Increased Symmetric Dimethylarginine Level Is Associated with Worse Hospital Outcomes through Altered Left Ventricular Ejection Fraction in Patients with Acute Myocardial Infarction

Abstract

ObjectivesWe aimed to investigate whether SDMA- symmetric dimethylarginine -the symmetrical stereoisomer of ADMA- might be a marker of left ventricular function in AMI.BackgroundAsymmetric dimethylarginine (ADMA) has been implicated in the prognosis after acute myocardial infarction (AMI) and heart failure (HF).MethodsCross sectional prospective study from 487 consecutive patients hospitalized <24 hours after AMI. Patients with HF on admission were excluded. Serum levels of ADMA, SDMA and L-arginine were determined using HPLC. Glomerular filtration rate (eGFR) was estimated based on creatinine levels. Outcomes were in-hospital severe HF, as defined by Killip class >2, and death.ResultsPatients were analysed based on SDMA tertiles. Sex, diabetes, dyslipidemia, and prior MI were similar for all tertiles. In contrast, age and hypertension increased across the tertiles (p<0.001). From the first to the last tertile, GRACE risk score was elevated while LVEF and eGFR was reduced. The rate of severe HF and death were gradually increased across the SDMA tertiles (from 0.6% to 7.4%, p = 0.006 and from 0.6% to 5.0%, p = 0.034, respectively). Backward logistic multivariate analysis showed that SDMA was an independent estimate of developing severe HF, even when adjusted for confounding (OR(95%CI): 8.2(3.0–22.5), p<0.001). Further, SDMA was associated with mortality, even after adjustment for GRACE risk score (OR(95%CI): 4.56(1.34–15.52), p = 0.015).ConclusionsOur study showed for the first time that SDMA is associated with hospital outcomes, through altered LVEF and may have biological activity beyond renal function.

Evaluation of the diagnostic value of the renal resistive index as a marker of the subclinical development of cardiorenal syndrome in MMVD dogs

“… 25 , 37 – 39 Finally, neurohormonal hyperactivity expressed as elevated RAAS leads to increased sodium reabsorption in the Henle loop, which results in dilatation of glomerular arterioles causing glomerular hyperperfusion. 40 This phenomenon occurs secondary to an increase in RRI, which is followed by increase in serum urea, creatinine, SDMA, and Cyst C as well as albuminuria. 40 , 41 We found that the RRI was correlated with albuminuria, which was consistent with other studies ( Figure 2 ).…”

“… 40 This phenomenon occurs secondary to an increase in RRI, which is followed by increase in serum urea, creatinine, SDMA, and Cyst C as well as albuminuria. 40 , 41 We found that the RRI was correlated with albuminuria, which was consistent with other studies ( Figure 2 ). There was no correlation between RRI and serum SDMA or Cyst C, which was surprising.…”

Symmetric dimethylarginine in dogs with myxomatous mitral valve disease at various stages of disease severity

“…The present results indicate that the CRS of humans [ 14 ], namely a specifically reduced renal function as a consequence of cardiac disease, is less likely to occur in dogs. In particular, humans with acute or chronic heart disease associated with a reduced ejection fraction, such as acute myocardial infarction and coronary artery disease, develop a progressive reduction in renal perfusion and, in turn, a decrease in GFR; the decreased renal function is accompanied by an increase in SDMA [ 27 , 39 , 40 ]. The absence of a strong evidence of CRS in dogs with MMVD could be explained by the differences in the major pathophysiologic mechanisms.…”

“…In humans, SDMA gradually increases with the progression of heart disease and is an independent predictor of the development of severe HF; moreover, it is associated with a worse outcome and mortality [27]. In dogs with MMVD, two studies evaluated SDMA as a biomarker of heart disease severity using an "old" clinical classification [28] or the less recent and stringent ACVIM guidelines [29].…”

Metabolomic Approach in STEMI-Patients Undergoing Left Ventricular Remodeling

“…Finally, endothelial metabolism could be affected. In fact, Lorin et al showed that SDMA—an enzyme involved in oxidative stress by inhibiting the activity of the endothelial nitric oxide synthase—was a marker of left ventricular dysfunction and in-hospital mortality after a myocardial infarction [21]. In a cohort of 487 patients presenting with myocardial infarction, an increased SDMA level at baseline was associated with worse clinical outcomes through altered LVEF during hospital stays.…”