Our study suggests that RV function significantly affects response to CRT. Poor LV reverse remodeling occurs after CRT in patients with HF having severe RV dysfunction at baseline.

A 53-year-old woman with no risk factors was admitted to our hospital in December 2006 because of worsening angina and positive exercise stress test. Two months earlier, she had been admitted to another hospital because of prolonged epigastrial pain without radiation, which had subsided just before she reached the hospital, that was associated with diagnostic elevation of troponin; she reported 3 episodes of the same pain lasting Ϸ5 minutes in the early morning hours over the preceding 3 weeks. A few hours after admission, she had a recurrence of pain with ST elevation on the inferior electrocardiogram (ECG) leads that responded to intravenous nitrates. Subsequent angiography failed to show lumen stenosis, irregularities, and thrombus deposition, but ventriculography showed akinesia of the basal inferior wall. The discharge diagnosis was inferior STelevation myocardial infarction (creatine kinase-MB peak, 112 U/L; troponin I peak, 9.74 ng/mL) with normal coronary arteries, and she was prescribed aspirin, calcium, antagonists, and ␤-blockers.She remained symptom free for about a month. Then, during a very stressful period of her life, she began to present with anginal pain during effort, sometimes on emotion. She insisted that the features of this new pain were completely different from those of the attacks leading to the previous

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