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

Abstract

We investigated the relationship between iodine-123-metaiodobenzylguanidine (123I-MIBG) findings and myocardial contractile reserve in patients with mild to moderate dilated cardiomyopathy (DCM). Little is known regarding the relationship between cardiac sympathetic nervous function and myocardial contractile reserve in DCM. 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). 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). 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.