Posted in Infrequently asked questions in cardiology (iFAQs), myocardial disease, tagged cardiology table, DCM, ischemic and idipathic dilated cardiomyopathy, ischemic vs idiopathic dialted cardiomyopathy on July 31, 2011| Leave a Comment »
This seemingly straight forward question is often asked in cardiology boards.
The answer to this question is important in the bedside as well ! Ironically , with sophisticated diagnostic modalities the complexities has also multiplied .
The following table attempts to simplify it. ( Mostly written with a personal knowledge and ignorance !)
Please click on the table to visualise a high resolution image.
Posted in Cardiology - Clinical, Cardiology-Land mark studies, Hemodynamics, Infrequently asked questions in cardiology (iFAQs), pericardial disease, tagged epicardial fat and constrictive pericarditis, epicardial fat pad, sub epicardial fat on July 4, 2011| Leave a Comment »
Constrictive pericarditis is a well known mechanical disorder of heart that occurs due to the compression by thickened pericardium .Constrictive pericarditis is the classical cause for severe diastolic dysfunction.
We know , lungs are prone for restrictive disorders due to chest wall , skeletal disorders. Does the heart get mechanically restricted in extreme obesity ?
Not really , one may reason out . Chest wall fat can have little effect on cardiac function but when excess fat accumulates within the layers of heart , it is indeed possible for the fatty layer to impede mechanical filling of heart. This may be considered rare as of now , but many times it is not recognised , as most of the dyspnea in morbid obesity is attributed to some other known factors.
Dyspnea in obestity can due to
Image courtesey : http://www.onlinejacc.org
Now, we have evidence for altered RV hemodynamics due to compressing effect of epicardial fat pad. It may be due to simple mechanical effect of epicardial fat over the distensiblity of RV or occasionally LV. (The distribution of epicardial fat is mainly over the right ventricle or septal areas.)
This paper from Korean circulatory journal succinctly describes this new possibility .
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2771803/pdf/kcj-39-116.pdf
Final message
Bed side cardiology continues to bring surprises , it never fails to fascinate us !
Heart is a dynamic organ , has a potential to get restricted by any layer that surrounds it. Constriction by pericardium got huge attention so far .We need to realise , the epicardium which is a part of pericardium has a variable fat depot . It can take a different avatar in an occasional obese individual and exert important hemodynamic impact.
Excess fat is excess load on heart . . . we have to unload it
It is possible , sucking out the epicardial fat in morbid obesity can bring important relief to those patients with unexplained dyspnea . We need to explore this possibility.
Posted in cardiology -congenital heart disease, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology congenital heart disese, cardiology-Anatomy, Infrequently asked questions in cardiology (iFAQs), tagged migraine and pfo, pfo, right to left shunt across pfo, vasoactive amines cross the pfo, young stroke and pfo on June 27, 2011| 1 Comment »
The link between migraine and PFO is . . .
Answer : One of the above is correct , but we do not know which one is !
There has been many patients with TIAs , cryptogenic strokes , who had documented PFO ,complain of prolonged head aches . This was the beginning of suspicion of PFO as a cause for migraine .Then the device industry foresaw a huge opportunity . Things began to unfold and the concept is currently as nebulous as it can be .
Mechanism of migraine in PFO
(All are presumptions )
Counter arguments
Where is the evidence ? The mystery called MIST study.
This study , done in UK generated more controversy , which it was supposed to remove . Still this study is considered to be a major evidence for the link between PFO and migraine . Star flex device was promoted by NMT medical Boston .
http://www.medscape.com/viewarticle/541260
Link to best review article on PFO
http://chestjournal.chestpubs.org/content/130/3/896.full.pdf+html
Final message
The link between migraine and PFO can be a fact or myth depending upon our belief in current methods of research in science. The issue is debatable . Of course , one issue is probably closed forever , even if they are linked casually (or seriously ) device closure can never be a sensible treatment option for migraine ! *
We expect a proof / disproof in this mysterious migraine -PFO hypothesis very shortly. Of course , many cardiologists already have their own conclusions !
*Please note , PFO device closure for stroke in young is a different story
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), tagged coronary blood flow, coronary hemodynamics, critical lad lesion, ffr, fractional flow reserve on May 18, 2011| 1 Comment »
Even as we make rapid strides in conquering coronary atherosclerosis by all those fancy gadgets , the fundamental coronary hemodynamic principle is poorly understood . Hence there is no surprise for the “perennial ambiguity” in the indication and effectiveness of coronary revascularization .
Why the hell , reliving a coronary obstruction may not provide the expected hemodynamic benefit or do not prevent future heart attack in many ? One of my patients asked ?
I told him . Wait , do not get excited , we also do not know . . .We are just beginning to understand mysteries of coronary circulation.
It is a well documented fact ( but a debatable ) that lesser the severiity of a lesion more likely it is prone for an acute coronary event .( Vulnerability , shearing stress or is it a simply a statistical mirage !) While the vulnerability aspect is complex , the hemodynamic impact of coronary lesions is relatively better understood. Here is an important documentation from Dr B . K Koo from Seoul , South Korea who has elegantly shown the behavior of fractional flow reserve (FFR ) in various grades of stenosis .This study was done in jailed side branches following PCI.
FFR shows a surprise relationship with severity of coronary stenosis . Even severe lesions showed equal if not more flow reserve ?
and mild lesions might have lost all its reserve.
How is it possible ? Can it be true ?
Yes , it is indeed a fact . God generally keeps a stong link between anatomy and physiology , structure and function . But he adds a rider and keeps a reserve in every human cell meant for emergency back up . FFR is one aspect of this , we have partially discovered . When we fail to understand this we are bound to get confused and make a wrong decision in cath lab.
Simply stated , flow across a coronary artery is much more depedent on the status of microvascualture than the hurdles they face in the epicardial highways !
Link to this original article from JACC .
How to do the FFR procedure ?
http://www.sjmprofessional.com/Clinical-Solutions/Intl/Radi-FFR.aspx
Soon to follow . . . If less severe lesions are more dangerous why we are ignoring it in cath lab ?
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology innovation, cardiology- coronary care, Cardiology-Coronary artery disese, Hemodynamics, Infrequently asked questions in cardiology (iFAQs), tagged 100% lad, 99% lad, bernouli principle in coroanry artery, coroanry doppler, coroanry perfusion pressure, coronary angiogram, coronary collateral circulation, coronary hemodynamics, coronary microvasculature, coronary stump with timi 3 flow, courage trial syntax score, distal coronary resistance, hanging the lad, intra coronary pressure, lad total timi 3 flow, ressitance in series, timi 3 flow on May 15, 2011| Leave a Comment »
Thousands of coronary angiograms are done every day. Cardiologist no longer get excited to see exotic coronary lesions .Still , some images can be striking and dramatic. Here is an angiogram from a middle aged man with stable angina , who was one among the routine early morning diagnostic studies in our cath lab.
Who chopped the neck of this LAD ?
How this man was able to fill up the distal LAD almost completely? (With a complete cut off right in the neck of LAD )
Are you sure there is antegrade flow ?
Do you get any clue ?
Yes . The first one is right . An almost invisible antegrade channel doing a exemplary job !
How is it possible ?
Realize an important fact . The distal flow beyond an obstruction is not primarily dependent on degree of obstruction but the status of the distal vascular bed . If it is normal even a hair-line patency can profusely perfuse the distal myocardial segment. This is what is happening to this man with a stable angina and perfectly normal micro vascular bed.
Lessens from this Image.
Do not get fooled by the lay man’s logic. Realise there is no simple relation between the degree of obstruction and degree of blood flow impediment.It can be linear , curvilinear , or even inverse depending upon the evolution and timing of obstruction , number of lesions , presence or absence of collateral support , finally and most importantly the integrity of microvascular bed .
The distal vascular bed drops its resistance drastically once it senses the problem in proximal segment . This is based on Bernoulli principle and is akin to how a garden hose pipe can simply increase the velocity by tightening the nozzle.*
* The garden hose analogy is a gross simplification of complex factors that determine coronary blood flow.But it effectively clarifies a point ie coronary blood flow is least dependent on coronary stenosis (until very late stages)
**Note further : This hemodynamic principle may not apply in acute occlusion as in STEMI , where acute obstruction often has a linear relationship with the quantum of blood flow.
By the way what happened to the above patient ?
Since he had significant angina there were no debates regarding management. He is posted for elective PCI this week-end .(We can’t get a stent just like that unless it is a real emergency .Ours is a Govt hospital !)
What is your take . Is it a going to be tough cross ?
I feel so , but my colleague Dr Gnanavelu strongly differs !
Let me post our experience during PCI shortly.
Posted in bio ethics, Infrequently asked questions in cardiology (iFAQs), tagged medical statistics on May 12, 2011| Leave a Comment »
In this world of evidence based medicine the funny bedside vocabulary of medical statistics has withstood the test of time. The following words are liberally used by physicians of all walks of life.
We never bother to find what these words mean to our patients !
Here is a crude and wild numerical attempt to decode these words.
Apart from the above there two hugely popular medical words used over million times every day in all walks of medical practice.
They are ” May” and “May not”
The greatness of these words lies in the fact it can convey any of the above 10 meanings in a single phrase without any fuss !
Further , the words may and may not are numberless un-quantified statistical jargons that can convey a deep meaning or . . . no meaning depending upon the circumstances !
Doctor , is there a possibility of my stent getting occluded as i have skipped the clopidgrel ,and aspirin for the past two weeks
You may be at risk . . . but you may not develop an heart attack immediately . I would advice you start the drug immediately .
Posted in cardiology -ECG, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged cardiac arrhythmias during epilepsy, ictal asystole, sbd vs scd, sudden brain death, sudden cardiac death during seizures, sudden cardiac death in epilepsy, sudden cardiac death in stroke on April 10, 2011| Leave a Comment »
Sudden cardiac death is the most common cause of instant death. We know , heart is also under massive neurological control . Still , heart can run for days even after brain dies , if respiration is supported.This implies , heart is independent neurologically ! what a paradox ! But this independence of brain function after death makes the human heart transplantation possible.
Even as we “wow” about this cardiac independence , we witness widespread deaths due to sudden neuro- cardiogenic deaths .This makes medicine . . . a wonderful puzzle and compels us to pursuit the eternal journey of knowledge !
When an area of brain fibrillates what will the heart do ?
When the brain suddenly discharges huge amount of electricity (Load shedding ) as in epilepsy or some other neurological injury , it may travel down and make sure the heart also shares the electrical insult .Sudden deaths have been reported in many epileptic individuals and in some forms of stroke .To distinguish sudden brain deaths from sudden cardiac death in such patients is a very difficult task.
The message is , hypo-functioning brain does not generally harm the heart (Men in coma live for years !) but , over -active brain can inflict major electrical damage to heart. This may indirectly explain , how an episode of severe mental stress could act as a trigger for acute coronary syndromes.
* We do not know , whether brain stem which has the cardiac high command can fibrillate independent of cerebral cortex .
Reference
Ictal asystole
Asystole during epilepsy could occur in significant numbers. As this review from France reveals
Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), myocardial disease, Uncategorized, tagged diabetic lvh, diabetic nephropathy, lv mass in diabetes, lvh in daibetes, microangioapthy, protenuria equivalent in heart on April 1, 2011| Leave a Comment »
Diabetes is a systemic disease affecting almost every cell that metabolises glucose .What begins as a minor functional impairment , worsens gradually and ultimately end up in severe structural changes.The basement membrane of cells face the brunt of the attack . (In the strict sense every cell has a basement but it is well developed only in kidneys ) . We also know , diabetes is able to inflict universal damage by targeting the vascular endothelial cells.
In the kidneys DM makes the glomerulus more porous causing protein leak* and ultimately damages the tubules and end up in CRF. In the retina it excretes the proteinaceous material into the vital layers and result in retinopathy and progressive visual loss.
* Micro/Macro albuminuria
In fact , there is a very close link between eyes and the kidneys Nephrologists hesitate to make a diagnosis of diabetic nephropathy without ocular changes. The peripheral vascular disease and diabetic foot are another expression of this microvascular dysfunction.
What is the impact on cardiac micro-circulation ?
Whenever significant diabetic nephropathy is present there must be a significant cardiac micro- angiopathy as well.This is now a fact than an assumption. We are not recognizing it rather ! (If only we have a cardiac creatinine we can easily identify diabetic myocardial protein leak !)
When kidneys lose protein , cardiac capillaries lose proteins to interstitial space and result in progressive fibrotic reaction . We know extravasaation of high osmolar proteins can play havoc in cardiac interstitium !
Proteins are the particles of life . . . but in wrong places it can transform into deadly molecules in a fraction of time !
Hence , the cardiac protein leak in diabetes can cause any of the following clinico -pathologic entities.
How to recognize cardiac protein leak ?
What about macro-vascular complications in diabetes ? How is it different from micro-vascular complications ?
Though we expect a direct link between micro and macro vascular complication , the later appears to a patho-genetically independent process . This will be addressed later.
Posted in echocardiography, Infrequently asked questions in cardiology (iFAQs), tagged critical aortic stenosis and low flow low gradient, dobutamine stress echo in aortic stenosis, low gradient sever aortic stenosis, waht determines aortic stenosis gradient on February 27, 2011| Leave a Comment »
New concepts are created to clear confusion and bring clarity. We know all along low gradient AS is a hall mark of severe LV dysfunction. Now we suddenly invented normally contracting LV can also cause low gradient due to low flow when the aortic valve orifice becomes very critically narrow .
How can it occur ? . . . few suspect it to be semantics !
The terminology that is often used in recent times when describing severe aortic stenosis.This is called Low gradient severe AS with preserved LV function .
But logic would say blood flow is required to produce gradient .If it falls extremely low the gradient is likely to fall.
If that is the case every severe AS patient will experience low flow at least in few beats . Is this the reason why we find it very difficult to reproduce the exact gradient ?
Low flow ,Low gradient aortic stenosis is not a new entity .It is the way we look at the data. It remains a fact , severe AS can be diagnosed with 2D features alone , without the help of Doppler.We also know Doppler is less reliable than 2D in many situations for various reasons .The most important being it’s dependence on angle of doppler intercept and LV contractile force.
Read the argument by Nikolaus Jander from Germany
http://eurheartjsupp.oxfordjournals.org/content/10/suppl_E/E11.full.pdf+html
Posted in cardiac surgery, Cardiology -Interventional -PCI, cardiology -Therapeutics, Infrequently asked questions in cardiology (iFAQs), tagged chronic total occlusion, coronary collateral circulation, idoe coronary collaterals support exertion, importance of coronary circualtion on February 3, 2011| 9 Comments »
Coronary collateral circulation is probably the most poorly understood circulation than any other.This is ignorance at it’s best , in spite of the life saving potential of this circulation. A popular (mis )perception is coronary collaterals can support only resting blood flow and it would struggle to compensate at times of exertion. This is based on few case studies and not based on large , authentic scientific data.
Does this reasoning mean , coronary collaterals can never / ever be complete ?
If we believe so . . .we are grossly underestimating the power of nature .(In fact , mankind was humiliated by the nature time and again !)
Lessons from a unique patient we have encountered.
Here is an example of total LAD/LCX occlusion with good collateral from RCA. He was having stable angina on medical management . This patient was not only asymptomatic and was also negative for exercise stress test at moderate work load .
There was an intense debate about the management when this angiogram was presented in the cath meeting .
Any answers . . .
He ultimately went on to receive CABG (By popular opinion ) , but the point here is the collaterals were good enough to support exertion.We have documented quiet a few similar patients with collateral circulation supporting exercise.
What happened to the collaterals and (of course ) the patient after surgery ?
I will post you the curious story soon . . .
Final message
Coronary collateral circulation , if well developed can provide hemo-dynamically useful support even at times of exertion *
* The existing literature is biased against this concept. It generalizes all grades of collaterals into a single entity. It is better if we spend more time to understand the nuances of coronary collateral circulation .
This is the message from our observation. Do not ever believe whatever is published as facts in scientific literature. Observe, analyse , create your own inference , and concepts. Mainstream cardiologists would brand it unscientific , Simply ignore it . Many times it is rewarding to our patients.
Dr.S.Venkatesan MD 
