Posted in Uncategorized, tagged annals of meicine, bmj, cancer, common cold, drsvenkatesan, jama, medicine, nejm on December 19, 2008| Leave a Comment »
The irony of medicine is unlimited ! 100 years of active clinical research failed to find a specific cure for the rhino virus mediated common cold.In fact US Govt stopped funding for this .
While , complete cure is possible for many of the cancers, especially hematological ones !
Message
In medicine there are thousands of disorder which have no cure !
Cancers , constitute only a fraction of them !
Posted in cardiology -Therapeutics, Cardiology hypertension, tagged allhat, ascot, atherosclerosis, bmj, coronary artery disese, diastolic blood presssure, hyperlipidemia, hypertension, jacc, jama, lancet, ldl, lipids, mayo clinc, nejm on December 14, 2008| Leave a Comment »
The tip for better vascular health is , all hypertensive patients should keep their lipids to optimal levels and all hyperlipidemia patients should keep their BP as low as possible .
“Keep your LDL as low as your diastolic blood pressure and let us keep it around 70 -80
Posted in bio ethics, Cardiology - Clinical, cardiology -Therapeutics, cardiology-ethics, Cardiology-Land mark studies, tagged accomplish, allhat, annals of internal medicine, bioethics, bmj, conflict of interest, diuretics, drsvenkatesan, drug trials, ethics, jama, jnc 7, lancet, nejm on December 10, 2008| Leave a Comment »
It is now mandatory for all journals to declare the conflict of interest by the authors who are involved in medical research .The purpose apparently is to make all transactions or links between the researchers and their funding agencies transparent .Even major journals do not go beyond this . Some ensure it , to appear in the first page of the article.
Most of journal articles are rejected for poor methodology, statistical analysis and so forth .We don’t know how often a paper is rejected due to a conflict issue per se.If this could happen ,bulk of drug trials would face a torrid time from the editors.
Why , even the leading scientific journals never indulge in grading the significance of the conflict ?
Here is an example .
The much hyped drug trial on Hypertension “ACCOMPLISH” was published in the world’s most prestigious medical journal recently .It left it to the readers to have their own assessment on the conflict issue.
The consequence of not , grading and investigating about the conflicts could have serious global health implications both financially and academically .
This study was designed, formulated, completed and published with a single hidden aim of neutralising the land mark trial of ALLHAT which recommended diuretics as a first line drug in HT.Apparently diuretics are very cheap , effective generic drugs.
Posted in cardiology -Therapeutics, Cardiology -unresolved questions, Infrequently asked questions in cardiology (iFAQs), tagged acc.aha, ace inhibitor, ameriican journal of hypertension, bmj, drsvenkatesan, hypertension, jama, kaplan, lancet, lvh, myocyte, myocytic hypertrophy, nejm, non myocytic hypertrophy, reanl hypertension, regression of lvh, sweeny, systemic hypertension on December 9, 2008| Leave a Comment »
Hypertension is the most common clinical cardiovascular entity.Left ventricular hypertrophy (LVH) is an important consequence of HT.In fact, it is considered as a end organ effect or damage. Others being brain, kidney, and peripheral vascular disease.Knowing about LVH is important because it has been linked to increased cardiovascular events.
Though LVH is considered as a close companion of HT it is surprising only a minority (15-30%) show evidence of LVH .Some experienced clinicians (Level C evidence) quote even lower < 10 % .Traditionally LVH was detected by ECG and now it is replaced by echocardiography.
It will be suprising to note , answer to this question is still not clear .
When we don’t know the answer to a question in medicine , the answer will generally will be inside the genes !
So in HT also the major determinant of LVH is in the genes that determine the myosin heavy chain response .
and also ACE gene polymorphism.ACE genes are involved in the expression of growth factors within the myocardium.
An excellent study on the issue http://www.nature.com/jhh/journal/v17/n3/full/1001523a.html#tbl1
It implicates , gender, age, race etc in the genesis of LVH
So , the myocardium does not respond with LVH in all patients with HT.It happens only in a minority* .Duration of HT can be an important determinant , but the major factor is the alteration of genetic switches within the myocytes How this switches are going to behave , is largely inherited .Regression of LVH is also not uniform again implying lesser role for hemodynamics. (Some studies revealed ACEI have maximum regression of LVH , later disputed )
*LVH is more consistently seen in hypertension due to reno vascular or parenchymal disorders .It is also an observed fact , a combination of diabetes and HT is more likely to result in LVH.
The other major issue that needs explanation in HT/LVH is , how much of LVH is due to myocyte hypertrophy perse and how much is contributed by interstitial cell hypertrophy(Non myocytic hypertrophy)
This issue will be discussed soon
Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged aging, blood pressure, bmj, cardiac output, drsvenkatesan, intra cerbral hypertension, intra coronary hypertension, jacc, jama, kaplan, lancet, nejm, peripheral vascular resistance, renal hypertension, systemic hypertension, venous system on November 14, 2008| Leave a Comment »
A normally functioning circulatory system is vital for our survival . We have about 6000 ml of blood, circulating all over the body in an approximate time of 15-20 seconds.The pressure at which this blood moves across the body is called the blood pressure . Hypertension or simply , high blood pressure is an undesirable hemodynamic disturbance in human circulatory system.Systemic hypertension is the most common type of hypertension. The blood pressure is primarily dependent on the status of the blood vessel(vascular resistance) and cardiac contractility. This regulation is under many neural and hormonal factors.Further the blood pressure varies depending upon the blood vessel calibre, and the local milieu.There is a progressive drop in blood pressure from major arteries to the small arteries .The pressure drop is maximum across the arterioles to reach the venules .The venous circulation has the lowest pressure, it ends up at right atrium with a mean pressure of 0- 5mmhg.
It should be realised , each organ has it’s own regulated blood pressure.The brain perfuses by the intracerebral pressure .The lungs decide how much should be the pulmonary arterial pressure.The kidney not only controls it’s own pressure but also has a major regulatory role in systemic pressure by rennin angiotensin system.The examples are numerous, portal system has it’s unique pressure controlling hepatic hemodynamics. The retinal blood vessels regulate intra ocular pressure. While the human circulatory system has a wide variation of blood pressure across the breadth and length of vascular system, it is ironical a single snap shot BP with a brachial cuff is used to define the normality and if it is normal every thing is thought to be hunky dory !
It is widely acknowledged now , aging of humanity is nothing but aging of our vascular system
So we should have new parameters to assess individual organ’s vascular health as well as the currently popular systemic vascular health.The single important factor that determine coronary endothelial damage is the intra coronary pressure.It is never taken into account in any of the cardivascular mortality studies. This is the prime reason for the widely prevalent conflict in the cardiology literature , namely : Controlling systemic blood pressure has poor correlation with cardiovascular outcome. Many of the so called normotensive individuals have serious hemodynamic injury in their coronary arteries.This was made apparent in the ASCOT LLA study , in which patients with near normal blood pressure also benefited from statin therapy , implying endothelial damage could occur at any level of systemic blood pressure.
The normal intracoronary pressure is around 40mmhg . Intra coronary hypertension as a clinical entity is yet to be recognised . There is no defintion available for intracoronary HT , intracerebral hypertension as well.
It’s still a long way to go , for the cardiology and neurology community to assess non invasively intracoronary pressures and intra cerebral arterial pressure to prevent coronary events ant strokes.
Simple risk prediction using brachial cuff blood pressure is a grossly unscientific method (Sorry, i really mean it ) to assess one’s vascular health.There has been few attempts like vascular endothelial health assessment by fore arm blood flow , central aortic pressure (Instead of brachial cuff pressure) as an index for risk predictment and assessment for hypertension is suggested.
Posted in cardiac surgery, Infrequently asked questions in cardiology (iFAQs), tagged annals of cardio thoracic surgery, beating heart surgery, bmj, bye pass surgery, bypass surgery, cabg, cardaic surgery, cass study, ctsnet, ctsnet.org, edrf, endothelium derived relaxing factor, gastro epiploic artery, graft, jama, lancet, lima, live graft, nejm, nitnitric oxide, opcam, radial artery, saphenous venous graft, triple vessel disaese on November 6, 2008| Leave a Comment »
During CABG arterial grafts are always preferred over venous grafts , for the simple reason the grafted vessel has to carry arterial blood and not the venous blood. Saphenous veins are tuned to carry venous blood at low pressure.The mean coronary arterial pressure is around 40mmhg and this will damage the saphenous venous endothelium more quickly. The reocculsion rate at 10 years for venous grafts can reach 60%.
Left internal mammary artery (LIMA) is the most commonly used arterial graft. This is usually anastamosed with LAD. The lumen of LAD & LIMA are more or less equal and they match well in character also !
The other advantage of LIMA graft is , blood tends to flow both during systole and diastole in a smooth fashion.. Since the venous graft which hangs from the root of aorta , the ostium of venous graft lacks the hemodynamic benefits of coronary sinus . (We know the coroanry sinus acts like a reservoir for the smooth release of blood flow into coronary arteries.)
Finally , the most important feature of LIMA is
It is a live graft
LIMA’s proximal origin from subclavian is left intact, so LIMA acts as a live vessel with it’s vasa vasorum intact , which means the endothlium derived relaxing factor (EDRF-Nitric oxide) secretion is not interrupted.This makes the LIMA an excellent graft , self protected against reocclusion.One may call it a drug eluting graft !
What is the patency rate for LIMA ?
LIMA patency rates at 10 years is nearly 90 % .But the graft patency depends on many factors , like diabetes, age, gender, surgical technique ,(Now , beating heart CABG is very popular , where the LIMA patency is said to be slightly lower than conventional CABG) Sequential LIMA grafts, free LIMA graft ( Which loses the advantage of being a live graft) have relatively lower patency rates.
What are the other arteries used in CABG ?
Other arteries that could be used are radial artery, right internal mammary artery, and gastro epiploic artery.The patency rates of all these arteries far less than LIMA .
A surgeon testing LIMA flow before Anastomosing it to LAD.
Image courtesy Dr.Mannoj Aggny .You tube
Posted in Cardiology -Interventional -PCI, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged bmj, cardiology, coronary, drsvenkatesan, failed thrombolysis, jacc, lancet, nejm, nstemi, stemi, streptokinase, tenekteplace, thrombolysis, tpa on November 2, 2008| Leave a Comment »
Which is the most important factor that determines thrombolysis failure in STEMI ?
Answer : 3 .(Though all 5 factors operate )
Failed thrmbolysis occur in about 40-50% after streptokinase and slightly less with TPA and TNK-TPA . Delayed arrival and late thrombolysis are most common cause of failed thrombolysis. As the time flies , the myocardium gets damaged and the intra coronary thrombus gets organised .Both these processes make delayed thrombolysis a futile exercise.
Not all STEMI patients have large thrombus burden. There need to be a critical load of thrombus for thrombolytic to be effective
Some may have a major mechanical lesion in the form of plaque fissure, prolapse and it simply blocks the coronary artery mechanically like a boulder on the road . The poor streptokinse or the rich Tenekteplace ! nothing can move this boulder .The only option here is emergency PCI .
It is impossible to know.That’s why primary PCI has a huge advantage. But still thrombolysis is useful as some amount of thrombus will be there in all patients with STEMI.Lysing this will provide at least a trickle of blood flow that will jeep the myocardium viable and enable us to take for early PCI.
The commonest cause for thrombolytic failure is the time of administration and the degree of underlying mechanical lesion . So it does not make sense to blame streptokinase always !
Posted in Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged acs, auto regulation, bmj, coronary angiogram, coronary risk factor, failed thrombolysis, hypertension, intra cerbral hemmorhage, intra coronary hypertension, intra coronary pressure, jacc, lancet, left ventricualr hypertrophy, myocardium, nejm, nstemi, stemi, streptokinase, stroke, systemic hypertension. cva, thrombolysis on November 2, 2008| Leave a Comment »
Hypertension is considered a major cardiovascular risk factor.Hypertension can have multiple physiological and pathological effects on heart . The common response to raised arterial pressure is the hypertrophy of the left ventricle ( LVH). This can increase the risk of heart failure in few ( Mainly diastolic failure) It is a leading cause for stroke and less often a coronary event.
Coronary artery disease is almost synonymous with atherosclerosis. There is no separate entity called hypertensive coronary artery disease. But HT can accelerate the process of atherosclerosis. It is widely understood, hypertension can cause physical endothelial damage and functional impairment of endothelial function.The physical damage ie enothelial disruption , or erosion is a very uncommon phenomenon . So currently there is sufficient clinical experience HT is considered dangerous for coronary artery only if it is with the company of diabetes and hyperlipidemia. (This will seem controversial as it is against the findings of iconic Framingham trial!)
What the medical community refers to hypertension , may not be really so inside for the coronary arteries.
The relationship between brachial cuff blood pressure and the intra coronary pressure has very little linear relationship. So one should recognise it is the intra coronary hypertension that has a immediate impact on the coronary events. Now only , we are beginning to understand the complexities of the relationship between HT and CAD. If we analyse a series of individuals HT per se is not a very serious risk factor for CAD* , but it is a number one risk factor for stroke.
While HT is notoriously common to result intracerebral hemorrhage, the same HT would not cause intramyocardial bleeds . Why ?
The exact mechanism is not clear.Acute surges of blood pressure can increase the risk of stroke many times but rarely precipitate a coronary event( But may cause a LVF) . The reasons could be the coronary endothelial shearing stress is less than the cerebral blood vessels.Both cerebral and coronary circulation has auto regulatory mechanism . The coronary auto regulation is more robust in that it does not allow intra coronary pressures to reach critical levels .There is no clinically relevant intra myocardial hemorrhage reported even during malignant hypertension.
*But a high intra coronary pressure can sometimes result in spontaneous coronary dissection and plaque fissure .Lipid mediated injury is vey much facilitated in a high pressure environment.
The answer is yes, ( But not an emphatic yes ! ) Some studies had been equivocal. It is very difficult to say , how much benefit is attributable to BP reduction per se and how much is attributable to indirect effect on atherosclerosis prevention.
High blood pressure during an episode of unstable angina or STEMI can increase the myocardial oxygen demand and worsen the ischemia. It requires optimal control with nitroglycerine ( Preferably ) or beta blocker and ACE inhibitors.Even though HT is commonly associated with ACS, one can not be sure the ACS is preciptated by HT. Many times the sympathetic surge during an ACS keeps the blood pressure high.It is a common experience the blood pressure suddenly dropping to normal or hypotensive levels once the pain and anxiety is controlled.
High blood pressure is a relative contraindication for thrombolysis.It need to be emphasised here, It is the the fear of stroke that make it contraindicated .The heart can tolerate thrombolytic agents delivered at high BP .In fact logically , hemodynamically and also practically it is obseved , thrombolytic agents administered at relatively high blood pressure (140-160 systolic) has better thrombolysis than a patient who is lysed at 100mmhg.
The coronary pressure head which contain the thrombolytic agent (streptokinase and others ) need to have pressure jet effect on the thrombus.So the mean coronary perfusion pressure becomes a critical determinant of success of thrombolysis.
It is a paradox of sorts , very high blood pressures are a relative contraindication for thrombolysis and at the same time normal pressure patients fare less well to thrombolysis.
Hypertension continues to be a major cardiovascular risk factor.It has direct and indirect effects on the heart.Generally HT is more of a risk factor for stroke than CAD.A slightly high BP ( Just around the upper limits of normal or just above it ) has a hemodynamic advantage during thrombolysis.(Class C evidence )
Posted in cardiology-ethics, tagged annals of internal medicine, bmj, cardiology, drsvenkatesan, ethics in medicine, herd behavior, lancet, medicine, nejm on October 31, 2008| Leave a Comment »
Herd behaviour describes how individuals in a group can act together without planned direction. The term pertains to the behaviour of animals in herds, flocks, and schools, and to human conduct during activities such as stock market bubbles and crashes, street demonstrations, sporting events, episodes of mob violence and even everyday decision making, judgement and opinion forming. This is very much applicable to medical profession also.(Ref:Wikipedia)
“surprise ! surprise ! There is very little difference noted , according to Hamilton”
Among humans for example when panicked individuals confined to a room with two equal and equidistant exits, a majority will favor one exit while the minority will favor the other.
The practicing habits of medical professionals move , symmetrically as a herd . When a top journal or a opinion leader utters something every one tend to move in that direction .
If a herd leader says a particular treatment is great, every one will say yes . If he says nay every one will say nay !
No one will really question the direction they move ? Unless the correction occurs from within the herd. No external forces usually are effective.Herding is also benefitial many times as rapid propogation of scientific facts needs such behavior ,but it needs constant scrutiny.
Herd behavior example 1 : The most typical example is the drug prescribing pattern of anti hypertensive agents over the past half century.The movement from diuretics to beta blocker , from beta blockers to calcium blockers and to ACE inhibitor and again to diuretic , then to ARBs and currently shying strongly away from beta blockers, in between have a brief encounter with alpha blockers and finally back to diuretics.
If a particular physician by his insight , had clinged onto diuretics ( Away from the herd ) for over three decades he is a real exemption , although branded old timed and unscientific , he has been the most scientific medical professional indeed !
Herd mentality example 2 : Every one says so ! so it must be true ! Hormone replacement therapy good or bad goes with the leader of the herd .
Herd mentality example 3: Very few cardiologists will be ready to agree the fact that , simple digoxin and diuretic ,ACEI, beta blocker, administration could be as effective as the costly cardiac resynchronisation therapy in atleast some of patients with wide QRS cardiac failure ( As we know up to 30 % wide QRS CHF population do not respond to CRT)
Defying Herd mentality resulted in major break throughs in medicine
When every one was saying beta blocker was harmful in CHF one person from Briton defied it ( Wagenstein, and now beta blockers are the mainstay in the management of CHF! )
There are hundreds of treatment modalities popularised by such herd behavior
Who is the watch dog , whether science is moving in the correct direction ?
Read this land mark article how medical research can be distorted by such learned behavior and how scientific research should not be done .
Click on the image .
This post is not intended to hurt anyone . It reflects , human beings are not fully evolved yet , in the onging process of evolutionary biology.
Dr.S.Venkatesan MD 
