Acute Thrombotic Coronary Occlusion Research Articles

Interobserver variability among experienced electrocardiogram readers to diagnose acute thrombotic coronary occlusion in patients with out of hospital cardiac arrest: Impact of metabolic milieu and angiographic culprit

ObjectivesWe sought to evaluate interobserver concordance among experienced electrocardiogram (ECG) readers in predicting acute thrombotic coronary occlusion (ATCO) in the context of abnormal metabolic milieu (AMM) following resuscitated out of hospital cardiac arrest (OHCA). MethodsOHCA patients with initial shockable rhythm who underwent invasive coronary angiography (ICA) were included. AMM was defined as one of: pH < 7.1, lactate > 2 mmol/L, serum potassium < 2.8 or >6.0 mEq/L. The initial ECG following ROSC but prior to ICA was adjudicated by 2 experienced readers using classic ST elevation myocardial infarction [STEMI] and expanded criteria and their combination to predict ATCO on ICA. Results152 consecutive patients (mean age 58 years, 76% male) met inclusion criteria. AMM was present in 77%; and 42% had ATCO on ICA. Sensitivity, specificity, PPV, NPV using classic STEMI criteria were 50%, 98%, 94%, 72% (c-statistic 0.74); whereas for combined (STEMI + expanded) criteria they were 69%, 88%, 81%, 79% respectively (c-statistic 0.79). Inter-observer agreement (kappa) was 0.7 for classic STEMI criteria, and 0.66 for combined criteria. Agreement between readers was consistently higher when ATCO was absent and with NMM (kappa 0.78), but lower in AMM (kappa 0.6). ConclusionsDespite experienced ECG readers, there was only modest overall concordance in predicting ATCO in the context of resuscitated OHCA. Significant interobserver variations were noted dependent on metabolic milieu and angiographic ATCO. These observations fundamentally question the role of the 12-lead ECG as primary triaging tool for early angiography among patients with OHCA.

AVR ST elevation myocardial infarction: A not so urgent cardiac emergency, the Ipoh experience

aVR STEMI is well recognised as a sign of acute occlusion of the left main stem (LMS) or proximal left anterior descending (LAD) coronary artery. However, whether aVR STEMI is always associated with acute thrombotic coronary occlusion is still debatable.

Prevalence, clinical characteristics, and in-hospital mortality of patients with angiographic acute total thrombotic occlusion presenting as non-ST-segment elevation myocardial infarction

Abstract Background The current paradigm in the treatment of acute coronary syndromes classifies patients according to the presence of persistent ST-segment elevation as a potential marker of total coronary thrombosis, in whom immediate fibrinolysis or primary PCI is appropriate. However, patients with NSTEMI may present with a total acute thrombotic coronary occlusion and may not be detected by this approach, therefore precluding the benefits of early reperfusion strategies. Purpose To identify the prevalence of total thrombotic occlusion elicited by coronary angiography in patients with NSTEMI, and to analyze their baseline characteristics and in-hospital mortality. Methods Retrospective cohort study including consecutive patients admitted with NSTEMI in a single center over a 15-year period. Patients with coronary angiography were further classified in three groups: patients with a total angiographic coronary thrombotic occlusion (TIMI thrombus V), patients with subtotal coronary thrombus (TIMI thrombus I–IV) and patients without angiographic thrombus. Baseline characteristics and in-hospital outcomes were compared among the three groups. Results A total of 4216 of NSTEMI patients were admitted within the study period, of whom 3191 underwent coronary angiography and constituted in the final analytic sample. In 211 patients (6.6%) a TIMI thrombus V was found. Table 1 summarizes the main characteristics among the three groups. In the group of patients with total thrombotic occlussion, a higher proportion were male, were more prone to be current smokers, had a lower prevalence of major cardiovascular risk factors and had suffered less cardiovascular events at enrollment. During hospital follow-up, 15 (7.1%) patients within the total thrombus group, 14 (4.3%) patients within the subtotal thrombus group and 112 (4.2%) patients within the no-thrombus group died. No statistically significant differences in hospital mortality were noted when comparing total thrombotic occlusion vs. no thrombus (HR 1.69, 95% CI 0.94–3.01, p=0.07) (Figure 1). Conclusions In our study, 6.6% of the patients with NSTEMI presented an acute total thrombotic occlusion in coronary angiography. Patients with total thrombotic occlusion showed a different risk-factor profile and a similar in-hospital mortality when compared with non-total thrombus or no thrombus. Funding Acknowledgement Type of funding sources: Public Institution(s). Main funding source(s): Ignacio Chavez National Heart Institute, Mexico City, Mexico Table 1. Baseline characteristicsFigure 1. In-hospital mortality

Do not disregard the initial 12 lead ECG after out-of-hospital cardiac arrest: It predicts angiographic culprit despite metabolic abnormalities

ObjectivesThe initial 12 lead electrocardiogram (ECG) following return of spontaneous circulation (ROSC) after out-of-hospital cardiac arrest (OHCA), is often disregarded by clinicians in ability to predict acute thrombotic coronary occlusion (ATCO) due to markedly abnormal metabolic milieu (AMM). We sought to evaluate the accuracy of initial vs. follow-up ECG prior to invasive coronary angiography (ICA) to predict ATCO following resuscitated OHCA. MethodsWe included OHCA patients with initial shockable rhythm who underwent invasive coronary angiography (ICA). AMM was defined as one of: pH ​< ​7.1, lactate >2 ​mmol/L, serum potassium <2.8 or >6.0 mEq/L. Two ECGs A (initial) and B (follow-up) following ROSC but prior to ICA were adjudicated by 2 experienced readers using expanded ECG criteria to predict angiographic ATCO on ICA. Results152 consecutive patients (mean age 58 years, 75% male) met inclusion criteria, 77% had AMM. Among those with both ECGs (n ​= ​102), overall accuracy, sensitivity, specificity, positive predictive value, negative predictive value for correctly predicting angiographic ATCO for ECG A was 72%, 63%, 81%, 61%, 83% and for ECG B was 71%, 50%, 91%, 73%, 80% respectively. Predictive accuracy for angiographic ATCO was similar between ECG A [odds ratio (OR) 7.31, CI 2.87–18.62, p ​< ​0.0001) and ECG B [OR 10.67; CI 3.6–31.61, p ​< ​0.0001], and consistent in AMM. ConclusionsIn OHCA, despite AMM, the initial post ROSC ECG retains a statistically significant, and similar accuracy as the follow-up ECG to predict angiographic ATCO using expanded criteria.

Pentadecapeptide BPC 157 resolves suprahepatic occlusion of the inferior caval vein, Budd-Chiari syndrome model in rats.

BACKGROUNDRecently, as a possible therapy resolving solution, pentadecapeptide BPC 157 therapy, has been used in alleviating various vascular occlusion disturbances. BPC 157 was previously reviewed as novel mediator of Robert cytoprotection and endothelium protection in the stomach, and gut-brain axis, beneficial therapy in gastrointestinal tract, with particular reference to vascular recruitment, ulcerative colitis and tumor cachexia, and other tissues healing. Here we raised new hypothesis about BPC 157 therapy in the Budd-Chiari syndrome in rats, rapid bypassing of the suprahepatic inferior caval vein occlusion, and rats recovery with the active and effective pharmacotherapy treatment.AIMTo investigate Budd-Chiari syndrome model (inferior caval vein suprahepatic occlusion) resolution, since BPC 157 resolves various rat vascular occlusion.METHODSWe assessed the activated bypassing pathways between the inferior and superior caval veins and portocaval shunt, counteracted caval/portal hypertension, aortal hypotension, venous/arterial thrombosis, electrocardiogram disturbances, liver and gastrointestinal lesions (i.e., stomach and duodenum hemorrhages, in particular, congestion). Rats with suprahepatic occlusion of the inferior vena cava by ligation were medicated at 1 min, 15 min, 24 h, or 48 h post-ligation. Medication consisted of 10 µg/kg BPC 157, 10 ng BPC 157 or 5 mL/kg saline, administered once as an abdominal bath or intragastric application. Gross and microscopic observations were made, in addition to assessments of electrical activity of the heart (electrocardiogram), portal and caval hypertension, aortal hypotension, thrombosis, hepatomegaly, splenomegaly and venography. Furthermore, levels of nitric oxide, malondialdehyde in the liver and serum enzymes were determined.RESULTSBPC 157 counteracted increased P wave amplitude, tachycardia and ST-elevation, i.e., right heart failure from acute thrombotic coronary occlusion. The bypassing pathway of the inferior vena cava-azygos (hemiazygos) vein-superior vena cava and portocaval shunt occurred rapidly. Even with severe caval ˃ portal hypertension, BPC 157 antagonized portal and caval hypertension and aortal hypotension, and also reduced refractory ascites. Thrombosis of portal vein tributaries, inferior vena cava, and hepatic and coronary arteries was attenuated. In addition, there was reduced pathology of the lungs (severe capillary congestion) and liver (dilated central veins and terminal portal venules), decreased intestine hemorrhagic lesions (substantial capillary congestion, submucosal edema and architecture loss), and increased liver and spleen weight. During the period of ligation, nitric oxide- and malondialdehyde-levels in the liver remained within normal healthy values, and increases in serum enzymes were markedly reduced.CONCLUSIONBPC 157 counteracts Budd Chiari syndrome in rats.

Acute Thrombotic Coronary Occlusion in a Patient with Coronary Artery Anomaly

Abstract Patients with coronary artery anomalies are more susceptible to develop acute thrombotic coronary occlusions due to the abnormal anatomy of these arteries and the disturbance of the pathophysiological mechanisms that lead to an accelerated atherosclerosis development. The following article presents the case of a 64-year-old female patient diagnosed with anterior ST-segment elevation myocardial infarction. The patient underwent primary percutaneous coronary intervention, which revealed the absence of the right coronary artery and separated origins of the left anterior descending artery and the left circumflex artery from the aorta.

Abstract 15825: Inter-reader Concordance and Variations in Interpretation of Post Resuscitation ECG in Abnormal vs Normal Metabolic Milieus Following Out-of-hospital Cardiac Arrest

Background: Among survivors of out of hospital cardiac arrest (OHCA), the post resuscitation 12-lead electrocardiogram (ECG) is a widely used tool to identify acute thrombotic coronary occlusion (ACTO) and for appropriate triage to the catheterization laboratory. It is unknown how a post-resuscitation abnormal metabolic milieu impacts ECG accuracy. We studied inter-reader concordance in ECG interpretation as well as same-patient variation in interpretation between abnormal (A) and normal (N) metabolic milieus (MM). Methods: We performed a retrospective analysis of 125 consecutive patients with OHCA with a shockable rhythm undergoing coronary angiography in a single institution. Patients with AMM were defined as pH &lt;7.1, K &lt;2.8 or &gt;6 mEq/L, vasoactive drug use or lactate &gt;2 ng/ml. All post resuscitation ECGs recorded in both AMM and NMM for each patient prior to any invasive intervention were blindly interpreted by 2 experienced readers, classified into two categories: diagnostic for ATCO (ATCO +) and not diagnostic for ATCO (ATCO -) and compared to angiographic ATCO. The Cohen’s kappa scale was used to measure concordance. Results: Concordance between readers was 0.69 (95% CI 0.56-0.84) in AMM and 0.82 (95% CI 0.64-0.99) in NMM. Of 35 ECGs interpreted as diagnostic for ATCO (+) in AMM, 27 (77%) were reclassified as ATCO (-) after metabolic correction. Among 90 ECGs initially diagnosed as ATCO (-) in AMM, 2 (2%) were reclassified as ATCO (+) whereas 88 (98%) remained as ATCO (-) in NMM. Most ATCO (-) ECGs were in the setting of angiographic ATCO; see table. Conclusions: Despite acceptable inter-reader concordance (moderate in AMM, high in NMM) between experienced ECG readers, a significant proportion of angiographic ATCO was missed on post resuscitation ECGs. A high percentage of patients with angiographic ATCO were reclassified on ECG from ATCO (+) in AMM to ATCO (-) in NMM, suggesting possible interim blunting/resolution of typical diagnostic ECG changes in NMM.

026 Left bundle branch block as an activation criterion for primary percutaneous coronary intervention: where is the evidence?

BackgroundThe activation criteria for primary percutaneous coronary intervention (PPCI) includes chest pain in association with either ST-segment elevation (STEMI) or new-onset left bundle branch block (LBBB) on the ECG. However,...

Time, Time, Time, see what's become of me; While I looked around for my possibilities; I was so hard to please. (From Simon and Garfunkel's Hazy Shade of Winter)

Acute Myocardial Infarct (AMI) due to acute thrombotic coronary occlusion is a synonym for a rapidly progressive necrosis of myocardium, with increasing damage to overall cardiac pump function. Whi...

A modified Anderson-Wilkins electrocardiographic acuteness score for anterior or inferior myocardial infarction

Background Optimal treatment of acute myocardial infarction (AMI) depends on the duration of the ischemia. The Anderson Wilkins (AW) electrocardiographic acuteness score has been shown to complement the historical timing in estimating the time interval from acute thrombotic coronary occlusion in patients presenting with chest pain and evolving myocardial infarction. The purposes of this study were to (1) compare the distributions of the previously developed AW acuteness score in a training population with either anterior or inferior AMI and (2) propose modifications to the formula to achieve distributions similar to the observed distributions of historical times from onset of pain. Methods Two hundred three and 177 patients were included as training and testing population, respectively. All patients had an anterior or an inferior AMI and were without confounding factors on the electrocardiogram. Results The training population had similar distributions of historical times from onset of pain, but differences in distributions of AW acuteness scores, between patients with anterior and inferior AMI ( P < .0001). Eighty percent of the inferior AMI group had the highest possible AW acuteness score. Modification of a Q-wave criterion from ≥30 to ≥20 ms resulted in similar distributions in patients with anterior and inferior AMI both in the training and an independent testing population. Conclusions These results suggest that a modified AW acuteness score using a lower Q-wave duration criterion provides similar AMI timing information in patients with anterior and inferior locations. Clinical use of the AW acuteness score will only be practical if the calculation is automated.

Platelet inhibition reduces cyclic flow variations and neointimal proliferation in normal and hypercholesterolemic-atherosclerotic canine coronary arteries.

Platelet-derived growth factors help stimulate the neointimal proliferation of restenosis after coronary interventions. Reducing platelet accumulation at treated sites may attenuate restenosis. We tested this hypothesis by inducing repetitive platelet aggregation at coronary angioplasty sites in dogs and measuring subsequent neointima formation. Cholesterol-sensitive dogs (n=74) received either 4% cholesterol-enriched diets for >8 months (n=29), creating visible atheromas, or normal canine diets (n=45). A coronary balloon angioplasty cyclic flow variation (CFV) model was used. One group of control dogs (group 1, n=8) had angioplasty with no arterial constriction applied and no drug treatment. Three other groups had arterial constrictors applied to provoke CFVs: group 2 (n=28) received no drug therapy, group 3 (n=18) received oral aspirin alone, and group 4 (n=20) received 3 oral antiplatelet agents: ridogrel, ketanserin, and clopidogrel (R+K+C) to simultaneously inhibit the thromboxane A(2), serotonin, and ADP pathways of platelet aggregation, respectively. Bleeding times were moderately prolonged in the aspirin-treated group (124+/-9 seconds after 3 weeks versus 76+/-6 seconds at baseline, P<0.01) and greatly prolonged on R+K+C (>600 versus 104+/-5 seconds, P<0.001). The frequency and severity of CFVs were inversely related to the degree of platelet inhibition and prolongation of bleeding times, as was sudden death due to acute thrombotic coronary occlusion. Quantitative histology at 8 weeks revealed increased intima-to-media ratio with CFVs: 0.89+/-0.14 in the untreated group 2 versus 0.11+/-0.04 in the control group (P<0.001). Intima-to-media ratio was significantly reduced with antiplatelet treatment (0.27+/-0.05 with aspirin treatment and 0.20+/-0.05 with R+K+C treatment, respectively, P<0.001). Cholesterol feeding did not appear to influence results. Repetitive platelet accumulation at coronary angioplasty sites caused enhanced neointimal proliferation by 8 weeks. Oral inhibitors of platelet aggregation attenuated platelet function, prolonged bleeding times, reduced or prevented cyclic flows and abrupt thrombotic occlusions, and thereby inhibited neointimal proliferation. Platelet inhibition should continue to receive attention in efforts to reduce restenosis after coronary interventions.

Comparison of an automated thrombolytic predictive instrument to both diagnostic software and an expert cardiologist for diagnosis of an ST elevation acute myocardial infarction

Because the electrocardiograms (ECGs) of patients with symptoms suggesting an acute thrombotic coronary occlusion are typically read by physicians relatively inexperienced in this skill, it is important to develop automated decision support. A Thrombolytic Predictive Instrument (TPI) is now available along with the standard diagnostic software in a commercially available electrocardiograph. This study evaluates the performance of the predictive software in comparison to both an expert cardiologist and standard diagnostic software. True sensitivity and specificity cannot be determined because acute coronary angiography was not performed. The specificities determined by this study were excellent (98% and 99%), and the sensitivities were very good (72% and 78%). These results that the TPI will be only rarely applied to patients who do not indeed have an acute coronary thrombosis. However, the reasons for even this small number of presumably falsely TPI positive patients should be determined and analyzed. It is unlikely that alterations of the thresholds for TPI activation will significantly improve on this very good level of sensitivity, without prohibitively decreasing specificity

Cardiac markers: present and future.

In the early twentieth century, acute myocardial infarction secondary to acute thrombotic coronary occlusion was considered a rare, fatal condition. Acute myocardial infarction is now one of the most-commmon serious illnesses in the industrialized world. Laboratory medicine now plays a crucial role in identifying risk factors, early events, and conditions triggering plaque rupture in coronary ischemic disease. However, the greatest progress in laboratory research has resulted from the discovery of new and more-promising biochemical markers of myocardial damage. The discovery of cardiac troponins, in particular, has heralded a new age in the diagnosis and treatment or management of a broad spectrum of diseases, grouped together under the heading of acute coronary syndrome, and including stable and unstable angina, and non-Q wave infarction to Q-wave infarction. Cardiac troponins, which are selectively released by damaged myocardiocytes, have a specificity that has not only allowed an improvement in the diagnosis of acute cardiac ischemic disorders, but has also enabled us to make a more-reliable stratification of risk and prediction of outcome. It is generally agreed that two biochemical markers should be used: an early marker (and we recommed myoglobin for this) and a definitive marker, which is cardiac troponin (I or T). Future research is likely to include the standardization of methods for measuring current markers, troponin I in particular, the assessment of rapid bedside tests, and the investigation of the relationship between cardiac markers and emerging immunological and coagulation parameters. Thrombogenesis is now recognized as important in the final process of coronary atherosclerosis, and new markers of thrombogenesis should be used to evaluate the risk of plaque rupture and to monitor the outcome of thrombolytic therapy. Moreover, recent vascular biology studies have provided information on the developmental stages of atherosclerosis and emphasized the importance of the endothelium as a modulator of vascular reactivity, atherogenesis, and plaque stability. The different types of laboratory test (biochemical, immunological, and coagulative) now available, should soon allow improvement in the diagnosis and therapy of ischemic coronary diseases.

Acute coronary artery occlusion likely due to thrombus occurring during coronary angiography: Report of a case

Twenty-five years ago, fatalities due to acute thrombotic coronary occlusion occurring during coronary angiography were reported not infrequently, but are thought to have been eliminated by changes in technique and equipment. We present a case with documentation of a normal coronary arterial tree just before the time of an abrupt occlusion, which had the angiographic features of clot. The likely source of the thrombus was the arterial sheath. Measures for prevention of this complication are discussed.

Influence of Ketanserin on Regional Myocardial Blood Flow After Myocardial Infarction in Baboons

Serotonin (5-hydroxytryptamine, 5-HT) mediates vasoconstriction and vasodilation in normal coronary circulation of various animal species. In the presence of coronary artery disease, serotonin may inhibit coronary collateral formation and stimulate predominantly vasoconstriction. We tested the effect of ketanserin, a selective 5-HT2 receptor antagonist and platelet aggregation inhibitor, on ischemic myocardium blood flow (BF) and collateral formation after coronary artery occlusion in primates. Fifteen baboons were subjected to left anterior descending coronary artery (LAD) ligation and thrombus formation. Hemodynamics and regional myocardial blood flow (RMBF) (microsphere technique) were measured before and 45 min and 1 week after coronary artery occlusion. There was no significant difference in the hemodynamic measurements, gross infarct size, or infarct-ischemic zone MBF in the experimental group (ketanserin 1 mg/kg daily, n = 9) as compared with the control group (injectable water, n = 6). Both groups had a significant increase in BF ratio of infarct-ischemic/normal myocardium at 1 week as compared with shortly after coronary occlusion. Thus, selective 5-HT2 receptor blockade has neither an adverse nor a protective effect on myocardial infarct resulting from acute thrombotic coronary occlusion in baboons.

Adjunctive thrombolytic therapy for angioplasty in ischemic rest angina: Results of a double-blind randomized pilot study

Objectives. A multicenter pilot study was instituted to assess the role of intracoronary thromholytic therapy during angioplasty for ischemic ress angina.Background. Acute thrombotic coronary occlusion is increased during angioplasty for unstable angina, and intracoronary thrombolytic agents have been used to maintain patency. Prophylactic use of intracoronary thrombolytic agents has been advocated in certain high risk subgroups, although no studies have randomized therapy.Methods. Ninety-three patients with either unstable angina and pain at rest (trial A, 66 patients) or postinfarction pain at rest (trial B, 27 patients) were randomized in double-blind fashion to administration of either intracoronary urokinase, 150,000 U, or saline solution placebo given immediately before angioplasty. Cineangiograms of the culprit lesion were recorded and analyzed in blinded fashion by a core laboratory for definite or possible (haziness) filling defects 15 min after angioplasty or after acute closure.Results. Urokinase decreased filling defects at 15 min after angioplasty in comparison, with placebo (14% vs. 29%, respectively, p = 0.08). Four patients in each treatment group developed acute vessel closure. However, although urokinase significantly reduced the incidence of filling defects in trial A (3% vs. 23%, p = 0.03), the drug had no effect at the selected dose in trial B (42% vs. 43%, respectively). Acute vessel closure occurrred significantly more frequently in trial B than in trial A, and urokinase at the selected dose also had no effect. Ischemic events after angioplasty appeared to be related more to dissection than to thrombosis, although redilation, which was more frequent after placebo administration, may have reduced their incidence as well as that of acute closure.Conclusions. These data suggest a possible role for intracoronary urokinase during angioplasty for unstable angina. The lack of effect after infarction may represent a greater thrombus burden or degree of plaque disruption. A trial utilizing higher doses of urokinase in a larger patient group is in progress.

Acute thrombotic coronary occlusion secondary to chest trauma treated with intracoronary thrombolysis

Acute thrombotic coronary occlusion secondary to chest trauma treated with intracoronary thrombolysis

Sudden death from coronary disease-the cardiac coundrum.

Five hundred sudden deaths ascribed to coronary sclerotic heart disease after complete autopsy have been studied and analyzed. A broad range of morbid cardiovascular and anatomic changes was observed. Approximately one-third of the hearts showed “new” disease in the form of acute thrombotic coronary occlusion, acute myocardial infarct, or both. The remainder of the victims died suddenly of the chronic disease without the participation of any recent recognizable change in the heart. A physiologic mechanism based on differential myocardial oxygenation is postulated as the death factor in these instances. The frequent finding of an entirely normal myocardium with “fatal” coronary disease raises the issue of “hearts too good to die” and points up the advisability of instituting positive action to restore the heart beat.