A 75-year-old woman who was told that she had premature ventricular contractions (PVC)
in a medical examination was transferred to our hospital with orthopnea and diagnosed
as acute decompensated heart failure. Electrocardiogram showed sinus tachycardia and
frequent PVC and echocardiogram showed severely reduced left ventricular (LV) ejection
fraction (17.8%) with dilated LV and severe mitral regurgitation (MR). We started
furosemide, spironolactone and tolvaptan for volume overload. She also had high blood
pressure, so nitroglycerin and ACE-inhibitor was started. Ambulatory electrocardiogram
revealed that PVC were 35,389 beats per day, and which were over 30% of total heart
beats. In coronary angiography, there was no significant stenosis, and cardiac magnetic
resonance imaging showed no late gadolinium enhancement of myocardium. Myocardial
biopsy showed nonspecific changes, so it was considered that LV dysfunction resulted
from both frequent PVC and severe MR. MR apparently deteriorated on PVC. We started
beta-blocker and amiodarone for PVC. However, PVC didn't decrease after medical treatment
and we also couldn't help stopping amiodarone because of liver dysfunction. We performed
radiofrequency catheter ablation for PVC. After procedure, MR significantly improved
as PVC decreased, and LV dysfunction was gradually improved. It is important to understand
mechanisms of mitral regurgitation and hemodynamic deterioration caused by frequent
PVC. We report this case with some literature reviews.
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