To answer some questions-
This is a very complicated history. I will try to address as best I can, and then list the full historical details.
My experience with Mitral Valve Prolpase was one of the worst nightmares possible. Since about the age of 24, I thought I was having serious heart issues, but was told time and again that MVP and these palpitations were harmless and there was no need to worry. I've had upwards of 10 cardiologists and 4 electrophysiologists look at my echoes my EKGs etc. Only one suggested a possible connection, but becuase my MVP was not severe, no action was taken. Then I went into Cardiac Arrest in March of 2009. Then again March 2010 and 3 weeks later in April of 2010. After an ablation where the focal site was determined to be the papillary muclle of the mitral valve, I asked the eletrophysiologist if we could associate the MVP with sudden cardiac arrest, he said he didn't think so. After several conversations I ended up being referred to the "Sudden Death Clinic" at Mayo in MN where I met with the Dr who is probably the authority on suddent cardiac death among young people and athletes. fairly depressing when you are being referred to the "sudden death clinic." Anyway, he agreed the MVP and sudden death was a somewhat controversial topic in the medical community, but he felt convinced that I was one of the "rare cases" where MVP can lead to a lethal cardiac arrest.
For me the next step was a no-brainer, get the MVP addressed.
And that brings me to where I am now - post MVP repair and thinking about my next move. And I am wondeing if anyone here with MVP has experienced serious ventricular arrhythmisas.
Thanks again-
Here medical history and timeline below.
1986 Aged 24 Sudden rush of fear and a sensation as if my heart had stopped
Lasted for about 5 seconds, felt like I was going to pass out
2nd event, similar feelings, about one month later
1987-2001 Felt palpitations on and off throughout late 1980s and 90s, but eventually started to ignore them.
September 22, 2001 Sensation of 2-3 very forceful and painful beats. Passed out during high level of exertion - was swimming in very rough ocean surf.
Felt palpitations for the next 6 months. Many days the palpitations quite frequent and bothersome.
March 2002 Visited local cardiologist. Got 24 halter monitor (noted occasional PVCs, numerous PACs, one 3 beat run of SVT)
(Local cardiologist reported it only showed I had "extra beats", "no reason for concern")
May 2002 Felt sudden tightness in chest, fluttering sensation, almost passed out while waiting for subway.
This was followed by 1 hour of intense palpitations, shortness of breath
Documented short run of ventricular tachycardia when admitted to local ER
Echo, Cardiac Cath, tilt table, and EP study all done after admitted to Hosp
Cardiac cath fine (no block), EP study induced VF but overall report was "polymorphic"/ "non specific"
Echo, MRI (MVP with MR mild-moderate) no structural abnornalities
ICD installed, 50 MG of toprol. Diagnosed as Idiopathic Ventricular Tachycardia
Minor palpitations on and off next two years, palpitations always most noticeable after eating. ICD Device recorded PVCs and isolated SVTs
December 2004 Paced out of VT by ICD, per interrogation
March/April 2007 8 second run of Ventricular Fibrillation, non sustained, per ICD interrogation Shock aborted. Very near syncope. Was a high level of exertion
2007 - 2008 Felt papitations on and off but again started to ignore them
March 22, 2009 Ventricular Fibrillation, syncope, ICD shock. Was a moderate level of exertion
May 2009 Cut out all caffeine. Immediately noticed far fewer palpitations. Thought that caffeine might have been culprit all along.
Also focused on better hydration with electrolytes during exercise.
March 8, 2010 Non sustained VT ( 8 beats) per device interrogation, during a 2 mile very slow jog HR approx 125.
March 14 2010 Ventricular Fibrillation, syncope, ICD shock, on first mile of what would have been a 10 mile run, moderate pace (target HR 135-140)
March 29 2010 Ventricular Fibrillation, syncope, ICD shock, very low level of exertion, HR probably around 90-100 max
April 2010 24 Hr Halter monitor showed polymorphic PVCs (3900 PVCS/day, a single run of 5 PVCs)
Treadmill stress test: many PVCs, 2 short runs VT (3 beats) once HR got to 120 BPM
Monitor compared with past EKGs, predominant location of PVC was observed (most PVCs but not all)
Genetic tests: CPVT. Long QT both Negative
May 2010 CAT Scan: Again no evidence of hypertrophic cardiomyopathy or other structural issues.
June 4, 2010 EP Study and ablation attempted
Able to induce VF, frequent ectopy - termed polymorphic
Predominant PVC located in papillary muscle by mitral valve, multiple lesions applied at high energy
Underlying cause still uncertain, but EP currently thinking along lines of CPVT
July 2010 Increased Toprol xl to 100mg
August 2 2010 5 second run of VF/Polymorphic VT, self terminating. Was not exercising
Sept 17 2010 5 second run of VF/Polymorphic VT, self terminating. Moderate level of exercise
Late September 2010 Had discussion with EP about options given apparent catecholamine trigger.
Asked if sympathetic denervation might be an option
Referred to Long QT/Sudden Death Clinic at Mayo Clinic in Minnesota.
Planned week visit, including full work up and sympathetic devernation procedure for end of week
Began a low dose of flecianide - immediately improved symptoms.
Follow-up 24 Holter showed dramatic decrease in PVCs and no more runs of PVCs after intro of flecianide
December 2010 Mayo Visit
Echo now showed MVP with very severe regurgitation
Severe left atrial enlargement, moderate left ventricular enlargement
No other structural issues noted on other tests
EP noted multifocal PVCs - but noted them coming from the papillary muscle region of the left ventricle
Mayo physicians felt there was a compelling case to link the MVP to the serious cardiac events.
Explained that MVP/Cardiac Arrest was rare, but observed in the MVP population
Denervation procedure postponed (for now)
Mitral valve repair performed - mininally invasive robotic assissted. No complications
Follow-up echo suggests repair successful, minimal MR
Future - Next 6 Mos Follow-up echoes and EKGs/24 hr
Reduce beta blocker and flecainide to see if PVCs remain dormant
Potential for future ablations also discussed if PVCs remain present