even in  2008 !  Now we clearly know, it is not the number of diseased vessels  that is important, but it’s location, severity , LV function, presence or absence of diabetes . Finally , the presence of revascularisation eligible myocardium must be documented in all post MI patients . (Technically referred to viable & ischemic myocardium ).              

              Currently , with the  PCI  & medical management has grown so much, CABG should be reserved only for, critical triple vessel disese , with at least one proximally located lesion (Mostly  LAD  or Left main ), especially in diabetic individuals.

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During acute  ischemia the most immediate requirement for the heart is

A.Blood

B.Oxygen

C.Glucose

D.High energy ATPs

E.Free fatty acid

Answer : A  will be considered  by most , as  correct answer .  A can provide B to E . But it is also a fact heart can survive without  A.  

Myocardium requires energy first  ! it does not in fact bother about from where it is coming at the time of crises.It may be right if you restore the coronary blood flow all other components (B-E) are made available to the heart .

The heart can survive off  the coronary circulation with only chemical support during cardiac surgery and also a during  heart transplantation  explanted  donor heart survives on a ice box during transit and till it is transplanted into the recipient heart

But ironically we spend much of our energy and efforts in restoring blood flow.One need to spare a thought about the quality of blood also . This is especially important  in the setting of ischmia  where a  metabolic centric approach will add further benefit.

Energy based approach to ischemia : Is it relevent ?

Heart is a fascinating  mechano biological organ  pumping   millions of  gallons of blood  .Fuel for this is self generated  on a continuous basis  from the circulation blood .So  the key to human survival is the coronary blood flow that supplies the fuel and nutrients to the heart. When this key supply line is under threat  during  acute coronary syndrome cardiologist have  the only option of restoring the compromised blood supply by any means . But during chronic ischemia there is  no  urgency. There has always been an option of enriching the  blood with energisers like ATPs,  glucose,  hemoglobin etc .Providing energy support to the failing heart has never captured the imagination of cardiac physicians until recently.Still most are skeptical about  the concept of biochemical ischemia.

Click to download full PPT presentation

Metabolic manipulation of  CAD( Will be available shortly)

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                            Amlodipine , the most popular anti hypertensive drug  used world wide has an very important action on coronary blood flow.When nifedipine was introduced three decades ago it was  known for it’s powerful anti anginal properties. Subsequently  amlodipine was introduced with almost similar action. But over the years, amlodipine was projected primarily as anti hypertensive drug and gradually many of the physicians are made to believe it is a drug that  should be used only if the blood pressure is high.The fear of reflex tachycardia in few was exaggerated.

                      

                              In fact a cross section of  today’s general physicians were queried  about amlodipine  and none of them acknowledged  using this drug as an anti anginal drug. And few of them went to the extent of withdrawing amlodipine if it was used for the purpose of angina relief !

Why amlodipine’s  anti anginal action is in doldrums ?

The single word answer is unfortunate!   Marketing bias ,coupled with  the fact  that mainstream cardiology texts have ignored this aspect.

Final message

                                    Amlodipine , can still be used as a antianginal drug especially  in a patient who has angina with associated bradycardia  , significant LV dysfunction . Some reserve amlodipine and nifedipine exclusively for vasospastic angina where beta blockers alone are theoretically contraindicated .

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