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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