Posted in Cardiology - Clinical, tagged 64 slice ct, cardiology, cardiology journals, ct coroanry calcium, ct scan, drsvenkatesan, mdct on February 4, 2010| Leave a Comment »
Now we have a dedicated journal for cardiovascular CT scan .
Does it surprise you ? For me . . . It is !
Link to the current journal page . Get updated !
Posted in Uncategorized, tagged cardiology on February 3, 2010| Leave a Comment »
STEMI is the major cardiac emergency .The acute mortality is about 20% (Both prehospital and in CCU ) STEMI occurs whenever a coronary artery is occluded suddenly in toto .We traditionally believe that STEMI occurs only in the major epicardial vessels. (LAD/LCX/RCA .)
The total length of coronary tree is much longer than the length of the three vessels put together.The diagonals , the ramus, the OMs ,the septals run for varied distances. The caliber of these vessels can be quite large.It is estimated the diameter of first diagonal , the first OM or the ramus can be as big as LAD proper in 30% of CAD population . Law of statistics tells us sudden occlusion can occur any where in the coronary tree in ACS prone patients.
What is the real incidence of side branch STEMI ?
The dogmatic answer is ” We do not know”
Will we ever know ?
How will a Diagonal / OM /Ramus or PDA STEMI behave ?
It is surprising this question is not addressed by us for so long . Some may even question the existence of such an entity(Side branch STEMI ). This is most likely , reflect our ignorance on the issue . We know bifurcation lesions at the side branch origin is very common . Further , thrombus can migrate from a main stem to a side branch immediately after formation .
Clinical presentation of side branch STEMI
It is very much possible , many of the side branch MIs may be wrongly diagnosed as unstable angina by us , for the simple reason the myocardial necrosis is not large enough to produce ST elevation .They may actually respond to thrombolysis , as there is total occlusion in the coronary artery. Since, they do not manifest ST elevation there is a lost opportunity here . This , probably is the population in TIMI 3B trial that showed some ( statistically insignificant ) benefit for thrombolysis in NSTEMI.
Is primary PCI justified in side branch STEMI ?
May not be . The chances of side branch STEMI to result in LV dysfunction and progressive adverse remodeling is considerably less . The hazards of primary PCI for exceeds the risks of MI due to a septal or diagonal branch lesion .
Final message
Counter point
* Identifying a side branch STEMI with confidence may be very difficult at bed side in an emergency . Implication of wrongly calling a STEMI as benign can be dangerous . So it will be argued , one need not do this exercise of traiging STEMI into main branch or side branch .
Image courtesey
Coronary tree : http://www.southcharlestoncardiology.com/64cta.html
Posted in bio ethics, Cardiology - Clinical, tagged african children, bmj, cardiology, climate summit, evidence based medicine, green house effect, health outcome analysis, hunger, knowledge disease, lancet, logic in medicine, malnourished, nejm, obesity, poverty, rich vs poor, unequal world, unlearning in medicine on December 26, 2009| Leave a Comment »
When we get contaminated with excess knowledge , we lose our ability to think ! & Common sense is the casuality . . .
Human beings differ from other forms of life by their sixth sense . Our planet is few billion years old . Life came into existence over a million years ago .Our life has evolved over many thousands of years .The average life span of human race is 75 years . We need to realise , our life constitutes only a fraction of our planet’s life (<.0000001% ) . A may fly , which lives a life of less than a day , does it in style , looking for the light throughout the night , says good bye , to earth by morning leaving it unharmed . Actually , in terms of time , the life of the fly is just a fraction less than human life span , when compared to our planet’s life !
When these children are longing for food , some of earthly humans go to spend millions for obesity surgery ! That is the progress of knowledge driven society . . .
It is extremely common to experience the following scenario in any corporate hospitals of both developing and developed country .A uninsured or half insured ! person is refused entry into a hospital even for an emergency care while a wealthy person is lying comfortably watching TV in a five star suit of the same hospital after an inappropriate coronary angioplasty for an innocuous lesion of his heart !
The irony is , in this short span of earthly life , we want to prevail over the nature and conquer the planet . God is watching this human behavior silently . And he is smiling . . .
With all our knowledge base , modern science have done the maximum possible damage to our planet .We have made many lives extinct. If we tend to think , with the help of 6th sense we can become immortal , it would be the ultimate foolishness. When every one of us , is obsessed with our own health , we are deaf to the silent cries of our beloved planet earth .
Now , all of a sudden we realise all the accumulated knowledge & development has actually worked against us. We find our knowledge is dissociating our thoughts and now , we are fighting vigorously over acquiring the rights to damage our planet .
So it seems , the more we learn, less wisdom we have ! We may need to learn important lessons of living from all those species which do not boast to have the 6th sense !
Read a related article , excellent one published in British medical journal nearly 2 decades ago
Knowledge disease BMJ. 1993 December 18; 307(6919): 1578.
Posted in cardiology -Therapeutics, cardiology-ethics, Uncategorized, tagged acute coronary syndrome, cardiology, drsvenkatesan, ethics in medicine, evidence based cardiology, hippocrates on December 16, 2009| 1 Comment »
Modern era of cardiology aims to treat ACS as and when it develops .That is , as soon as the vulnerable plaque ruptures or a thrombus blocks the victim’s coronary artery.
But this can be achieved only if the patient reacts to this event.We know 20% of ACS can be totally silent. Some produce very vague symptoms especially in elderly and diabetics. ECG and enzyme changes may help us in patients who do not have clear symptoms.There are variety of markers available for STEMI & UNSTEMI.(CPK-MB, Troponin T , myoglobin etc) Now we are working at finding a marker for ischemia without necrosis. Ischemia modified albumin is one such molecule that is showing promise.
The ER department world over have vigorous screening protocols to diagnose ACS for the patients with chest pain. There are thousands of triaging protocol in the emergency management of chest pain.In spite of the highest awareness and availability of scientific expertise , knowledge base the error rate of diagnosing ACS stands at an astonishing 58%. This may seem odd , but this is what this land mark article in NEJM tell us (Data from Boston , Milwaukee etc).
Out of 10500 patients with suspected ACS. Only 17 % had real ACS. 55% were admitted initially as ACS later turned out to be non cardiac .This may seem acceptable for many even if it is an act of unnecessary admission and investigation. It gives us , a sense of satisfaction for not missing a diagnosis of ACS. But it has it’s own risk of complication arising out of unnecessary investigations.It is a chain reaction of suspicion that may end up in a coronary angiogram in many ! .It is also a well recognised fact these patients spend atleast an average of 2 days to get rid of the ACS tag over their necks .
Experience has taught us simple presence of a human being as a patient within an ICU ( however short the stay may be ) can be a health hazard and risk . This 55 % error , which does exactly this to our patients with chest pain who reach the ER never bothers us This is because we feel credited both academically as well as financially .
In the same study 2.3 % (About 25 patients) with true ACS were sent home after a missed diagnosis . Paradoxically this 2.3% has worried the medical professionals too much . . . This happens , even as we do not have proper data on how many of them had a real adverse event after a missed ACS.
So the message here is even in best centres both missed and wrong diagnosis are rampant. while wrong diagnosis (25 fold more here ) is easily accepted by the medical community .We can justify this as a screening camp for ACS , akin to arresting a group of suspected criminals in a preventive raid , later releasing for want of evidence.
In the morals of criminal judiciary , it is often said one can afford to lose a real offender from the clutches of law , but a innocent should never be punished in any circumstance .
In medical parlance this goes something like this . . . Thousand patients shall die because of his or her illness but not even a single healthy person should die due to unnecessary treatment.
The above thoughts were in response to the excellent original article on missed diagnosis of ACS from NEJM. http://content.nejm.org/cgi/content/full/342/16/1163?ijkey=652d8337709a8bf84c813f4c9d685863ee053162
Final message : (Sorry for the lengthy message !)
Can we afford to miss an ACS in emergency room ?
“Definitely not” . . .but do we succeed in that ? The answer is same “definitely not “
When we are able to accept with pride every time we make a wrong diagnosis of ACS in perfectly normal people , It may to provocative to say we can also afford to do the same when we occasionally miss a diagnosis of ACS as well . Law of statistics dictates for every correct diagnosis made there is many fold number of wrong or missed diagnosis takes place. May be , reducing that is the only aim of medicine.
We need to realise with even with a 55% of false positive initial diagnosis 2% real ACS escape net !The only fool proof method for not missing , even a single case of ACS is to label every patient with chest pain as ACS .
In this vexing issue , we should realise , in field of medical decision making , errors due to acts of commission ( Making an inappropriate drug/procedure /surgery is easily accepted by medical professionals as well as the court of law !) . But acts of omission , like missing a diagnosis or failure to prescribe a drug or perform a procedure is rarely accepted and is considered a great negligence and bring intense guilty feeling among the physicians .
This perception is definitely not warranted in this greatest profession of glorious uncertainties ! Both acts of commission and omission cause significant damage to patients . In this modern era , we have clear statistics that reveal , acts of commission leads far ahead over it’ s counterpart in injuring our people .
Hippocrates got it right over 2000 years ago . First let us do no harm . . .
Posted in Cardiology - Clinical, Great websites in cardiology, tagged cardiology, dr s venkatesan, drsvenkatesan, madras medical college, top cardiology websites on December 16, 2009| Leave a Comment »
A good collection of resources dedicated to cardiology
Posted in Cardiology -unresolved questions, Cardiology hypertension, cardiology- coronary care, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, Uncategorized, tagged ARBS, bmj, bnp, cardiology, chronic total occlusion, coronary care units, cost effectiveness, cpk mb, CRT, cto, ebm, ethics, ethics in cardiology, ethics in medicine, evidence based medicine, fondaparinux, heparin, hippocrates, hypertension, jacc, jama, jnc6, jnc7, lmwh, nejm, nstemi, pci, ptca, rescue pci, seminars in cardiology, stemi, troponin on August 19, 2009| Leave a Comment »
Coming soon : 10 more ways to increase cost of cardiology care . . .beyond common man’s reach
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, Uncategorized, tagged acetyl choline, atropine, av block, bradycardia, cardiology, cath lab, complete heart blcok, m2 receptors, muscarnic receptor blocker, pci on August 15, 2009| 2 Comments »
Atropine , the extract from the Belladona plant is an important cardiovascular drug. It’s presence is vital in every crash carts . This unassuming molecule probably has saved more cardiac lifes than any other drug . It provides immediate remedy for many of the bradycardias .It works like a magic. The physician buys time with this molecule and proceed on to resuscitate or plan other interventional procedures. It is most powerful antiarrhytmic agent known .It is an irony , many of the standard cardiac texts do not even mention this while discussing anti arrhythmic agents .
In this era of hyped cardiac care , the sartans , 2b3a inhitors , the fondaparinux’s making merry ! we have no spare time to realise , more cardiac deaths have been prevented by atropine than all these drugs put together. It is still working like a bull across the coronary care units and cath lab world over. While many mediocre drugs enjoy a big bash time for possibly saving few occasional lives , the atropine like drugs never get the due recognition among cardiac literature for the simple reason , it being a cheap generic drug.This drug is available for few rupees , no marketing no advertisements, no celebrations.
Mechanism of action
The biochemical mediator : Acetyl choline
Site of action : It blocks the M2 (Muscaranic receptors) .
We will confine to the cardiovascular actions.
Effect on ECG
Sinus tachycardia
Short PR interval
Life saving situations in cath labs in CCU.
Vagus nerve richly innervate the heart and blood vessels . Acute coronary syndromes especially involving the infero posterior territory raises the vagal tone , and can in severe bradycardia and hypotension. In cath labs , as we manipulate cardiac structures with wires and catheters there is always a potential to elicit the vascular reflex .It can occur any where between the access point , femoral or radial artery to coronary arteries .
Further , whenever the pain intensity is more , the central pain integrating centre in brain stem and thalamus has a spill over effect into the vagal nucleus .
What happens if a vaso vagal reaction is left untreated ?
We have often made the term “vaso vagal reaction” appear as an innocuous entity. The main reason for this perception is due to the common occurrence of “vaso vagal syncope” which is largely a benign entity in the general population .This fact has sensitised our brains . One should distinctly realise the vaso vagal syncope that occurs in healthy people standing in erect posture , from vagal reactions that occurs in lying patient with a diseased heart in a cath lab or CCU.In the classical vaso vagal syncope , assuming the recumbent posture is the treatment and it counters the hemodyanmic imbalance .No drug is required here. So the common vagal syncope can never be compared with potentially dangerous vagal reflex that occur in CCUs and cath labs. If not recognised earlier and immediately countered it can lead on to asystole and death .Many of the delayed deaths post PCI during sheath removal or an episode of vomiting are directly related to this.
Atropine is the Savior here . Can you imagine a world without atropine .
The other reason we had always considered vaso vagal reactions lightly is that the poor atropine is always available in the side selfs and it acts rapidly and promptly with almost 100 % success reversing the vagal action in less than 60 seconds .
How often we here this “Oh it’s a brady . . . push 2cc atropine . . . given sir, the rate has picked up . . .”
If only atropine has a failure rate of say 50% we would have realised the full impact of vaso vagal shocks (See … how we struggle with No reflow with no effective drug available !)
Is there any other alternative treatment for vaso vagal shock other than atropine ?
No. (I guess so . . .Readers may correct me )
Other uses of atropine in cardiac practice
Non cardiac uses.
Ophthalmology, pre anesthetic medication, bronchial asthma, various poisoning.
What is the future for this molecule ?
Remain bright . But only very few companies make this molecule. It is a drug that can not fill the cash boxes but it is a drug to keep the human heart running at times of crises . The only threat to this drug is the possibility of it being replaced with a modified patented version of this great molecule !
Final message
The evolution of medicine is based on strong foundations put upon by clinical acumen by great medical men of past generation. Atropine was developed by such people and it has withstood the test of time. This drug probably has saved ( and continue to save) many lives than any other drug in cardiology . It should be recalled , another great cardiac drug called digoxin has almost succumbed to modern medical forces .Let us keep developing new molecules , we shall also pay tributes to some of the unassuming drugs in cardiology .
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, tagged arterial shock, cardiology, circualtory failure vs cardiac failure, circulation, distriubutive shock, effective circulatory volume, gram negative shock, metarteriole, micro circulation in shock, myocardial depression in septic shock, persistent hypotension, post operative shocks, refractory hypotension, septic shock, shock, shock in ccu, shock in intensive cares units, spinal shock, third space, vascualr shcok, vasodilatory shock, venous shock, venules on August 12, 2009| 2 Comments »
Human circulatory system consists of the heart , the arterial and the venous systems . Together they constitute the three important limbs of circulatory system namely , the pumping, delivering and retrieval systems .In physiological conditions approximately 6 liters of blood has to traverse the entire circuit every minute . The purpose of the circulatory system is not simply circulating the blood within the body, but it has to perfuse different vital organs like brain, kidney, liver . Of course , the heart has to self perfuse the coronaries by it’s own contraction.The organ perfusion is determined by local and systemic regulatory mechanism. A gamut of intrinsic and extrinsic neuro humoral modulators take up this job. A functionally intact autonomic nervous system is an absolute necessity to maintain tissue perfusion. The perfusion pressure is highly variable in different organs and different cells. Similarly the ability to with stand ischemia and hypoxia also varies. Shock is a general term used to imply , circulation is seriously compromised.Here we will confine our self to the intricacies of peripheral circulatory shock
Traditionally shock is classified as
The hemodynamics of the first two are straight forward and easily understood. In cardiogenic shock , the pumping action of heart is primarily affected .In hypovolemic shock there is no structural defect in any of the circulatory limbs but there is a loading defect due to low blood volume as in hemorhagic shock .
The term vasodilatory shock or redistributive shock is most poorly understood and most difficult to treat.
The concept is further confounded as combinations of above three mechanism in a same a pateint can occur . ( More commoner than we believe !) . An example could be a septic patient with an internal bleed and myocardial depression either due to preexisting LV dysfunction or circulating toxins.
Since we have always perceived heart as the sole vital component of circulatory system , our understanding of the role of the vascular tree which is primarily responsible for delivering the blood is largely undermined and neglected. We are always happy if the EF % is normal.
Classical features of circulatory failure ?
The cardiac contraction is good.This is documented by normally contracting LV by echocardiography. The pulmonary capillary wedge pressure is normal (<12mmhg).Still the patient is in hypotension with evidence for vital organ under perfusion like oliguria and reduced mentation.
What is vascular tone ? What sustains the flow of blood into the tissues ?
The entire vascular tree could form a few 100 kilometer length.(Capillary /arterioles /venules included). While , it is easy to percieve heart as a dynamic pumping organ , it is a less recognised fact the entire vascular tree is also pulsating to every beat. That is the rhythm of life. What makes the vascular tree to pulsate ? Apart from contraction of the heart , there is an intrinsic tone for the large , small arteries and the arterioles and veins .This tone is vital for pushing the bllood into various organs and return into venous circulation and subsequently back into the heart.
The millions of perivascular cuffings and the artreriolar smooth muscles can be considered as small micro pumping stations situated along side every cell.
It is very important to emphasize here, if tone in these microcirculation is less than optimal , the patient’s circulatory system can never complete the desired circuit even if the heart has 75% EF . This exactly is happening in circulatory shock . The vascular tree fails to accept and return the pumped blood in timely fashion.
What controls this tone ?
It is chiefly under the control of autonomic nervous system.The endogenous vasoconstrictors , the adrenergic nervous system, the endothelins , the angoitensins constrict the vascular smmoth muscles while endothelial relaxing factors ,( EDRF -nitric oxide relaxes it ). There is a delicate balance between these forces.
A cardiovascular health of a person is not simply having a healthy heart , he has to have a healthy vascular system with intact biological activity.The fact that , not every one with sepsis react with poor vascular tone indicate inherent capacity to neutralise toxic vasodilatory neuro transmitters.
Is there a invisible parameter called vascular ejection fraction in circulatory system?
Yes. It must be . We rarely discuss it . The vascular tree has an important role for pumping the blood into the tissues. It needs micro manometers to assess the systolic and diastolic dimensions of small arteries and arterioles . But what we know is , it is grossly impaired in circulatory failure.The vessels especially the arteriolar smooth muscles which determine the perfusion pressure of cells go into state of permanent relaxation. The vascular smooth muscles lose control from autonomic innervation and become flabby. It is the DCM equivalent for blood vessels. The arterioles no longer regulate blood flow and fluids get sequestrated in various viscera,( often called thrid spaces) and organ dysfucntion sets in. The resultant hypoxia aggarvates the tissue stagnation by producing still unnamed vasodialtory mediators.
What are the pharmocological approches to increase the vascular tone of a failing vascular tree ?
It is a very difficult problem even in this modern era of vascular medcine. Once set in , these patients invariably go downhill .The primary underlying problem , often sepsis need to be corrected. Usually these patients need multi organ support.Vasoconstrictors like epinephrine,nor epinephrine , dopamine can sustain vasoconstriction temporarily . As we know the vascualr smooth msucles can not be kept on this assited contrection mode for long.It is bound to fail .Patients native autonomic function has to recover fast to wean of this support.
What is normal circualtorty time .How is it altered in circualtory failure ?
The normal circualtory time is 15-20 seconds.It is many times prolonged in circualtory failure inspite of the cardiac contraction being normal
What is effective circulatory volume ?
The body fluid compartment is divided into ICF,ECF & interstitial spaces.At a given time , the fluid in the extracellular space can only take part in circulation. A good blood pressure does not always mean a good tissue perusion why ? This is very important to realise as blood pool has to dynamically exchange with intra cellullar compartment. At times of shock the blood can bye- pass the cells through the alternate circuits in the periphery of micro circulation. So what is circulating in the system may not be taking part in tissue perfusion .This is the concept of effective circulatory volume.This is especially noted in hepatic shocks and in some terminally ill malignancy.
Is there a venous shock syndrome ?
Cardiologists often show a step motherly attitude to venous disorders. In fact many of the cardiovascular specialists think their job is taking care of heart ( Of course , a little bit of aorta and venacava !) .It is surprising to know, there is little scientific data on determinants venular and venous tone (Both small and large veins).
The power of venous system should not be under estimated as it pumps many litres of blood every minute defying gravity ! For this to happen it needs a vigorous tone .Where do it get from ? : The same autonomic nervous system that controls the heart. Remember , in pathological states there is a great chance for this to go out of control. So venous shock is a clinically distinct possibility. In fact inappropriate administration of nitrates which reduces the venous tone has resulted in many adverse events in RV shock.In a patient with circulatory shock , we would never know how much is contributed by venous side and how much by arterial side .This is important as in circulatory shock we administer all vital drugs through veins.Now it is thought systemic venous dysfunction also contribute to shock state.
Bacterial shocks
Viral shocks
Dengue/Swine flu etc
Others*
* Idiopathic unexplained persistent hypotension , with difficulty to wean off from vasoconstrictive agents is a commonly encountered problem in any intensive care unit.The exact mechanism is not known.When we are not clear about the mechanism we generally blame it on the the autonomic nervous system !
How common is the mixed shock syndrome ?
This is more common than we realise .The classical description of multisystem failure is a direct consequence of this.
Can a cardiogenic shock transform into a peripheral circulatory shock ?
Such a scenario is possible .A resuscitated cardiac arrest may end up with a recovered heart but a loss of vascular tone possibly due to hypoxic vascular damage. .Many times cardiac patients are kept (Post PCI/CABG ) on large doses of vasoconstrictors or IABP that can induce tachyphylaxis. It may result in difficulty in weaning these drugs.
How can circulatory shock result compromised cardiac function ?
The common effect of any shock is reduced organ perfusion.So even in peripheral shock , the coronary blood flow gets compromised especially if these patients have a silent coronary lesions which are otherwise not significant , becomes sites of hemodynamic hurdles during hypotension.This may result in global contractile dysfunction, or a coronary event.
What is vasoconstrictive shock ?
Epinephrine and nor epinephrine are very potent vasoconstrictors .If levels of these becomes excessively high , the blood vessels go in for sustained spastic state that can impair the micro circulation .Some times this results in a good blood pressure in the major vessels but severely compromised tissue perfusion.This particular situation has been reported after scorpion envenomation , and in rare cases of pheochromocytoma .
Final message
Primary circulatory failure or shock (With largely intact cardiac function without hypovolemia) is a common problem in critically ill. The entire macro and micro vascular tree goes for a stunning reaction and goes for a sleep in a semi dilated state . It can be termed as Arterial or Arteriolar shock. Contrary to all those hi-tech mechanical stuff for supporting a failing heart (LV assist, Impalla, Abiomed , ) the available options are very little here . The response to vasoconstrictive agents are also unpredictable. Correcting the multi organ failure and targeting the primary cause is the only hope.
Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology-ethics, Hemodynamics, Top ten in cardiology, tagged breaking news in cardiology, cardiology, cardiology breakthrough, cardiology of 2oth century, cardiology top ten, echocardiography, frusemide, great cardiology drugs, gruentzig, heparin, lasix, pci, prosthetic valves, ptca, statins, ten great inventions in cardiology on December 24, 2008| 1 Comment »
Selected on the basis of , impact on survival , relief of human suffering index and also innovation
10.Percuateneous interventions
9. Electrocardiography
8 . Hemodynamics of cardiovascular system
7.Fruesemide
6.Thrombolysis
5.Pacemakers
4.Defibrillation
3.Heparin
2.Prosthetic valves
1.Coronary care units
Concept of vascular biology
Statins
RF ablation
Nitric oxide
Total Artifitial heart
Echocardiography
Ten least important concepts and inventions in cardiology
Selected based on duplication of research, futile scientific concepts and of course impact on survival
10.Low molecular weight heparins
9.Cardiac resynchronisation
8.Rotablator
7.Multi chamber pacing
6.Newer ARBs
5.C reactive protein
4.Three dimensional echocardiography
3.
Comments welcome and please contibute
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged acc.aha, angina grading, angina pectoris, beta blockers, braunwwald, canadian cardiovascualr society classifcation, cardiology, ccsc, chronic stable angina, drsvenkatesan, heberdeen, intermediate coronary syndrome, jacc, jama, lancet, nejm, nstemi, post infarct angina, post pci angina, ptca, rest angina, stable angina, stemi, unstable angina on November 11, 2008| 1 Comment »
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)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.In patients with systemic hypertension and LVH or cardiomyopathy resting ST depression may not indicate UA
Dr.S.Venkatesan MD 