Coronary arteries are the major site for human atherosclerosis .CAD is considered the ultimate determinant of cardio vascualr health of our global population.Coronary atherosclerosis has a predilection for proximal sites and branching points.Typically it occurs in leftmain, LAD ostium, LCX ostium, proximal LAD, diagonal origins, OMs RCA and its branches .
Septal branches , even though divide very early from the LAD , it is uncommon to get affected by coronary atherosclerosis. Even for an experienced interventional cardiologist , it would be very rare to have performed a PCI for septal disease.
Why septal branches of LAD is rare to suffer from atherosclerosis ?
We don’t know the answer yet.
But , it is thought,septal branches are near perpendicular branches .The branching angle and incidence of atherosclerosis has a peculiar relationship.IAt any bifurcation point , the atherosclerosis tend to occur , if the angle is more acute , and is less common in abtuse angles .It is almost rare , if branching happens at exact 90 degree angle or so !
The other reason for septal branches being immune to atherosclerosis is , it runs within the muscle in its major course. The constant squeezing action(. . . and possibly bridging also) makes it difficult for the process of atherosclerosis to sustain and grow .
Can you still get a septal CAD ?
Yes, usually as a component of bifurcation or trifurcation lesion. Some times a diagonal and septal are very close together and atherosclerosis involves both ostia.
What is the implication for the cardiologist to perform a PCI with stenting in a septal branch of LAD ?
PCI and stenting in the septal branches are more prone for crushing and fracture as it is constantly exposed to the mechanical effects of muscle contraction.
Any other significance for septal branches of LAD ?
Isolated septal myocardial infarction can occur.This could be even a embolic manifestation.
Septal branches of LAD are potential target for therapeutic embolisation (By injecting alcohol) in patients with hypertrophic obstructive cardiomyopathy(HOCM) .This manover aims to produce a controlled septal myocardial infarction and thus paralysing the left ventricular outflow tract and reduce the dynamic LVOT gradient. This form of treatment, was glorified till recently now considered experimental !
Aortic dissection is a complex cardiac problem and a killer disease .Even though it is a fancier to make a diagnosis of aortic dissection in any intractable chest (or back )pain the most common error committed by physicians is failure to recognise it .
Is it possible to diagnose or atleast suspect aortic dissection by a rapid screening biochemical test ?
Yes, it seems so,
D Dimer , a product released consequent to intravascular thrombosis is elevated by >500ng in most of the patients with dissection.
Aortic smooth muscle heavy chain estimation is the other option.
What happens once a diagnosis of aortic dissection is made ?
It is not a great achievement to make a diagnosis of aortic dissection.It is only, a beginning of a long and often tedious decision making process . A real tough task , on hand for the cardiothoracic surgeons. It is a team work , needs the interaction of cardiologists, radiologists and cardiac surgeons to bring an optimal outcome.
The major issues are
Never try to manage this problem in a small hospital or facility. Always send the patient to a teaching hospital ( of course , not all teaching hospital can tackle this either , so enquire about their expertise ! )
No credits for making a simple diagnosis of dissection.One has to exactly locate the entry point and exit points if any.
Aortic root and arch involvement is of major importance in determining the modality of therapy.
Debaky classification is not of academic interest ! it has a purpose . Generally type A dissection(Proximal ) require emergency surgery
Differentiating true lumen from false lumen is of critical importance , it needs a meticulous transesophageal echocardiogram.( Some times one may , never be sure which is true and which is false lumen , funnily .in descending aortic dissection it may never matter for the patient !) Self healing of many dissections with thrombus is possible.
Controlling hypertension with powerful parentral antihypertenive drugs (Labetalol . . . ideally ) is vital.
Side branch involvement (spiral dissections) especially arch vessels and renal arteries make this entity much more complex
Isolated distal dissections and some low risk proximal dissections can indeed be managed conservatively(Also called non surgical ! ) Some cardiologists or even institutions hesitate to put a aortic dissection with medical management .They feel it is inferior form of treatment . . . but realise , it is not necessarily so !)
What is the other bichemical marker for disscetion ?
The aortic smooth Muscle Myosin Heavy Chain was proposed as a useful marker for diagnoisng dissection.
Diagnostic Implications of Elevated Levels of Smooth-Muscle Myosin Heavy-Chain Protein in Acute Aortic Dissection: The Smooth Muscle Myosin Heavy Chain Study Toru Suzuki, MD; Hirohisa Katoh, PhD; Yasuhiro Tsuchio, MD; Annals of internal medicine 3 October 2000 | Volume 133 Issue 7 | Pages 537-541
The abstract from annlas of internal medicine follows Readers from India can get the full text article free
Drug eluting stents : A slap on the face of Evidence based cardiology . . .
Click the BMJ link or read below
It is often said science is sacred and unfortunately we forget , science is not a heavenly creation and it is the creation of scientist of varying grades of integrity fueled by the vested interest of medical industry . It has been a almost a daily affair , some of the devices and drugs are recalled or found to be unsafe on patients.
Now the big cat has come out .The Drug eluting stent has fallen from Hero to Zero in a short span of 5 years. It was projected to have zero percent restenosis in 2002 . And now we realize it is Zero percent truth.
What has started as anecdotal reports of late stent thrombosis has indeed become an epidemic in all DES patients. The five studies that has been published in the NEJM this month (March 2007) has convincingly proved how unsafe these stents are in most of the coronary population .
Millions of patients in whom this stent was implanted will carry an impending stent thrombosis and possibly an SCD . Who is to take care of them ?
The DES story is a clear cut case of getting premature approval for a dangerous form of treatment inside human coronary arteries.
It is amazing how the scientist’s eyes are shut by the illusion of knowledge and lure of wealth. How foolish they were to think drug which was administered via the stent will selectively prevent vascularisation and leave the normal endothelium intact . Now they realized , one should not suppress the endothelial growth around the stent and got the fundamental point wrong. Which was the key reason for the astonishing episodes of late stent thrombosis. When we play with biology of nature we have to be little more careful .God has created man and his heart for over a million years . One can not alter it by a 6 month follow up study of DES .
When ICDs were exposed last year , of similar disastrous outcome they were recalled and explanted . How are we going to unstent the millions of coronary arteries ?
Somewhere along the line the medical professionals have lost the battle against the Wall street and NASDAQ . Or how else we can explain repetition of similar events.
The wages for the modern technology , the patients have to pay a heavy price.
Let us all hope common man with common sense will reign supreme over the sixth sense of the uncommon man . . .
“Ignorance is better than illusion of knowledge”
Dr Venkatesan Sangareddi MD , Assistant Professor of cardiology , Madras medical college Chennai, India
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.
The growth of medical science has been phenomenal .It is estimated , the quantum of break throughs and development in the last 50 years is nearly equal to 2000 years of evolution of our knowledge put together. Along with this growth , came the unavoidable misuse , and abuse of medical science. This is mainly due to contamination of medicine with commerce . Federal drug authority (FDA) and it’s variants were formed in all countries to monitor the proper usage of these technologies for the benefit of mankind. It has an authority to ban a drug or device , if it is found to bring more injury or side effects than benefit !
But , unfortunately there is no legal authority to ban an an investigation which is potentially or (really harmful )
or used extensively without any valid purpose .
The list of such investigation is increasing in every speciality
In cardiology
Doing a Troponin assay in patients wuth classical STEMI
MDCT in general population
Pro BNP in all suspected cardiac failure
Routine C reactive protein for CAD
Central venous catheters for all pateints with shock.
Is there a case for banning an investigation (Like banning a drug) for the benefit of our patients ?
Looking superficially , it may seem ironical. But we realise many seemingly innocuous investigations are responsible for uncontrolled misery for many patients.
This especially true in people who throng the wellness clinic (Also called master health check up)
A incidentally high C – reactive protein can lead on to forearm blood flow assessment of endothelial dysfunction and carotid intimal plaque that could lead onto carotid stents ! and life long anticoagulation , and an excess INR and sudden cerebral bleed and death !
This is one sample story in one particular speciality
There is a definite case for banning ( Either total or partial) some of the questionable investigations which are done routinely !
Just because these investigation do not have any physical , visible , adverse reactions like a drug , it should not be allowed to be abused .The consequence of false positive results of these investigations could be terrible and worse than the real disese itself !
Coronary arterial circulation is the life line for the human heart and it’s survival.Typically it is supplied by two coronary arteries, left and right coronary artery.Both, together carry about 250ml of blood every minute.( Approxinately equal to a cup of coke ! ).These coronary arteries generally divide in a predetermined fashion , and have multiple branches . It is a mystery , what decides this branching pattern
Is it like a our palmar crease ? or the cerebral gyri ?
However , it does follow a certain rule, one major coronary artery will follow the four important grooves of heart. In the left side , left main coronary artery (LM) originates in the left coronary sinus (Size varying between 1mm -20mm) and usually bifurcates into LAD and LCX. The left anterior descending artery (LAD) runs in anterior interventricular groove while , the right atrio ventriculo groove carries the right coronary artery(RCA) .Left circumflex artery (LCX) traverses the left atrio ventricular groove.The most inconstant branch is the posterior descending artery (PDA) which runs in the posterior interventricular groove.PDA can arise from either RCA, LCX or both or even from LAD.
The major branches of LAD are called diagonal and septal while the branches of LCX are called obtuse marginal(OM).There can be two to three diagonal and OMs.
What is ramus intermedius coronary artery ? What is the incidence of Ramus ?
The left main coronary artery instead of bifurcating into two , it trifurcates into three vessels.(LAD, LCX, Ramus)
The real incidence could vary betweenn (10% to 30%) depending upon the series.
What course it takes ?
It generally goes in the angle between the LAD and the LCX.It may either behave like a large OM or a diagonal branch.It supplies the lateral free wall of the LV many times.The peculiarity of this vessel is it does not run in a anatomical groove .It simply slides over the free surface of LV.Rarely, a very abnormal course of ramus, criss cross the aorta and pulmonary artery .
How common is atherosclerosis within Ramus ?
We don’t know yet. But it is very likely since it is an early branch from left main, it might have a predilection for atherosclerosis as like LAD or LCX ostium.In fact now we recognise more of trifurcation lesions involving three branches of left main .
What would be the ECG finding if a large ramus is the culpirit vessel during STEMI ?
This scenario could be rare.
ACS in ramus could present as ST elevation in 1/Avl /V5,V6
Lateral MI
Apical MI
High lateral MI
But it is realised , whenever the ECG changes are not fitting with typical ASMI or a lateral MI one should suspect a ramus lesion
What is the significance of ramus for an interventional cardiologist ?
PCI in ramus is a rare opportunity for a cardiologist .The issue here is, if ramus is involved adjacent LAD and LCX is also likely to be involved .So it would logically be a multivessel , complex angioplasty.Isolated ramus lesion could be tackled easily.Another issue here could be ,since this vessel is not within any anatomical groove stent deployment would have a poor support and prone for mobilisation and migration .
Stents are mechanical devices like a spring , used to keep an artery open after a PTCA or PCI.
Bare metal stents(BMS) were found to have restenois rate of about 25%. So it was perceived a stent should have it’s own protective coat , so that it won’t get restenosed.For this the researchers thought anti cancer drugs are ideal as they block cell proliferation and thus neovascualrisation and restenosis.Alas, they were found dismally wrong , after all , neointiaml proliferation is only a part of the problem of restenosis and simple blocking of cell growth is insufficient . The issue doesn’t stop with that, the anti cancer drugs incorporated within the stent simply can not differentiate normal from abnormal cells and
DES effectively blocks the normal endothelisation over the stents and make this highly vulnerable for acute stent thrombosis .
This complication is unique to DES and can result in SCD.Further ,during the last 6 years of DES , we recognised the restenosis rate has increased form the much hyped O % to almost 15% and it’s still growing . These complications has made a huge question mark over the future of drug eluting stents !
The concept of DES may not die , but which drug it should elute should be answered ! This again is going to be a long battle. So it is currently adviced, based on common sense ( With due respects to those RCTs funded by industry )
Whenever you encounter a block within the coronary artery* Ask the following questions in sequence ,
Whether we can leave it alone with medical therapy , if the answer is no , proceed to the next step !
Is there a possibility for plain balloon angioplasty in a given vessel (POBA, Yes ! the concept is not dead yet !)
If you decide a stent is required , Will the bare metal do the job ?
In multivessel CAD , Did the issue of increased metal load on the long term outcome was considered ?
If lesions appear complex, should we notstrongly consider CABG as an option ?
However if we have the habit of ask ing the following question you are likely to deviate from scientific approach
Is it possible to put a stent across the block ?
Yes , will be the answer most of the time ,and the patient will invariably get one or more stents and carry a life long stent related problems.
*The rule does not apply in Acute coronary syndromes
Also read this letter posted by the author published in British medical journal
One of the important principles of post PCI care is, we need to be very careful till the metal struts are fully endothelialised . This is of vital importance as improper endothelialisation is a powerful trigger and nidus for a imminent thrombosis and acute coronary syndrome.
It is a billion dollor irony , the much hyped DES does exactly what we don’t want ! and still it’s usage is increasing world wide . The drugs (Anti cancer agents) which coat the DES are the villains as it prevents the metal struts from being endothelialised and keep the metal surface raw and vulnerable , while the much maligned bare metal stents allow this natural endothelialisation process without any interruption ! So right now it is mandatory to administer dual antiplatelet agents life long( life of the stent !) for the patients with DES.
Just look , at the following image of a stent in vitro at 30 days follow up
Department of cardiology, Madras Medical College, Chennai.
Radial artery has become the major accesssite for the interventional cardiologist in recent years. Radial approach has provided increased patient comfort and less access site complication. Many of the complications are unique to radial approach mostly due to anomalies of origin, and course while others are hardware related .Unlike femoral arterial access , compromise of blood supply to hand is never considered a threat because of dual blood supply to hand .But the factis that, it could be sub-clinical and the hand is rarely assessed for vascular insufficiency after a radial procedure.
The aim of the study is to assess the impact ofradial procedures on the blood flowtohand . 20 patients who had undergone routine radial coronaryangiogramformed the study population. All patients had negative Allen’s test prior to the procedure. The mean procedure time was 25mts (18-45) .Standardhardwares were used. Difficulty in crossing at forearm and subclavianwas observed in4 patients. Extravasation of dye in forearm was observed in two. Allen test wasdone 24 hours after sheath removal andrepeated 48 hours after the procedure .4 patients showed positive Allen testat 24hrs. One patientregained Allen negativity at48hours. The incidence of positive Allen test at24 hours is 20%. The compromised blood flow was correlated with theprocedure time, and a difficult catheter course .
We propose, radial procedures especially , when prolonged has a potential to compromise palmar arch flow .This phenomenon is either permanent or transient andmay be attributable to enhancedendothelial tone and sheath related injury. Irreversiblecompromiseof blood flow to palmar arch mayalso occurin radial dominant hands. Further enhanced sympathetic tone can spill over to ulnar artery as well .
It is concluded, interventions through radial route has hitherto unreported adverse effectof “Post procedural positive Allen test” . It implies , radialprocedurescould convert a dual blood supply pattern of the hand to ulnar dependentuni-modal blood flowin a significantsubset of patients. This is important to recognise, as it precludes further radial procedures in the same patient.
Final message
Hand function could be as vital as our heart’s , please handle with care to avoid this complication
The science of medicine has evolved over 2000 years since the stone age days.It has currently reached a glorious era with cutting edge scientifc technology .Today one can map the entire human genetic blue print and intervene in the disease even before they manifest .One can keep dying people alive for years with multi organ transplantation. Modern medicine has taught us how human sufferings can be prevented and life can be prolonged (with or without purpose !)
The term conservative management conveys two different
meanings for medical professionals.
For other group of physicians
Ever since the days of application of leech over the head for treating migraine and a crude knife abdominotomy for emergency exit of babies from pregnant mothers in distress , healer’s mind has always perceived “something has to be done urgently when some body suffers” this sort of reaction is probably inherited and is related to the primitive flight or fight response .
This may be true in some of the emergencies but it is untrue in many of the non emergencies.
Unfortunately , our mind finds it difficult to differentiate between these situations . With constant exposure to dramatic medical breakthroughs , modern day physician is made to believe “Some thing is always better than nothing when illness strikes. Human body is a wonderful machine which has it’s own service station ! in the form autoregulation and the meticulous homeostatic mechanisms. Only if the disease process overwhelms, it needs intervention.( Typical example:In the routine viral fever , you don’t adminster Acyclovir or other antiviral for all of them !)
The problem with early aggressive approach is, it fails to give an oppurtunity for the body’s natural defence forces to respond. Further , we will never ever knowhow the administered treatment is going to fare vis a viz the natural response.( With due respects to RCTs). While the field of medicine has so much evolved , our thought process, especially the aspect of clinical reasoning has always been lagging behind .It is now considered as inferior or even unscientific treatment if some one follows a conservative approach to a problem even if it provides same outcome of that of an invasive or aggressive approach ( The classical example is PCI for chronic stable angina The COURAGE study).
The other major issue is the hazards of unwarrnted invesitigations , drugs and procedures
Classical example:No one knows how much morbidity or mortality the routine Swan ganz catheter caused when it was rampantly used for over two decades to monitor central venous pressure .It is estimated that in modern medicine there are at least few drugs or devices in each speciality waiting for the same fate as that of the swan ganz catheter.
No body knows when it will be exposed .Our EBM will take it’s own time . . .Till that time humanity need to suffer.
This thinking is not new The concept “First do no harm is over 2000 years old”
Questions in search of answers
Does law of conservation of energy applicable to human body and medicine ?
Can we defy death with modern medicine ?
Final message
Conservative management is still a great medical concept in many situations and one should not allow it to die by the whims and fancies of the modern scientific forces.
Whatever you do on the patent’s body do it , only if it is going to helpful for him /her. If you are unsure Whether a given treatment is going to help or not ask this question to an expert .
The widely prevailing dogma of aggression is always better than non aggression has absolutely no evidence.
So approach a clinical issue disease by disease , individual by individual.
Now , in this era high tech medicine , It is lot more tougher to choose a conservative path as the pressure to do more and more looms larger ! It is easier to follow the crowd than a path of your own .
Always remember it needs a stronger mind to act according to our conscience !
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