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Sulfido‐peptide leukotrienes in coronary heart disease – relationship with disease instability and myocardial ischaemia
Author(s) -
De Caterina R.,
Giannessi D.,
Lazzerini G.,
Bernini W.,
Sicari R.,
Cupelli F.,
Lenzi S.,
Rugolotto M. M.,
Madonna R.,
Maclouf J.
Publication year - 2010
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1111/j.1365-2362.2010.02261.x
Subject(s) - medicine , creatinine , unstable angina , excretion , cardiology , myocardial infarction , angina , endocrinology , acute coronary syndrome
Eur J Clin Invest 2010; 40 (3): 258–272 Abstract Background  Urinary excretion of leukotriene (LT) E 4 is an index of LTC 4 biosynthesis and platelet–neutrophil interactions, which may occur in coronary heart disease and contribute to myocardial ischaemia. Enhanced LTC 4 biosynthesis may be a consequence of myocardial ischaemia or be linked to its pathogenetic substrate. Methods and results  Overnight urine collections were obtained from 17 patients with chronic stable angina, three patients with Prinzmetal’s angina, 16 patients with non ST‐elevation acute coronary syndromes (NSTE‐ACS) and six patients with acute ST‐elevation myocardial infarction (STEMI). LTE 4 excretion was measured by enzyme immunoassay after HPLC separation. Compared with healthy controls (51·1 ± 21·3 pg mg −1 creatinine, mean ± SD, n  = 11) and with non‐coronary cardiac controls (36·6 ± 9·8 pg mg −1 creatinine, n  = 9), LTE 4 excretion was unchanged in stable angina (40·5 ± 25·8 pg mg −1 creatinine), but significantly ( P  < 0·01) increased in NSTE‐ACS (122·7 ± 137·2 pg mg −1 creatinine) and STEMI (213·4 ± 172·4 pg mg −1 creatinine). In these patients, LTE 4 excretion rapidly dropped after day 1, consistent with effective coronary reperfusion. In patients with NSTE‐ACS, the increase in LTE 4 excretion was entirely restricted to patients with recent (< 48 h) spontaneous anginal episodes. Myocardial ischaemia elicited by a positive exercise stress test was not accompanied by any detectable increase in LTE 4 excretion, while a significant ( P  < 0·01) increase was detected after a single‐vessel percutaneous coronary interventions (PCI) procedure ( n  = 10), as compared with diagnostic angiography ( n  = 9). Conclusions  In coronary heart disease, increased LTC 4 biosynthesis is restricted to ACS and not linked to myocardial ischaemia per se , but likely to the occurrence of plaque disruption.

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