Published: 2018-03-21

Markers of inflammation following percutaneous coronary intervention (PCI) and its effect on adverse events

Nalin Kumar Mahesh, Prafull Sharma, Ankush Gupta, Keshavamurthy Ganapathy Bhat, Niket Verma


Background: Number of markers of inflammation has been associated with coronary artery disease and various studies have shown increased levels during chronic stable angina, acute myocardial infarction, and percutaneous coronary intervention. However, co-relation to final outcomes of percutaneous coronary intervention with these markers has not been studied. Aim of this study was to try and find a correlation between markers of inflammation released during percutaneous coronary intervention and incidence of restenosis on follow up at 06 moths on patients undergoing percutaneous coronary intervention with Bare Metal Stent (BMS).

Methods: 36 consecutive only Bare Metal Stent (BMS) angioplasties done at our centre between July 2015 and June 2016 were analysed for markers of inflammation from peripheral venous sample before the procedure and coronary sinus sample after the procedure. Pts were kept on follow up for 6 months and assessed as per their clinical symptoms and Coronary Angiogram was done where indicated and results tabulated.

Results: There was increase in the studied markers of inflammation post percutaneous coronary intervention but they did not correlate with or predict possible restenosis.

Conclusions: This study showed that markers of inflammation are elevated during percutaneous coronary intervention but none of these markers correlates with subsequent restenosis.


Acute coronary syndrome, Coronary artery disease, Inflammatory markers, Percutaneous coronary intervention

Full Text:



Göran K. Hansson,Inflammation, Atherosclerosis, and Coronary Artery Disease NEJM. 2005;352:1685-95.

Stary HC, Chandler AB, Dinsmore RE. A definition of advanced types of atherosclerotic lesions and a histological classification of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation 1995;92:1355-74.

Stary HC, Chandler B, Glagov S. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis: a report from the Committee on Vascular Lesions of the Council on Arteriosclerosis, American Heart Association. Circulation. 1994;89:2462-78.

van der Wal AC, Becker AE, van der Loos CM, Das PK. Site of intimal rupture or erosion of thrombosed coronary atherosclerotic plaques is characterized by an inflammatory process irrespective of the dominant plaque morphology. Circulation. 1994;89:36-44.

Falk E, Shah PK, Fuster V. Coronary plaque disruption. Circulation. 1995;92:657-71.

Saikku P, Leinonen M, Mattila K. Serological evidence of an association of a novel Chlamydia, TWAR, with chronic coronary heart disease and acute myocardial infarction. Lancet. 1988;2:983-6.

Moreno PR, Falk E, Palacios IF, Newell JB, Fuster V, Fallon JT. Macrophage infiltration in acute coronary syndromes: implications for plaque rupture. Circulation. 1994;90:775-8.

Libby P, Aikawa M. Stabilization of atherosclerotic plaques: new mechanisms and clinical targets. Nat Med. 2002;8:1257-62.

Christopher H, Dimmeler S. Serum Level of the Antiinflammatory Cytokine Interleukin-10 Is an Important Prognostic Determinant in Patients with Acute Coronary Syndromes Circulation. 2003;107:2109.

Liuzzo G, Baisucci LM, Gallimore JR, Caligiuri G, Buffon A, Rebuzzi AG, et al. Enhanced inflammatory response in patients with preinfarction unstable angina. J Am Coll Cardiol. 1999;34:1696-703.

Ramadan MM, Kodama M. Impact of percutaneous coronary intervention on the levels of interleukin-6 and C-reactive protein in the coronary circulation of subjects with coronary artery disease AJC. 2006;98,:915-7.

Wojakowski W, Maslankiewicz K. The pro- and anti-inflammatory markers in patients with acute myocardial infarction and chronic stable angina International journal of molecular medicine. 2004;14,317-22.

Mizia-Stec K, Gasior Z. Serum tumour necrosis factor-[alpha], interleukin-2 and interleukin-10 activation in stable angina and acute coronary syndromes. Pathophysiology and Natural History Coronary Artery Disease. 200;14(6):431-8.

Ali Ozeren CA, Mustafa A, Mehmet T. Levels of serum IL-1b, IL-2, IL-8 and tumor necrosis factor-a in patients with unstable angina pectoris Mediators of Inflammation. 2003;12(6):361-5.