Cardiac sympathetic dysfunction correlates with abnormal myocardial contractile reserve in dilated cardiomyopathy patients

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 Ca ²⁺-ATPase (SERCA2) mRNA levels were significantly more reduced in patients with a delayed HMR ≤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.