[Embolic central retinal artery occlusion as a complication of percutaneous coronary angioplasty--case report]. / Zator tetnicy srodkowej siatkówki jako powiklanie przezskórnej angioplastyki wiencowej--opis przypadku.

Procedures of the percutaneous coronary intervention are more often carried out in patients with coronary heart disease (CHD) because they are not very invasive and very effective. Even though a lot of procedures of this type are carried out, reports on the ophthalmic complications connected to them,are rarely found. The authors present the case of the 78-years-old patient in whom disturbances of the right eye vision occurred after coronary angiography combined with angioplasty of the narrowed artery with stent implantation. Ophthalmic examination revealed features of the central retinal artery occlusion. Even though an immediate treatment was applied, the function of the right eye was not improved. When general condition of the patient was normalized, the diagnosis was confirmed by the Color Doppler ultrasonography in the vessels supplying eye. The photographic documentation was prepared. The literature data indicate the necessity of immediate diagnosis of even mild vision disturbances in the course of and after the percutaneous coronary intervention because only an immediate treatment can protect the patient from a permanent vision decrease, due to the embolism of the retinal vessels.

Myocardial perfusion assessed by contrast echocardiography correlates with angiographic perfusion parameters in patients with a first acute myocardial infarction successfully treated with angioplasty.

BACKGROUND: Angiographic flow in an epicardial artery does not define perfusion at the microvascular level. AIM: To compare myocardial contrast echocardiography (MCE) with angiographic methods of assessing microvascular reperfusion in patients with acute myocardial infarction (AMI). METHODS: One hundred consecutive patients with a first ST segment elevation myocardial infarction and single-vessel disease were successfully treated with primary percutaneous coronary intervention. Regional contrast score index (RCSI), corrected Thrombolysis In Myocardial Infarction (TIMI) frame count (cTFC), TIMI myocardial perfusion grade (TMPG) and myocardial blush grade were evaluated. RESULTS: Among 717 asynergic segments on MCE, 168 revealed a lack of perfusion. TMPG and cTFC correlated significantly with RCSI (P=0.031 and P=0.027, respectively). Myocardial blush grade did not correlate with RCSI (P=0.067). Patients with anterior AMI had significantly more segments with a perfusion defect on MCE than patients with inferior AMI (P=0.0001). CONCLUSIONS: MCE results correlate with angiographic methods of perfusion assessment such as TMPG and cTFC. Anterior AMI is associated with a greater extent of perfusion defect. MCE results correlate also with recovery of systolic left ventricular function and clinical outcome at six month follow-up.

Is transport with platelet GP IIb/IIIa inhibition for primary percutaneous coronary intervention more efficient than on-site thrombolysis in patients with STEMI admitted to community hospitals? Randomised study. Early results.

INTRODUCTION: 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. METHODS: The studied group comprised patients with STEMI (infarct duration time <12 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. RESULTS: 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. (p <0.0001). 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, p <0.0001). 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). CONCLUSIONS: 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.

Safety and feasibility of a novel dosing regimen of tirofiban administered in patients with acute myocardial infarction with ST elevation before primary coronary angioplasty: a pilot study.

BACKGROUND: Intravenous glycoprotein GP IIb/IIIa receptor antagonists administered to patients with acute coronary syndromes limit platelet-dependent thrombus formation and vasoconstriction and lower the complication rate of PCI. The efficacy of glycoprotein IIb/IIIa inhibitors critically depends on appropriate suppression of platelet aggregation. A growing body of evidence indicates that regimen of tirofiban used in several recent trials may be suboptimal. We investigated if a novel regimen of dosage of tirofiban administered to patients with acute myocardial infarction with ST elevation (STEMI) before primary angioplasty is safe, feasible and whether such treatment improves coronary flow in infarct-related artery. METHODS: It was an open-label, non-randomized, prospective observational study. 253 consecutive patients with STEMI, qualified to PCI were included. 104 of patients (group 1) received heparin plus tirofiban at a novel regimen (10 microg/kg bolus, followed by 0.4 microg/kg/min for 30 min and then 0.1 microg/kg/min for 12-24 hours) and the remaining 149 of the patients (group 2) received a standard dose of heparin prior to PCI. Bleeding complications were recorded. The primary end point of the study was combined TIMI 1 + 2 + 3 grade flow at the time of first contrast medium injection during angiography for primary PCI. RESULTS: Heparin was administered 50.3 +/- 58.1 minutes (group 1) or 62.3 +/- 67.3 minutes (group 2) ( p = 0.205). Tirofiban was administered for an average of 14.5 +/- 14.4 minutes before TIMI assessment (group 1). In patients treated with heparin + tirofiban the rate of combined TIMI 1 + 2 + 3 coronary flow was higher (38.4% vs. 24.8%, p = 0.020) as compared to patients treated with heparin alone. The difference in the rate of TIMI > or = 2 coronary blood flow between the groups 1 and 2 (24.0% vs. 20.1%) has not reached statistical significance ( p = 0.459). At the same time the significant difference in the rate of TIMI 1 coronary blood flow between the groups 1 and 2 was noted (14.4 vs. 4.7%, p = 0.007). In hospital mortality in the groups 1 and 2 was similar (5.3 vs. 4.8%, p = 0.838). Significant difference was noted between the groups 1 and 2 with regard to minor bleeding complications (17.3 vs. 8.7%, p = 0.041). CONCLUSION: In patients undergoing primary angioplasty for acute myocardial infarction the novel regimen of tirofiban is well tolerated and feasible, and is associated with improvement in coronary blood flow in the infarct related artery. Larger studies assessing the effects of tirofiban on clinical outcomes of patients with AMI undergoing primary angioplasty seem worthwhile.

Platelet inhibition by increased tirofiban dosing during primary coronary angioplasty for ST elevation myocardial infarction.

BACKGROUND: 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. AIM: 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). METHODS: 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. RESULTS: 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 inhibition <90% was found in only 3 (11%) patients. Eight hours from the initiation of tirofiban, platelet inhibition <70% was found in 3 (11%) patients; of them, two had platelet inhibition <95% when measured 10 minutes from the onset of therapy with tirofiban. CONCLUSIONS: 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.