Natale PVI

Hi All,
The folowing post disappeared from the bb due to the early March difficulties. So here it is again.

Hi all,

On February 20, Dr. Natale performed my PVI at Marin General Hospital. I have already posted praises for the hospital and the staff and will now report my follow-up experiences. I would appreciate any feedback on 4 issues numbered below.
First, during the surgery I had monomorphic nonsustained ventricular tachycardia, an unexpected finding. This is apparently dangerous and will require another ablation. I have not studied this problem yet and so would appreciate comments either on the board or personally (issue number 1).
The atrial fib ablation is viewed currently as “successful”. To be more precise, successful means that I do not have atrial fib but I have not been in sustained NSR since Wednesday February 25. I have nearly continuous “ectopics” (first for the same recordings, I was told that I had afib, then ventricular bigemeny and then finally “ectopics”). I hope that final diagnosis is correct. I wonder if anyone else who has had an ablation has had nearly continuous ectopics after surgery and whether it resolved itself (issue number 2).
I am taking 200 mg of flecanide, 50 mg of toprol, 20 mg of lipitor and coumadin and am nearly comatose sleeping as much as 16 hours a day. I was told that I will be on the toprol for 2 months and then it will be eliminated to “see if the atrial fib ablation has worked”. I am to stay on the flecanide until the next surgery. So I asked how we would know whether the PVI has worked if I remain on flecanide and was told that afib breaks through flecanide. I do not think this is the general experience of folks on the board. I would appreciate comments on this point (issue number 3).
Alarmingly, I have pain upon taking a deep breath, have a dry cough and am much too tired to exercise. All the symptoms nearly disappear when I sit or stand up and worsen when I lie down. I had a TEE and wonder if these are the result of the TEE because I have soreness along the entire trachea when I raise my head and had a large haematoma near my collarbone at the hollow in my neck (not near the ICE bruises at all) as if someone ran the TEE into the inside of my throat. Does anyone know what the symptoms of a badly executed TEE are? (issue number 4).
Marin General has largely ignored my complaints about my breathing pain and I am hoping to go to my local cardiologist this afternoon in case I have some iatrogenic problem. Does anyone know what stenosis symptoms are? (issue number 5).
At this point, I am stuck in hope- maybe the symptoms will abate and the heart return to NSR as it heals. I guess that I should be grateful that Dr. Natale discovered the ventricular tachycardia but I cannot help but wonder if the chemicals to which I was exposed during the surgery somehow generated it. Any comments? (issue number 6).
I am sorry to bring a less than cheerful post to this board because I think that for most people the helpful nature of the posts here are a real lifeline. Even now, I am so grateful not to have had a stroke, a mitral valve problem, or tamponade during the surgery that I do consider myself to be well off, but still I am stuck in hope for a better future.
Lynn

Lynn- I developed bigeminy after my ablation and my resting HR is often close to 100 BPM. When I had the 30 day event monitor after 3 months I bounced around from having about 20 PVC'S/minute to just a few. My pulse is so faint that I don't trust my judgement about what's going on now. So I'm still a little uneasy about this. But I'm off all meds(halleluia!). no afib that I know of and feel better for the most part.

Hang in there. Will be praying for NSR.

Lynn,

I assume you were on flecainide prior to your ablation. If not, keep in mind
that flecainide can, in many cases, have the paradoxical effect of increasing the frequency of episodes but greatly shortens duration. In my case,
flec. on a daily basis caused a big jump in frequency. I stopped the daily
intake and agreed with my EP to use only on demand. I have an episode
every two to three weeks and the flec. converts me overnight every time.
Based on your seemingly strong technical knowledge evidenced in your post, I am sure you are aware of this concept and that daily flec. was of help to you prior to your surgery. If not, then I would reconsider the use of this drug on a daily basis.

Kerry
How much were you taking on a daily basis. Taking 50mg twice daily made events more frequent however I have just started taking 100mg twice daily for the last few days and it seems to be holding.On demand my system went mad attacks all over the place thus I'm waiting for my system to stabalise before decreasing the Flec and reverting back to on demand , but limiting the amount taken. Seeing Cardio next Friday , that should be interesting.
Be well
Chris H

Hi Kerry,
I had never taken Flecanide prior to the ablation. I am taking it now to reduce the VT which I am presumed to have. Apparently Dr. Natale does not think that the VT was induced due to the surgery. Nonethelss, I have never passed out from VT before the surgeyr and am perplexed therefore as to why the Flecanide is really necessary beyond the 2 month time frame. I will consult with my local cardiologist since I would like to stop the Flecanide at least for a while before the next surgery now scheduled in June.
I am also confused about taking a drug which can be proarrhythmic without knowing whether it is the surgery or the drug which could be causing arrhythmias.
Thanks Kerry,
Lynn

Hi Carol,
I am sorry that you are not in sustained NSR at 70 bpm but glad that at least you feel better than before the surgery.
I have "attacks" of PVCs that seem to be continuous for hours at a time (4-8). Recently they do seem to be interleaved with NSR. I am experimenting with various foods to see if they produce the PVCs and think that I might beon to something. Also, I think that I recall that Hans posted that copper and magnesium often eliminate PVCs. I am not sure that I remember this accurately and think that you and I might contact Hans to ask about the studies supporting this view.
Here's hoping,
Lynn

Hi Lynn

Sorry to hear about all your sufferings. I found this case study (seems quite similar to your problems) and thought it might be of interest to you - in that you may be able to avoid the VT with postural change. But then again ... Any way this story has a good outcome, and so will yours.

[www.annals.org]

In patients without structural heart disease, recurrent orthostatic syncope is often caused by hypovolemia, autonomic insufficiency, or vasodepressor syncope. Only rarely has postural ventricular tachycardia been reported to cause syncope. In this case report, we describe an unusual variant of idiopathic ventricular tachycardia reproducibly triggered by upright posture.


Case Report

A 66-year-old woman with no previous history of cardiac disease or symptomatic arrhythmia began having dyspnea on exertion. Three weeks later, she sought medical attention when she developed severe substernal chest pressure, postural syncope, and near-syncope.

In the emergency department, the patient's supine blood pressure, measured using an arm cuff, was 142/78 mm Hg. Monitoring documented sinus rhythm at 82 beats per minute with episodes of ventricular bigeminy, unifocal couplets, and 10- to 14-beat runs of nonsustained monomorphic ventricular tachycardia. This tachycardia had a right bundle-branch heart block morphology, left-axis deviation, and a cycle length of 280 ms. The electrocardiogram was otherwise normal, with a QTc interval of 410 ms. Electrolyte levels were within normal limits. The patient was treated with lidocaine, heparin, and aspirin. During the subsequent 24 hours, she continued to have short episodes of nonsustained ventricular tachycardia elicited by upright posture. Her systolic blood pressure remained greater than 90 mm Hg during ventricular tachycardia. Creatinine kinase plasma concentrations were not elevated, and no serial changes were seen on electrocardiogram.

The day after admission, while supine, the patient had isolated, unifocal premature ventricular complexes and bigeminy. She had a Bruce protocol thallium exercise test. After 1 minute of exercise, she developed episodes of nonsustained monomorphic ventricular tachycardia associated with near-syncope that were identical to her previous episodes of nonsustained ventricular tachycardia. The ventricular tachycardia resolved after the patient lay down.

Coronary angiography showed normal coronary arteries. The left ventricular ejection fraction was normal, and there were no wall-motion abnormalities on the biplane left ventriculogram. The left ventricular end-diastolic pressure was 11 mm Hg. The episodes of ventricular tachycardia began to increase in frequency and became more easily provoked with simple activity, such as rising from bed. The patient was transferred to the University of Michigan for further management.

On the evening of hospital admission, the patient continued to have bouts of nonsustained and sustained ventricular tachycardia with any activity. To prevent the tachycardia, she refused to move from a supine position. Her electrocardiogram and electrolyte level remained normal. Her vital signs while supine and the results of her physical examination were normal except for an S4 gallop.

During a continuous 12-lead electrocardiogram recording, the head of the patient's bed was gradually raised while the patient's feet dangled over the side of the bed. As the angle of the head of the bed approached 90 degrees, the ventricular ectopy progressed from bigeminy, to couplets and triplets, to nonsustained monomorphic ventricular tachycardia, and finally to sustained ventricular tachycardia Figure 1. During the tachycardia, the patient's symptoms were reproduced. The patient became lightheaded and developed chest pressure; her blood pressure was 88/56 mm Hg. As the head of the bed was lowered to the supine position, the severity of the tachycardia progressively diminished from sustained ventricular tachycardia to bigeminy and unifocal premature ventricular contractions. This phenomenon of postural ventricular tachycardia was reproducibly induced by changes in the position of the head of the bed. The morphology of the ventricular tachycardia was identical to that of the previous bouts of sustained and nonsustained ventricular tachycardia and was a right bundle-branch heart block pattern with left-axis deviation. The QRS duration was 130 ms, and the cycle length was 280 ms. Although the ventricular tachycardia prohibited assessment of the upright sinus rate, no physical findings suggested hypovolemia. The patient remained in bed, and an electrophysiology test was done.

When the patient arrived in the electrophysiology laboratory, her rhythm was ventricular bigeminy. After informed consent was obtained, three 6-Fr diagnostic quadripolar electrode catheters (Mansfield EP, Watertown, Massachusetts) were inserted into a femoral vein and positioned in the high right atrium, the His bundle position, and the right ventricular apex. Ventricular tachycardia was not inducible by programmed atrial or ventricular stimulation. During an infusion of isoproterenol (2 mu g/min), spontaneous episodes of nonsustained ventricular tachycardia occurred. The morphology of the ventricular tachycardia was identical to that of the clinical ventricular tachycardia.

A 7-Fr quadripolar electrode catheter with a 4-mm tip electrode (Mansfield EP) was placed in the right femoral artery, intravenous heparin was administered in a bolus of 5000 U, and the catheter was advanced into the left ventricle. Pace mapping showed the site of origin of the ventricular tachycardia to be along the septal aspect of the inferobasal left ventricle. Two applications of radiofrequency energy at this site successfully eliminated all ventricular ectopy. No ectopy occurred during a 6 mu g/min infusion of isoproterenol or during upright posture.

The patient remained on a telemetry unit for 48 hours and had no recurrence of ventricular arrhythmia. A treadmill test was done, and the patient exercised for 8 minutes of a Bruce protocol and had no ventricular ectopy during or after exercise. At 1 year of follow-up, the patient had no recurrence of dyspnea, chest pain, or syncope, and no recurrence of the clinical ventricular ectopy on a 24-hour ambulatory monitor.

Hi Fran,
Thanks for the optimistic note. I think that I am indeed headed for a ventricular ablation. I was told that my BP dropped to 80/60 when I had the vtach in the OR. I still cannot help but wonder whether the vtach was induced by the surgery in some way since I hvae neer felt faint or passed out prioir to Feb 20.
By the by, I am still on the paleolithic diet and think that it does help. I did eat cheese on Wednesday and paid for it I think with a bout of PVCs. I

Hi Fran,
Thanks for the optimistic note. I think that I am indeed headed for a ventricular ablation. I was told that my BP dropped to 80/60 when I had the vtach in the OR. I still cannot help but wonder whether the vtach was induced by the surgery in some way since I hvae neer felt faint or passed out prioir to Feb 20.
By the by, I am still on the paleolithic diet and think that it does help. I did eat cheese on Wednesday and paid for it I think with a bout of PVCs. I

Hi Fran,
Thanks for the optimistic note. I think that I am indeed headed for a ventricular ablation. I was told that my BP dropped to 80/60 when I had the vtach in the OR. I still cannot help but wonder whether the vtach was induced by the surgery in some way since I hvae neer felt faint or passed out prioir to Feb 20.
By the by, I am still on the paleolithic diet and think that it does help. I did eat cheese on Wednesday and paid for it I think with a bout of PVCs. I

Hi Fran,
Thanks for the optimistic note. I think that I am indeed headed for a ventricular ablation. I was told that my BP dropped to 80/60 when I had the vtach in the OR. I still cannot help but wonder whether the vtach was induced by the surgery in some way since I hvae neer felt faint or passed out prioir to Feb 20.
By the by, I am still on the paleolithic diet and think that it does help. I did eat cheese on Wednesday and paid for it I think with a bout of PVCs. I

Hi Fran,
Thanks for the optimistic note. I think that I am indeed headed for a ventricular ablation. I was told that my BP dropped to 80/60 when I had the vtach in the OR. I still cannot help but wonder whether the vtach was induced by the surgery in some way since I hvae neer felt faint or passed out prioir to Feb 20.
By the by, I am still on the paleolithic diet and think that it does help. I did eat cheese on Wednesday and paid for it I think with a bout of PVCs. I

Lynn

I'm convinced that many arrhythmias are more to do with chemical changes and downright invasive proceedures on the heart than something that was always there and just manifested itself. Something changed for it to manifest itself and I would think similar to you in that it might have been due to surgery - or some drug they were treating you with whilst under.... It just didn't happen by itself. I do believe that some of us are much more sensitive to chemicals/meds than the majority of the population (who they do the trials on ) and suspect the underlying problem is the OP poisoning which makes our bodies react differently to others. I suffered the passing out and funny arrhythmias for many years... and, by the method I stopped it all, I have to say it was caused purely by what I personally (with the help of Dr's too) put into my own body.

Trial and error is the best way for finding food culprits. I would never have believed the change in me when going paleo. And like everyone else I have fallen by the wayside and suffered again. Each time I cheat and eat dairy or grains the outcome reinforces the reason why I have to avoid them.

Best of luck to you Lynn. The VT ablation seems much more successful than the AF one.

Fran

Fran,
you're a very smart cookie!

Lynn:

Do you have any documentation that what you have is truly V Tach and not isolated PVCs or runs of afib. This line puzzles me:
"I have "attacks" of PVCs that seem to be continuous for hours at a time (4-8)." Do you mean that you have 4-8 Ventricular beats in a row or 4-8 ventricular beats interspersed in a minute of NSR. Are you sure they are ventricular? Have you had this proven by an event recorder or holter monitor? I would want to be sure of that before going into another ablation attempt, although I think that ventricular ablations are more successful with a lower rate of complications. You cannot tell by how they feel whether they are atrial or ventricular. I have been lying in the hospital and having both PACs and PVCs and cannot tell them apart by how they feel, just by how they look running across the screen. I have seen people have a run of V Tach during a cardiac catherization just secondary to the invasiveness and irritation to the endocardium. These people don't otherwise have ventricular arrhythmias.

Wow Lynn, I'm glad your ablation was so successful. Good for you. I would want to be off Flecainide and have an event monitor for about a month. Phone in anything you feel, especially if symptomatic and know for sure that you have V Tach. If the only proof ON PAPER was the one during the ablation procedure, I would want proof that what you're feeling is definately V Tach. At least your rid of the afib. V Tach has a lethal potential, and if all of what you're feeling is V Tach, they wouldn't let you out of the hospital.

As far as the throat pain from the TEE, I never had it at all. I had a slight sore throat for a few hours. I think you should ask your regular doctor about that.

Hope you feel better, Lynn, and please post some more specific info on documentation of the new arrhythmia.

All the best, Lynn,
Pam