AIMS: Many patients with idiopathic dilated cardiomyopathy (DCM) have been diagnosed on the basis of the exclusion of significant coronary stenosis and the presence of left ventricular (LV) dysfunction. In the present study, we investigated the possibility that coronary multispasm is one of the mechanisms leading to diffuse idiopathic DCM-like LV dysfunction. METHODS AND RESULTS: Forty-two patients with severely depressed LV function but without significant coronary stenosis were enrolled (baseline LV ejection fraction, 33 ± 11%). An acetylcholine (ACh) provocation test was performed at the time of coronary angiography. In patients with a positive ACh provocation test (n = 20), coronary angiography revealed multivessel diffuse coronary spasm with marked electrocardiogram changes. In patients with a negative ACh provocation test (n = 22), significant findings compatible with idiopathic DCM were more frequently observed on magnetic resonance imaging (MRI) or in LV biopsies compared with the ACh-positive group (MRI, 73% vs. 12%; and LV biopsy, 71% vs. 0%, respectively; P < 0.01). In the ACh-positive group, LV function significantly improved after the administration of calcium channel blockers (LV ejection fraction, 34 ± 12% vs. 54 ± 10%; and brain natriuretic peptide, 803 ± 482 pg/mL vs. 69 ± 84 pg/mL, at baseline and 1 year, respectively; P < 0.01). CONCLUSIONS: Our results raise the possibility that patients with LV dysfunction due to repeated coronary multispasm are being diagnosed as idiopathic DCM, and that calcium channel blockers may prove to be a promising therapeutic strategy in those patients.
AIMS: Many patients with idiopathic dilated cardiomyopathy (DCM) have been diagnosed on the basis of the exclusion of significant coronary stenosis and the presence of left ventricular (LV) dysfunction. In the present study, we investigated the possibility that coronary multispasm is one of the mechanisms leading to diffuse idiopathic DCM-like LV dysfunction. METHODS AND RESULTS: Forty-two patients with severely depressed LV function but without significant coronary stenosis were enrolled (baseline LV ejection fraction, 33 ± 11%). An acetylcholine (ACh) provocation test was performed at the time of coronary angiography. In patients with a positive ACh provocation test (n = 20), coronary angiography revealed multivessel diffuse coronary spasm with marked electrocardiogram changes. In patients with a negative ACh provocation test (n = 22), significant findings compatible with idiopathic DCM were more frequently observed on magnetic resonance imaging (MRI) or in LV biopsies compared with the ACh-positive group (MRI, 73% vs. 12%; and LV biopsy, 71% vs. 0%, respectively; P < 0.01). In the ACh-positive group, LV function significantly improved after the administration of calcium channel blockers (LV ejection fraction, 34 ± 12% vs. 54 ± 10%; and brain natriuretic peptide, 803 ± 482 pg/mL vs. 69 ± 84 pg/mL, at baseline and 1 year, respectively; P < 0.01). CONCLUSIONS: Our results raise the possibility that patients with LV dysfunction due to repeated coronary multispasm are being diagnosed as idiopathic DCM, and that calcium channel blockers may prove to be a promising therapeutic strategy in those patients.