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The failing heart enlarges progressively and attain a globular shape . What looks for the naked eye as a simple global hypokinesia of LV , when analysed , reveal multiple forms regional desynchronisation .This is especially true if the QRS complex is wide.
It is generally divided into three groups
In our search for improving CHF mortality and morbidity , we have stumbled upon this concept of restoring the lost synchrony of the heart. Cardiac resynchronisation therapy has become ( Rather projected to become !) a great modality for patients with cardiac failure.It was initially advocated only for severe forms of cardiac failure , now advised even for class 1 CHF. (CRT-MADIT 2009)
Restoring the lost synchrony by rewiring the cardiac conducting system with multiple leads and optimally timed pacing increases the effectiveness of cardiac contractility.It can improve EF, and also regress mitral regurgitation.
The above concept was perfect on paper , but was very difficult to replicate on real patients. CRT was ineffective in 30% of patients. Many had partial effect. Few had adverse effect .
The reason for the poor efficacy is technical in many . Identifying the optimal sites for positioning the leads and the futility of such an exercise as the LV epicardial lead is pre- selected by the patients coronary venous anatomy are the major issues.An electrically ideal site for pacing can contain a mechanically dysfunctional scar. While these technical issues may be addressed in due course what worries us is the conceptual flaws.
Emerging facts indicate timing of asynchrony could be vitally important.
What is the incidence desynchrony with reference to the cardiac cycle ?
One major reason that was overlooked totally was the presumption cardiac dysynchrony occur only during systole. It is a less recognised fact is the ventricular relaxation is not uniform and synchronous.A failing ventricle can not be expected to relax systematically and coherently for the simple reason the myocytic calcium reuptake into the sarcoplasmic reticulum is grossly impaired. This is directly responsible for the diastolic dysfunction observed in dilated cardiomyopathy . If this impairment occur uniformly throughout the left ventricle it can be termed global diastolic dysfunction which is little easier to correct .But what really happens is the defect in calcium reuptake occurs in a random fashion with lot of regional variation. This is called regional diastolic wall motion defect or regional diastolic dysfunction.The above mechanisms result in the typical restrictive filling pattern of many of the advanced patients with DCM . CRT as a concept should need to address this issue.
How to diagnose Diastolic WMD?
The fact is ,we have not mastered the quantification of systolic WMD as yet. It may take years before decoding the nuances of diastolic wall motion defects. At least we need to know such a thing exists.Tissue doppler strain rates , velocity vector imaging could be useful tools. As such they are not clinical tools.
Final message
Cardiac resynchronisation as a concept is good on paper . Heart need to be synchronous both during systole and diastole .This becomes especially important in an advanced stages of heart failure. Without proper follow up and potential adverse effects of CRT on diastolic WMD , CRT concept has miles to travel ! . Some pessimistic thinking cardiologists ( Me . . . !) would even argue it as a case of prematurely released device into the patient domain. Of course there is lot of scientifc data that will vouch for its beneficial effects .(The latest being from the prestigious NEJM , CRT-MADIT) but it has to prove it’s worth in individual patients. Physicians must exercise caution before embarking on heroic attempts to provide resynchrony of failing hearts .
Reference
This study from France published in JACC 2005 by Iris Schuster,
http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109705021005/fulltext
Coming soon
ICDs are better bet than CRT
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Left ventricular hypertrophy (LVH) is one of the most common structural heart disease.Systemic hypertension, aortic valve disease are responsible for the bulk of the cases .Some of the LVH occur due to cardiomyopathy (HCM/Non HCM variants).Athlete’s heart is a physiological response to exercise and it is largely a normal entity.
How many patients with SHT develop LVH ?
It is surprising to note , not every patient with SHT develop LVH .In fact estimates suggest only about 30-40% of chronic hypertensive individuals develop SHT .
What are the determinants of LVH in SHT ?
While any of the above factors may operate in determining LVH
none of the above are important than this
“Genetic susceptibility ”
The myosin isoforms are determined by the genes .The re expression of fetal isoforms in adults is responsible for LVH in many .This is determined by the genetic homogeneity
LVH in renal disease
Secondary hypertension due to renal dysfunction is a major determinant of LVH. This is espcially true if the pateints are dialysis dependent.The mechanism are not clear .
Diabetes and SHT : LVH friendly forces
When diabetes alone and SHT alone is less likely to result in LVH the combination of these two entities greatly increase the likely hood of LVH.DM induced microangitis amplifies the after load effect of HT and result in early LVH.Further this LVH is different from pure forms of hypertensive LVH in that the interstitium goes for hypertrophy and in some cases neovascualrisation. In hypertensive LVH it is predominately myocyte hypertrophy with little interstitial proliferation. this has important therapeutic implication as any drug which reduce the blood pressure can regress pure myocytic hypertrophy, while in diabetic LVH regression is difficult to achieve .
Lipid levels inversely related to LVH ?
There is no consistent relation between lipids and LVH .Occasional reports suggest a negative correlation.
Which LVH is associated with diastolic dysfunction ?
It is a well known fact , LVH has major effect on LV diastolic function.But it is also a fact only some forms of LVH develop this. Now it is clear only if the interstitial hypertrophy occur diastolic dysfunction is manifested. Even as the as the hypertrophied myocyte continue to relax the interstitium do not have molecular mechanisms to relax .Hence, as discussed earlier , diabetic hypertensive patient often develop diastolic dysfunction .
Final message
LVH is not a simple expression of raised after load.It has major non hemodynamic determinants which if identified , could have important therapeutic implication.
Coming soon . . .
Can coronary artery disease induce LVH in the absence of SHT or DM ?
//
Posted in Cardiology -Mechnisms of disease, Hypertension, Infrequently asked questions in cardiology (iFAQs) | Tagged determinants of lvh, genetic aspects of LVH, left ventricular hypertrophy, lvh, mechansim of lvh, systemic hypertension | Leave a Comment »
The quantum of electrical energy reaching the surface of the chest wall varies widely .It depends upon myocardial mass, proximity to the chest wall and the thickness of chest wall.
Apart from this , the amount of blood within the left ventricle also determine the QRS voltage of ECG.
In dilated LV due to a regurgitant lesion , the LVEDV is increased . Since blood is a very good conductor of electricity , it amplifies the transmural activation front and results in high voltage QRS complex.This is referred to as Brody’s effect.
Where else , we can visualise the Brody effect ?
During excercise stress testing , when the heart rate and the LV diastolic volume increases .There is a significant increase in QRS voltage in leads facing LV, especially V5 and V6.
This is usually a benign response in healthy individuals. However in patients with preexisting CAD and LV dysfunction an increase in R wave amplitude may be a marker of exercise induced LV dilatation which could predict an adverse outcome .
Is there a reversed Brody effect , where Q waves get deepened on exercise ?
This has not been described in literature , but it is seen often in patients with post MI stress testing .Q gets deepened .If the q gets minimised* it could indicate presence of significant viable tissue , as it gets recruited during the excercise induced positive inotrpism mediated by catecholamine .Lengthening or deepening of Q indicate less viable tissue.
*Study in progress : Will be referenced shortly .
Brody effect is a complex phenomenon.
Advanced readers follow the link for illustration on Brody effect
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Human body is made up of trillions of cells. Some of these cells are specialised and connected together to form various organs.The cells that connect each other provides the structural support and maintain the organ shape and function. Traditionally these supporting cells were thought to have little functional role. Now it is well recognised these cells could be as important as the myocytes or hepatocyte . God has never created any of the human cells with out any purpose . They may have important paracrine function. Healthiness of these interstitial cells are vital for the intercellular communication, cell nutrition and it’s proper function . These cells are called by various names , the old terminology could be the connective tissue -the tissue that connects cells. Many times fibroblasts is the common name given to all interstitial cells . Interstitium is not only filled with some bizarre mesenchymal cells it is also a depot of sticky molecules. Now we have deeper knowledge about these , and identified various intercellular adhesion molecules, matrix metallo proteins , vitronectins, etc.
It is a great medical paradox the specialised the myocytes, hepatocytes, axonal cells are given due respect, while the role of cells and molecules that bind them together is least appreciated . In fact in any given organ the functional cells constitute only one third of it’s weight.In the heart myocytes form only 30% of it’s weight. It is a clear cut case of discriminating the majority !
Interstitial disorders and diseases
In the lung Interstitium becomes very much important because the gas exchange has to traverse the interstitium and enter the alveloar cells. So any abnormality here is immediate and profound.The diffusion capacity reduces .Patients develop progressive COPD.
In the kidneys , interstitium has a functional component as the absorbed fluid and electrolytes has to reach the blood circulation .Hence acute and chronic interstitial nephritis are distinct clinical entities .
In the brain dysfunctional inter neuronal cells can interfere with various CNS functions dementia the major disorder id thought mainly contributed by the interstitial fibrosis.
So when each of the vital organ has a potential to suffer from interstitial pathology How can heart alone escape ?
No, it does not . The currently popular entity , heart failure with normal ejection fraction could be nothing but chronic interstitial carditis. or chronic progressive interstitial fibrosis. Hypertensive heart disease is a major cause . CAD can also contribute .
The interstitial fibrosis is also a feature of dilated and restrictive cardiomyopathies. (Classical amyloid heart disease ) .Initially these fibrosis do not affect the contractile function of myocyte .In later stages it encroach upon the contractile cells and impair the EF. This explains the natural history of many of the RCMs which go for dilatation and contractile dysfucntion in terminal state.
What is the difference between myocyte relaxtion and cardiac relaxation ?
How to overcome interstitial fibrosis and stiffness ? Anti fibrotic drugs ? .
We are in search for such a universal anitifibrotic drug that can work in liver fibrosis ( Cirrhosis ) lung and myocardial fibrois. D penicillamine has showed some promise. How to make the interstitial interface more flexible ? Collagenolytic agents , elastase MMP inhibitors etc may become the future targets. A much established way to regress myocardial fibrotic process is , with ACEI and aldosternoe antogonists. (EPESUS, RALES study) .Some of the anti myocardial remodelling action of ACEI is attributable to it’s anti growth factor properties and can the resultant regression of interstitial fibrosis.
Apart from the look out for sophisticated drugs , applying common sense can do a “great deal of good “for the myocardium in diastolic cardiac failure . A stiff skeletal muscle need physiotherapy. A stiff cardiac muscle will also need exactly this. For cardiac muscle physiotherpy can not be administered by a therapist ! , we have to do it , regular exercises to make it contract and relax fast . So , it is important to recognise exercise prescription and training could be the most important modality for preventing progression of diastolic heart failure.
Clinical situations where cardiac interstitial pathology is relevant
Final messge
Deep dissections of pathological hearts in pursuit of culprit cells has surprisingly , lead us not into myocytes and conducting cells but into inter cellular spaces” . There is big secret world over there within the cardiac interstitum.Young scientists and students argued to explore and unravel the mysteries !
Reference
A landmark article in Circulation 1991
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ST segment depression is the classical response to stress during excercise stress testing. (EST)Not all types of ST segment are pathological.The ST segment should depress atleast 1 mm below the isoelectric segment and it should be depressed for 80msec from the J point.
It must satisfy two criteria .
Always pathological slopes
Most often pathological
Non pathological slope
Horizontal or down sloping ST segment is easily recognised .When there is junctional ST depression with a ST segment that is climbing upwards , it is some times difficult to interpret.
How do you measure the slope of ST segment ?
We don’t have the trouble of measuring it as the computer does this job automatically. But a cardiology fellow need to know how it is measured !
A slow upsloping ST segment( <1.5mv.sec )can be a significant marker of ischemia.This is especially true in established CAD or individuals at high risk . For so slow up sloping a .5mm allowance is given to filter out false positive (ie to improve sensitivity) . So for slow up sloping ST segment , to be reported as positive it should depress atleast 1.5mm or some times 2mm.
Available evidence suggest a rapidly upsloping ST segment (> 1.5mv /Sec) is a non ischemic response irrespective of the quantum of ST depression at 80msec. However , a rapidly upsloping ST is rarely depressed beyond 2mm .( This is because , the geometric hyperbolic curve of ST segment does not allow a situation of 3mm ST depression at 80msec with rapid upsloping )
What is the angiographic correlation of slow upsloping ST segment depression?
Few studies are availbale to address the issue. It is believed slow up sloping of ST depression is often associated with CAD but it is very rare to find a critical and proximally located CAD.Left main disease is almost never manifest with slow upsloping ST depression.
What is the significance of slow upsloping ST in clinical situations like unstable angina ?
It is rare for cardiologist to diagnose or “even look for” slow or rapid up sloping ECGs in coronary care units. But , a patient with stable CAD , sinus tachycardia , angina can exactly mimic a stress test situation .
Some of the low risk UA , mainly secondary UA due to increase demand situations manifest with slow upsloping ST depression , while classical thrombotic occlusions produce the typical horizontal or downsloping ST segment depression.
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Primary ventricular fibrillation is the number one killer in STEMI.It is believed to occur ( Rather it occurs really !) in up to 25 % of all patients with STEMI before they reach the hospital and another 4% after reaching the hospital.
What triggers this primary VF ?
Easily answered : It is the acute ischemia in majority.
Why it triggers in only in some patients? The rest reach the ER safely and some casually walk in to the OPD few days after a STEMI
This can never be answered with our current knowledge base. Some call this as fate !
Scientists should work hard on this issue, if we know the answer we could possibly prevent the number one killer of the mankind at bay.
Many factors are being analysed to find the reasons for primary VF
If nothing explains the VF it is always safe to blame it on susceptibility and inherited risk for primary VF , which of course is very much likely as the K+ channel activity and it’s response to ischemia is largely inherited
Is there any hot spots in the heart that are hypersensitive to ischemia ?
Some studies have clearly documented increased incidence of primary VF in infero posterior MI , and RV MI
than anterior MI . J Am Coll Cardiol 2001; 37: 37-43
Why ischemia of a certain location of heart should be more prone for primary VF ?
The answer is any body’s guess.
Some intriguing possibilities are ,
Related video by the author
Ignorance based cardiology -You tube
Potential research areas
Genetic susceptibility
Environmental Energy flows and primary VF
Some believe a role for astrological forces and VF
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Traditionally we believed VT can originate only from the ventricular myocardial cells . Then we realised many of the VTs shared the characteristics of SVT. When these were analysed , it was found VTs , after all , do not have a big deal of difference wth SVT s ! especially when it arises from the high septum .Contary to the conventional teaching the AV node is not a anatomically distinct and discrete structure .Instead it is made up of thousands of specialised cells located in AV junctional area .These cells ramify both superiorly and inferiorly like an octopus . Hence , it does not require great academics to understand AV Nodal properties extend downward into the IVS for some distance . In some individuals clusters of cells with slow conducting property (Which is a hall mark of AV nodal tissue ) may invade deep into the IVS .The interface of these slow conducting tissue with that of fast septal purkinje fibres , make it a perfect platform for the potential slow-fast reentry within IVS. This forms the basis of fascicular VT.
Clinical features
Note:
Fascicular tachycardia is also known in several names.
It forms the bulk of the causes for idiopathic left ventricular VTs .Other being LVOT VT.
Described first by Cohen in 1974 , followed by Zipes , when they noticed it was possible to reproduce atrial induction of VT.
Belhassen in 1984 found the verapamil sensitivity of this VT
Other synonyms some times used are
Download high resolution table
Fascicular tachycardia
Posted in Cardiology - Clinical, cardiology- coronary care, Tutorial in clinical cardiology | Tagged anterior fascicular tachycardia, bbr, belhassen ventricular tacycardia, fascicular tacycardia, inter fascicular tacycardia, narrow qrs ventricular tachycardia, narrow qrs vt, posterior fascicular tachycardia, RF ablation, upper septal tachycardia, ventricular tachycardia, verapamil sensitive vt, wide qrs tacycardia | Leave a Comment »
Ventricular tachycardias , especially incessant ones not controlled by drugs are very troublesome . Radio frequency ablation is the treatment of choice currently. Principles of electrophysiology would demand acccurate localisation of the tachycardia focus and then ablate it with RF energy .This requires induction of the clinical arrhythmia on the EP table, mapping , identifying the circuits and ablate the optimal points of reentry or slow conduction or P potentials
In reality , some times ( or Is it many times !) , tentative ablation
in the ” V-tach Zone” without mapping is more easier and surprisingly more effective than the much scientific approach of localising the circuit and inducing the arrhythmia.This is referred to as primary ablation
Is it not a crude method to blindly burn cardiac tissues ?
No, we are not worried by the crudeness , as long as it is safe and effective. Experience have made us clever, inducing a VT in the EP lab can be very demanding to our senses and it is a true stress test for the cardiologist’s patience and endurance.Primary ablation has reduced fluroscopic time, procedural time and most unexpectedly increased the success rate!
So even a relatively unscientific blind burn may be better than a scientific burn ?
Yes. It seems to be , at least in idiopathic VTs of fasicular origin and some VTs in RVOT.
Heart is a 400gram organ , it can afford to lose few grams of tissue , especially when it is pathological and behave aberrantly
Reference:
A nice paper from India
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It is often said life is a cycle , time machine rolls without rest and reach the same point again and again . This is applicable for the knowledge cycle as well .
We live a life , which is infact a “fraction of a time”(<100years) when we consider the evolution of life in our planet for over 4 million years.
Man has survived and succumbed to various natural and self inflicted diseases & disasters. Currently, in this brief phase of life , CAD is the major epidemic , that confronts modern man.It determines the ultimate life expectancy . The fact that , CAD is a new age disease and it was not this rampant , in our ancestors is well known .The disease has evolved with man’s pursuit for knowledge and wealth.
A simple example of how the management of CAD over 50 years will help assess the importance of “Time in medical therapeutics”
So the CAD therapeutic journey found it’s true destination , where it started in 1960s.
Final message
Every new option of therapy must be tested against every past option .There are other reverse cycles in cardiology that includes the role of diuretics in SHT , beta blockers in CHF etc. It is ironical , we are in the era of rediscovering common sense with sophisticated research methodology .What our ancestors know centuries ago , is perceived to be great scientific breakthroughs . It takes a pan continental , triple blinded randomised trial to prove physical activity is good for the heart .(INTERHEART , MONICA studies etc) .
Medical profession is bound to experience hard times in the decades to come , unless we look back in time and “constantly scrutinize” the so called scientific breakthroughs and look for genuine treasures for a great future !
Common sense protects more humans than modern science and it comes free of cost too . . .
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Dr.S.Venkatesan MD 