Percutaneous plug-based vascular closure device in 1000 consecutive transfemoral transcatheter aortic valve implantations.

BACKGROUND: Arterial access-site related complications constitute a large proportion of adverse events related to cardiac interventions requiring large-bore devices and have significant implications on morbidity, mortality and hospital cost. AIMS: To evaluate the safety and effectiveness of a novel percutaneous plug-based vascular closure device (VCD) in 1000 consecutive patients undergoing transfemoral transcatheter aortic valve implantation (TAVI). METHODS: A single-center observational study evaluating a plug-based VCD (MANTA, Teleflex/Essential Medical Inc., Malvern, Pennsylvania, USA) in patients undergoing TAVI at the Karolinska University Hospital, Stockholm, Sweden. The primary outcome was VCD-related major vascular complication according to the criteria of the Valve Academic Research Consortium (VARC)-2. RESULTS: From May 2017 to September 2020 a total of 1000 consecutive patients underwent transfemoral TAVI with arterial access-site management using the MANTA VCD. VARC-2 major vascular complications occurred in 42 (4.2%) patients: 17 (1.7%) patients intraoperatively received a covered stent, 17 (1.7%) patients underwent surgical repair during hospital stay, 3 (0.3%) patients underwent vascular surgery after discharge, 3 (0.3%) patients had major bleeding and 2 (0.2%) patients had symptoms of claudication with conservative treatment. No significant differences in major complications were seen between individual interventionists irrespective of experience with the device. A larger sheath outer diameter to femoral artery inner diameter ratio was the only factor associated with a significant increase of VCD-related major vascular complications. CONCLUSION: This largest ever real-world evaluation of MANTA for large-bore arteriotomy closure in transfemoral TAVI patients indicates effective and safe arterial access-site management with low complication rates and short learning curve. CLINICAL TRIAL REGISTRATION: http://www. CLINICALTRIALS: gov. Unique identifier: NCT04392492.

Heart failure is a common complication after acute myocardial infarction in patients with diabetes: A nationwide study in the SWEDEHEART registry.

BACKGROUND: Several glucose lowering drugs with preventive effects on heart failure and death have entered the market, however, still used in low proportions after acute myocardial infarction. We explored the complication rates of heart failure and death after acute myocardial infarction in patients with and without diabetes. METHODS: All patients (N = 73,959) with acute myocardial infarction admitted for coronary angiography included in the SWEDEHEART registry during the years 2012-2017 were followed for heart failure (until 31 December 2017) and mortality (until 30 June 2018); mean follow-up time 1223 (SD ± 623) days. RESULTS: Mean age was 69 years (SD ± 12), 69% were male and 24% had diabetes. Heart failure occurred more often in diabetes (22% vs. 12% if no diabetes), especially if previous MI (33% vs. 23%). Patients with diabetes had increased risk of HF regardless of previous myocardial infarction (MI); with previous MI adjusted hazard ratio 2.09 (95% confidence interval 1.96-2.20) and without MI 1.52 (1.44-1.61) respectively when non-diabetes patients with first MI served as reference. In patients with no previous heart failure or MI and discharged with left ventricular ejection fraction ≥50% the risk of heart failure was particularly high in those with diabetes (1.56; 1.39-1.76) when compared with those without. Similar findings were seen for death and combined event (heart failure and death). CONCLUSIONS: Heart failure is a common complication after acute myocardial infarction in diabetes, increasing the risk by 50-60% regardless of previous heart failure or MI. This risk is present even with normal reported left ventricular ejection fraction, indicating the existence of a large diabetes population at heart failure risk after acute myocardial infarction.

Retrograde Snare Technique to Overcome Hostile Aortic Arch Anatomy During Transcatheter Aortic Valve Implantation.

Percutaneous valve implantation is a recognized therapy for calcific aortic stenosis in those patients who are inoperable or at high surgical risk. The transfemoral approach is the most frequently used method for device delivery, but a tortuous calcific aorta and the inflexibility of large-caliber endovascular equipment can impede progress or even cause the procedure to be abandoned. Herein, the use of a technique employing a snare to safely overcome device obstruction in the aortic arch of an elderly female patient is described. The technique may be of practical value whenever any large-caliber device is obstructed in the circulation.

A Path to Avoid during Transcatheter Aortic Valve Implantation: Case Report.

Collateral pathways in vascular disease are important natural "bypass" conduits that protect against ischemia. Endovascular diagnostic and therapeutic procedures via peripheral access sites are performed frequently. This case report underlines the importance of being aware of collateral circulation in patients with chronic aortoiliac occlusive disease undergoing subclavian transcatheter aortic valve implantation to avoid acute limb ischemia. (©) RSNA, 2016.

Femoral access-related complications during percutaneous transcatheter aortic valve implantation comparing single versus double Prostar XL device closure.

OBJECTIVES: To evaluate the efficacy and safety of a double Prostar XL suture-based closure technique compared to a conventional single Prostar XL technique in elective transcatheter aortic valve implantation (TAVI) via the common femoral artery. BACKGROUND: TAVI is recommended as a treatment for symptomatic severe aortic stenosis for those who are at high or prohibitive risk of surgical valve replacement. Vascular complications remain the most frequent category of procedural complication. The most efficacious and safest percutaneous suture-based closure technique is unknown. METHODS: Prospective observational study of Prostar XL device closures used in 126 consecutive patients between 2012 and 2014. Single Prostar XL closure was used in 63 patients and double Prostar XL closure in a further 63 patients. Outcomes from the groups were compared. All patients were treated transfemorally through an 18Fr sheath. Technical success was defined as hemostasis not requiring interventional or surgical repair during hospital admission. Bleeding and vascular complications were defined using the second consensus of the valvular academic research consortium (VARC-2) criteria. RESULTS: The cohort was aged 83+/-6 and 48% were female with a logistic Euroscore of 24+/-11.6. Technical success was 86% and 98% respectively (P = 0.017) with systematic single and double Prostar XL closure. Composite VARC-2 vascular and bleeding complications occurred more frequently in the single Prostar XL group compared to the double Prostar XL group (10 [16%] v 3 [5%] P < 0.04, and 17 [27%] v 6 [10%] P < 0.004). CONCLUSION: A systematic double Prostar XL closure technique for large caliber arterial access sites during TAVI is feasible, safe and associated with fewer technical failures, fewer vascular complications, and less bleeding compared with single Prostar XL.

High event rate after a first percutaneous coronary intervention in patients with diabetes mellitus: results from the Swedish coronary angiography and angioplasty registry.

BACKGROUND: Patients with diabetes mellitus have reduced longevity after acute coronary syndromes and revascularization. However, knowledge of the long-term complication rates and patterns from an everyday life setting is lacking. METHODS AND RESULTS: Consecutive patients undergoing percutaneous coronary intervention included in the Swedish Coronary Angiography Angioplasty Registry (SCAAR) between 2006 and 2010 and with no previous revascularization were prospectively followed up for combined cardiovascular events (first of all-cause mortality, myocardial infarction, stroke, and heart failure) until December 31, 2010. The mean follow-up period was 920 days (SD, 530 days). Differences in background and procedural characteristics were adjusted for in a multivariate Cox regression model. Of 58 891 patients, mean age 67 years, 19% had diabetes mellitus; 27% of them were on diet treatment, 33% on oral glucose lowering, and 40% on insulin treatment. At admission, cardiovascular risk factors, multiple coronary vessel, and left main stem disease were more frequent in patients with diabetes mellitus and their revascularization was less often complete. The adjusted risk for combined cardiovascular events was higher in patients on insulin (hazard ratio [95% confidence interval], 1.63 [1.55-1.72]), on oral treatment (1.23 [1.15-1.31]), and on diet alone (1.21 [1.12-1.29]) compared with patients without diabetes mellitus. Insulin-treated patients ran an increased risk of restenosis (1.54 [1.39-1.71]) and stent thrombosis (1.56 [1.25-1.96]). CONCLUSIONS: The prognosis after a first percutaneous coronary intervention is more severe in patients with diabetes mellitus, in particular, in patients treated with insulin, with higher rates of mortality, cardiovascular events, and stent thrombosis over the following 5 years.

Long-term impact of postconditioning on infarct size and left ventricular ejection fraction in patients with ST-elevation myocardial infarction.

BACKGROUND: Ischemic postconditioning (PostC), reperfusion in brief cycles, is known to induce short-term reduction in infarct size in patients with ST elevation myocardial infarction (STEMI), especially among those with large myocardium at risk (MaR). The aim of the present study was to investigate the long-term effect of PostC on infarct size and left ventricular ejection fraction (LVEF). METHODS: Sixty-eight patients with a first STEMI were randomised to primary percutaneous coronary intervention (PCI) (n = 35) or PCI followed by PostC (n = 33). MaR was determined as abnormally contracting segments on left ventricular angiogram. Cardiac magnetic resonance was performed at 3 and 12 months for the determination of infarct size and LVEF. RESULTS: Overall there was no difference in infarct size expressed in percentage of MaR between patients randomised to the control (31%; 23, 41) and PostC (31%; 23, 43) groups at 12 months. Likewise there was no difference in LVEF between control (49%; 41, 55) and PostC (52%; 45, 55). In contrast, patients in the PostC group with MaR in the upper quartile had a significantly smaller infarct size (29%; 18, 38) than those in the control group (40%; 34, 48; p < 0.05) at 12 months. In these patients LVEF was higher in the PostC (47%; 43, 50) compared to the control group (38%; 34, 42; p < 0.01). CONCLUSIONS: In this long-term follow-up study PostC did not reduce infarct size in relation to MaR or improved LVEF in the overall study population. However, the present data suggest that PostC exerts long-term beneficial effects in patients with large MaR thereby extending previously published short-term observations. TRIAL REGISTRATION: Karolinska Clinical Trial Registration (http://www.kctr.se). Unique identifier: CT20080014.

Effect of stent inflation pressure and post-dilatation on the outcome of coronary artery intervention. A report of more than 90,000 stent implantations.

BACKGROUND: Percutaneous coronary intervention (PCI) stent inflation pressure correlates to angiographic lumen improvement and stent expansion but the relation to outcome is not clarified. Using comprehensive registry data our aim was to evaluate how stent inflation pressure influences restenosis, stent thrombosis and death following PCI. METHODS: We evaluated all consecutive coronary stent implantations in Sweden during 46 months from 2008 using data from the Swedish Coronary Angiography and Angioplasty Registry (SCAAR). We used logistic regression and Cox proportional hazard modeling to estimate risk of outcomes with different balloon pressures. RESULTS: In total, 93 697 stents were eligible for analysis and divided into five different pressure interval groups: ≤15 atm, 16-17 atm, 18-19 atm, 20-21 atm and ≥22 atm. The risks of stent thrombosis and restenosis were significantly higher in the ≤15 atm, 18-19 atm and ≥22 atm groups (but not in the 16-17 atm group) compared to the 20-21 atm group. There were no differences in mortality. Post-dilatation was associated with a higher restenosis risk ratio (RR) of 1.22 (95% confidence interval (CI) 1.14-1.32, P<0.001) but stent thrombosis did not differ statistically between procedures with or without post-dilatation. The risk of death was lower following post-dilatation (RR 0.81 (CI 0.71-0.93) P = 0.003) and the difference compared to no post-dilatation was seen immediately after PCI. CONCLUSION: Our retrospective study of stent inflation pressure identified a possible biological pattern--the risks of stent thrombosis and of restenosis appeared to be higher with low and very high pressures. Post-dilatation might increase restenosis risk.

Effects of myocardial postconditioning on the recruitment of endothelial progenitor cells.

BACKGROUND: Ischemic postconditioning (PostC), brief repetitive cycles of ischemia and reperfusion during early reperfusion, is suggested to protect the myocardium in patients with stent thrombosis-elevation myocardial infarction (STEMI) by improved endothelial dysfunction and alteration of cytokine release. These mechanisms are also of importance for the recruitment of endothelial progenitor cells (EPC), an endogenous repair mechanism for re-endothelialization and neoangiogenesis. The aim of this study was to investigate the effect of PostC on recruitment of EPC. METHODS: EPC were analyzed in 20 patients with STEMI randomized to receive four cycles of PostC following percutaneous coronary intervention (PCI) or conventional PCI. Different subpopulations of EPC were quantified immediately and on day 4 using flow cytometry. Myocardium at risk, and infarct size was determined by cardiovascular magnetic resonance. RESULTS: There was no influence of PostC on the number of different EPC (CD34(+) , CD133(+) , CD34(+) CD133(+) , CD34(+) KDR(+) , CD34(-) CD133(+) KDR(+) , CD34(+) CD133(+) KDR(+) ). Left ventricular ejection fraction, myocardium at risk, and infarct size did not correlate to the mobilization of EPC. There was an inverse correlation between the symptom-to-balloon time and the mobilization of progenitor precursor cells (CD34(+) cells: R =-0.527, P = 0.02; CD133(+) cells: R =-0.624, P = 0.004; CD34(+) CD133(+) cells: R =-0.466, P = 0.04). DISCUSSION: Ischemic PostC did not result in improved mobilization of EPC in STEMI patients. The recruitment of progenitor cells seems to be related to the duration of ischemia rather than the size of the ischemic myocardial area. More effort is needed to understand the changes of endothelial surface markers by PostC and their role in EPC recruitment and homing.

Circulating endothelial and platelet derived microparticles reflect the size of myocardium at risk in patients with ST-elevation myocardial infarction.

OBJECTIVES: Microparticles (MP) are small membrane vesicles, released from activated, damaged and apoptotic endothelial cells (EMP) or platelets (PMP) that may actively modulate inflammation, coagulation and vascular function. We tested the hypothesis that the number of circulating EMP or PMP in acute myocardial infarction correlates with the myocardium at risk (MaR) and infarct size (IS). METHODS: EMP were quantified in plasma samples of 36 patients (age: 63±10 years) with first time ST-elevation myocardial infarction (STEMI) using flow cytometry. EMP were defined as CD31(+)/CD42(-) MP and CD144(+) MP and PMP as CD31(+)/CD42(+) MP. MaR and IS was determined by cardiovascular magnetic resonance imaging one week after the index event. RESULTS: Plasma levels of CD31(+)/CD42(-) EMP were 251.0±178.8/µl and CD144(+) 106.3±33.7/µl. PMP levels were 579.2±631.8/µl. MaR was 31.0±11.2% of the left ventricle and IS was 11.4±7.1% of the left ventricle. Patients with STEMI in the left anterior descending artery had higher levels of CD31(+)/CD42(-) EMP and PMP than those with other infarct-related arteries (p<0.05). The numbers of CD31(+)/CD42(-) EMP and PMP correlated to MaR, but not to IS. CONCLUSIONS: Circulating EMP and PMP correlate to the size of MaR in patients with STEMI suggesting that they reflect the severity of the endothelial injury and platelet activation during myocardial ischemia.

The predictive value of inflammatory activity and markers of the adipo-insular axis on restenosis in patients with type 2 diabetes.

AIMS: Patients with type 2 diabetes (T2DM) have a high restenosis rate after percutaneous coronary intervention (PCI). This study investigated whether markers of inflammation and the adipo-insular axis associated with T2DM and poor metabolic control were able to predict restenosis after PCI in T2DM patients. METHODS AND RESULTS: The predictive value of traditional and non-traditional risk markers, including IL-1ß, IL-6, TNF-α, hsCRP, interferon gamma, leptin, IGF-I, insulin, proinsulin and NT-proBNP, was investigated in 82 patients with T2DM. A re-angiography 6 months after the index percutaneous coronary intervention (PCI) revealed that 43% of the patients had a restenosis. In a multiple regression analysis, the only independent predictors of restenosis were fasting glucose before the PCI and previous myocardial infarction (odds ratio [OR] 1.44, 95% confidence interval [CI] 1.07-1.92; p = 0.015 and OR 8.00, 95% CI 2.49-25.67; p ≤ 0.001, respectively). None of the other markers remained as significant predictors. CONCLUSION: Fasting glucose prior to the PCI was an independent predictor of restenosis in patients with T2DM while analyses of a variety of markers related to inflammation and the adipo-insular axis did not add any further information.

Long-term mortality after PCI in patients with diabetes mellitus: results from the Swedish Coronary Angiography and Angioplasty Registry.

AIMS: Patients with diabetes mellitus have poorer outcome following acute coronary syndromes and coronary revascularisation. Knowledge of long-term outcome after revascularisation in real-life situations is though limited was analysed. METHODS AND RESULTS: Patients included in the Swedish Coronary Angiography Angioplasty Registry (SCAAR) in 2002-2007 with no previous revascularisation were followed for mortality after a first PCI until the end of 2007 (mean follow-up time 1,059 days). Differences in background and procedural characteristics were adjusted for in a multivariable Cox regression model. Of 57,708 patients, 18.8% had diabetes. Absolute mortality rate after four years follow-up was after STEMI, non-ST-elevation ACS and stable CAD respectively 23.2%, 17.8% and 12.7% for persons with diabetes and 14.4%, 8.4% and 5.7% for persons without diabetes. Adjusted relative risk for long-term mortality after first PCI was higher in patients with diabetes compared with those without; RR (95% CI); 1.66 (1.33-1.72), and after all three different PCI indications; RR (95% CI) for CAD; 2.01 (1.69-2.40), non-ST-elevation ACS 1.73 (1.58-1.90) and STEMI 1.44(1.30-1.59). CONCLUSIONS: Long-term mortality is higher in diabetic patients compared with those without, after a first PCI and this mortality gap increases with follow-up time. Intensive secondary preventive measures are needed to improve this situation.

Assessment of myocardium at risk with contrast enhanced steady-state free precession cine cardiovascular magnetic resonance compared to single-photon emission computed tomography.

BACKGROUND: Final infarct size following coronary occlusion is determined by the duration of ischemia, the size of myocardium at risk (MaR) and reperfusion injury. The reference method for determining MaR, single-photon emission computed tomography (SPECT) before reperfusion, is impractical in an acute setting. The aim of the present study was to evaluate whether MaR can be determined from the contrast enhanced myocardium using steady-state free precession (SSFP) cine cardiovascular magnetic resonance (CMR) performed one week after the acute event in ST-elevation myocardial infarction (STEMI) patients with total coronary occlusion. RESULTS: Sixteen patients with STEMI (age 64 +/- 8 years) received intravenous 99 m-Tc immediately before primary percutaneous coronary intervention. SPECT was performed within four hours. MaR was defined as the non-perfused myocardial volume derived with SPECT. CMR was performed 7.8 +/- 1.2 days after the myocardial infarction using a protocol in which the contrast agent was administered before acquisition of short-axis SSFP cines. MaR was evaluated as the contrast enhanced myocardial volume in the cines by two blinded observers. MaR determined from the enhanced region on cine CMR correlated significantly with that derived with SPECT (r2 = 0.78, p < 0.001). The difference in MaR determined by CMR and SPECT was 0.5 +/- 5.1% (mean +/- SD). The interobserver variability of contrast enhanced cine SSFP measurements was 1.6 +/- 3.7% (mean +/- SD) of the left ventricle wall volume. CONCLUSIONS: Contrast enhanced SSFP cine CMR performed one week after acute infarction accurately depicts MaR prior to reperfusion in STEMI patients with total occlusion undergoing primary PCI. This suggests that a single CMR examination might be performed for determination of MaR and infarct size.

Serum C-reactive protein response to percutaneous coronary intervention in patients with unstable or stable angina pectoris is associated with the risk of clinical restenosis.

BACKGROUND: Inflammation plays a pivotal role in the pathogenesis of atherosclerosis. Previous reports have used vaccination as a model to stimulate inflammation. The aim of the present study was to investigate the role of C-reactive protein response to PCI in the risk of clinical restenosis or new coronary stenosis, considering PCI as a model to stimulate inflammation. MATERIAL AND METHODS: Eight hundred and ninety-one patients with stable or unstable angina pectoris and with normal serum troponin T

Usefulness of preprocedural serum N-terminal pro-brain natriuretic peptide levels to predict long-term outcome after percutaneous coronary intervention in patients with normal troponin T levels.

Our objective was to evaluate the prognostic information of preprocedural serum N-terminus pro-brain natriuretic peptide (NT-pro-BNP) levels to predict the long-term outcome after percutaneous coronary intervention (PCI). A total of 891 consecutive patients with stable or unstable angina pectoris with normal serum troponin T levels (< or =0.03 microg/L) undergoing PCI were investigated. For each patient with a cardiovascular event (death or nonfatal myocardial infarction), 2 event-free patients were used as controls. The procedure was successful in all patients, and follow-up was complete. By the end of the follow-up period (mean 2.6 years), 75 patients had had a cardiovascular event (41 deaths and 34 nonfatal myocardial infarctions). On multivariate analysis, lesion severity, diabetes mellitus, and NT-pro-BNP levels in the highest quartile (>490 mg/L) were identified as independent factors for death or nonfatal myocardial infarction after PCI. In conclusion, preprocedural NT-pro-BNP levels are associated with long-term outcome after PCI. The use of NT-pro-BNP can be of value in risk stratification in patients undergoing PCI.

Response of serum C-reactive protein to percutaneous coronary intervention has prognostic value.

BACKGROUND: Data are sparse regarding the association between C-reactive protein (CRP) and percutaneous coronary intervention (PCI) in long-term prognosis. Previous studies have shown that PCI evokes an inflammatory response. We tested the hypothesis that the CRP response to PCI has a prognostic value. METHODS: We investigated 891 consecutive patients presenting with stable or unstable angina pectoris, with serum concentrations of cardiac troponin T < or =0.03 microg/L, who were undergoing a variety of PCIs. Serum concentrations of CRP and cardiac troponin T were determined before and the day after PCI. The mean follow-up time after PCI was 2.6 years, and the endpoint was death or nonfatal myocardial infarction. RESULTS: Seventy-six patients reached the endpoint (4.6% death, 3.9% nonfatal myocardial infarction), whereas 21% developed myocardial infarction during the procedure. CRP increased more than 2-fold after the procedure. Patients in the third tertile of the CRP response to PCI had an increased risk for death or nonfatal myocardial infarction in multivariate analysis. CONCLUSIONS: Increased serum CRP in response to PCI is an independent predictor of death or nonfatal myocardial infarction independent of myocardial injury during the procedure. CRP determinations might be of value in risk stratification after PCI.

Stent implantation, but not pathogen burden, is associated with plasma C-reactive protein and interleukin-6 levels after percutaneous coronary intervention in patients with stable angina pectoris.

BACKGROUND: The systemic inflammatory response to percutaneous coronary intervention (PCI) is associated with recurrent cardiac events; however, the pathophysiology of this inflammatory response is not well understood. The present study was performed to investigate the role of pathogen burden of infection in determining the magnitude of C-reactive protein (CRP) and interleukin 6 (IL-6) response to PCI. METHODS: One hundred patients with stable angina pectoris undergoing elective PCI at a single center were recruited. Antibodies against cytomegalovirus, Chlamydia pneumoniae , Epstein-Barr virus, Helicobacter pylori , and herpes simplex virus types 1 and 2 were determined before PCI. Plasma CRP and IL-6 levels were measured before and 6, 24, 48, 72 hours after PCI and data presented as area under the curve. RESULTS: Plasma CRP and IL-6 concentrations increased significantly after PCI. Neither antibodies against single nor multiple pathogens were associated with the CRP or IL-6 response to PCI. No correlations were found between the inflammatory markers and troponin T levels after PCI. With the exception for CRP and body mass index (R = 0.20, P < .05), neither risk factors for coronary heart disease nor medication but stent implantation was associated with increased plasma CRP (76 vs 61 mg/L, P < .005) and IL-6 (74 vs 64 pg/mL, P < .005) levels after PCI. CONCLUSION: Stent implantation, but not pathogen burden, is associated with the plasma CRP and IL-6 response to PCI.

Comparison of effects of a thrombin-based femoral artery closure device with those of a mechanical compression device on serum C-reactive protein and amyloid A after percutaneous coronary intervention.

The present study evaluates whether the closing procedure of the femoral artery after percutaneous coronary intervention influences the degree of inflammation related to the procedure as measured by C-reactive protein (CRP) and serum amyloid A (SAA). A thrombin-based device (Duett sealing device) was compared with a mechanical compression device (FemoStop).

Platelet function and myocardial injury during percutaneous coronary intervention.

BACKGROUND: Several studies have shown that inhibition of the glycoprotein IIb/IIIa receptor can reduce myocardial injury during percutaneous coronary intervention (PCI). The present study was performed to investigate platelet function, using a bedside diagnostic system, to test the hypothesis that patients with activated platelets have an increased risk for myocardial injury during PCI. Such information would be valuable to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor during and after the procedure. METHODS: 155 consecutive patients undergoing PCI were included in the study. 94 of the patients had stable angina pectoris and the remaining patients had unstable angina pectoris or ongoing myocardial infarction. Troponin T levels were measured in serum before PCI and at 6 am the day after PCI by an immunoassay. Platelet function was analyzed in arterial blood before PCI using the platelet function analyzer PFA-100(R) by Dade Behring. RESULTS: The platelet function analyzer PFA-100(R) could not discriminate between patients with or without myocardial injury during the procedure but between patients with or without acetyl salicylic acid. CONCLUSION: The platelet function analyzer PFA-100(R) cannot be used to guide the PCI operator to whom he or she should give a glycoprotein IIb/IIIa inhibitor but the results indicate that PFA-100(R) can be used to monitor platelet effects of ASA therapy.