Posted in Brugada syndrome, cardiology -ECG, Cardiology-Arrhythmias, early repolarisation syndrome, ECG -Basics, tagged brugada syndrome and ers pattern overlap, ers pattern, Fear of J waves in ECG, j point in ecg, j wave beingn waves, j wave syndrome, Jitter waves in ecg, junctional point in ecg on April 26, 2015|
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J point is a critical point in the ECG when the ventricles hand over the baton in the electrical relay race from depolarization to repolarization .This the time the sodium channels extinguish itself and the potassium current begins its activity from Phase 0 to 1 .
If the potassium channels activate little early and snatch the baton prematurely from sodium , we get early repolarization pattern .When this happens , the J point of ECG show a conspicuous wave called J wave , originally denoting Junctional wave between QRS/ST segment (Now perceived as Jitter waves ?) The other implication of premature K+ activity is , lifting up of ST segment , making it the most common cause of non ischemic ST elevation.
* J wave in hypothermia is referred to as Osborne wave and may not be not related to ERS(Ref.4)
The Ito current is responsible for the phase 1 of action potential (AP), where a rapid outward k + ion flux take place and draws the dome of AP . The dynamics of Ito is complex .It depends upon the density of epicardial K + channels , which are clustered in a heterogeneous manner .There seems to be a concentration gradient along the epicardium and endocardium , making the wave appear prominent in some. This is especially true in healthy, athletic male population where we have some evidence for androgen to play a role on how these channels will behave.Here comes the overlap between Brugada syndrome and ERS as well.
The subset of patients with J wave pattern were recently shown to have increased risk of primary VF due to phase 2 reentry , when they develop ACS. (Rather J wave pattern was more common in patients who had primary VF following STEMI(Ref 1).This resulted in a spate of worrying articles .Now we know , the fear is largely unfounded ,the risk is far less.
Current thinking is, persons who have asymptomatic ERS pattern with prominent J waves should not be investigated electro-physiologically . (Please remember , every human heart can be induced to VF in EP lab if appropriately stimulated ! )
In fact , I used to tell the young men who harbor prominent J wave , as a marker of healthy heart rather. Let us not fear them with a remote risk that could be as negligible as risk of intercontinental flight crashing into the ocean !
1.Haissaguerre M, Derval N, Sacher F, et al. Sudden cardiac arrest associated with early repolarization. N Engl J Med. 2008;358:2016–2023.
2.Idiopathic Ventricular Fibrillation “Le Syndrome d’Haïssaguerre” and the Fear of J Waves , J Am Coll Cardiol. 2009;53(7):620-622. 11
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Have you felt like this query any time in your office ?
If “Yes” is your answer, then you are not alone .There was a unique conference that took place in 2010 to answer the same query in Rome , Italy on behalf of Italian cardiology society , where this entity is researched more than any other place.Its worth going through this.
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PTMC involves a critical step , where one has to cross the IAS to reach the LA.The septal puncture remains somewhat a blind procedure in fluoroscopy .(Echo can still assist us. )
Stitch effect is a rare complication where the needle pierces the intrapericardial space from the right atrial side and re-enter the left atria .This wrong way entry into LA may not be recognised untill the sheath is withdrawn and a cardiac tamponade ensues after removal.
Where exactly the stitch occurs ? What are the anatomical planes ?
This usually happens in the superior aspects of IAS , abutting the roof of RA and LA . The alignment of IAS with reference to RA and LA is key a determinant.We know in mitral stenosis LA can outgrow the RA , bringing superior aspect of LA in a different plane with reference to IAS .The IAS puncture site may overshoot , enter the pericardial space and stitches the non IAS aspect of RA and LA together , of course still guiding us into LA through a false pericardial track (Which is not recognized )
Note : The intra-pericardial track can be more complex than we realise as a significant part of posterior LA is extra-pericardial and transverse sinus of pericardium can get involved as well.
Our understanding(mis ?) suggests at least four different stitches are possible
- IAS-Pericardial space -LA roof
- RA-Pericardial space -LA roof
Other complex tracts (Based on theoretical assumptions . Please note , in some of the fatal punctures the exact route was not identified by surgeons even under direct vision . )
3.RA-Pericardial space -Extra cardiac-Reenter LA
4.RA-IAS -Pericardial space-Extracardiac -Reenter LA ?
What are the possible bleeding sites in stitch effect ?
There can be two sites of active bleeding .One from RA exit point and other from LA entry point of needle.Extra-cardiac oozing can also occur if the needle has pierced the outer pericardium before entering LA.
- Recognition is the key. It requires extra anatomic acumen to diagnose the false track before we insert and withdraw the sheath.Echocardiography should be liberally used if you suspect a false track .
- Tamponade is to be drained promptly and emergency surgery is usually required if re-accumulation occurs.
- Closing the puncture site with devices has been successfully attempted in few patients .A small ASD device (or a Plug ? ) is expected to close the site of puncture . Since the anatomy can be complex ,one may need to close with two devices , one on LA side and other one RA side .The radial force that closes the tear and long term retention of these device are not known .
Other mechanisms of cardiac tamponade during PTMC
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Mconnell’s sign is a distinct echocardiographic sign that occurs in Acute pulmonary embolism , where RA and RV dilates. RV shows a distinct regional wall motion abnormality in which RV free wall shows akinesia (or severe hypokinesia ) with well-preserved RV apical contraction.This is visible in apical 4 chamber view.
This sign is explained by both anatomic and hemo-dyanmic reasons.
- RV when exposed to sudden pressure overload it not only dilates , it’s wall stress increases (Laplace law : Wall tension = P x Radius ) and end up mechanically stunned . But , since the RV has a complex shape the distribution of this stress is not uniform .As the RV assumes more spherical shape the apical part is not exposed to this stress as it tend to abut under LV.
- RV apex is anatomically tethered with LV apex and share significant amount of circumferential fibres .In patients with acute pulmonary embolism , LV usually is hyperkinteic due to tachycardia .This pulls the RV apex along with it for a proxy contraction .
- Rarely , primary RV ischemia due to RCA under perfusion* may be responsible for this unique wall motion defect . Since RV apex is mostly supplied by LAD it is free from ischemia . (*Acute elevation of RV intramural pressure due to PHT , compromising RCA perfusion pressure )
1.McConnell MV, Solomon SD, Rayan ME, Come PC, Goldhaber SZ, Lee RT. Regional right ventricular dysfunction detected by echocardiography in acute pulmonary embolism. Am J Cardiol. 1996; 78: 469–473.
2. Rachel P. Sosland, Kamal Gupta,McConnell’s Sign circulation. 2008; 118: e517-e518
3. Link to the Echo clipping of McConnell sign in echocardiography
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During exercise stress test , systolic pressures should raise at least by 20-40mmhg.(Max 60 mm from baseline ) Diastolic BP will remain at baseline or show a marginal elevation or even a miniscule fall.This is primarily due to increased cardiac out-put , mediated by demand and dilatation of musculature in exercising muscle.
If the systolic BP falls or does not raise during exercise , it implies either poor LV function , vascular insufficiency or autonomic dysfunction.
If there is a fall of > 20mm , even in the first stage, accompanied by chest discomfort or giddiness with ECG changes ,it could be an ominous sign of serious left main or a tight proximal LAD disease and test should be terminated immediately.
Paradoxically , If BP raises more then 200 at any time we call it hypertensive response and may be a risk factor for future onset systemic HT or even a stroke. ( Stress test not only help us detect ischemia of heart ,it also can reveal how the vascular system would handle and adopt to increased cardiac output at time of hemodynamic demands)
Physical de-conditioning is an important cause for hypertensive response , as the entire vascular system lacks dynamism (Vascular tone ) , a precursor for hypertension, endothelial dysfunction and cardio vascular events..
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