Posted in Uncategorized, tagged belhassen vt, classification of VT, galavardin, ILVT, left ventricular tachycardia, lvot vt, narrow qrs vt, septal vt, vt on February 24, 2011 |
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How to name a ventricular tachycardia ?
This continues to be a favorite past & present time of modern-day cardiologists. Especially , VTs associated with structurally normal heart suffers with this protracted problem .Widespread use of EP study has not solved the issue as yet.
The VTs that arise from the left ventricle in an apparently normal heart has been referred by various terms.
- VT with structurally normal heart
- Idiopathic left ventricular tachycardia
- Verapamil sensitive VT
- Septal VT (It can be either myocardial /non myocardial origin)
- Narrow qrs VT
- Fasicular VT
- LVOT tachycardia
- Hemodynamically stable VT
- Belhassen VT
Now we have still more exotic VTs like Cuspal , mitral annular , etc . All of the above can mean anything , or same thing in different centers , different cardiologists in different times .
* RVOT tachycardias also have many synonyms.( Adenosine sensitive, Adrenergic, Gallavardin, Parkinson Pop, etc )
VTs associated with CAD , valvular , myocardial diseases generally devoid of nomenclature problems. Ischemic VT is yet to be classified in a proper fashion.
The confusion in classifying VT is not due to the complexity of heart disease. It is due to the general comprehension failure as every VT can be described with reference to clinical , ECG morphology, hemodynamics and presence or absence of underlying heart disease. A simplified and clinically useful VT classification is being prepared in this forum .Will be published shortly .
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Posted in Cardiology - Clinical, tagged bundle brancg reentry, cardiac arhhythmias, dc shock, defibrillator, ICD, ischemic vt, lvot vt, madit, madit 2, naspe, nstemi, pace, ventricular fibrillation, ventricular tachycardia, vf, vt, vt in unstable angina on May 10, 2009 |
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Acute coronary syndrome is the commonest cardiac emergency. STEMI and NSTEMI are the two clinical limbs of ACS. Generally they have distinct clinical, ECG, angiographic features.(Ofcourse, with some degree of overlap) . It is a mystery , both clinical presentations differ so much inspite of the common denominator , namely , an injured plaque with add on thrombus within the coronary artery.
The mystery is since decoded , the primary difference between these two entities is STEMI the occlusion occurs sudden and complete and in NSTEMI it occurs slow and incomplete
In STEMI , most of the clinical features and , need for emergent treatment , response to thrombolysis /PCI are dictated by the time dependent risk to myocardial loss .
Cardiac arrhythmias in ACS
It is a much published factoid for many decades only one third of STEMI patients reach the hospital alive ! The reason being , STEMI is very much prone for primary VF.
Contrary to this , almost all patients with NSTEMI reach the hospital alive ! How ?
Both are ACS, if ischemia is a powerful trigger for dangerous ventricular arrhythmia’s , NSTEMI should also behave similarly .
So what protects against arrhythmias in NSTEMI ?
- We realise , by observational experience (Not EBM !) It is the suddenness and totality of ischemia that trigger dangerous form of arrhythmia .
- Further, a balanced ischemia in two contralateral segments (or global ischemia) some how protects against development of ventricular fibrillation .This may be due to preservation of electrical homogeneity , and the spherical VT spiral waves are not sustainable.
- In contrast , STEMI has a sudden focal , ischemic zone that initiates the VT and ischemia free contralateral segment welcoming and sustaining the reentrant wavelet.
- The observation of primarily single vessel disese in STEMI and multivessel disease in NSTEMI also give credence to this concept.
- Further , ischemic preconditioning can exert an important anti arrhythmic effect in NSTEMI as patients with unstable angina have slow, repetitive episodes of ischemia prior to the index event .
- Post MI scar mediated VT/VF is independent of degree of overall ischemia
- It is also established , a sub group of STEMI pateints who had preinfarction angina( ie . a brief period of UA/NSTEMI) have very low risk of SCD supporting the concept of sensitising the myocardium against ventricular arrhythmias.
Even though , there is a convincing concept of ischemia induced cardiac arrhythmia in literature , in real patients it is very difficult to link the two.
UA/NSTEMI is the most common acute ischemic event but the incidence of VT/VF here, is far less than one would expect.
In ACS , focal , total ischemia is more likely to precipitate a VT/VF than multifocal and global ischemia.
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Posted in Cardiology - Electrophysiology -Pacemaker, cardiology- coronary care, Infrequently asked questions in cardiology (iFAQs), tagged bmj, fasicular tachycardia, heart rhythm, Hemodynamics, ischemic vt, jama, lancet, lvot vt, myocardial VT, nrjm, pace, ventricular tachycardia, verapamil sensitive vt on October 3, 2008 |
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Ventricular tachycardia is considered as one of the most dangerous cardiac arrhythmia .It is often the word VT spreads more fear than the arrhythmia itself. It is also a well known fact many patients with VT walk into hospital.But the fact of matter is VT will always be a sinister arrhythmia as long as it carries a risk of degenerating into ventricular fibrillation.
What determines hemodynamic stability in VT ?
- Origin and location of VT
- The ventricular rate
- Impact on mitral inflow pattern
- Associated left ventricular dysfunction or valvular heart disease.
- VT in the setting of acute coronary syndrome.(Ischemic VT)
- Inappropriate drug selection
Origin and location
VTs originating high up in the ventricle( High septal VT,Proximal VTs) have more organised ventricular contraction and they are more stable.Distal VT originating in the myocardium away from the conducting systm has chaotic myocyte to myocyte conduction.These are very unstable.
The term fascicular VT is nothing but VTs originating in the His bundle and it’s branches( Can also be termed Septal VT ).These VTs are also stable and some of them respond well to calcium blockers indicating that they are very close to the AV junction and carry the properties of junctional tachycardia. QRS width gives a rough estimate about the location of VT. Narrower the VT higher it’s origin.( But remember even in VT , qrs can further widen on it’s way downhill !)
This is probably the most important determinant of the outcome in VT. Patients with severe LV dysfunction (EF <30%) fare badly .Hence the land mark concepts from MADIT 1& 2 demanded ICDs in these patients.The most common clinical setting is dilated cardiomyopathy.SomE of them have bundle branch re entry(BBR).This particular VT can be stable for many hours.
Usually VT has a rate between 120-200.Higher the rate of VT more the chances of instability .This rule is also not always true as fascicular VT can be well tolerated at high rates.So location of VT focus and LV dysfunction usually over rides the impact of ventricular rate.
Mitral inflow pattern
Proper left ventricular filling is the key to hemodynamic stability in VT. In proximal, septal,fascicular, LVOT VTs doppler studies suggest (ACC /AHA Type C evidence : Personal observations in CCU during VT) near normal preservation of bi modal filling of mitral valve inflow.In ischemic myocardial VT the mitral inflow profile is critically affected . There is no distinctive forward filling was observed .In fact at rapid rates a short pulsatile MR jets are noted instead.
Associated valvular diseases
It is obvious, aortic valve and mitral valve disorders can aggravate the hemodyanmic instability.
The clinical behaviour of ventricular tachycardia is widely variable and dependent on multiple factors.
Associated LV dysfunction and structural heart disease ultimately determine the outcome.
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