The Relationship between Plasma BNP Level and the Myocardial Phosphocreatine/Adenosine Triphosphate Ratio Determined by Phosphorus-31 Magnetic Resonance Spectroscopy in Patients with Dilated Cardiomyopathy

Abstract

The purpose of this study was to evaluate the correlation between the plasma B-type natriuretic peptide (BNP) level and the myocardial phosphocreatine/adenosine triphosphate ratio determined using rapid phosphorus-31 magnetic resonance spectroscopy (³¹P-MRS) in patients with dilated cardiomyopathy (DCM). Thirteen DCM patients, who had slight or moderate heart failure, were examined. The plasma BNP was measured on a day close to the rapid ³¹P-MRS study. ³¹P-MRS measurements were conducted with a 1.5-T MR instrument. The plasma BNP levels tended to be correlated negatively with the myocardial phosphocreatine/adenosine triphosphate, although the correlation did not reach statistical significance (r = –0.54, p =0.06). By contrast, the log of the plasma BNP levels was correlated negatively with the myocardial phosphocreatine/adenosine triphosphate (r = –0.73, p < 0.01). Our results indicate that the myocardial energy metabolism evaluated using ³¹P-MRS tends to be correlated with the severity of heart failure and left ventricular dysfunction estimated using the plasma BNP levels in DCM patients. This paper provides additional information regarding the relationship between the BNP and myocardial energy metabolism in DCM patients.

The Effect of Exogenous Creatine Phosphate on Myocardial Injury After Percutaneous Coronary Intervention

“…It does this by reducing adenosine monophosphate (AMP) degradation by inhibiting 5-nucleotide as well as increasing AMP synthesis by countering the inhibition of phosphoribose-pyrophosphate synthase by adenosine diphosphate (ADP). [10][11][12] In addition to providing energy for calcium channels, CP can also promote the homogeneous distribution of calcium ions to prevent conversion of xanthine dehydrogenase to xanthine oxidase otherwise mediated by excessive calcium ions, thus reducing peroxidation-induced myocardial injury by decreasing the production of oxygen free radicals in myocardial ischemia-/reperfusion. 26 At the same time, CP promotes the recovery of myocardial contractility by avoiding myocardial contracture due to strong binding of contractile proteins induced by the excessive calcium load.…”

“…In recent studies, CP was shown to protect mitochondria and thus reduce apoptosis by inhibiting the opening of mitochondrial permeability transition pores after passing through cell membranes. [10][11][12] This study was designed to evaluate the effect of exogenous CP on myocardial injury after PCI in patients with coronary heart disease.…”

Creatine Phosphate Administration in Cell Energy Impairment Conditions: A Summary of Past and Present Research

“…New studies performed with biochemical heart failure markers, like plasma B-type natriuretic peptide level [16], have demonstrated that the CrP/ATP ratio negatively correlates with the severity of heart failure.…”

Determinaciones de niveles de creatina y lípidos mediante espectroscopia por resonancia magnética en miocardio de pacientes con insuficiencia cardiaca no isquémica

“…Uno de los mecanismos que explican su disminución es la baja disponibilidad (downregulation) del cotransportador sodio-creatina (na-cr), el cual es responsable del ingreso de cr al miocito 7 . Por otra parte, un estudio reciente demostró en pacientes con miocardiopatía dilatada no isquémica, una disminución del índice fosfocreatina (Pcr)/AtP determinado mediante el uso de antenas de fosforo-31 con medición de los niveles de fosfocreatina y AtP 8 . Del mismo modo, se ha reportado que en los pacientes portadores de miocardiopatía hipertrófica presentan una depleción de cr en comparación con individuos sanos pero sus niveles se encuentran por sobre los pacientes con miocardiopatía dilatada 4 .…”