Thank you again for this wonderful forum. I posted a couple of days ago, and thought maybe my question was missed. Sorry if this caused any inconvenience. F/45/cauc/slight build/normal wt/BP normally 100-110/55-70; 20+ year HX of MVP/MR and PVCs.
TEE ('00) MVP (anter > post) moderate 2-3+ post. directed MR;
normalNormal saline flush LV function; EF 55%.
Stress echo ('01) functional capacity
normalNormal saline flush; no signs of
ischemiaHepatic ischemia
Ischemic colitis
Mesenteric artery ischemia
Testicular torsion
Vertebrobasilar circulatory disorders present. EF 55%.
HolterHolter monitor (24h) ('01) showed 92459 QRS complexes, 22531
VentricularParoxysmal supraventricular tachycardia (psvt)
Ultrasound, ventricular septal defect - heartbeat
Ventricular assist device
Ventricular fibrillation
Ventricular septal defect
Ventricular tachycardia ectopicsEctopic pregnancy; 4419 isolated; 2517 couplets; 4 triplets; MANY episodes of bigeminy.
Stress echo (Dec. '02) functional capacity normal; no signs of ischemia; max HR 97%; 8.5 METS; level of stress achieved, imaging showed evidene of a cardiomyopathic process in the entire left ventricle; baseline EF 40%; stress ejection fraction increased; at rest, there is evidence for mild post. leaflet MVP and at least mod. MR on color doppler. Info is consistent with cardiomyopathy.
Began Flecainide in hosp. (Dec readings may have been affected by frequency of PVCs). Repeat echo -EF 45%. Normal stress test.
Potassium/magnesium good.
Are you aware of any study that frequent PVCs can lead to cardiomyopathy? Staying on RX and repeating echo in April. Dr. will decide what next (ace inhibitor/flecainide/ablation/other). I have had MVP MR and frequent, consecutive PVC complexes for years, but EF has always been normal. Dr. said because EF increased upon exercise, MVP was not the cause. I have an event monitor for any new arrythmias or unusual feelings. Appreciate any comments/suggestions. THANK YOU : )