An Unconventional Approach to Overcome the Extreme Angulation of LAD: A Challenging Percutaneous Coronary Intervention.

We herein describe a challenging acute anterior ST-elevation myocardial infarction (STEMI) case. The patient was hemodynamically unstable during the procedure and the extremely angulated culprit vessel hindered our repeated attempts of wiring. Procedural complexity and risks were increased not only due to angulation but also the bifurcational nature of the culprit lesion. We report an innovative solution that enabled the successful revascularisation of such a complex situation, after the failure of multiple attempts of conventional methods for wiring. We also briefly review the literature about recommended methods for such severely angulated vessels. Key Words: Angulation, infarction, Vessel, Angiography.

Does the level of myocardial injury differ in primary angioplasty patients loaded first with clopidogrel and the ones with ticagrelor?

OBJECTIVE: In daily clinical practice, we encounter ST segment elevation myocardial infarction (STEMI) patients loaded with clopidogrel upon admission to primary angioplasty. These patients are loaded with ticagrelor, if there is no contraindication. This study aimed to compare the level of injury between STEMI patients who were first loaded with clopidogrel and the ones first loaded with ticagrelor. Although patients were switched from clopidogrel to ticagrelor at the first hour of angioplasty, antiplatelet action may still be lower than the others. METHODS: This study included STEMI patients with angina onset of ≤3 h and who had primary angioplasty to proximal segment of one coronary artery. All patients had total thrombotic occlusion at the proximal segment. Δtroponin level (6th-hour troponin-admission troponin) was calculated to compare the level of myocardial injury. RESULTS: A total of 105 patients were included; 52 were loaded with ticagrelor and 53 with clopidogrel first and switched to ticagrelor. Baseline characteristics were similar in the two groups, except from type B2 lesions being more common in the ticagrelor-loaded group. Δtroponin levels were significantly higher in the clopidogrel-loaded group compared with the ticagrelor-loaded group (p=0.013). Major bleeding and in-hospital MACE rates were similar in both groups. CONCLUSION: In STEMI patients, the degree of troponin rise was more prominent in clopidogrel-loaded patients, despite the switch to ticagrelor in the first hour of intervention. Clopidogrel is slow and modest, and variable platelet inhibition may continue to be a negative factor for protection from myocardial injury, even after switching to ticagrelor.

Prevention of minor myocardial injury after elective percutaneous coronary intervention: comparison of ticagrelor versus clopidogrel.

BACKGROUND: Elective percutaneous coronary intervention (ePCI) may cause minor elevation of cardiac enzymes, so-called minor myocardial injury (MMI) which can be due to different pathophysiological mechanism (e.g. distal embolisation, side branch occlusion, increased platelet activation triggered by the intracoronary metallic stents). We aimed to compare the effectiveness of ticagrelor versus clopidogrel for the prevention of MMI and major adverse clinical events (MACEs) after ePCI. METHODS: Study population consisted of two groups of patients based on the treatment: Group I, receiving clopidogrel (n = 104), Group II, receiving ticagrelor (n = 96). Cardiac troponin I (cTnI), CK-MB were studied before and 12 hours after the procedure. Elevation of cTnI greater than 0.06 ng/ml was considered as MMI. All patients were also evaluated for the MACEs (death, myocardial infarction, stroke and transient ischaemic attack). RESULTS: Fifty-two of 200 patients (26%) had MMI after the procedure. The minor myocardial injury was significantly more prevalent in clopidogrel group than that of ticagrelor group (33% vs. 19%, p = .03). Myocardial infarction (MI) and MACEs were significantly higher in the clopidogrel group (15% vs. 6%, for MI, p = .04; 16% vs. 6%, for MACEs, p = .03, respectively). Multivariate analysis demonstrated antiplatelet treatment, saphenous graft intervention, type-C lesion as independent predictors of MMI. CONCLUSIONS: Present study showed that the combination of ticagrelor and aspirin was more effective than combination of clopidogrel and aspirin in decreasing MMI and MACEs after elective stenting.

Effect of Diltiazem on Coronary Artery Flow and Myocardial Perfusion in Patients With Isolated Coronary Artery Ectasia and Either Stable Angina Pectoris or Positive Myocardial Ischemic Stress Test.

Isolated coronary artery ectasia (CAE) may be associated with stable or unstable coronary events despite the absence of epicardial coronary stenosis. Impaired coronary flow dynamics and myocardial perfusion have been demonstrated in stable patients with ectatic coronary arteries. We aimed to assess whether epicardial flow and tissue-level perfusion would be improved by diltiazem in myocardial regions subtended by the ectatic coronary arteries in patients with isolated CAE. A total of 60 patients with isolated CAE were identified of 9,780 patients who underwent elective coronary angiography. Patients were randomized to 5 mg of intracoronary diltiazem or saline. Coronary blood flow of the microvascular network was assessed using myocardial blush grade (MBG) technique. The thrombolysis in myocardial infarction (TIMI) flow grade and TIMI frame count (TFC) were used to assess epicardial coronary flow. MBG (from 2.4 to 2.6, p = 0.02), TIMI flow grades (from 2.4 to 2.8, p <0.001), and TFC (from 35 to 26, p <0.001) were significantly improved after diltiazem, whereas no significant change was noticed after saline (from 2.4 to 2.4, p = 0.86 for MBG; from 2.3 to 2.3, p = 0.71 for TIMI flow grade; and from 35 to 33, p = 0.43 for TFC). Diltiazem provided amelioration of the altered coronary flow dynamics, which was suggested as the pathophysiological influence of CAE. In conclusion, the favorable effects of the diltiazem on myocardial perfusion were observed at both epicardial and tissue levels.

The relationship between coronary collateral artery development and inflammatory markers.

OBJECTIVE: This study aims to show the effect of myeloperoxidase (MPO), hsCRP, TNF-alpha values and leukocyte count on the development of coronary collateral arteries in patients with severely diseased coronary arteries. METHODS: Current study is an observational cross-sectional study. In the study, 295 patients who had functional obstruction or total coronary occlusion at least 1 month on their angiograms were included. We divided the study population into two groups according to their collateral grade as good collateral (Group 1) (169 patients) and poor collateral (Group 2) (126 patients). Multiple logistic regression analysis was used for independent variables associated with the coronary collateral grade. RESULTS: History of stable angina pectoris was statistically more prevalent in good collateral group (61.5% and 48.4%, p=0.025). Furthermore, MPO activation was higher in good collateral group and the difference was statistically significant (3.7 U/mL and 3.0 U/mL p=0.001). In multiple logistic regression analysis, stable angina pectoris [OR 1.7, 95% CI (1.05-2.8), p=0.03] and high MPO levels [OR 2.7, 95% CI (1.7-4.3), p<0.001] were found to be independent predictors of good collateral development. CONCLUSION: We think that proinflammatory enzymes and cytokines released from these cells rather than inflammatory cells themselves may play an important role on the collateral development.

Effect of hypertension on coronary remodeling patterns in angiographically normal or minimally atherosclerotic coronary arteries: an intravascular ultrasound study.

Whether there is any particular role of hypertension in remodeling process has not been completely understood yet. The aim of this study was to assess the association between hypertension and remodeling patterns in normal or minimally atherosclerotic coronary arteries. Seventy-nine patients who were free of significant coronary atherosclerosis were divided into two groups according to the absence (n = 39) or presence (n = 40) of hypertension; and standard intravascular ultrasound examination was performed in 145 segments. To determine the remodeling pattern in early atherosclerotic process, patients were also analyzed according to the level of plaque burden at the lesion site after the analysis of remodeling patterns. Positive remodeling was more prevalent in the hypertensive group (52.5% vs. 12.8%; P < .001) whereas negative remodeling was more common in diabetic patients (53.6% vs. 27.4%; P = .03). Mean remodeling index was 1.04 for hypertensives and 0.96 for normotensives (P = .03). There were no correlations between remodeling patterns and other risk factors such as age, family history, and hypercholesterolemia. Early atherosclerotic lesions (< 30%) exhibited more negative remodeling characteristics while intermediate pattern was observed more frequently in patients with high plaque burden (P = .006 and .02, respectively). Positive remodeling showed no association in this context (P = .07). This study demonstrated that minimal atherosclerotic lesions in hypertensives had a tendency for compensatory arterial enlargement. Positive remodeling may result from local adaptive processes within vessel wall or hemodynamic effects of blood pressure itself.

Anticalcifying nanoparticle antibody titer is an independent risk factor for coronary artery calcification.

BACKGROUND: Calcium phosphate deposition is present even in the early phases of the atherosclerotic plaque formation. Calcifying nanoparticles (CNPs), previously known as nanobacteria, have emerged as a potential causative agent for pathological calcification in human vasculature. This study investigates the relationship between the anti-CNPs antibody titers and the extent of coronary calcification. METHODS: A total of 197 consecutive patients undergoing multidetector computed tomography were enrolled in this study. The patients with coronary artery calcification (CAC; n=103) were included in the CAC group, and those without calcification (n=94) were determined as controls. The commercially available enzyme-linked immunosorbent assay kits were used to detect IgG antibodies against CNPs in serum samples. RESULTS: Mean titers of anti-CNPs antibodies were higher in individuals with CAC than in the control group (0.4 ± 0.4 vs. 0.19 ± 0.21U; P<0.0001). Multivariate logistic regression analysis revealed that high anti-CNPs antibody levels were an independent correlate of CAC in addition to conventional risk factors such as age, hypertension, diabetes mellitus, and low levels of high-density lipoprotein cholesterol. When the CAC scores were subcategorized: score 0, 1-100, 101-400, and more than 400, they still correlated significantly with the anti-CNPs antibody, especially in the group having CAC scores greater than 400 (P<0.0001). CONCLUSION: Anti-CNPs antibodies are an independent risk factor for CAC and the antibody levels correlate with CAC scores.

[Percutaneous treatment of Lutembacher syndrome: a case report]. / Lutembacher sendromlu bir olguda perkütan tedavi.

Lutembacher syndrome is a rare combination of congenital atrial septal defect (ASD) and acquired mitral stenosis (MS). Although it is traditionally corrected by surgical treatment, both conditions are amenable to transcatheter treatment without the need for surgery. We present a 49-year-old woman with Lutembacher syndrome. On pretreatment transthoracic echocardiography, planimetric mitral valve area was 1.5 cm(2), maximum diastolic gradient was 17 mmHg, and mean diastolic gradient was 9 mmHg. Combined percutaneous treatment was performed including balloon valvuloplasty for MS and closure of the ASD with the Amplatzer septal occluder. The patient was discharged uneventfully. Transthoracic echocardiography performed a week later showed planimetric mitral valve area as 2.1 cm(2), maximum diastolic gradient as 9 mmHg, and mean diastolic gradient as 4 mmHg. Complete closure of the ASD was achieved. Transcatheter treatment may be an effective alternative to surgery in selected patients with Lutembacher syndrome.

Facilitation of radial artery cannulation by periradial subcutaneous administration of nitroglycerin.

PURPOSE: To determine whether subcutaneous administration of nitroglycerin mixed with local anesthetic agent results in effective vasodilation of the radial artery, and whether this technique improves access time and decreases complications. MATERIALS AND METHODS: This prospective study consisted of two consecutive investigations. In the first (n = 30), only local anesthetic agent (prilocaine 2%) was injected into one arm, and local anesthetic agent plus 500 microg nitroglycerin was injected into the other arm. Radial artery diameters before and after injections were measured by ultrasonography. In the second, 33 patients received local anesthetic agent (prilocaine 2%) plus 500 microg nitroglycerin (group A) and 30 received only local anesthetic agent (group B) to determine whether the addition of nitroglycerin would improve radial artery access time, duration of angiography, perception of arterial pulse (ie, pulse score), number of punctures before successful cannulation, and complication rates. RESULTS: In the first investigation, radial artery diameter increased significantly in the nitroglycerin-treated arm (2.3 mm +/- 0.4 vs 2.9 mm +/- 0.5; P = .05). In the second, there were no significant differences between groups with respect to age, sex, duration of angiography, and number of punctures before cannulation. However, the pulse score increased and radial artery access time improved significantly after addition of nitroglycerin (79% vs 10% [P < .001] and 75 sec +/- 47 vs 132 sec +/- 100 [P = .005], respectively). Radial artery spasm and thrombosis were less frequently observed in group A, albeit to an insignificant extent (P = .39 and P = .49, respectively). CONCLUSIONS: Subcutaneous administration of nitroglycerin significantly increased radial artery diameter, which can lead to facilitation of catheterization of the radial artery for arteriography and interventions.

The relation between endothelial dependent flow mediated dilation of the brachial artery and coronary collateral development - a cross sectional study.

BACKGROUND: Endothelial dysfunction is thought to be a potential mechanism for the decreased presence of coronary collaterals. The aim of the study was to investigate the association between systemic endothelial function and the extent of coronary collaterals. METHODS: We investigated the association between endothelial function assessed via flow mediated dilation (FMD) of the brachial artery following reactive hyperemia and the extent of coronary collaterals graded from 0 to 3 according to Rentrop classification in a cohort of 171 consecutive patients who had high grade coronary stenosis or occlusion on their angiograms. RESULTS: Mean age was 61 years and 75% were males. Of the 171 patients 88 (51%) had well developed collaterals (grades of 2 or 3) whereas 83 (49%) had impaired collateral development (grades of 0 or 1). Patients with poor collaterals were significantly more likely to have diabetes (p = 0.001), but less likely to have used statins (p = 0.083). FMD measurements were not significantly different among good and poor collateral groups (11.5 +/- 5.6 vs. 10.4 +/- 6.2% respectively, p = 0.214). Nitroglycerin mediated dilation was also similar (13.4 +/- 5.9 vs. 12.8 +/- 6.5%, p = 0.521). CONCLUSION: No significant association was found between the extent of angiographically visible coronary collaterals and systemic endothelial function assessed by FMD of the brachial artery.

Total blush score: a new index for the assessment of microvascular perfusion in idiopathic dilated cardiomyopathy.

BACKGROUND: The aim of this study was to evaluate tissue-level perfusion in patients with idiopathic dilated cardiomyopathy (IDC), using the myocardial blush grade technique. METHOD: The study population consisted of 26 prospectively enrolled IDC patients (15 women and 11 men; mean age, 59+/-8.8 years) and 26 control subjects (11 women and 15 men; mean age, 54.9+/-10.6 years), whose angiographic films were technically adequate for myocardial blush grade analysis. After grading, we measured total blush score (TBS) for both groups. TBS was determined as the sum of the blush grades of each coronary territory. RESULTS: A total of 156 coronary territories in both groups were assessed. Average of TBS was significantly lower in patients with IDC than in control group (7.6+/-1.2 vs. 8.8+/-0.4; P<0.0001). The TBS significantly and inversely correlated with New York Heart Association class, heart rate, left ventricular end-systolic dimension, and left ventricular end-diastolic pressure, and positively correlated with left ventricular ejection fraction (r=-0.76, P<0.001; r=-0.61, P=0.001; r=-0.77, P<0.0001; r=-0.68, P<0.0001; and r=0.67, P<0.0001, respectively). CONCLUSION: In IDC, decreased TBS might be assumed to be a surrogate marker for a diseased microvascular network in the catheterization laboratory. The relationship between reduced TBS and IDC severity suggests that this index might have prognostic significance.

The association of elevated white blood cell count and C-reactive protein with endothelial dysfunction in cardiac syndrome X.

BACKGROUND: The aim of the study is to evaluate the association of inflammatory markers with endothelial function in syndrome X. METHODS: The study population consisted of 59 prospectively enrolled patients (28 women and 31 men; mean age, 50.29 +/- 6.48 years) and 51 healty control subjects (18 women and 33 men; mean age, 51.04 +/- 7.25 years). High-sensitive CRP (hs-CRP), white blood cell (WBC) count and its subtypes [neutrophil (N), lymphocyte (L) and monocyte (M)] were measured in each subject. Endothelial function was assessed with the brachial artery flow-mediated dilatation (FMD) technique. RESULTS: WBC counts and hs-CRP levels were significantly higher in patients who had syndrome X than in control subjects (7.53 +/- 1.52 x 10(9) cells/L versus 6.21 +/- 1.17 x 10(9) cells/L, P = 0.0001, and 3.11 +/- 0.63 mg/L versus 2.68 +/- 0.76 mg/L, P = 0.002, respectively). Neutrophil count and N/L ratio was significantly increased in syndrome X when compared with the control subjects (5.14 +/- 1.10 x 10(9) cells/L versus 4.11 +/- 0.76 x 10(9) cells/L, P = 0.0001 and 2.75 +/- 1.06 versus 2.37 +/- 0.65, P = 0.02, repectively). Other subtype counts were similar between the groups. FMD was impaired significantly in patients who had syndrome X in comparison with the control subjects (5.71 +/- 4.08% versus 16.02 +/- 4.13%, P = 0.0001). There was a significant correlation between hs-CRP levels and FMD measurements (r = -0.44; P = 0.0001). Furthermore, the correlation between WBC count and FMD measurements were also significant (r = -0.48; P = 0.0001). CONCLUSIONS: The present study showed that hs-CRP and WBC count were higher in patients with syndrome X than in control subjects. Furthermore, endothelial function was impaired significantly in patients with syndrome X.The increased levels of hs-CRP and WBC count may suggest that these markers may be used in clinical practice for the assessment of the inflammatory status of the endothelium in syndrome X.

Good collaterals predict viable myocardium.

The authors undertook this study to see whether highly developed coronary collaterals at an area shed by a totally occluded coronary artery predicts myocardial viability. Percutaneous coronary intervention (PCI) of a totally occluded coronary artery has been debated since its introduction. It is recommended to search for viable myocardium before opening a totally occluded coronary artery; however, there is no practical yet sensitive method of assessing myocardial viability in the catheterization laboratory. Forty-seven consecutive patients (12 women, 25.5%; 35 men, 74.5%), each with 1 totally occluded coronary artery, were prospectively enrolled to the study. After the diagnostic coronary angiography, all patients underwent dobutamine stress echocardiography to determine viable myocardium at the territory of the totally occluded coronary artery, and the status of angiographic coronary collaterals was assessed. Patients were then divided into 2 groups according to the presence (Group A) or absence (Group B) of viable myocardium by stress echocardiography. Eighteen patients (38.3%) had viable myocardium (Group A) in the area shed by the totally occluded coronary artery and 29 patients (61.7%) had nonviable myocardium (Group B). The incidences of significant coronary collateral circulation to the viable (Group A) and nonviable (Group B) areas were 66.7% (12 patients) and 20.7% (6 patients), respectively (p = 0.002). Logistic regression analysis was used to evaluate the independent factors for viable myocardium, and only significant coronary collateral circulation was found to be an independent factor for the detection of viable myocardium (p = 0.006, OR 16.7, 95% CI 2.25 to 124.4). The sensitivity and specificity of good collateral circulation for the detection of viable myocardium were 75% and 65.7%, respectively. The positive predictive and negative predictive values of the good coronary collateral circulation in detecting viable myocardium were 75% and 79%, respectively. The authors conclude that good coronary collaterals have a high sensitivity and positive predictive value for the prediction of viability as shown by dobutamine echocardiography, and only by assessing the coronary collateral circulation can one decide for percutaneous coronary revascularization, if not for coronary artery bypass surgery.

Association between proliferative scars and in-stent restenosis.

BACKGROUND: Keloid and hypertrophic scars are two types of proliferative scars at sites of cutaneous injury that form as a result of an abnormal wound-healing process. Proliferative scar formation after skin injury and restenosis after coronary stenting have common features. The aim of this study was to investigate the association of proliferative scars with coronary stent restenosis. METHODS: Patients with previous open heart surgery with median sternotomy who had coronary stenting after the surgery and were admitted for control angiography were included in the study. The patients were divided into two groups according to the presence or absence of proliferative scars. The primary end point was the incidence of angiographic restenosis in patient groups. RESULTS: The study group consisted of 80 patients (64 men; mean age 64 + or - 9 years). Twenty-three patients (29%) have a proliferative scar. In general, two groups were comparable with regard to baseline lipid profiles, demographics, and cardiovascular risk factors. Restenosis was significantly more prevalent in patients with proliferative scars than with controls (p = .04). By multivariate logistic regression analysis, stent length (odds ratio [OR] 1.12, p = .005), diabetes (OR 3.3, p = .03), and proliferative scar (OR 4.2, p = .02) independently predicted in-stent restenosis. CONCLUSION: The findings of this study suggest that patients with proliferative scars may have a higher risk of in-stent restenosis.

The relationship of chronic angiotensin converting enzyme inhibitor use and coronary collateral vessel development.

BACKGROUND: Angiotensin II induces various growth factors such as vascular endothelial growth factor, platelet-derived growth factor, and fibroblast growth factor, and recent studies suggest that the expression of these growth factors promotes collateral growth. We hypothesized that the blockage of angiotensin II production by ACE inhibitors might interfere with collateral development in patients with coronary occlusion. METHODS: The study group consisted of 187 patients (114 males, mean ages, 62 +/- 11 years) who had chronic (> 1 month) coronary occlusion (TIMI flow grade < or = 1) in one of 3 epicardial coronary arteries. Collaterals were graded using the Rentrop classification, and the patients were divided into 2 groups according to having good (grade 2 and 3) or poor (grade 0 and 1) collaterals (n = 127 and 60, respectively). Clinical and angiographic characteristics were compared in the 2 groups. RESULTS: ACE inhibitor use (52% versus 35%, P = 0.04) and the prevalence of diabetes mellitus (DM) (43% versus 27%, P = 0.02) was higher in patients with poor collaterals. Patients with poor collaterals had a higher frequency of circumflex artery (Cx) occlusion, worse wall motion, and lower ejection fraction. In multivariate analysis, ACE inhibitor use (OR: 2.4; 95% CI = 1.23-4.68, P = 0.01) and the occlusion of Cx (OR: 3.3, 95% CI; 1.33-8.12, P = 0.01) were found to be independent predictors for poor collateral development, whereas there was a trend for DM as a predictor for poor collaterals (OR: 1.9, 95% CI = 0.97-3.8, P = 0.06). CONCLUSION: The findings suggest that ACE inhibitor therapy may contribute to poor collateral development in patients with coronary occlusion.

Relationship between angiotensin-converting enzyme gene polymorphism and severity of aortic valve calcification.

OBJECTIVE: To investigate the role of angiotensin-converting enzyme (ACE) gene polymorphism in patients with degenerative aortic valve calcification (AVC). PATIENTS AND METHODS: Our study consisted of 305 Turkish patients of European descent (139 male, 166 female; mean plus or minus age, 68 plus or minus 9 years) referred to our echocardiography laboratory for aortic valve evaluation between June 2, 2003, and April 29, 2005. The severity of AVC was graded from 1 to 6 by echocardiography. We used polymerase chain reaction to determine ACE gene polymorphism. RESULTS: The ACE insertion/deletion genotype distributions for the study population were in Hardy-Weinberg equilibrium (chi square equals 3.5, P equals .18). The study population was divided into 3 groups based on the severity of AVC: those with grade 1 calcification were in group 1, those with grades 2 to 4 in group 2, and those with grades 5 to 6 in group 3. Group 1 patients were significantly younger, less likely to have hypertension and diabetes, and had higher high-density lipoprotein cholesterol levels. The genotype frequencies were significantly different among groups, with the insertion/insertion genotype being less prevalent in group 3 patients. In multivariate analysis, independent predictors of severe AVC were hypertension (odds ratio [OR], 5.6; 95% confidence interval [CI], 2.8 to 11.0; P less than .001), low high-density lipoprotein cholesterol (OR, 2.7; 95 percent CI, 1.5 to 4.9; P equals .001), and the deletion/deletion and insertion/deletion vs insertion/insertion genotype (OR, 3.2; 95 percent CI, 1.5 to 7.2; P equals .004). CONCLUSION: These results suggest that ACE gene polymorphism may be associated with severe AVC.

Naproxen treatment prevents periprocedural inflammatory response but not myocardial injury after percutaneous coronary intervention.

BACKGROUND AND AIM: Recent studies have documented that elevation of C-reactive protein (CRP) levels after percutaneous coronary intervention (PCI) have been predictive of adverse outcome. This study was performed to test the hypothesis that preprocedural use of naproxen sodium is associated with a reduction in the extent of inflammatory response and myocardial injury after PCI. METHODS: Ninety-seven patients who were scheduled for elective PCI were randomized either for naproxen sodium (500 mg bid) (n:39, 75% male, 59+/-10 years) or control (n:58, 76% male, 60+/-10 years). All patients were troponin negative before the procedure. Blood samples for CRP, Troponin I and CK-MB were collected at baseline and after the procedure. RESULTS: The characteristics were similar between the two groups. After coronary stenting, the rise in CRP levels was significantly higher in controls than those treated with naproxen (DeltaCRP=6.4 mg/L in the controls and 0.43 mg/L in the naproxen group, p<0.0001). The incidence of any troponin I elevation or CK-MB elevation above upper limit of normal was not statistically different between groups. During follow up (12+/-2 months), major cardiac adverse events (death, myocardial infarction, and revascularization of target lesion) was similar between groups. CONCLUSION: Our data show that naproxen pretreatment leads to significant suppression in PCI related CRP elevation. However this improvement in CRP levels was not associated with any significant reduction in post-PCI myonecrosis.