Poster presentation | Open | Published:
Serum nitric oxide in patients with acute coronary syndromes: correlation with the extent of myocardial ischemia and role of diabetes mellitus
Critical Carevolume 8, Article number: P80 (2004)
An intact endothelium releases nitric oxide (NO), which acts through cyclic GMP to mediate coronary dilatation, whereas a diseased endothelium releases less NO and more endothelin and poorly reduces the vasomotor tone. Release of NO is indirectly assessed by the measurement of NO synthase and the end product metabolites of NO (i.e. nitrites and nitrates). Diabetic patients (patients) with the potential of diabetic microangiopathy and endothelial dysfunction are theoretically expected to be poor secretors of NO. The aim of the present study is to correlate the serum level of NO in patients with acute coronary syndromes (ACS) (i.e. unstable angina, nonST segment elevation myocardial ischemia [NSTEMI], and ST segment elevation myocardial ischemia) in correlation with the extent of the total ischemic burden in relation to the presence or absence of diabetes mellitus. To achieve this aim we studied 59 patients, 20 diabetics and 39 nondiabetics (53 males, six females), with ACS (unstable angina in 20 patients, NSTEMI in five patients and acute myocardial ischemia in 34 patients). Before any therapeutic intervention, arterial blood samples were withdrawn to assess the serum NO metabolites level by the Griess reaction. Acute myocardial perfusion imaging with gated SPECT study was carried out by injecting 10 mci 99mTC SestaMIBI IV during chest pain with acquisition of the first set of SPECT images to asses the area of myocardium at risk (MAR), and to estimate of the initial ejection fraction. The second set was acquired 72 hours later to assess the extent of myocardial salvage achieved by different therapeutic modalities (PTCA, SK, etc.). A twenty-segment scoring system was applied for both sets of images to estimate the salvage index (SI): SI = [(MAR - second score) / MAR] × 100. A control group of 20 patients matched for age and sex were also studied.
Compared with the control group patients with acute ischemic syndromes had a significantly lower level of serum NO metabolites (mean 24 ± 10 Ug/l vs 39 ± 11 Ug/l, P < 0.05). The initial perfusion score averaged 27 ± 15. The second score averaged 15 ± 5 and the SI averaged 40%. Compared with the control group, diabetic patients had significantly lower level of serum NO metabolites with no significant difference between diabetic and nondiabetic patients.
Significantly lower serum levels of serum NO metabolites in patients with acute ischemic syndromes are a marker of substantial endothelial dysfunction with consequent impaired coronary perfusion. Despite the key role of NO in maintaining the normal vasomotor tone and coronary flow, therapeutic inhalation of NO would not be expected to improve coronary flow in acute coronary syndromes as extrapolated from our data showing poor correlation between the serum level of NO and the extent of myocardial salvage. Adverse effects of diabetes mellitus on endothelial function in ischemic patients are not apparently mediated solely by the NO pathway, as shown by little difference between diabetic and nondiabetic patients.