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Coronary endothelial dysfunction in patients with acute-onset idiopathic dilated cardiomyopathy

^a Cardiac Unit, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts, USA

View larger version (13K): [in a new window]   Figure 1 Epicardial CSA response to graded intracoronary doses of acetylcholine (Ach) and a 5% dextrose control infusion (C1) in patients with acute-onset DCM and in control patients (CTRL). Acetylcholine infusion produced no change in CSA in control patients but a significant epicardial constriction in patients with DCM. *p < 0.05, p < 0.01 versus C1. p < 0.05 versus control patients.

View larger version (13K): [in a new window]   Figure 2 CBF response to graded intracoronary doses of acetylcholine (Ach) and a 5% dextrose control infusion (C1) in patients with acute-onset DCM and in control patients (CTRL). Acetylcholine infusion produced an increase in CBF in control patients but no change in patients with DCM. *p < 0.01 versus C1. p < 0.05 versus patients with DCM.

View larger version (12K): [in a new window]   Figure 3 CSA and CBF responses to intracoronary infusion of 10–4 mol/liter adenosine and a 0.9% NaCl control infusion (C2) in patients with acute-onset DCM and control patients (CTRL). Adenosine infusion produced significant increases in CSA and CBF in both groups. The magnitude of the responses did not differ between DCM and control patients.

View larger version (16K): [in a new window]   Figure 4 Plots of the relation between coronary responses to acetylcholine infusion and a 5% dextrose control infusion (C1) and subsequent improvement in LVEF in patients with acute-onset dilated cardiomyopathy. Left, Association between the epicardial CSA response during infusion of 10–6 mol/liter acetylcholine and improvement in LVEF on follow-up. Right, Association between the CBF response during infusion of 10–6 mol/liter acetylcholine and improvement in LVEF at follow-up.