Objectives: We investigated the relationship between iodine-123-metaiodobenzylguanidine (123I-MIBG) findings and myocardial contractile reserve in patients with mild to moderate dilated cardiomyopathy (DCM).
Background: Little is known regarding the relationship between cardiac sympathetic nervous function and myocardial contractile reserve in DCM.
Methods: Twenty-four DCM patients who showed sinus rhythm underwent echocardiography, biventricular catheterization, and myocardial 123I-MIBG scintigraphy. Left ventricular (LV) pressures were measured using a micromanometer-tipped catheter. The myocardial contractile function (LV dP/dt(max)) was determined at rest and during atrial pacing. The messenger ribonucleic acid (mRNA) expressions of intracellular Ca2+-regulatory proteins were analyzed by real-time quantitative reverse transcription-polymerase chain reaction. Myocardial 123I-MIBG accumulation was quantified as a heart-mediastinum ratio (HMR).
Results: A significant correlation was observed between the delayed 123I-MIBG HMR and the percentage change in LV dP/dt(max) from the baseline to the peak or critical heart rate (r = 0.64; p < 0.001). The delayed 123I-MIBG HMR was significantly lower in patients showing a worsening change in LV dP/dt(max) than in those showing a favorable change (p < 0.005). The maximum LV dP/dt(max) during pacing and the sarcoplasmic reticulum Ca2+-ATPase (SERCA2) mRNA levels were significantly more reduced in patients with a delayed HMR < or =1.8 than in those with a delayed HMR >1.8 (p < 0.05, respectively).
Conclusions: Abnormal myocardial 123I-MIBG accumulation is related to an impaired myocardial contractile reserve and down-regulation of SERCA2 mRNA in DCM. Myocardial 123I-MIBG scintigraphy can be useful in noninvasively evaluating myocardial contractile reserve in patients with mild to moderate DCM.