Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction

Giampaolo Niccoli, Felicita Andreotti, Francesca Marzo, Silvia Cecchetti, Eleonora Santucci, Domenico D'Amario, Teodosio Pafundi, Nicola Cosentino, Filippo Crea

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Background In models of acute ischaemia, erythropoietin (EPO) administration has been found to attenuate vascular injury largely through reduced apoptosis, suppressed inflammation and increased nitric oxide availability. We studied the association between circulating endogenous EPO and no-reflow in patients with first ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods Blood sampling was performed before PPCI. Consecutive patients with (n=24) or without (n=24) evidence of angiographic no-reflow after PPCI were enrolled. Angiographic no-reflow was defined as Thrombolysis in Myocardial Infarction (TIMI) flow ≤2 or as TIMI flow=3 but with myocardial blush grade -1, P=0·001, and 4·0 (0·6-7·1) vs. 9·3 (1·0-12·6) mIUmL -1, P=0·01, respectively]. At multivariable analysis, decreasing EPO tertiles and left anterior descending as the infarct-related artery were the only factors that predicted both angiographic and ECG no-reflow (P=0·017 and P=0·02 for EPO; P0·05 for left anterior descending artery, respectively). Conclusions We found an independent, graded, inverse relation between endogenous EPO levels and angiographic and ECG no-reflow following PPCI. In animal models of ischaemia, EPO has been found to be protective. In humans, endogenous EPO may contribute to offset the mechanisms responsible for no-reflow.

Original languageEnglish
Pages (from-to)1210-1219
Number of pages10
JournalEuropean Journal of Clinical Investigation
Volume41
Issue number11
DOIs
Publication statusPublished - Nov 2011

Fingerprint

Erythropoietin
Percutaneous Coronary Intervention
Serum
Electrocardiography
Ischemia
Arteries
Myocardial Infarction
Vascular System Injuries
ST Elevation Myocardial Infarction
Nitric Oxide
Animals
Blood
Animal Models
Availability
Apoptosis
Sampling
Inflammation

Keywords

  • Acute myocardial infarction
  • Erythropoietin
  • No-reflow
  • Primary PCI

ASJC Scopus subject areas

  • Medicine(all)
  • Clinical Biochemistry
  • Biochemistry

Cite this

Niccoli, G., Andreotti, F., Marzo, F., Cecchetti, S., Santucci, E., D'Amario, D., ... Crea, F. (2011). Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction. European Journal of Clinical Investigation, 41(11), 1210-1219. https://doi.org/10.1111/j.1365-2362.2011.02528.x

Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction. / Niccoli, Giampaolo; Andreotti, Felicita; Marzo, Francesca; Cecchetti, Silvia; Santucci, Eleonora; D'Amario, Domenico; Pafundi, Teodosio; Cosentino, Nicola; Crea, Filippo.

In: European Journal of Clinical Investigation, Vol. 41, No. 11, 11.2011, p. 1210-1219.

Research output: Contribution to journalArticle

Niccoli, G, Andreotti, F, Marzo, F, Cecchetti, S, Santucci, E, D'Amario, D, Pafundi, T, Cosentino, N & Crea, F 2011, 'Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction', European Journal of Clinical Investigation, vol. 41, no. 11, pp. 1210-1219. https://doi.org/10.1111/j.1365-2362.2011.02528.x
Niccoli, Giampaolo ; Andreotti, Felicita ; Marzo, Francesca ; Cecchetti, Silvia ; Santucci, Eleonora ; D'Amario, Domenico ; Pafundi, Teodosio ; Cosentino, Nicola ; Crea, Filippo. / Endogenous serum erythropoietin and no-reflow in patients with ST-elevation myocardial infarction. In: European Journal of Clinical Investigation. 2011 ; Vol. 41, No. 11. pp. 1210-1219.
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AU - Andreotti, Felicita

AU - Marzo, Francesca

AU - Cecchetti, Silvia

AU - Santucci, Eleonora

AU - D'Amario, Domenico

AU - Pafundi, Teodosio

AU - Cosentino, Nicola

AU - Crea, Filippo

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N2 - Background In models of acute ischaemia, erythropoietin (EPO) administration has been found to attenuate vascular injury largely through reduced apoptosis, suppressed inflammation and increased nitric oxide availability. We studied the association between circulating endogenous EPO and no-reflow in patients with first ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods Blood sampling was performed before PPCI. Consecutive patients with (n=24) or without (n=24) evidence of angiographic no-reflow after PPCI were enrolled. Angiographic no-reflow was defined as Thrombolysis in Myocardial Infarction (TIMI) flow ≤2 or as TIMI flow=3 but with myocardial blush grade -1, P=0·001, and 4·0 (0·6-7·1) vs. 9·3 (1·0-12·6) mIUmL -1, P=0·01, respectively]. At multivariable analysis, decreasing EPO tertiles and left anterior descending as the infarct-related artery were the only factors that predicted both angiographic and ECG no-reflow (P=0·017 and P=0·02 for EPO; P0·05 for left anterior descending artery, respectively). Conclusions We found an independent, graded, inverse relation between endogenous EPO levels and angiographic and ECG no-reflow following PPCI. In animal models of ischaemia, EPO has been found to be protective. In humans, endogenous EPO may contribute to offset the mechanisms responsible for no-reflow.

AB - Background In models of acute ischaemia, erythropoietin (EPO) administration has been found to attenuate vascular injury largely through reduced apoptosis, suppressed inflammation and increased nitric oxide availability. We studied the association between circulating endogenous EPO and no-reflow in patients with first ST-elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). Methods Blood sampling was performed before PPCI. Consecutive patients with (n=24) or without (n=24) evidence of angiographic no-reflow after PPCI were enrolled. Angiographic no-reflow was defined as Thrombolysis in Myocardial Infarction (TIMI) flow ≤2 or as TIMI flow=3 but with myocardial blush grade -1, P=0·001, and 4·0 (0·6-7·1) vs. 9·3 (1·0-12·6) mIUmL -1, P=0·01, respectively]. At multivariable analysis, decreasing EPO tertiles and left anterior descending as the infarct-related artery were the only factors that predicted both angiographic and ECG no-reflow (P=0·017 and P=0·02 for EPO; P0·05 for left anterior descending artery, respectively). Conclusions We found an independent, graded, inverse relation between endogenous EPO levels and angiographic and ECG no-reflow following PPCI. In animal models of ischaemia, EPO has been found to be protective. In humans, endogenous EPO may contribute to offset the mechanisms responsible for no-reflow.

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KW - Erythropoietin

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