Intracoronary Thrombus Formation Research Articles

Fibrinogen and Intracoronary Thrombus as Predictors of Major Adverse Cardiovascular Events In-Hospital in St-Elevation Myocardial Infarction (STEMI) Patients Undergoing Primary Percutaneous Coronary Intervention

Background: Fibrinogen is an acute phase reactant involved in inflammation and coagulation in STEMI. Rupture of atherosclerotic plaque can cause the formation of intracoronary thrombus. Despite undergoing primary percutaneous coronary intervention (PCI), patients are at risk of experiencing major adverse cardiovascular events (MACE). Method: The research design used a prospective cohort. The independent variables are fibrinogen and intracoronary thrombus. Fibrinogen levels are examined when the patient arrives at the cardiac emergency unit. Intracoronary thrombus examination is carried out when the patient undergoes primary PCI. The outcomes studied were MACE during treatment in the form of cardiovascular death, cardiogenic shock, acute heart failure, malignant arrhythmias and persistent chest pain. Results: A total of 62 samples were involved in this research. There were 29 patients (46.7%) with high fibrinogen and 38 patients (61.3%) with large intracoronary thrombus. During follow-up during treatment, 26 patients (41.9%) experienced MACE. The cut-off fibrinogen value was 341.6 mg dl (AUC 0.809; 95% CI 0.696-0.923; p<0.001). Cox regression analysis using the backward log rank method showed that high fibrinogen (adjusted HR 3.45; 95% CI 1.29-9.23; p=0.13) and large intracoronary thrombus (adjusted HR 4.30; 95% CI 1.24-14.90; p=0.021) were independent predictors of MACE during hospitalization. Combined analysis of high fibrinogen and large intracoronary thrombus showed that 81.0% of patients experienced MACE during hospitalization (adjusted RR 2.87; 95% CI 1.12-7.35; Cohran and Mantel-Haenzel p=0.002). Conclusion: High fibrinogen and large intracoronary thrombus are independent predictors of MACE during hospitalization and can be applied as additional data for risk stratification in STEMI patients undergoing primary PCI.

P226 A STRANGE CASE OF ISOLATED RIGHT VENTRICULAR DYSFUNCTION

Abstract Introduction In Europe, approximately 29% of the population aged between 15 and 64 have used illicit drugs. Italy is at the top of this ranking. Description 45–year–old female, no previous cardiology events. She enters the Emergency Department for typical chest pain following alcohol and cocaine abuse. EKG (see figure 1) detects sinus tachycardia and mild non–specific changes in ventricular repolarization. Blood tests reveal an increase in Troponin T levels (305 ng/L, NV < 14 ng/L, then decreased with subsequent measurements) and D–dimer (902 mg/mL, NV < 500 mg/mL). Echocardiography reveals a non–dilated right ventricle with severe systolic dysfunction (TAPSE 11 mm). No signs of pulmonary hypertension but a dilated and hypocollapsing inferior vena cava is noted. Abnormal motion of the interventricular septum with systolic d–shape is present (see figure 2). Left ventricle appears normal. Pulmonary angio–Tc was negative for embolic phenomena and coronary angiography detects no lesions on coronary arteries. At discharge, right ventricular systolic dysfunction and septal d–shape were completely regressed (see Figure 3). Discussion Cocaine is a strong systemic adrenergic agonist, which can cause vasospasm of small arterioles of the cardiac microcirculation with possible formation of intracoronary thrombi. Peculiarity of this case is the selective and reversible involvement of the right ventricle, an extremely rare presentation as evidenced by the almost absence of scientific literature on the subject (there is only a similar case report published on the American Journal of Emergency Medicine in 2015). Reversible damage from vasospasm and/or intracoronary thrombosis localized to the marginal branch of the right coronary artery, induced by cocaine use, is conceivable. D–shape of the interventricular septum associated with right ventricular dilatation is likely caused by acute right ventricular failure causing volume overload in the right sections. Take home message Drugs abuse is a widespread problem among the population. Cocaine intake is associated with important adverse cardiovascular effects. A rare presentation can be isolated right ventricular ischemia associated with acute right heart failure.

Outcome of Intracoronary Tirofiban administration at Primary Percutaneous Coronary Intervention in St-Elevation Myocardial Infarction Patients

Background: ST-elevation myocardial infarction results from obstruction of coronary flow due to intracoronary thrombus formation. Primary PCI is the gold standard and class-I indication for revascularization following STEMI. Investigators in this study aimed to evaluate the TIMI flow and myocardial blush grade after intracoronary Tirofiban administration in patients with STEMI during the primary percutaneous coronary intervention (PPCI) and its outcome.
 Methodology: This Cohort study was conducted at Cardiology Department, Niazi Medical & Dental College, Sargodha, after getting informed consent from patients with STEMI. Primary PCI was done in these patients, and two groups were formed. Tirofiban and Non-tirofiban group on basis of Tirofiban administration. Variables included TIMI Grade flow, myocardial blush, major bleeding, minor bleeding, hematoma, MACE, and mortality. P<0.05 was considered statistically significant.
 Results: The mean age of the study groups was 41.64 ± 12.30 years, with 74% (N=250) males. It was seen that 39 (31.2%) vs 41 (32.8%) with p-value of 0.786 were hypertensive, 28 (22.4%) vs 34 (27.2%) diabetic were having p-value of 0.380 whereas 34 (27.2%) vs 37 (29.6%) with p-value of 0.674 were smokers. TIMI flow grades in both groups were not similar and showed significant differences, indicating that both groups were independent, with a p-value <0.05. The myocardial blush grade was compared in the two groups and the results showed that the score in both the groups was not similar, having significant differences as the p-value was 0.001; major bleeding compared with minor showed statistical insignificance, which indicated that there is a relationship between the two groups. (p-value=0.625 & 0.705 respectively).
 Conclusion: Administration of intracoronary Tirofiban was associated with superior clinical prognosis in terms of TIMI flow and myocardial blush grades compared with the other group at primary PCI.

Pathophysiology and mechanisms of Acute Coronary Syndromes: athero-thrombosis, immune-inflammation and beyond

Introduction The pathophysiology of atherosclerosis and its acute complications, such as the Acute Coronary Syndromes (ACS), is continuously under investigation. Immunity and inflammation seem to play a pivotal role in promoting formation and grow of atherosclerotic plaques. At the same time, plaque rupture followed by both platelets’ activation and coagulation cascade induction lead to intracoronary thrombus formation. Although these phenomena might be considered responsible of about 90% of ACS, in up to 5-10% of acute syndromes a non-obstructive coronary artery disease (MINOCA) might be documented. This paper gives an overview on athero-thrombosis and immuno-inflammation processes involved in ACS pathophysiology also emphasizing the pathological mechanisms potentially involved in MINOCA. Areas Covered The relationship between immuno-inflammation and atherothrombosis is continuously updated by recent findings. At the same time, pathophysiology of MINOCA still remains a partially unexplored field, stimulating the research of potential links between these two aspects of ACS pathophysiology. Expert opinion Pathophysyiology of ACS has been extensively investigated; however, several grey areas still remain. MINOCA represents one of these areas. At the same time, many aspects of immune-inflammation processes are still unknown. Thus, research should be continued to shed a brighter light on both these sides of “ACS” moon.

Intracoronary Thrombogenicity in Patients with Vasospastic Angina: An Observation Using Coronary Angioscopy.

Background: Despite significant interest in intracoronary thrombi in patients with vasospastic angina (VSA), the phenomenon remains unclarified. Therefore, we investigated a possible relationship using coronary angioscopy (CAS) in VSA patients. Methods: Sixty patients with VSA, for whom we could assess the spastic segment using CAS, were retrospectively studied. An intracoronary thrombus on CAS was a white thrombus and an erosion-like red thrombus. We verified the clinical characteristics and lesional characteristics as they determined the risk of intracoronary thrombus formation. Results: There were 18 (30%) patients with intracoronary thrombi. More of the patients with intracoronary thrombi were male, current smokers and had severe concomitant symptoms; however, no statistically significant difference was observed upon logistic regression analysis. There were 18 (26%) coronary arteries with intracoronary thrombi out of 70 coronary arteries recognised in the spastic segments. Furthermore, atherosclerotic changes and segmental spasms were significant factors responsible for such lesions. Conclusion: Intracoronary thrombi occurred in 30% of VSA patients and much attention should be paid to the intracoronary thrombogenicity of VSA patients.

Association of stress hyperglycemia ratio with intracoronary thrombus burden in diabetic patients with ST-segment elevation myocardial infarction.

BackgroundLarge intracoronary thrombus burden is not rare during primary percutaneous coronary intervention (PCI) in patients with acute ST-segment elevation myocardial infarction (STEMI). Stress hyperglycemia is independently associated with poor prognosis. However, the underlying relationship between stress hyperglycemia and thrombus burden remains unknown. This study aims to investigate the association of stress hyperglycemia, evaluated by the combination of acute and chronic glycemic levels, with intracoronary thrombus burden in diabetic patients with STEMI.MethodsWe enrolled 227 consecutive diabetic patients with STEMI undergoing primary PCI within 12 hours after symptom onset. Stress hyperglycemia was estimated using the stress hyperglycemia ratio (SHR), which was calculated as admission glycemia divided by estimated average glucose derived from glycosylated hemoglobin. Based on reclassified angiographic thrombolysis in myocardial infarction (TIMI) thrombus grades, patients were divided into small thrombus burden (STB) group (TIMI thrombus grades <4) and large thrombus burden (LTB) group (TIMI thrombus grades 4 or 5).ResultsOf the entire study population, 77 (33.9%) patients were categorized as LTB group, whereas 150 (66.1%) patients presented with STB. The mean age was 64.1 years, and 80.6% of the patients were male. The SHR levels were significantly higher in patients with LTB than in those with STB [1.31; interquartile range (IQR): 1.13–1.48 versus 1.11; IQR: 0.96–1.32; P<0.001]. The predictive performance of SHR for LTB was moderate (area under the curve: 0.669; 95% confidence interval: 0.604–0.730; P<0.001), with the best cut-off value 1.19 (sensitivity 71.4%, specificity 64.7%). The incidence of LTB with SHR ≥1.19 was significantly higher compared with SHR <1.19 (50.9% versus 18.5%; P<0.001). Based on the multivariable logistic regression analysis, the high SHR (≥1.19) was found to be an independent predictor of LTB following adjustment for baseline clinical confounders.ConclusionsA high SHR value was independently associated with large thrombus burden and has a better predictive value than glycemia at admission in diabetic patients with STEMI undergoing primary PCI. Stress hyperglycemia may play an important role on the intracoronary thrombus formation.

Role of Intracoronary Fibrinolytic Therapy in Contemporary PCI Practice.

Plaque rupture or plaque erosion leads to intracoronary thrombus formation resulting in coronary artery occlusion and ST-segment elevation myocardial infarction. Early restoration of blood flow in occluded coronary artery is the mainstay of therapy and it can be achieved by either thrombolytic therapy or primary percutaneous coronary intervention (P-PCI) or a combination of these two in many different ways. It has been proved that primary PCI is better than thrombolytic therapy in establishing early and effective recanalization of infarct related artery, reducing major adverse cardiovascular events (MACE) and increasing survival. There have been tremendous advances in PCI techniques over the years with newer stents, thrombectomy devices, and adjunctive pharmacotherapy. However, intracoronary thrombus continues to be the bane of interventional cardiologists. Failure of recanalization, suboptimal results, distal embolization, no reflow and impaired myocardial perfusion are some of the unresolved difficulties, regularly seen during PCI of patients with large intracoronary thrombus burden indicating an unmet need. This review focuses on emerging evidence about the usefulness of intracoronary thrombolytic therapy as an adjunct to PCI in patients with large intracoronary thrombus burden.

Spatially Organized Structure of Coronary Thrombus in Acute Myocardial Infarction

IntroductionThe use of thromboaspiration in primary percutaneous intervention (PCI) for ST-segment elevation myocardial infarction (STEMI) has offered a unique opportunity to study thrombus composition, its dynamic formation, and architecture in vivo. There has been, however, several limitations, not least the fact that the technique has not yet allowed a precise transversal analysis from one side of the artery to the other, as is done in histological analysis. The dynamic process of intracoronary thrombus formation in STEMI patients is thus still not well understood. Ischemic time was hypothesized to be among the strongest independent correlates of thrombus architecture. In time the platelets are decreasing its proportion and fibrin proportion is increasing (J Silvain, J-P Collet, JW Weisel et al, J Am Coll Cardiol 2011; 57:1359). However, no real report on the internal structures of the in vivo formed thrombi has been shown so far. Therefore, we investigated both the surface and the composition of longitudinally freeze-fractured thrombi.MethodsThrombi were collected by PCI from 119 STEMI patients. Out of the patients there were "early comers " (>12 h from symptom onset; 23 patients) and "late comers" (more than 720 min; 29 patients). The mean age of all patients was 64 years, 70% of patients were males, 51% were smokers, 50% had arterial hypertension, 20% were diabetics and 23% had chronic renal insufficiency.Scanning electron microscopy; collected thrombi obtained by PCI were thoroughly washed in saline solution and stored in 4% formaldehyde prior dehydration. To reveal the internal structures of the thrombi selected samples were longitudinally freeze fractured in liquid nitrogen and coated with platinum. Samples were examined in SEM Vega Plus TS 5135 (Tescan s.r.o., Brno, Czech Republic). Whole areas of the freeze-fractured thrombi were scanned.Results and discussionThe thrombus composition of longitudinally freeze-fractured thrombi was compared between groups of "early-comers" and "late-comers. The distribution of the components in the "early comers" thrombi freeze-fracture seemed to be uniform. Platelets were far the main component (about 75 % in proportion) of the "early comers" thrombus, followed by fibrin and other compounds. The amount of red blood cells was negligible (about 2 - 8 %). We did not observe any significant differences between the thrombi in the group of early comers.Thrombi of the "late-comers" group were composed mainly of red blood cells; platelets and fibrin formed only minority of the thrombi. In contrast to the "early comers" the distribution of the main thrombus components in the "late comers" thrombi was dramatically different between individual parts of the thrombus. The number of platelets and red blood cells varied from 0% to almost 99% and vice versa. It was possible to estimate the initiating place of the thrombus as well as the direction of the growth. Each thrombus could be divided into parts formed mainly either by platelets or by red blood cells. It seems that thrombus develops a regional architecture defined by the extent of platelet activation and packing density. It has been reported that in contracted clots and thrombi, erythrocytes are compressed to close-packed polyhedral structures with platelets and fibrin on the surface demonstrating how contracted clots form an impermeable barrier important for hemostasis and wound healing (D Cines, T Lebedeva, J Weisel et al, Blood 2014; 123:1596). Our investigation of the composition of the in vivo formed thrombi supports these results and helps to explain how fibrinolysis is greatly retarded as clots grow and contract.We have found that on the surfaces of late-comers thrombi fibrin thick fibrils were present. It has been shown that the association of soluble fibrinogen with the fibrin clot results in the reduced adhesiveness of such fibrinogen/fibrin matrices toward leukocytes and platelets (VK Lishko, T Burke, T Ugarova, Blood 2007; 109:1541). Fibrinopeptides A are less accessible for thrombin in surface bound fibrinogen which thus provides additional level of protection of thrombi from premature dissolution (T Riedel, L Medved, JE Dyr, Blood 2011; 117:1700). These findings may have great impact on our knowledge of pathophysiology of the thrombus growth and possible therapeutic consequences related to the time of symptom onset. DisclosuresNo relevant conflicts of interest to declare.

Inflammatory cell content of coronary thrombi is dependent on thrombus age in patients with ST-elevation myocardial infarction

BackgroundST-elevation myocardial infarction (STEMI) is typically caused by an occlusive coronary thrombus. The process of intracoronary thrombus formation is poorly understood. It is known that inflammatory cells play a role in the formation and resolution of venous thrombi, however their role in coronary thrombosis is not clear. We therefore analyzed inflammatory cells in thrombi derived from patients with STEMI in relation to histologically classified thrombus age. MethodsThrombus aspirates of 113 patients treated with primary percutaneous coronary intervention were prospectively collected and classified (fresh, lytic, or organized) based on hematoxylin and eosin staining. The density of inflammatory cells neutrophils (MPO), monocytes/macrophages (CD68), lymphocytes (CD45), and the platelet area (CD31), were visualized using immunohistochemistry. Patients’ history, medication, and laboratory data were registered. ResultsFresh thrombi (76.1%) were the most abundant as compared to lytic (16.8%) and organized (7.1%) thrombi. Neutrophils were significantly less present in organized (169cells/mm2) compared to fresh (327 cells/mm2) and lytic thrombi (311 cells/mm2). Monocytes/macrophages were significantly more present in lytic (471 cells/mm2) than in fresh (312 cells/mm2) thrombi. We additionally found that thrombi from patients aged <50 years as compared to >50 years old contained significantly more neutrophils and monocytes/macrophages irrespective of thrombus age. Furthermore platelet area was smaller in patients on aspirin again irrespective of thrombus age. No gender differences were found. ConclusionsThe composition of inflammatory cells differs with thrombus age in thrombosuction material of STEMI patients that in part depends on patient age and medication.

Intracoronary thrombus formation on a guide wire: who is to blame?

Case report: A 77-year-old man with stable angina and known left main coronary artery (LMCA) disease was admitted for elective percutaneous coronary intervention (PCI). Dual antiplatelet therapy with aspirin and clopidogrel had been instituted 7 days before the PCI, accompanied by administration of unfractionated heparin (UHF) during the procedure. For the PCI planning purpose, intravascular ultrasound was performed to evaluate the anatomy and the size of the LMCA and the morphology of the left anterior descending artery-first diagonal (LAD-D1) bifurcation lesion that had appeared only moderately stenotic on angiography. Minimal lumen diameter of the middle LAD segment and LMCA was 1.6 mm and 2.6 mm, respectively, indicating the severity of both lesions. After predilatation with the semicompliant balloon, a successful provisional stenting of the LAD-D1 bifurcation lesion using drug-eluting stent (DES) was performed, followed by high-pressure postdilatation to optimize stent deployment. At that time, the thrombus formation on a guide wire within the LMCA was noted, giving rise to distal LAD embolization. Direct stenting of the proximal LMCA with DES 4.0/9 mm was then performed and the intracoronary bolus of eptifibatide was given, leading to complete LMCA thrombus resolution, with residual thrombi seen in the distal LAD segments. Due to chest pain aggravation, a second-look angiography was performed 2 hours after the index procedure, showing non-occlusive dissection at the distal end of the LMCA stent. Additional DES 4.0/9 mm was implanted with optimal result and Thrombolysis In Myocardial Infarction 3 flow. Clopidogrel was replaced with ticagrelor. The 6-month follow-up was uneventful. Discussion: Pharmacotherapy during PCI is used to mitigate the sequel of iatrogenic plaque rupture and to reduce the risk of thrombus formation on intravascular PCI equipment. Iatrogenic damage to the endothelium leads to increased expression of tissue factor and activation of the coagulation cascade, ultimately leading to thrombus formation 1

ST-Segment Elevation Myocardial Infarction as a Result of Coronary Artery Ectasia-Related Intracoronary Thrombus in a Patient with Liver Cirrhosis

Coronary artery ectasia (CAE) is a rare condition defined as the dilatation of coronary artery to at least 1.5 times larger than the normal adjacent coronary artery. Clinical manifestations of CAE vary, ranging from asymptomatic to ST-segment elevation myocardial infarction (STEMI). Because of its rarity and clinical diversity, the best treatment strategy and prognosis for CAE remain unclear. We describe a case of STEMI caused by intracoronary thrombus formation within an ectatic area in a patient with liver cirrhosis (LC). The patient was successfully managed by thrombus aspiration only, without balloon angioplasty or stent implantation, and maintained by dual antiplatelet therapy with aspirin and ticagrelor, a potent new P2Y12 inhibitor.

Markers of thrombin generation are associated with myocardial necrosis and left ventricular impairment in patients with ST-elevation myocardial infarction.

IntroductionPlatelet activation, thrombin generation and fibrin formation play important roles in intracoronary thrombus formation, which may lead to acute myocardial infarction.We investigated whether the prothrombotic markers D-dimer, pro-thrombin fragment 1 + 2 (F1 + 2) and endogenous thrombin potential (ETP) are associated with myocardial necrosis assessed by Troponin T (TnT), and left ventricular impairment assessed by left ventricular ejection fraction (LVEF) and N-terminal pro b-type natriuretic peptide (NT-proBNP).Materials/MethodsPatients (n = 987) with ST-elevation mycardial infarction (STEMI) were included. Blood samples were drawn at a median time of 24 h after onset of symptoms.ResultsStatistically significant correlations were found between both peak TnT and D-dimer (p < 0.001) and F1 + 2 (p < 0.001), and between NT-proBNP and D-dimer (p = 0.001) and F1 + 2 (p < 0.001). When dividing TnT and NT-proBNP levels into quartiles there were significant trends for increased levels of both markers across quartiles (all p < 0.001) D-dimer remained significantly associated with NT-proBNP after adjustments for covariates (p = 0.001) whereas the association between NTproBNP and F1 + 2 was no longer statistically significant (p = 0.324).A significant inverse correlation was found between LVEF and D-dimer (p < 0.001) and F1 + 2 (p = 0.013). When dichotomizing LVEF levels at 40 %, we observed significantly higher levels of both D-dimer (p < 0.001) and F1 + 2 (p = 0.016) in the group with low EF (n = 147).Summary/conclusionIn our cohort of STEMI patients we demonstrated that levels of D-dimer and F1 + 2 were significantly associated with myocardial necrosis as assessed by peak TnT. High levels of these coagulation markers in patients with low LVEF and high NTproBNP may indicate a hypercoagulable state in patients with impaired myocardial function.

Thrombolytic therapy in a patient with inferolateral myocardial infarction after carbon monoxide poisoning.

ST segment elevation myocardial infarction (STEMI) due to coronary artery occlusion caused by intracoronary thrombosis in the setting of acute carbon monoxide (CO) poisoning is a very rare presentation. We present a case of intracoronary large and mobile thrombus formation after CO poisoning. A previously healthy 50-year-old woman was referred for CO poisoning. She had chest pain after exposure to CO. Her initial mental status was preoccupied with chest pain. Her initial CO fraction was 28.1%, and initial laboratory data showed creatine kinase-myocardial isoenzyme of 134 U/L (upper limit 25 U/L) and troponin I of >50 ng/mL (upper limit 0.06 ng/mL). Electrocardiography was carried out on admission, revealing an ST segment elevation in the inferolateral leads. After initial evaluation, coronary angiography was performed and an intracoronary large mobile thrombus was seen in the proximal left anterior descending (LAD) artery with no significant stenosis. We administered tenecteplase with heparin. After the thrombolytic therapy, ST elevation in the inferolateral leads resolved. Repeat angiography was performed after 24 h; the thrombus in LAD had resolved. The patient was discharged after 5 days, with persistent Q wave in the inferior leads and mild hypokinesia of the inferoposterior wall suggesting myocardial injury. We describe intracoronary thrombus formation induced by CO poisoning. Because intracoronary thrombus can result in myocardial infarction, its consideration following CO poisoning is important. Patients with CO poisoning who have symptoms of STEMI should be carefully evaluated with serial electrocardiograms, cardiac biomarkers, and an echocardiogram. When there is evidence of acute myocardial injury, a primer in coronary angiography can determine which patients could benefit from intervention.

Factor XIII-A dynamics in acute myocardial infarction: a novel prognostic biomarker?

After acute myocardial infarction (MI) the damaged heart has to be repaired. Factor XIII (FXIII) is considered a key molecule in promoting heart healing. FXIII deficiency was associated to cardiac rupture and anomalous remodelling in MI. During MI, FXIII contributes firstly to the intracoronary thrombus formation and shortly after to heal the myocardial lesion. To quantify the real contribution of FXIII in this process, and to explore its possible prognostic role, we monitored the FXIII-A subunit levels in 350 acute MI patients during the first six days (d0-d5) plus a control at 30-60 days (d30). A one-year follow-up was performed for all the patients. A transient drop in the FXIII-A mean level was noted in the whole cohort of patients (FXIII-Ad0 99.48 ± 30.5 vs FXIII-Ad5 76.51 ± 27.02; p< 0.0001). Interestingly, those who developed post-MI heart failure showed the highest drop (FXIII-Ad5 52.1 ± 25.2) and they already presented with low levels at recruitment. Similarly, those who died showed the same FXIII-A dynamic (FXIII-Ad5 54.0 ± 22.5). Conversely, patients who remained free of major adverse cardiac events, had lower consuming (FXIII-Ad0 103.6 ± 29.1 vs FXIII-Ad5 84.4 ± 24.5; p< 0.0001). Interestingly, the FXIII-A drop was independent from the amount of injury assessed by TnT and CKMB levels. The survival analysis ascribed an increased probability of early death or heart failure inversely related to FXIII-A quartiles (FXIII-A25th< 59.5 %; hazard ratio 4.25; 2.2-5.1; p< 0.0001). Different FXIII-A dynamics and levels could be utilised as early prognostic indicators during acute MI, revealing the individual potential to heal and suggesting tailored treatments to avoid heart failure or its extreme consequence.

Extensive Fatal Intracoronary Thrombosis During Percutaneous Coronary Intervention With Bivalirudin

The authors describe 2 cases of extensive intracoronary thrombus formation leading to acute closure of the left main where bivalirudin (Angiomax) was used as the anticoagulant during percutaneous coronary intervention leading to mortality. Both cases had similarity in the cascade of complications of coronary dissection leading to slow flow and prolonged procedure time with compromise of antegrade flow in the coronary artery and a final catastrophic development of extensive intracoronary thrombosis extending into the left main and nonintervened vessel (left anterior descending or circumflex) followed by ventricular fibrillation and death. Bivalirudin has reversible anticoagulant pharmacodynamics because the bivalirudin molecule is cleaved by the thrombin molecule. In situations when the antegrade flow is compromised, delivery of fresh circulating bivalirudin to replenish the catalysis of bivalirudin by thrombin is diminished, allowing thrombin activity to regenerate, thereby creating a prothrombotic milieu in these coronary segments. This can lead to extensive intracoronary thrombus formation in situations of slow flow precipitated by coronary dissection and prolonged dwell time with intracoronary hardware (wires, balloons, and stents). Interventionalists should be aware of the potential risk of this fatal complication and should be proactive in recognizing the scenarios where this is likely to occur. In such anticipated circumstances, the interventionalist may judiciously switch the anticoagulant to heparin and/or use additional glycoprotein IIb/IIIa inhibitor because freshly formed intracoronary thrombus is susceptible to lysis by glycoprotein IIb/IIIa inhibitors.

Cardiac tamponade due to coronary perforation during percutaneous interventions successfully treated with microspheres

In recent years, new techniques and materials in interventional cardiology have improved patient safety significantly. This led to the ability to perform more and more complex coronary interventions with a minimal risk for relevant complications. However, perforation of distal coronary vessels by guide wires is still observed and can lead to a life-threatening pericardial tamponade. Various treatment options have been described but management of this particular complication remains a challenge for the interventional cardiologist. So far, the treatment of choice for many cardiologists is the application of coils [1, 2]. But coils have some major disadvantages; they are sometimes difficult to position and are often not routinely available in cath labs. Other proposed methods include long inflation of over-the-wire balloons which is easy to handle and can be considered as a temporary solution to gain time, but is often not sufficient to stop the bleeding [3]. Implantation of covered stents can also be considered, but is not suitable in small vessels or lesions not reachable with a stent for other reasons [4, 5]. Administration of protamine might facilitate measures to seal a coronary perforation but might also lead to intracoronary thrombus formation or even stent thrombosis [6]. Microspheres are small spherical particles made of various materials with diameters ranging between 1 and 1,500 lm. Such particles are used for a broad spectrum of percutaneous interventions. They found their way into interventional cardiology as an alternative to ethanol for transcoronary ablation of septal hypertrophy (TASH) in hypertrophic obstructive cardiomyopathy (HOCM) [7]. Despite the fact that some authors suggested the use of different kinds of microspheres for coronary perforation, this technique did not find its way into clinical routine so far [8, 9]. This might partially be due the fact that the optimal size and material of microspheres remain uncertain. Patient #1 was admitted to the emergency department with ST-elevation myocardial infarction and was transferred to the cath lab immediately after admission. Emergency coronary angiography revealed an ostial occlusion of the left circumflex artery (LCX) which was treated with balloon angioplasty and implantation of an everolimus eluting coronary stent. For this purpose, a PT Graphix guide wire was placed distally in a marginal branch. The patient was provided with a loading dose of aspirin and ticagrelor. In addition to that, due to a heavy thrombus burden, abciximab was administered intravenously. After successful revascularization, the patient was referred to the intensive care unit for further surveillance. Two hours later the patient became hemodynamically unstable and had to be treated with catecholamines. Echocardiographic evaluation revealed cardiac tamponade as the underlying cause. Pericardial paracentesis was performed immediately and led to hemodynamic stabilization by drainage of 500 ml blood. As a coronary perforation seemed the most likely cause, coronary angiography was performed, showing a leak of contrast dye into the pericardium at the marginal branch of the LCX in which the wire was positioned during the prior intervention. Occlusion of the lesion by balloons did not lead to a sustained sealing. Therefore, decision was made to inject in total 3 ml of 75 lm Embozene microspheres (CeloNova BioSciences, San Antonio, TX, USA) F. Meincke (&) K.-H. Kuck M. W. Bergmann Department of Cardiology, Asklepios Klinik St. Georg, Lohmuehlenstrasse 5, 20099 Hamburg, Germany e-mail: f.meincke@yahoo.com

冠動脈内血栓形成における冠攣縮の関与

冠動脈内血栓形成における冠攣縮の関与

Systemic lupus erythematosus and small vessel coronary infarction: who's to blame?

Systemic lupus erythematosus (SLE) with or without accompanying antiphospholipid antibody syndrome (APLS) is known to cause myocardial ischemia via multiple mechanisms, including accelerated coronary atherosclerosis, impaired coronary vasomotor function, spontaneous intracoronary thrombus formation, or endothelial dysfunction in the context of cardiac syndrome X (CSX). We present the case of a young woman with SLE and APLS who presented with myocardial ischemia and peculiar echocardiographic evidence of multiple small septal perforator infarcts despite a normal coronary angiogram, a rare combination.

Rare occurrence of simultaneous coronary artery perforation and intracoronary thrombus formation following angioplasty.

Both coronary artery perforation and intracoronary thrombus formation are life-threatening complications of percutaneous coronary interventions, which rarely occur simultaneously during angioplasty. We herein report a case of stent-related, left circumflex artery perforation, and subsequently acute left main artery thrombosis after the leakage was embolized with 7 microcoils. Intracoronary thromboectomy and systemic anticoagulant therapy were carefully used with good results. This case also represents some of our uncertainties regarding the best management of the patient.

Fatal Subacute Stent Thrombosis Induced by Guidewire Fracture with Retained Filaments in the Coronary Artery

During percutaneous coronary intervention, guidewire fractures are very exceptionally encountered in medical practice, but can cause fatal complications such as intracoronary thrombus formation, embolization and perforation. Removal of the remnant segments of guidewire is important for the prognosis. There are several methods being recommended for the treatment of fractured guidewire remnants. However, the best treatment of remnant guidewire filament is still unclear. Herein, we present a case where we did not completely remove remnant guidewire filaments that caused fatal coronary thrombosis.