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Introduction. Dual left anterior descending (LAD) artery is a very rare inherited anomaly. It can be incidentally revealed during primary percutaneous coronary intervention (pPCI) and may produce difficulties in detecting and treating the culprit lesion. Case report. We presented a 52-year-old male patient with ST-segment elevation myocardial infarction (STEMI) of inferior wall, in whom dual LAD anomaly was revealed during pPCI: a short LAD artery originated from the left main coronary artery and a long LAD artery originated from the proximal part of the right coronary artery (RCA). A bare metal stent was successfully implanted in the place of the culprit lesion in RCA and ST-segment resolution was achieved in ECG. After two hours, the patient was referred again to the catheter lab due to new STEMI of anteroseptal wall. Another bare metal stent was implanted in new infarction related artery, this time it was proximal part of the short LAD. Conclusion. Careful and correct interpretation of ECG is very helpful in detection and treatment of the culprit lesion in cases with dual LAD. [ABSTRACT FROM AUTHOR]

Introduction. The left main stem (MS) coronary artery (CA) (MSCA) thrombosis is a rare but potentially lethal manifestation of acute coronary syndrome. The standard approach in treating such patients is the primary percutaneous coronary intervention (pPCI) or CA bypass graft surgery. In some cases, depending on the morphological appearance of the thrombus, findings and flow rates assessed on coronary angiography (CAn), clinical conditions, and cardiologist's experiences, another possible method of treatment can be the conservative approach using antithrombotic therapy. Case report. A 37-year-old male was admitted to the emergency room with symptoms of an acute myocardial infarction with an ST elevation in diaphragmal localization. Using an emergency CAn, we have visualized a thrombus at the ostial and proximal part of the left MSCA, with no complete obstruction of the blood flow. Initially, dual antithrombotic therapy (ticagrelor and acetylsalicylic acid) was applied, and in the further procedure, it was decided to introduce glycoprotein IIb/IIIa platelet receptor inhibitor (tirofiban) as an intracoronary bolus (0.3 µg/kg) and later as a continuous infusion (0.1 µg/kg/min). Four days later, a control CAn and intravascular echocardiography were performed, and it was decided to continue the treatment using conservative therapy without a pPCI procedure. The patient was discharged in good condition with no signs of illness on the eighth day after hospital admission for home recovery, with planned frequent follow-ups in the future. Conclusion. In the case of non-obstructive thrombotic masses without significant atherosclerotic stenotic lesions, conservative treatment modality with the use of aggressive antithrombotic therapy may be considered. [ABSTRACT FROM AUTHOR]

Background/Aim. It is not know which factors influence no-reflow phenomenon after successful primary percutaneous intervention (pPCI) in patients with myocardial infarction with ST elevation (STEMI). The aim of this study was to estimate predictive value of some admission characteristics of patients with STEMI, who underwent pPCI, for the development of no-reflow phenomenon. Worse clinical outcome in patients with no-reflow points to importance of selection and aggressive treatment in a group at high risk. Methods. This was retrospective and partly prospective study which included 491 consecutive patients with STEMI, admitted to a single centre, during the period from 2000 to September 2015, who underwent pPCI. Descriptive characteristics of the patients, presence of classical risk factors for cardiovascular disease, total ischemic time and clinical features at admission were all estimated as predictors for the development of no-reflow phenomenon. No-reflow phenomenon is defined as the presence of thrombolysis in myocardial infarction (TIMI) < 3 coronary flow at the end of the pPCI procedure, or ST-segment resolution by less than 50% in the first hours after the procedure. The significance of the predictive value of some parameters was evaluated by univariate and multivariate regression analysis. In univariate analysis, we used the χ² test and Mann Whitney and Student's t-tests. Results. No-reflow phenomenon was detected in 84 (17.1%) patients (criteria used: TIMI < 3 coronary flow) and in 144 (29.3%) patients (criteria used: ST-sement resolution < 50%). Patients older than 75 years [odds ratio (OR) = 2.53; 95% confidence interval (CI) 1.48-4.33; p = 0.001] and those who had Killip class at admission higher than 1 had increased risk to achieve TIMI-3 flow after pPCI. Killip class higher than 1 (OR 1.59; 95% CI 1.23-2.04; p < 0.001), left anterior descendent artery (LAD) as infarct related artery (IRA) and total ischemic time higher than 4 hour were associated with increased risk to failure of rapid ST segment resolution after pPCI. Conclusion. Older age and Killip class were main predictors of TIMI < 3 flow, and Killip class, LAD as IRA and longer total ischemic time were predictors for the failure of rapid ST segment resolution after pPCI. [ABSTRACT FROM AUTHOR]

Introduction. Stent thrombosis (ST) in clinical practice can be classified according to time of onset as early (0-30 days after stent implantation), which is further divided into acute (< 24 hours) and subacute (1-30 days), late (> 30 days) and very late (> 12 months). Myocardial reinfaction due to very late ST in a patient receiving antithrombotic therapy is very rare, and potentially fatal. The procedure alone and related mechanical factors seem to be associated with acute/subacute ST. On the other hand, in-stent neoatherosclerosis, inflammation, premature cessation of antiplatelet therapy, as well as stent fracture, stent malapposition, uncovered stent struts may play role in late/very late ST. Some findings implicate that the etiology of very late ST of baremetal stent (BMS) is quite different from those following drug-eluting stent (DES) implantation. Case report. We presented a 56-year old male with acute inferoposterior ST segment elevation myocardial infarction (STEMI) related to very late stent thrombosis, 9 years after BMS implantation, despite antithrombotic therapy. Thrombus aspiration was successfully performed followed by percutaneous coronary intervention (PCI) with implantation of DES into the previously implanted two stents to solve the instent restenosis. Conclusion. Very late stent thrombosis, although fortunately very rare, not completely understood, might cause myocardial reinfaction, but could be successfully treated with thrombus aspiration followed by primary PCI. Very late ST in the presented patient might be connected with neointimal plaque rupture, followed by thrombotic events. [ABSTRACT FROM AUTHOR]

Introduction. Spontaneous coronary artery dissection (SCAD) is a very rare disease with poor prognosis. It mainly affects young women free of risk factors for coronary artery disease (CAD) and women during the peripartum period. The prognosis for myocardial infarction caused by SCAD is poor, management is often difficult and guidelines still missing. Case report. We presented a woman with acute myocardial infarction of anterior wall of the left ventricle, caused by spontaneous dissection of medial segment of the left anterior descending coronary artery. We treated the patient with thrombolytic therapy and performed coronary angiography after that. Finally we decided to do nothing more. Two years later we performed coronary angiography again and founded the coronary artery normal. We also analyzed 19 cases publiched from 1996 to 2012 when coronary artery dissection had been treated with thrombolytic agent. Analysis revealed only one case of 19, with complication after treating SCAD with thrombolysis. Conclusion. Sometimes, regarding myocardial infarction in young women with no risk factors for CAD, especially in young women in peripartum, we should think about SCAD. The presented case, like eight others, demonstrates that good clinical outcomes can be achieved with thrombolysis. In spite of all this, we still need more data to verify that thrombolysis does not have to harm the therapy for SCAD. For the time being thrombolytic therapy could be an option. [ABSTRACT FROM AUTHOR]