February 8, 2009 by dr s venkatesan
Ventricular tachycardia is considered as a dangerous electrical rhythm abnormality .It can immediately degenrate into ventricular fibrillation and result in SCD in many.Ironically, it is also a fact , a patient with VT can present silently without any symptom .Some VTs are slow and recurrent without much affecting The hemodyanmics.
In chronic recurrent, beningn VT (Some may consider it , ” height of absurdity ” to call a VT beningn ! but it is a reality , the term beningn denotes – very remote chance of converting into VF) ” Is there any other therapeutic option other than convertng into sinus rhythm. “( Read related topics)
The following paper was presented in the Annual scientific sessions of Cardiological society of India, Kochi , seven years ago in 2002
VENTRICULAR RATE CONTROL IN VENTRICULAR TACHYCARDIA
S.Venkatesan,,. Madras Medical College. Chennai
Mangement of hemodynamically stable recurrent ventricular tachycardia remains a delicate clinical problem. Reverting to sinus rhythm is considered as the only aim of treating VT.While rate control is accepted as a therapeutic option in atrial fibrillation, it is not so, for ventricular tachycardia.In this context we attempted to analyse the effect of Amiodarone on ventricular rate in stable ventricular tachycardia which fail to convert to sinus rhythm.
The study cohort consisted of 49 patients with stable VT who were admitted in the coronary care unit of Govt. General Hospital between 1998 to 2002.The criteria for inclusion were systolic BP>100mmHg and absence of hypoperfusion of vital organs The mean age was 52 years (range 26-68) with a male female ratio of 4:1. Of the study group 36 patients were either reverted with IV lignocaine , Amiodarone ( 150-300mg bolus ) or DC cardioversion . 13 patients who did not respond to either of these were followed up with Amiodaroneinfusion(1000mg) for 24 hours. The baseline diagnosis were old MI (6)) DCM (3) Arrhythmogenic RV displasia(2). Idiopathic VT was diagnosed in 2 patients.All these patients had VT during most part of the 24 hour follow up.
The pre Amiodarone mean ventricular rate was 152 (124 –196). Post amiadaorne (at 24hrs) mean ventricular rate was 128(88-142). The time taken for 50% heart rate reduction was 6.6h (4-24h). The average systolic blood pressure improved from 100 to 112mmhg . These patients were discharged in stable clinical status with oral Amiodarone and were referred for EP study.
It is concluded that Amiodarone, apart from it’s cardioverting ability , has a distinct ventricular rate controlling effect which can be of therapeutic value in at least certain subset of chronic recurrent VT.
Final message
Some of the patients with VT carry a very low risk of VF and SCD .In these patients , the only other major aim is to prevent tachycardiac cardiomyopathy that can be done with drugs which controls the ventricular rate whenever VT occurs !
Corrrecting the primary cause like cardiac failire , revascularisation ,detailed EP study ,tachycardia mapping , followed by RF ablation and ICD implantation is the state of the art approch in the management of VTs.But this small clinical observation was made to impress rate control could also be an option in patients in whom these procedures are contraindicated or not available .
Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, Infrequently asked questions in cardiology (iFAQs), My presentations | Tagged amiodarone, arvd, cardaic arrhythmias, electro physiology, ep study, heart rhythm, naspe, podrid, rate control, rvot, ventricular tachycardia, wellens, wide qrs tachycardia, zipes | Leave a Comment »
February 1, 2009 by dr s venkatesan
Ventricular tachycardia (VT) is one of the dangerous form of cardiac arrhythmias.
When it occurs , it may present in many ways
- Cardiac arrest with immediate degeneration into ventricular fibrillation.
- Pulseless VT in a conscious patient but in in shock.
- With pulse, relatively stable , not much fall in blood pressure.
- Incidentally detected.*(Rare)
This , gives us an idea that VT as an electrical abnormality has wide clinical presentations , life threatening at one end and, patient walking into the hospital with minimal palpitation on the other hand !
The management issues
- In patients with hemodynamic instability , decision making is easy as there is only option of DC shock.
- In patients with stable VT, it is natural for the physicians to get tentative or even confused.This is because , dangers of shocking a stable patient has to be weighed against the currently available excellent antiarrhytmic drugs( Amiodarone, Ibutilide etc) .
The major issue here is in ruling out underlying structural heart disease.
Never shock a stable VT, without knowing the myocardial and valvular function.There has been many occasions underlying severe LV dysfunction is missed and they may go for asystole.
VT in the setting of cardiomyopathy, Post MI(Scar mediated) are often refractory even to DC shocks.It is the drugs that will ultimately control the arrhythmia.DC shock is just used to terminate the VT.
VT structurally normal heart , especially arising the outflow tracts of LV or RV behave very differently (Fortunately they are more benign)
- Have less hemodynamic impact as it involves the outflow tract and not over the the pumping zone of LV as in conventional ischemic myocardial VT .
- They respond to calcium blockers verapamil to be precise (As they share properties of SVTs)
- Sensitivity to verapamil by no way convey a meaning of Amiodarone resistance.Out flow tract VTs will also respond to Amiodarone many times.
- Degeneration into VF is rare.
Also read Therapeutic issues in stable ventricular tachycardia
Presented and published in Indian heart journal
Related topics
Why some ventricular tachycardias are resistant , even to multiple DC shocks ?
Posted in Uncategorized | Tagged cardaic arrhythmias, cartp, ECG, electrophysiology, endosense, heart rhythm, naspe, ventricualr tachycardia | Leave a Comment »
January 28, 2009 by dr s venkatesan
Lignocaine , probably has saved more lifes world over than any other cardiac drug .
It was the only choice for ventricular tachycardia till 1990s, both in pre and post thrombolytic era.Every coornary care unit has reverted tens of thousands of unstable VTs with this simple and cheap intravenous drug.the utility value of lignocaine is not limited to ischemic VT alone it is effective in in almost all forms of VT.It was classically administered in two or more boluses followed by an infusion.
What happened to this wonder drug with great performance record ?
The power of statistics , and inappropriate interpretation by the scientific community has left a serious blow to this wonder drug .Now the drug has been made redundant, and mainstream cardiac literature has made everyone feel guilty , if anybody uses this drug for VT .
Why did lignocaine lose the battle ? The reason is three fold
- The advent of much fancied Amiodarone
- One negative study for antiarrhythmic drugs in post MI period (CAST)
- And two so called positive studies for Amiodarone (ALIVE & ARREST) has sounded the death bell for this drug which has resuscitated millions of life !
CAST study http://content.nejm.org/cgi/content/abstract/321/6/406
All , CAST said was routine suppression of asymptomatic ventricular arrhythmias in the post MI period is unwarranted. But you know , how this world interpreted it “Lignocaine has no role in ventricular arrhythmias in post MI setting ” The most funny thing was lignocine was never used in CAST study .
The studies involving one to one comparison of Lignocaine and Amiodarone (ALIVE and ARREST study) was also not interpreted properly.These studied only shock resistant VTs. What about the role of lignocaine where defibrillator was not available ?
Link to ALIVE and ARREST read and make your own conclusion.
http://content.nejm.org/cgi/content/abstract/346/12/884
http://content.nejm.org/cgi/content/full/341/12/871?ijkey=8fa241f3cebb86a177632ec6ccadfb5a3ded7bc2
Final message
- Lignocaine is not only a topical anesthetic , it is powerful and gentle myocardial anesthetic when administered in post MI period.
- With this property it successfully cardioverts and prevents dangerous ventricular arrhythmias.
- Time tested and worthiness proven.
- While , we are made to believe the success rate of Amiodarone in VT is far superior than ligncaine .It is a falsehood.
- Any experienced cardiologists will recognise , many times even Amiodarone resistant VTs often respond to Lignocaine .
- The fact of the matter is , without a good quality one to one study , lignocaine was ditched. One reason for this could be Lignocaine , is a generic drug and has no market value.
Let us take home , the message (scientific or unscientific ! ) Lignocaine still has a great role to play in the management of dangerous ventricular arrhythmias .The only caution is , it should not be used routinely and indiscriminately in all asymptomatic patients with VPDs or nonsustained VT . (Acknowledging CAST conclusion.)
Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Arrhythmias, Cardiology-Coronary artery disese | Tagged alive study, amiodarone, arrest study, cast study, ccu, ICD, lignocaine, lignociane vs amiodarone, ventricualr tachycardia, xylocard | Leave a Comment »
January 27, 2009 by dr s venkatesan
Cannon waves occur classically, during ventricular ectopic beats .(Commonly irregular) regular cannon waves occur during Junctional tachycardias with 1:1 VA conduction
Cannon like wave may appear in the jugular vein if the VPDs is timed in a such a fashion ,the atrial systole occurs with a closed AV ( Tricuspid and mitral valve ) so the atrial contractile wave is reflected back into the veins.This not only happen in right atrium but also in the left atrium , but the cannon waves are sent into the pulmonary veins , which is not visible. As by tradition cannon waves are meant to be seen only in neck veins , we rarely realise the importance of such waves in the pulmonary veins.
There must be some significance for this abnormal pulmonary venous waves which travel in a retrograde fashion.In fact , with the advent of echocardiography, we realise pulmonary flow reversal is an important contribution for raised PCWP.
The dyspnea during multiple VPDs can be due to
1.Transient Mitral regurgitation and resultant elevation of PCWP.
2.Pulmonary venous cannon waves and it’s effect on J receptors.
3.Many of the intermittent episodes of dyspnea (Especially paroxysmal nocturnal dyspnea ) , other wise unexplained could be due to this pulmonary venous cannon waves.
4.It also need to be studied how this pulmonary venous cannon waves distribute themself into the 4 pulmonary veins.
//
Posted in Cardiology - Clinical, Cardiology -unresolved questions | Tagged cannon waves, cannon waves in pulmonary viens, left atrial cannon waves, mechanism of cannon waves, pulmonary cannons | Leave a Comment »
January 26, 2009 by dr s venkatesan
Angina is classified in many ways .The most useful , clinical classification is stable and unstable angina . While ,the former generally is considered innocuous the later conveys a sinister signal to the patient as well as the physician.
Why stable angina is stable ?
In stable angina
- The patient knows how the pain is going to behave by his past experience.
- Very predictable .The patient knows at what distance it’s going to come
- He also knows when it will disappear.(For some , with rest for others with nitrates)
- He also knows where the chest pain will radiate.
- If some thing is unusual it is unlikely to be stable angina , also any first episode of angina is considered unstable as one wouldn’t know how the angina is going to behave !
How is that stable angina has such a learned behaviour ?
The main reason for the beningn nature of stable angina is the coronary artery has “stable plaques”
Stable plaques produce stable angina ,Unstable plaques cause unstable angina
Stable plaque s restrict blood flow only at times of increased demand( ie supply side ischemia.) There is no thrombus in these plaques.As soon as the exertion ends the angina is relieved.So in chronic stable angina, the patient is stable, the angina is stable , the palque is stable , the coronary blood flow is stable.
Unstable palques have erosion and thrombus , and it interferes with blood flow even at rest .So in unstable angina, not only the angina is unstable , the plaque is unstable ,coronary blood flow is unstable. So it is obvious unstable angina , may not be relieved by bed rest.It needs intensive treatment.
Is there a overlap between stable and unstable angina?
Yes. In fact it is more common than we realise.
Read this post https://drsvenkatesan.wordpress.com/wp-admin/post.php?action=edit&post=2177
Related topics
How is a stable palque converts into a unstable plaque ?
How do you identify these vulnerable plaques ?
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Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged acc.aha, angina, plaque, stable angina, unstable angina | Leave a Comment »
January 25, 2009 by dr s venkatesan
Competence of mitral valve is vital for proper hemodynamics of heart .A trivial mitral regurgitation ,is observed in nearly 10-20% of normal population detected by doppler echocardiograpgy .This is other wise clinically insignificant. In fact , it is expected , the sonographers do not report this, as it might increase the patient anxiety.
Can a mildly incompetent mitral valve be a hemodynamic advantage ?
Left ventricle , physiologically can have only one exit, namely LVOT and aortic valve.If there is normal impedance , at this level (LV after load ) it is refered to as physiological .In disease states , as in cardiac failure there is raised after load or LV wall stress.this makes the LV struggle to pump blood into aorta.The more the dilatation the more the wall stress (Laplace law). more the wall stress more the after load.
The main principle of management of cardiac failure for decades has been promoting LV inotropism .Now we have realised this is fundamentally a wrong concept, (Except in acute heart failure). Hence the main option available now is to reduce the after load , ACEI do that most effectively and proven to improve survival.
What is the effect of trivial or mild MR on LV after load ?
It is a hemodynamic fact for MR to increase LV contractility and Dp/Dt due to a relative reduction of after load.
In patients with cardiac failure , even a mild improvement in LV contractility can give a symptomatic improvement .
Can mitral valve act as controlled safety valve allowing only a trivial or mild MR ?
This may be difficult . But it happens naturally in many of our patents in cardiac failure .
Probably , these are same patients who come under the 20% incidence of physiological doppler MR .Other group could form the functional MR*
We have found, patients with DCM with mild mitral regurgitation tolerate excercise better than patients who have very competent and rigid mitral valve.It is presumed a mitral valve which gives in a little bit , decompresses the LV with a symptomatic benefit.But if the MR , is occurs in an eccentric path or it results in significant volume burden the potential advantage becomes a liability.
Related issues
*Functional mitral regurgitation. Functional MR is said to occur , when patients with cardiac failure, and resultant dilatation of mitral annular ring, and lack of opposition of leaflets
While milder forms of MR are well tolerarted , when it occurs acutely ( even if it is mild) , it can be dangerous and result in sudden pulmonary edema .This usually happens in acute MI or infective endocarditis etc.
Final message
- Minimal or mild mitral regurgitation without any significant volume overloding in some of the patients with dilated cardiomyopathy could bring a hemodynamic advantage .
- So one may not unduly worry about , a mild MR (central jet) in patients with DCM.It could be after all a safety exit for overstrained LV
We will report the results of the ongoing study about the impact of presence /absence of mild MR on the 6 minute walk test in patients with dilated cardiomyopathy.
Posted in Cardiology - Clinical, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged cardiac failure, central jet mr, DCM, dilated cardiomyopathy, doppler mitral regurgitation, eccentric jet, functional MR, lap;ace lae, lv wall stress, lvedp, mitral valve, mittral regurgitation | Leave a Comment »
January 20, 2009 by dr s venkatesan
- Gastric pain is a great mimicker of cardiac pain.
- It may have , almost all the typical characters of angina . . . in some cases ECG changes too.
- The confusion is complete , as esophageal pain can also be relieved by sublingual nitrates !
- The issue is further complicated, when esophagus and coronary artery share the same neural codecs, and each may induce spasm among themselves !
- It is thought , of course with some evidence ! many of the syndrome X patients ( positive stress test with normal coronary arteries ) have esophageal motility disorders.
- The ST segment depression during EST in these patients is apparently attributed to stress induced esophageal spasm !
- And many of the patients with variant angina , have associated esophageal sapsm .
Read this land mark concept paper documenting the neural link between esophagus and the coronary artery
Click on the article
Final message
- Don’t ever forget the esophagus in your scheme of things when evaluating CAD.
- Realise that esophageal disorders not only cause non cardiac pain but also cause ischemic chest pain (Also called linked angina)
- EsophagEal smooth muscle cell can exert electrical influence on the ST segment of cardiac ECG !(After all every cell
has an action potential )
Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged ECG, esophagus | Leave a Comment »
January 19, 2009 by dr s venkatesan
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 !
Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, Cardiology -unresolved questions, cardiology- coronary care | Tagged coronary angiogram, diagonal, left anterior descending, septal coronary artery | Leave a Comment »
January 19, 2009 by dr s venkatesan
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.
Read this original article by Patrick Ohlmaan
Click on the link
http://www.medscape.com/viewarticle/530783_print Courtesy Medscape
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
- http://www.annals.org/cgi/content/abstract/133/7/537
- http://www.annals.org/cgi/content/full/133/7/537
Posted in cardiac surgery, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Uncategorized | Tagged aortic dissection, biochemical diagnosis of dissection, d dimer, de baky, intima, media, patrick ohlmaan, type b dissection | Leave a Comment »
January 18, 2009 by dr s venkatesan
Drugs are poisons , whenever it is administered without valid purpose. it can enter human body in many ways (Oral, intravenous, percutaneous etc ) And now we have another route namely intracoronary !
In quest for prevention of restenosis, many of the anti cancer drugs are now delivered directly inside the coronary arteries .These drugs are secreted like a sustained release tablet from the drug coated stents.These drugs are expected to prevent restenosis within the stented segment.But, after years of intense debate and research , we realised that , drugs eluted from the stent could damage the distal coronary vascular bed and coronary microcirculation.( And thus came the epidemic of acute stent thrombosis ! )
The tender and sensitive coronary microvasculature is constantly exposed to these powerful anticancer and immmunosuppresive drugs .It is a great surprise , no body thought of this dangerous drug -coronary artery interaction ! It required the genius of Renu virmani and others to point out this.
But still , the cardiology community by and large , fails to consider this an important issue.This is proven by the fact, usage of DES is still increasing and used mainly as an off label indication.
Read this land mark article from circulation
http://circ.ahajournals.org/cgi/content/full/115/8/1051?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&author1=renu+virmani&andorexacttitle=and&andorexacttitleabs=and&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2007&tdate=12/31/2007&resourcetype=HWCIT
Questions that need to be answered
- What is the long term effects of drugging a coronary artery ?
- Is no reflow or slow flow more common after DES , because of the adverse drug reaction in the distal vascular bed ?
- If a patient with DES undergoes a CABG later what would be the impact of the drug on the graft ? Will the functional vasodilatation affected ?
Final message
A drug , to get a legal clearance it has to undergo hundreds of rigorous tests . Finally it is cleared for that specific indication for which it is tested .Just because a drug is cleared for one purpose ( Paclitaxel for malignancy ) it does not mean it is safe to use for any other purpose for which it is deemed to be useful . Exactly the opposite is happening in the the field of interventional cardiology . No body wondered to think what would be the effect of these drugs on the normal coronary endothelial cells and vasculature.Is it not a crime , without analysing this particular issue , dozens of drug eluting stents have been released in the market . And now, sounds of crying foul is heard world wide !
Let us thank , the so called negative forces in cardiology for making this an issue . In science , the watch dogs should bark at times of danger not wag the tail !
Posted in Uncategorized | Tagged acc.aha, acs, angioplasty, bmj, circulation, cypher, des, drug abuse, ethics, europcr, evidence based cardiology, long stent, medical auditing, nejm, nstemi guidelines, pci, primary pci, ptca, rescue pci, scai, sirius, sirolimus, stemi guidelines, stents, sub acute stent thrombosis, taxus, tctmd, thrombolysis | Leave a Comment »
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Dr.S.Venkatesan MD 