Abstract

Abstract In recent works, it has been observed that cardiac sympathetic innervation contributes to the hemodynamic adaptations of the cardiovascular system, in relation to numerous needs. Orimo et al, through the use of scintigraphy with MIBG, showed in Parkinson‘s patients a marked reduction in myocardial uptake of MIBG corresponding to cardiac sympathomimetic denervation, in relation to the severity of the disease. The aim of this work was to evaluate the morpho–functional variations of the heart at a programmed sympathomimetic stimulus (dopamine test), both in healthy patients and in those suffering from Parkinson‘s disease. Materials and Methods At the University Cardiology “La Sapienza” of Rome, Pontine Polo, 10 patients affected by PD (age 56±5,5, of which 6 M and 4 W) and 10 healthy (54±6,4, of which 6M,4W)were tested in the absence of cardiovascular FR; all patients performed: blood chemistry, ECG, chest x–ray, Eco–TSA, tilt test, echocardio– Dopamine (2D–stress) and MIBG Scintigraphy. 2D–stress echocardiogradia was assessed by t–student of F.acc + EF + left and right diastolic times + GLS + Tapse + PAPS at 10, 20.30.40 µ dopa and their correlation (r–pearson) in the two groups. Discussion The observation of the data in the two groups of patients, in the absence of ongoing and remote cardiological pathology, showed a behavior of the values in the range both in basal conditions and during dopa stimulation. The comparison of the two groups both basal and during progressive dose stimulation that a statistical difference (P < 0.05) is observed on both systolic and diastolic function. The comparison in the two groups in the different stimulus phases showed a parallel growth behavior but with a different speed (Dp / Dv). There is no single explanation for these results: certainly the central role is played by the poor representation of post–ganglionic nerve endings as well as by the significant reduction of cardiac adrenergic receptors in Parkison. Conclusion The small number of patients and the data observed, stimulates researchers to continue the study, to better understand which pathophysiological mechanisms underlie these observations and verify the presence of an inverse relationship between PD and all those cardiological pathologies caused by catecholaminergic hyperstimulus.

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