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Background GRACE, TIMI, Zwolle, and CADILLAC are risk scores designed for predicting short-term outcome after acute coronary syndromes. The aim of our study was to test their utility for a prognosis of 5-year survival in a "real-life" population of patients with ST-elevation myocardial infarction (STEMI) treated with primary percutaneous coronary interventions (pPCI). Methods Our registry consisted of consecutive patients with STEMI treated with pPCI. Five-year follow-up was performed with all-cause mortality as the end-point. Results Out of 505 patients (mean age 58.6±11.3years) 32 died during the first 30days (6.3%) and an additional 74 within 5years (15.6%). PCI was successful in 95.2% ( n =481). Prognostic values ( c statistics) for predicting 5-year mortality equaled: 0.742 (CI 0.69–0.79) for the GRACE risk score, 0.727 (CI 0.67–0.78) for TIMI, 0.72 (CI 0.67–0.77) for Zwolle, and 0.687 (CI 0.63–0.74) for CADILLAC. In a univariate analysis all the scores were associated with the 5-year outcome. Conclusions GRACE, TIMI, and Zwolle risk scores predicted well 5-year all-cause mortality in patients with STEMI treated with pPCI. Our data show that the usefulness of initial bedside risk assessment can be further extended for long-term follow-up.

Aims Our study aimed to compare two reperfusion strategies in patients with ST-elevation myocardial infarction (STEMI) admitted initially to a community hospital without catheterization facilities. Methods and results Four hundred and one patients with STEMI admitted to community hospital (13 hospitals, radius 20–150 km from cath-lab) were randomized to on-site thrombolysis or to transport with tirofiban (10 µg/kg bolus i.v. + i.v. infusion 0.1 µg/kg/min) for primary PCI in single invasive centre. Primary endpoints were total mortality, recurrent MI (re-AMI), and stroke during 1 year follow-up. Delay to reperfusion defined as interval between admission and start of fibrinolysis or primary PCI was 35 and 145 min ( P < 0.0001). Mean time of tirofiban administration to PCI in transfer group was: 122.3 ± 35.7 min. Mortality was not different during hospitalization and at 30th-day, with trend towards lower mortality at 1 year in transport group (12.5 vs. 7.0%, P = 0.061). There were no differences in the rate of re-AMI and stroke, with trend towards lower incidence of re-AMI in transfer group at 1 year (7.5 vs. 3.5%, P = 0.073). Composite of death/re-AMI/stroke was higher in on-site group during follow-up (15.5 vs. 8.0%, P = 0.019; 21.5 vs. 11.4%, P = 0.006, respectively, at 30th-day and 1 year). Conclusion Outcomes at 1 year follow-up suggest that transportation with adjunctive therapy with GP IIb/IIIa inhibitor tirofiban for primary PCI is superior to on-site thrombolysis for patient with STEMI presenting to hospital without catheterization facilities.

Background The significance of dynamic changes in a depressed ST-segment in the reciprocal changes after percutaneous coronary intervention (PCI) of patients with ST-elevation myocardial infarction (STEMI) is unknown, so the aim of this study was to evaluate the significance of reciprocal ST-segment depression normalization (STN) on long-term mortality in patients with STEMI treated with primary PCI. Methods and Results Data for 247 consecutive patients with STEMI were analyzed; 84 patients were excluded because of exclusion or incomplete inclusion criteria, so finally, 163 patients successfully treated with primary PCI were included. The study group was divided into 3 subgroups according to percentage of STN: poor STN ( 70%). Complete STN occurred in 63%, partial in 24% and poor in 13% of patients. STN correlated with late mortality (15% vs 28% vs 38% respectively, p=0.012). Patients who died during the follow-up period had a lower mean percentage reduction of initial ST-segment depression after PCI (50% vs 75%, p=0.001). Percentage reduction of initial ST-segment depression after PCI was a significant and independent risk factor of long-term mortality (odds ratio 1.01; 95% confidence interval: 1.00-1.02; p=0.02). Conclusions These data revealed the use of reciprocal changes normalization as a novel tool for assessment of long-term risk of death in patients after successful primary PCI for STEMI. (Circ J 2007; 71: 1851 - 1856)

Background: Left main stenosis (LMS) occurs in 5–7% of patients with coronary artery disease. Half of patients with left main coronary artery (LMCA) disease die within few years after the diagnosis. Aim: To evaluate survival of patients with LMCA disease treated with coronary artery bypass grafting (CABG), percutaneous coronary intervention (PCI), or managed medically due to lack of consent for CABG or being considered unsuitable candidatesfor CABG/PCI. Methods: In 2006–2008, a significant LMS was found in 257 (5.14%) patients, and 98.44% of these patients were followed upfor on average 15.1 months. The patients were divided into 5 groups according to the treatment used. CABG was performedin 67% of patients, PCI of an unprotected LMS in 8% of patients, and 12% of patients were treated with PCI after a previous CABG (protected LMS). The remaining patients were managed medically: 4% were not considered suitable for CABG, and9% did not give their consent for CABG. Results: Total mortality in the overall study group (n = 253) was 14.6%. Multivessel disease was more frequent in the CABG group (60.9% vs. 15.8%, p < 0.001). Mortality in CABG and PCI groups was comparable (11.4% vs. 15.8%). Patients in the PCI group were more frequently hospitalised due to recurrent angina (21.1% vs. 3.0%, p < 0.001) and the need for repeated revascularisation (15.8% vs. 1.2%, p < 0.001). Compared to the CABG group, patients considered not suitable for CABG hadlower left ventricular ejection fraction (LVEF) (36.55% vs. 51.04%, p < 0.001) and a higher mortality risk as estimated by the EuroScore. Mortality among patients deemed unsuitable for CABG was 54.6% (p < 0.001) and myocardial infarctions were observed more frequently in this group (18.2% vs. 2.4%, p < 0.01). In comparison to the CABG group, patients who did not consent to CABG were older (71.04 vs. 65.99 years, p = 0.027), had lower LVEF (44.05% vs. 51.04%, p = 0.004), were less frequently hospitalised due to acute coronary syndromes (17.4% vs. 40.8%, p = 0.03), and had a smaller degree of LMS (63%vs. 71%, p = 0.027). Mortality in this group was comparable to the CABG group (17.4% vs. 11.4%). The majority of patients who underwent previous CABG needed repeated revascularisation: PCI of a protected LMS was performed in 27% of patients,PCI of other native coronary arteries in 39% of patients, and PCI of a bypass graft in 7% of patients. Conclusions: PCI of unprotected LMCA may be an equally effective revascularisation method as CABG. High mortality (55%) due to concomitant diseases was observed among patients with LMS who were deemed unsuitable candidates for CABG. Prognosis among patients who declined CABG was relatively good and might have been related to the small number of patients and different patient characteristics in this group.

Left main disease (LMD) is a severe form of coronary artery disease (CAD). Fifty percent of patients with LMD treated conservatively die within 3-5 years of diagnosis. The aim of the study was to assess the influence of type 2 diabetes on early and late (2-year) prognosis and the risk of complications after coronary artery by-pass graft (CABG) surgery in patients with LMD.We enrolled 257 patients diagnosed with LMD. 169 (67%) underwent CABG, 19 (8%) percutaneous coronary intervention (PCI) without left main stem protection. 30 (12%) patients had CABG previously. Patients treated with CABG were divided into two groups - with and without diabetes. There were 43 (25.4%) patients with diabetes and 126 (74.6%) without diabetes.We observed more complications with wound healing (40.5% vs. 12.8%, p0.001) and sternal dehiscence (23.8% vs. 4.0%, p0.001) after CABG in patients with diabetes. There were no differences in 7-day, 30-day, 3-month and 1-year mortality. 2-Year mortality was also similar in both groups (11.6% vs. 11.1%, p=0.928). Patients with diabetes were more frequently hospitalized due to other reasons than angina (39.5% vs. 20.6%, p=0.014).Patients with diabetes and LMD had more often complications with wound healing and sternal dehiscence after CABG than patients without diabetes. Type 2 diabetes did not influence early and late mortality in patients with LMD treated with cardiac surgery, but the presence of diabetes was associated with more frequent hospitalizations.

The progress which has been made in interventional cardiology contributes to the gradual improvement of the results of CHD (coronary heart disease) therapy. The aim of the study was the assessment of early and long-term prognosis in all the patients with CHD treated invasively in one large-volume PCI center in 2005.1390 consecutive patients with CHD treated with PCI in 2005 were included in the analysis. Patients with ST-elevation myocardial infarction (STEMI) accounted for 50% of cases, patients with stable angina (SA) amounted to 25%, and patients with non-ST elevation acute coronary syndromes (NSTE-ACS) constituted 25%. Mean follow-up was 738 (±237) days.The highest mortality during the hospitalization was noted within the STEMI group(SA vs. NSTE-ACS vs. STEMI; 0% vs. 0.3% vs. 4.1%, respectively; p0.001). The highest mortality during a 2-year follow-up was also observed in the STEMI group (SA vs. NSTE-ACS vs. STEMI, 6.3% vs. 8.5% vs. 13.8%, respectively; p0.001). Multiple regression model showed that independent risk factors for death during the follow-up were: age, glycaemia at admission, heart rate, blood pressure, ejection fraction, STEMI, ineffective PCI (R=0.3613; F(10.131)=19.672; p0.0001 for the model).The highest relative increase of mortality after the discharge of patients with CHD undergoing PCI referred to the patients with NSTE-ACS. However, in the real life PCI practice STEMI patients have the worst hospital and long-term prognosis. Well recognized risk factors for death in patients with CHD are still of great importance in negative prognosis of patients undergoing PCI.

Rotational atherectomy is a valuable technique complementary to PCI in complex calcified coronary artery stenoses. A case of a 65 year-old man with non-ST elevation acute myocardial infarction (NSTEMI) treated with PCI with rotational atherectomy followed by two drug eluting stents (DES) implantation is presented.

We hypothesize that higher morbidity of patients with ST-segment elevation myocardial infarction (STEMI) in the out-of-office hours differences in outcome after myocardial infarction may depend on the concentrations of inflammatory cytokines. The aim of the study was to determine the relation between the time of percutaneous coronary intervention (PCI) and local concentration of interleukin 6 (IL-6) and its soluble receptors (sIL-6R and sgp130) in patients with STEMI. Methods and results: The study included 32 patients with invasively treated left anterior descending artery occlusion and no significant co-morbidities. Blood samples were drawn from coronary sinus and aorta before and after intervention. Patients admitted in the afternoon (13–20) presented significantly higher mean IL-6 levels in all samples than patients admitted in the morning. There was a positive correlation between time of intervention and concentrations of IL-6 in all samplings, but also with transcardiac IL-6 gradient at the end of procedure and IL-6 increase during PCI. We did not find any significant association between time of PCI and concentrations of sIL-6R and sgp130, time from pain to balloon, angiographic parameters or medical history. Conclusions: Coronary concentration of IL-6 in patients with STEMI is significantly higher in the afternoon than in the morning. This might be involved in increased morbidity of those patients.

Coronary stenting may create local inflammatory reaction. Interleukin 6 effects depend on the presence of soluble receptors (sIL-6R and sgp130) that facilitate or impede interleukin 6 signal transduction. Concentrations of interleukin 6 and its soluble receptors were assessed in aorta and coronary sinus after stenting in optimally treated stable angina patients scheduled for elective stenting. Baseline levels of interleukin 6 and its soluble receptors in patients did not differ from healthy controls. Initial levels of sIL-6R in aorta were significantly higher than in coronary sinus but this difference disappeared after intervention. Stenting caused interleukin 6 concentration increase to a similar extent both in coronary sinus and in aorta. Moreover, there was significantly higher sgp130 concentration in coronary sinus than in aorta. Coronary intervention increases concentration of interleukin 6 in patients with stable angina. It affects the cardiac level of interleukin 6 soluble receptors what may influence the local inflammatory reaction.

Interleukin 6 (IL-6) is a pleiotropic cytokine involved in both inflammatory reaction and myocardial response to stress. Its effects largely depend on the concentration of the soluble receptors (sIL-6R and sgp130). We investigated the production of IL-6, sIL-6R and sgp130 by the heart during ischemia and reperfusion. Methods: The levels of IL-6 were determined in blood of 34 patients with first myocardial infarction (STEMI), left anterior descending (LAD) artery occlusion, otherwise normal coronaries, without significant co-morbidities and 16 comparable subjects with stable ischemic heart disease and lesion in LAD. Blood samples from coronary sinus (CS) and aorta (Ao) were drawn before percutaneous intervention (PCI), immediately after and at the end of the procedure. Venous blood from 30 healthy volunteers served as control. Results: STEMI patients presented high IL-6 concentrations that increased further after reperfusion when its levels in CS became significantly higher than in Ao. In both groups prior to the PCI there were significantly higher concentrations of sIL-6R in Ao than in CS. This difference disappeared immediately after reperfusion. STEMI patients who experienced cardiovascular complications had higher IL-6 concentration and higher transcardiac sIL-6R gradient than patients with event-free hospitalisation. This association was confirmed in multivariate logistic regression analysis. Myocardial infarction increases concentration of IL-6 that is further elevated by reperfusion. A transcardiac gradient of sIL-6R during ischemia may indicate that large amounts of soluble IL-6 receptors are bound to the infarcted heart and thus affect signal transduction. IL-6 and initial sIL-6R gradient may portend complications in STEMI patients.

Reperfusion of ischemic myocardium evokes rapid release of free radicals in experimental models. The aim of the study was to investigate the oxidative stress and antioxidative defense during first minutes after reopening of the infarct related artery in patients treated for acute myocardial infarction. The study group consisted of 15 patients with first ST elevation myocardial infarction (STEMI) due to left anterior descending artery occlusion. The control group included ten patients with stable ischemic heart disease (IHD). Blood samples from coronary sinus were drawn before, immediately after and about 15 min after angioplasty. Activity of superoxide dysmutase (SOD), concentration of glutathione as well as the concentrations of lipid peroxides, malodialdehyde (MDA) and 4-hydroxy-2-nonenal (HNE) were measured. There was significantly higher concentration of MDA and HNE and higher SOD activity in STEMI patients before the reperfusion, as compared to the stable IHD group. After the reperfusion concentration of HNE in erythrocytes from STEMI patients was higher than in IHD group. At the same time the activity of SOD significantly decreased in patients with impaired tissue perfusion (myocardial blush grade

TIMI Risk Score for ST-elevation myocardial infarction (STEMI) was developed in a cohort of patients treated with fibrinolysis. It was though to predict in-hospital and short-term prognosis. Later studies validated this approach in large cohorts of patients, regardless of the applied treatment and presented its good power to predict 30-day mortality.We applied the TIMI Risk Score to our registry of STEMI patients treated with primary percutaneous intervention (pPCI) to validate the possibility to predict one-year survival.Our registry comprised 494 consecutive patients (mean age 58.5+/-11.3 years) with STEMI treated with pPCI who were followed for approximately one year. STEMI was diagnosed based on typical criteria: chest pain, ECG changes and rise in myocardial necrosis markers. In all patients TIMI Risk Score for STEMI was calculated and they were divided into three groups: low risk (0-5 points), medium risk (6-7) and high risk (7 points). Multivariate logistic regression analysis, Kaplan-Meier survival analysis with Cox and log-rank tests as well as c statistics from receiver-operator curves (ROC) were used for statistical analysis.TIMI 3 flow was obtained in 95.5% of patients. Median TIMI risk score was 4 (ranging from 0 to 10). During follow-up there were 47 deaths (9.5%). There was a statistically significant difference in survival between all risk groups both in 30-day and one-year follow-up (p0.001 log-rank test). TIMI Risk Score had good power to predict 30-day (c statistic 0.834, 95% CI 0.757-0.91, p0.0001) as well as one-year mortality (c statistic 0.809, 95% CI 0.739-0.878, p0.0001). Interestingly, when we excluded from the analysis all patients who died during the first 30 days, TIMI Risk score maintained its very good prognostic value. All analysed risk groups significantly differed between each other with respect to mortality (p0.05, log-rank test) and the c statistic was 0.745 (95% CI 0.612-0.879, p0.0002). In multivariate logistic regression analysis TIMI Risk Score was one of the independent risk factors of death during one-year follow-up (OR 1.59, p0.001).TIMI Risk Score accurately defines the population of STEMI patients who are at high risk of death not only during the first 30 days, but also during a long-term follow-up. This simple score should be included in the discharge letters because it contains very useful information for further care.

The advantage of primary percutaneous coronary intervention (pPCI) in the management of ST-elevation myocardial infarction (STEMI) over thrombolytic therapy has been demonstrated. However, an optimal medical treatment of STEMI patients admitted to regional hospitals without catheterisation facilities has not yet been established. Delay in initiation of pPCI resulting from transportation to the catheterisation laboratory may diminish the benefits of such therapy in comparison with thrombolysis administered in a regional hospital. Early initiation of therapy with platelet glycoprotein IIb/IIIa receptor inhibitor, which provides protection for the transportation, may be a reasonable solution to maintain the advantage of pPCI over thrombolysis alone in STEMI patients.The studied group comprised patients with STEMI (infarct duration time12 hours, typical clinical and electrocardiographic criteria of MI) who were randomly assigned in 13 regional hospitals located 20 to 150 km from invasive centre to one of two subgroups, either to thrombolysis in the community hospital or to transport after thrombolysis initiation with platelet GP IIb/IIIa receptor inhibitor (tirofiban; 10 mg/kg in intravenous bolus in the emergency room of the community hospital followed by continuous intravenous infusion of 0.1 mg/kg/min during transport as well as coronary procedure) in order to receive pPCI. All patients with cardiogenic shock on admission were routinely treated with PCI and were excluded from the study.341 patients were included in the study (169 were randomised to receive thrombolytic therapy and 172--transport with intention to perform PCI). Mean time between onset of MI and randomisation was similar in the transport and thrombolysis groups, (139+/-133 min. vs 143+/-117 min., respectively, p=0.94). Mean infusion time of tirofiban to the beginning of PCI in the transport group was 121+/-36 min. Anterior MI was present in 42.6% of patients in the PCI group and in 41.5% in the thrombolytic group (p=0.085). Mean time from randomisation to pPCI was 158+/-60 min., and to thrombolysis initiation in 44+/-43 min. (p0.0001). None of the patients died during transfer. In a 30-day follow-up we noted (pPCI vs thrombolytic group, respectively): mortality 3.49% vs 8.88% (p=0.04); reinfarction 1.16% vs 5.92% (p=0.02), stroke 0.58% vs 1.18% (p=0.55). In-hospital stay was significantly shorter in the transport group (9+/-3 days vs 14+/-7 days, p0.0001). During hospitalisation, 17 (10.05%) patients initially assigned to thrombolysis alone had to be transferred to the catheterisation laboratory to undergo PCI (rescue PCI or PCI for postinfarction angina). Combined end-point (death/reinfarction/stroke) was reached more frequently in the thrombolytic group (15.98% vs 5.23%, p=0.001).A strategy of invasive therapy involving transport with GP IIb/IIIa receptor inhibitor and pPCI in STEMI patients admitted to hospital without catheterisation facilities was found to be more effective than thrombolytic therapy alone employed in the regional hospitals.

Coronary stenting is associated with acute inflammation within the arterial wall followed by neointimal growth. Acute inflammatory response is expressed by a marked systemic elevation of the inflammatory biomarker C-reactive protein (CRP). It has been shown that the degree and extent of CRP increase may be related to clinical presentation or periprocedural treatment.To investigate whether an increase in CRP level is associated with the extent of arterial injury during stent deployment.CRP levels were measured with a high-sensitivity CRP (hsCRP) assay. Seventy-three patients (51 males) with normal baseline plasma CRP (3 mg/L) underwent percutaneous coronary intervention (PCI) with stent implantation for stable coronary disease. Blood samples for hsCRP were drawn before the intervention, and 6, 12 and 24 hours after the procedure. Both quantitative (single vs multivessel coronary intervention) and qualitative analyses (including lesion classification according to the ACC/AHA grading system) were performed in all patients. The examined angiographic parameters and procedural data obtained included reference diameter, lesion location, lesion length, total stented segment length, diameter of stent after deployment, maximal deployment pressure, total inflation number and duration.The mean hsCRP level increased in all patients between baseline and 24 hours (1.36+/-0.93 mg/L and 4.34+/-3.3 mg/L, p0.0001). Single vessel procedure was performed in 51 patients and multivessel coronary intervention in 22 patients. Mean hsCRP was similar at baseline and after 6 hours in both groups and the increase after 12 and 24 hours was higher among patients with multivessel coronary intervention compared to patients with single vessel procedure (2.69+/-2.48 vs 4.15+/-3.17; p=0.039 and 3.76+/-3.13 vs 5.69+/-3.38; p=0.021, respectively). There was no correlation between hsCRP and the degree of lesion complexity. Multiple regression analysis showed that the total stented segment length (p=0.01) contributed to the hsCRP increase after 24 hours.The inflammatory response expressed by hsCRP levels is higher in patients with multivessel coronary intervention with longer total segment stented.

Platelet receptor IIb/IIIa inhibition during percutaneous coronary interventions (PCI) decreases incidence of major adverse cardiac events (MACE). These effects directly result from the level of platelet inhibition. Due to existing data indicating that standard dosing of tirofiban is insufficient for optimal platelet inhibition, we proposed a novel, experimental dosing.In this study we assessed, with the use of Ultegra Rapid Platelet Function Assay (RFPA), the level of platelet inhibition with increased tirofiban dosing during primary PCI for ST elevation myocardial infarction (STEMI).Twenty eight patients (22 males, 6 females, mean age 63 years, range 32-78 years) with STEMI were included into the study. All patients received 300 mg of aspirin, iv. heparin in a dose of 10 000 IU, which was followed by platelet receptor GP IIb/IIIa inhibitor tirofiban - 10 micro g/kg iv bolus, 0.4 micro g/kg/min for 30 min and infusion 0.1 micro g/kg/min continued for 12-24 h. Platelet function was assessed with RFPA before tirofiban administration and after 10, 30, 90 minutes as well as 8 hours from the initial dose of tirofiban. Baseline fibrinogen binding to platelet receptor IIb/IIIa was defined as PAU (platelet aggregation unit) and the effects of tirofiban on platelets were expressed as a percentage of platelet inhibition.During in-hospital stay, no deaths, re-infarction nor recurrences of ischaemia requiring intervention were noted. The mean total duration of tirofiban administration was 21 hours. Thrombocytopenia was not observed in any patient. Bleeding complications occurred in 5 (17.9%) patients. Blood transfusion was required in three patients. The percentages of platelet inhibition measured at the pre-specified time-points were 95%, 94%, 91% and 87%, respectively. In 32% of patients an inhibition of platelet exceeding 95%, measured 10 minutes from the onset of tirofiban infusion, was not achieved. At the same time, platelet inhibition90% was found in only 3 (11%) patients. Eight hours from the initiation of tirofiban, platelet inhibition70% was found in 3 (11%) patients; of them, two had platelet inhibition95% when measured 10 minutes from the onset of therapy with tirofiban.1. Increased dosing of tirofiban resulted in an enhanced platelet inhibition. 2. Optimal platelet inhibition, especially during first minutes of drug administration, was not achieved in a substantial number of patients. 3. Increased IIb/IIIa inhibitor dosing resulted in a high partial and normal baseline coronary flow in an infarct-related artery. 4. Increased tirofiban dosing resulted in a relatively high bleeding complications rate.