The main goals in the treatment of acute coronary syndrome are to prevent myocardial ischemia, damage, and possible complications. Accordingly, we evaluated the predictive value of glypican-6 (GPC6) for cardiac remodeling after myocardial infarction (MI). Baseline plasma GPC6 levels were measured in patients who underwent primary percutaneous coronary intervention (PCI) for acute MI. Left ventricular ejection fraction (LVEF) was measured at baseline and at 6 months with transthoracic echocardiography. Reduced LVEF persisted in 89 out of 276 patients after 6 months. The majority of the patients were male (n = 198, 72%) and the mean age was 57.8 ± 10.8 years. Glypican-6, N-terminal pro-brain natriuretic peptide (NT-proBNP), and high-sensitive troponin levels were significantly lower in the improved LVEF group compared with the low LVEF group (10.54 ± 4.46 vs 6.98 ± 3.34 ng/mL, P < .001; 500 pg/mL [range, 300-600 pg/mL] vs 350 pg/mL [range, 200-550 pg/mL], P = .008; 396 pg/mL [range, 159-579 pg/mL] vs 300 pg/mL [range, 100-500 pg/mL], P = .016, respectively). Logistic regression analysis revealed the SYNTAX Score 2, GPC6, and NT-proBNP as significant independent predictors of low LVEF (hazard ratio [HR]: 1.064, P = .041; HR: 1.215, P < .001; HR: 1.179, P < .001). Glypican-6 may prove to be useful for the detection of low LVEF development in patients undergoing PCI following MI.
PichéMEPoirierPLemieuxI, et al.Overview of Epidemiology and Contribution of Obesity and Body Fat Distribution to Cardiovascular Disease: An Update. Prog Cardiovasc Dis. 2018;61(2):103–13.
2.
CamiciPG. Hibernation and heart failure. Heart. 2004;90(2):141–3.
3.
StegPGJamesSKAtarD, et al.ESC Guidelines for the management of acute myocardial infarction in patients presenting with ST-segment elevation. Eur Heart J. 2012;33(20):2569–619.
4.
RoffiMPatronoCColletJP, et al.2015 ESC Guidelines for the management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: Task Force for the Management of Acute Coronary Syndromes in Patients Presenting without Persistent ST-Segment Elevation of the European Society of Cardiology (ESC). Eur Heart J. 2016;37(3):267–315.
5.
AmsterdamEAWengerNKBrindisRG, et al.2014 AHA/ACC Guideline for the Management of Patients with Non-ST-Elevation Acute Coronary Syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014;64(24): e139–e228.
6.
O’GaraPTKushnerFGAscheimDD, et al.2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines. Circulation. 2013;127(4): e362–425.
7.
PfefferMABraunwaldE.Ventricular remodeling after myocardial infarction. Experimental observations and clinical implications. Circulation. 1990;81(4):1161–72.
8.
OpieLHCommerfordPJGershBJ, et al.Controversies in ventricular remodelling. The Lancet. 2006;367(9507):356–67.
9.
SchironeLForteMPalmerioS, et al.A Review of the Molecular Mechanisms Underlying the Development and Progression of Cardiac Remodeling. Oxid Med Cell Longev. 2017;2017:3920195.
10.
GreenbergBQuinonesMAKoilpillaiC, et al.Effects of long-term enalapril therapy on cardiac structure and function in patients with left ventricular dysfunction: results of the SOLVD echocardiography substudy. Circulation. 1995;91(10):2573–81.
11.
DoughtyRNWhalleyGAGambleG, et al.Left ventricular remodeling with carvedilol in patients with congestive heart failure due to ischemic heart disease. Journal of the American College of Cardiology. 1997;29(5):1060–6.
12.
GroenningBANilssonJCSondergaardL, et al.Antiremodeling effects on the left ventricle during beta-blockade with metoprolol in the treatment of chronic heart failure. Journal of the American College of Cardiology. 2000;36(7):2072–80.
13.
BraunwaldEPerloffJMannD, et al.The history and physical examination: An evidence-based approach. Braunwald’s Heart Disease: A Textbook of Cardiovascular Medicine. 10th edPhiladelphia, PA: Elsevier Saunders. 2014:95–113.
14.
Kirn-SafranCFarach-CarsonMCCarsonDD. Multifunctionality of extracellular and cell surface heparan sulfate proteoglycans. Cellular and Molecular Life Sciences. 2009;66(21):3421–34.
15.
HäckerUNybakkenKPerrimonN. Heparan sulphate proteoglycans: the sweet side of development. Nature reviews Molecular cell biology. 2005;6(7):530–41.
16.
HoKAndersonKMKannelWB, et al.Survival after the onset of congestive heart failure in Framingham Heart Study subjects. Circulation. 1993;88(1):107–15.
17.
MaytinMColucciWS. Molecular and cellular mechanisms of myocardial remodeling. Journal of nuclear cardiology. 2002;9(3):319–27.
18.
DornGWMannDL. Signaling pathways involved in left ventricular remodeling: summation. Journal of cardiac failure. 2002;8(6): S387–S8.
19.
BaxJJBaumgartnerHCeconiC, et al.Third universal definition of myocardial infarction. Journal of the American College of Cardiology. 2012;60(16):1581–98.
20.
LeamanDMBrowerRWMeesterGT, et al.Coronary artery atherosclerosis: severity of the disease, severity of angina pectoris and compromised left ventricular function. Circulation. 1981;63(2):285–99.
21.
LangRMBadanoLPMor-AviV, et al.Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. European Heart Journal-Cardiovascular Imaging. 2015;16(3):233–71.
22.
HunterJJChienKR. Signaling pathways for cardiac hypertrophy and failure. New England Journal of Medicine. 1999;341(17):1276–83.
23.
FilmusJSelleckSB. Glypicans: proteoglycans with a surprise. The Journal of clinical investigation. 2001;108(4):497–501.
24.
BaumhoerDTornilloLStadlmannS, et al.Glypican 3 expression in human nonneoplastic, preneoplastic, and neoplastic tissues: a tissue microarray analysis of 4,387 tissue samples. American journal of clinical pathology. 2008;129(6):899–906.
25.
BülowHEHobertO. The molecular diversity of glycosaminoglycans shapes animal development. Annu Rev Cell Dev Biol. 2006;22:375–407.
26.
PiliaGHughes-BenzieRMMacKenzieA, et al.Mutations in GPC3, a glypican gene, cause the Simpson-Golabi-Behmel overgrowth syndrome. Nature genetics. 1996;12(3):241–7.
27.
Campos-XavierABMartinetDBatemanJ, et al.Mutations in the heparan-sulfate proteoglycan glypican 6 (GPC6) impair endochondral ossification and cause recessive omodysplasia. The American Journal of Human Genetics. 2009;84(6):760–70.
28.
Cano-GauciDFSongHHYangH, et al.Glypican-3–deficient mice exhibit developmental overgrowth and some of the abnormalities typical of Simpson-Golabi-Behmel syndrome. The Journal of cell biology. 1999;146(1):255–64.
29.
MellebyAOStrandMERomaineA, et al.The heparan sulfate proteoglycan glypican-6 is upregulated in the failing heart, and regulates cardiomyocyte growth through ERK1/2 signaling. PloS one. 2016;11(10): e0165079.
30.
PiperHMMeuterKSchäferC. Cellular mechanisms of ischemia-reperfusion injury. The Annals of thoracic surgery. 2003;75(2): S644–S8.
31.
BodorGS. Biochemical markers of myocardial damage. Ejifcc. 2016;27(2):95.
32.
ParkKCGazeDCCollinsonPO, et al.Cardiac troponins: from myocardial infarction to chronic disease. Cardiovascular research. 2017;113(14):1708–18.
33.
KolhPWindeckerSAlfonsoF, et al.2014 ESC/EACTS Guidelines on myocardial revascularization: the Task Force on Myocardial Revascularization of the European Society of Cardiology (ESC) and the European Association for Cardio-Thoracic Surgery (EACTS) Developed with the special contribution of the European Association of Percutaneous Cardiovascular Interventions (EAPCI). European Journal of Cardio-Thoracic Surgery. 2014;46(4):517–92.
34.
RossR. Atherosclerosis—an inflammatory disease. New England journal of medicine. 1999;340(2):115–26.
35.
PearsonTAMensahGAAlexanderRW, et al.Markers of inflammation and cardiovascular disease: application to clinical and public health practice: a statement for healthcare professionals from the centers for disease control and prevention and the American heart association. circulation. 2003;107(3):499–511.
36.
BlakeGJRidkerPM. C-reactive protein and other inflammatory risk markers in acute coronary syndromes. Journal of the American College of Cardiology. 2003;41(4 Supplement): S37–S42.
37.
LibbyPRidkerPM. Novel inflammatory markers of coronary risk: theory versus practice. Am Heart Assoc. 1999.
38.
RidkerPM. C-reactive protein and the prediction of cardiovascular events among those at intermediate risk: moving an inflammatory hypothesis toward consensus. Journal of the American College of Cardiology. 2007;49(21):2129–38.
39.
ChenZ-WYuZ-QYangH-B, et al.Rapid predictors for the occurrence of reduced left ventricular ejection fraction between LAD and non-LAD related ST-elevation myocardial infarction. BMC cardiovascular disorders. 2016;16(1):1–8.
