Effect of Serum Gamma-Glutamyl Transferase Levels on Myocardial Perfusion and Long-Term Prognosis after Primary Angioplasty in Patients with Acute ST-Elevation Myocardial Infarction
Restricted accessResearch articleFirst published online December, 2012
Effect of Serum Gamma-Glutamyl Transferase Levels on Myocardial Perfusion and Long-Term Prognosis after Primary Angioplasty in Patients with Acute ST-Elevation Myocardial Infarction
Gamma-glutamyl transferase (GGT) level was found to be elevated in plasma of patients with cardiovascular risk factors. The aim of our study was to assess the relationship between serum GGT levels and the occurrence of no-reflow as well as to evaluate the prognostic value of GGT in ST-segment elevation myocardial infarction (STEMI) population.
Methods and Results
One hundred sixty-eight consecutive patients with STEMI who underwent percutaneous coronary intervention (PCI) were enrolled in the study. Patients with STEMI were grouped into tertiles according to their admission serum GGT levels. No-reflow after PCI was assessed both angiographically (thrombolysis in myocardial infarction [TIMI] flow and myocardial blush grade) and electrocardiographically (ST resolution). Gamma-glutamyl transferase levels were higher in patients with STEMI compared to the elective PCI group subjects. Patients with angiographically (TIMI flow ≤2 or TIMI flow 3 with final myocardial bush grade ≤2 after PCI) and electrocardiographically (ST resolution <30%) detected no-reflow were increased in number across the GGT tertiles. In addition, 1-year mortality rates showed a significant increase across the tertile groups (4% vs 11% vs 23%, P < 0.01). Multivariable logistic regression analysis revealed that GGT levels on admission were a significant predictor of long-term mortality of myocardial blush grade–detected no-reflow phenomenon. High GGT level on admission was a significant predictor for long-term mortality and major adverse cardiac events.
Conclusions
In patients with STEMI undergoing primary PCI, high GGT levels at admission were found to be associated with no-reflow phenomenon and increased long-term mortality.
RahmanI, MacNeeW. Oxidative stress and regulation of glutathione in lung inflammation. Eur Respir J. 2000; 16: 534–554.
2.
PaolicchiA, EmdinM, GhliozeniE, . Images in cardiovascular medicine. Human atherosclerotic plaques contain gamma-glutamyl transpeptidase enzyme activity. Circulation. 2004; 109: 1440.
3.
PaolicchiA, EmdinM, PassinoC, . Beta-lipoprotein- and LDL-associated serum gamma-glutamyltransferase in patients with coronary atherosclerosis. Atherosclerosis. 2006; 186: 80–85.
4.
PompellaA, EmdinM, PassinoC, . The significance of serum gamma-glutamyltransferase in cardiovascular diseases. Clin Chem Lab Med. 2004; 42: 1085–1091.
5.
LeeDS, EvansJC, RobinsSJ, . Gamma glutamyl transferase and metabolic syndrome, cardiovascular disease, and mortality risk: the Framingham Heart Study. Arterioscler Thromb Vasc Biol. 2007; 27: 127–133.
6.
LeeDH, HaMH, KimJH, . Gamma-glutamyltransferase and diabetes-a 4 year follow-up study. Diabetologia. 2003; 46: 359–364.
7.
LeeDH, HaMH, KimJR, . Gamma-glutamyltransferase, alcohol, and blood pressure. A four year follow-up study. Ann Epidemiol. 2002; 12: 90–96.
8.
LeeDH, JacobsDRJr, GrossM, . Gamma-glutamyltransferase is a predictor of incident diabetes and hypertension: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Clin Chem. 2003; 49: 1358–1366.
9.
Van de WerfF, BaxJ, BetriuA, . Management of acute myocardial infarction in patients presenting with persistent ST-segment elevation: the Task Force on the Management of ST-Segment Elevation Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2008; 29: 2909–2945.
10.
KeeleyEC, BouraJA, GrinesCL. Primary angioplasty versus intravenous thrombolytic therapy for acute myocardial infarction: a quantitative review of 23 randomised trials. Lancet. 2003; 361: 13–20.
11.
KlonerRA, GanoteCE, JenningsRB. The “no-reflow” phenomenon after temporary coronary occlusion in the dog. J Clin Invest. 1974; 54: 1496–1508.
12.
NiccoliG, BurzottaF, GaliutoL, . Myocardial no-reflow in humans. J Am Coll Cardiol. 2009; 54: 281–292.
13.
KingSB3rd, SmithSCJr, HirshfeldJWJr, . 2007 focused update of the ACC/AHA/SCAI 2005 guideline update for percutaneous coronary intervention: a report of the American College of Cardiology/American Heart Association Task Force on Practice guidelines. J Am Coll Cardiol. 2008; 51: 172–209.
14.
MorishimaI, SoneT, MokunoS, . Clinical significance of no-reflow phenomenon observed on angiography after successful treatment of acute myocardial infarction with percutaneous transluminal coronary angioplasty. Am Heart J. 1995; 130: 239–243.
15.
MorishimaI, SoneT, OkumuraK, . Angiographic no-reflow phenomenon as a predictor of adverse long-term outcome in patients treated with percutaneous transluminal coronary angioplasty for first acute myocardial infarction. J Am Coll Cardiol. 2000; 36: 1202–1209.
16.
Vande Werf F, ArdissinoD, BetriuA, . Management of acute myocardial infarction in patients presenting with ST-segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003; 24: 28–66.
17.
AndersenHR, NielsenTT, RasmussenK, . A comparison of coronary angioplasty with fibrinolytic therapy in acute myocardial infarction. N Engl J Med. 2003; 349: 733–742.
18.
MorrowDA, AntmanEM, CharlesworthA, . TIMI risk score for ST-elevation myocardial infarction: a convenient, bedside, clinical score for risk assessment at presentation: an intravenous nPA for treatment of infarcting myocardium early II trial substudy. Circulation. 2000; 102: 2031–2037.
19.
The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group. N Engl J Med. 1985; 312: 932–936.
20.
van ‘t HofAW, LiemA, SuryapranataH, . Angiographic assessment of myocardial reperfusion in patients treated with primary angioplasty for acute myocardial infarction: myocardial blush grade. Zwolle Myocardial Infarction Study Group. Circulation. 1998; 97: 2302–2306.
21.
GibsonCM, MurphySA, MorrowDA, . Angiographic perfusion score: an angiographic variable that integrates both epicardial and tissue level perfusion before and after facilitated percutaneous coronary intervention in acute myocardial infarction. Am Heart J. 2004; 148: 336–340.
22.
SchroderR. Prognostic impact of early ST-segment resolution in acute ST-elevation myocardial infarction. Circulation. 2004; 110: e506–e510.
23.
GibsonCM, KarhaJ, MurphySA, . Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the thrombolysis in myocardial infarction trials. J Am Coll Cardiol. 2003; 42: 7–16.
24.
CutlipDE, WindeckerS, MehranR, . Clinical end points in coronary stent trials: a case for standardized definitions. Circulation. 2007; 115: 2344–2351.
25.
EmdinM, PassinoC, MichelassiC, . Prognostic value of serum gamma-glutamyl transferase activity after myocardial infarction. Eur Heart J. 2001; 22: 1802–1807.
26.
WannametheeG, EbrahimS, ShaperAG. Gamma-glutamyltransferase: determinants and association with mortality from ischemic heart disease and all causes. Am J Epidemiol. 1995; 142: 699–708.
27.
RuttmannE, BrantLJ, ConcinH, . Gamma-glutamyltransferase as a risk factor for cardiovascular disease mortality: an epidemiological investigation in a cohort of 163,944 Austrian adults. Circulation. 2005; 112: 2130–2137.
28.
MeisingerC, DoringA, SchneiderA, . Serum gamma-glutamyltransferase is a predictor of incident coronary events in apparently healthy men from the general population. Atherosclerosis. 2006; 189: 297–302.
29.
LazzeriC, ValenteS, TarquiniR, . The prognostic role of gamma-glutamyltransferase activity in non-diabetic ST-elevation myocardial infarction. Intern Emerg Med. 2011; 6: 213–219.
30.
AkpekM, ElcikD, KalayN, . The prognostic value of serum gamma glutamyl transferase activity on admission in patients with STEMI undergoing primary PCI. Angiology. 2012Jan10. [Epub ahead of print].
31.
LeeDH, JacobsDRJr. Association between serum gamma-glutamyl transferase and C-reactive protein. Atherosclerosis. 2005; 178: 327–330.
32.
JeanJC, LiuY, BrownLA, . Gamma-glutamyl transferase deficiency results in lung oxidant stress in normoxia. Am J Physiol Lung Cell Mol Physiol. 2002; 283: L766–L776.
33.
Joyce-BradyM, TakahashiY, OakesSM, . Synthesis and release of amphipathic gamma-glutamyl transferase by the pulmonary alveolar type 2 cell. Its redistribution throughout the gas exchange portion of the lung indicates a new role for surfactant. J Biol Chem. 1994; 269: 14219–14226.
34.
PaolicchiA, MinottiG, TonarelliP, . Gamma-glutamyl transpeptidase-dependent iron reduction and LDL oxidation—a potential mechanism in atherosclerosis. J Investig Med. 1999; 47: 151–160.
YoshidaT, MaulikN, EngelmanRM, . Glutathione peroxidase knockout mice are susceptible to myocardial ischemia reperfusion injury. Circulation. 1997; 96: II-216–II-220.
37.
MatsumotoH, InoueN, TakaokaH, . Depletion of antioxidants is associated with no-reflow phenomenon in acute myocardial infarction. Clin Cardiol. 2004; 27: 466–470.
38.
SorajjaP, GershBJ, CostantiniC, . Combined prognostic utility of ST-segment recovery and myocardial blush after primary percutaneous coronary intervention in acute myocardial infarction. Eur Heart J. 2005; 26: 667–674.
39.
GiuglianoRP, SabatineMS, GibsonCM, . Combined assessment of thrombolysis in myocardial infarction flow grade, myocardial perfusion grade, and ST-segment resolution to evaluate epicardial and myocardial reperfusion. Am J Cardiol. 2004; 93: 1362–1367, A5–A6.
40.
LindL. Circulating markers of inflammation and atherosclerosis. Atherosclerosis. 2003; 169: 203–214.
41.
BlakeGJ, RidkerPM. C-reactive protein and other inflammatory risk markers in acute coronary syndromes. J Am Coll Cardiol. 2003; 41: 37S–42S.
42.
KilicT, UralD, UralE, . Relation between proinflammatory to anti-inflammatory cytokine ratios and long-term prognosis in patients with non-ST elevation acute coronary syndrome. Heart. 2006; 92: 1041–1046.
43.
BoS, GambinoR, DurazzoM, . Associations between gamma-glutamyl transferase, metabolic abnormalities and inflammation in healthy subjects from a population-based cohort: a possible implication for oxidative stress. World J Gastroenterol. 2005; 11: 7109–7117.
44.
SaijoY, UtsugiM, YoshiokaE, . The relationship of gamma-glutamyltransferase to C-reactive protein and arterial stiffness. Nutr Metab Cardiovasc Dis. 2008; 18: 211–219.
45.
PleinerJ, MittermayerF, SchallerG, . Inflammation-induced vasoconstrictor hyporeactivity is caused by oxidative stress. J Am Coll Cardiol. 2003; 42: 1656–1662.
