Anterolateral Infarction Research Articles

PERCUTANEOUS MITRAL PLICATION FOR WEANING BY VA–ECMO IN PATIENT WITH OBSTRUCTIVE SAM ASSOCIATED WITH PRECLINICAL PHENOTYPE OF HYPERTROPHIC CARDIOMYOPATHY AND STEMI COMPLICATED BY CARDIOGENIC SHOCK

Abstract A 53–year–old man with a history of hypertrophic obstructive cardiomyopathy with a preclinical phenotype, classified at low risk of sudden cardiac death (HCM–SCD risk score 2.98%), and cardiac arrest (OHCA) in the absence of a shockable rhythm. The patient underwent cardiopulmonary resuscitation for more than 30 minutes before the diagnosis of complete atrioventricular block, masked by concomitant atrial stand–still, resolved after transcutaneous pacing. After temporary trans–venous cardiac pacing was obtained, the electrocardiogram revealed signs of an extensive anterolateral occlusive infarction (OMI), treated with primary angioplasty during percutaneous ventricular support (Impella CP). The ICU course was characterized by several ineffective attempts to wean from mechanical assistance to the circulation finally made possible by correction of outflow obstruction from mitral SAM, achieved by percutaneous mitral plication with MitraClip system. This case, in addition to suggesting an alternative strategy of weaning from mechanical assistance to the circulation in patients with a similar hemodynamic profile (SCAI D stage cardiogenic shock by dual mechanism: pump dysfunction and outflow obstruction), offers important insights into the management of OCHA in the absence of a shockable rhythm.

Anatomic and MRI bases for medullary infarctions with patients’ presentation

ObjectiveThere is a low incidence of the medullary infarctions and sparse data about the vascular territories, as well as a correlation among the anatomic, magnetic resonance imaging (MRI) and neurologic signs. Materials and methodsArteries of the 10 right and left sides of the brain stem were injected with India ink, fixed in formalin and microdissected. The enrolled 34 patients with medullary infarctions underwent a neurologic, MRI and Doppler examination. ResultsFour types of the infarctions were distinguished according to the involved vascular territories. The isolated medial medullary infarctions (MMIs) were present in 14.7%. The complete MMIs comprised one bilateral infarction (2.9%), whilst the incomplete and partial MMIs were observed in 5.9% and 8.9%, respectively. The anterolateral infarctions (ALMIs) were very rare (2.9%). The complete and incomplete lateral infarctions (LMIs), noted in 35.3%, comprised 11.8% and 23.6%, respectively, that is, the anterior (5.9%), posterior (8.9%), deep (2.9%), and peripheral (5.9%). Dorsal ischemic lesions (DMIs) occurred in 11.8%, either as a complete (2.9%), or isolated lateral (5.9%) or medial infarctions (2.9%). The remaining ischemic regions belonged to various combined infarctions of the MMI, ALMI, LMI and DMI (35.3%). The infarctions most often affected the upper medulla (47.1%), middle (11.8%), or both (29.5%). Several motor and sensory signs were manifested following infarctions, including vestibular, cerebellar, ocular, sympathetic, respiratory and auditory symptoms. ConclusionsThere was a good correlation among the vascular territories, MRI ischemia features, and neurologic findings regarding the medullary infarctions.

Early Left Ventricular Thrombus Following Ventricular Fibrillation/Ventricular Tachycardia Electrical Storm.

Left ventricular thrombus (LVT) formation is a serious clinical complication of low-flow states that may be seen in an ischaemic, arrhythmic heart. While LVT formation has a poor prognosis, in the setting of myocardial infarction it is usually a result of post-infarct sequelae such as left ventricle aneurysms, and inflammatory changes from damaged tissue, with the LVT taking several days to form. Arrythmias such as ventricular tachycardia (VT) or ventricular fibrillation (VF) may also lead to thrombus formation, as they contribute to stasis due to decreased cardiac output. Large anterolateral myocardial infarctions can cause electrical or arrhythmic storm, characterized by more than three episodes of VT or VF in a 24-hour period. This prolonged state of dyskinesis further increases the risk of thrombosis, creating a compounding effect. Here, we report the case of a patient who had a VF cardiac arrest with electrical storm secondary to anterolateral myocardial infarction complicated with LVT formation found on echocardiogram after the cardiac arrest, which was absent on presentation. This thrombus formation occurred particularly early during the course of the patient’s arrest, possibly due to the compounding factors increasing the risk of thrombosis. Herein, we discuss in detail the risk factors for LVT formation, its mechanism and management options. A review of the literature also shows that LVT formation in the acute phase of arrest, as seen in our patient, is rare.LEARNING POINTSLeft ventricular thrombus (LVT) formation occurs 3–14 days after myocardial infarction, but in the setting of concomitant ventricular fibrillation arrest, may occur within the first 24 hours.Risk factors for LVT formation include a large infarct, anterior/anterior apical infarction, decreased ejection fraction (particularly <30–35%), left ventricular aneurysm, and delayed time to revascularization.Although diagnosis is generally made on transthoracic echocardiography with intravenous contrast, cardiac MRI with contrast has better sensitivity and specificity.Treatment consists of anticoagulation with a vitamin K antagonist or heparin for 3–6 months with a repeat echocardiogram to confirm the thrombus has organized or resolved. Further trials are needed to assess the efficacy of direct oral anticoagulants.

Acute myeloid leukemia causing acute thrombosis of the\xa0coronary arteries: a\xa0case report

BackgroundThis case report demonstrates acute myeloid leukemia causing acute thrombosis of coronary arteries with anterolateral ST elevation myocardial infarction and ventricular tachycardia in an otherwise healthy woman. Few case reports have been documented on patients with concomitant conditions of acute myeloid leukemia and acute myocardial infarction, and it is important to note that prognosis for patients with both is worse than that of either condition. While both conditions together are rare, other non-atherosclerotic causes of acute coronary syndromes are likewise important considerations in the context of myocardial ischemia.Case presentationA 59-year-old Caucasian woman with no notable past medical history presented to her primary care provider with 2 weeks of severe fatigue, anorexia, and malaise, associated with chills, night sweats, and myalgias. Peripheral blood smear identified 92% blasts consistent with acute myeloid leukemia and computed tomography identified a right segmental pulmonary embolism and thrombotic infarcts in the spleen, bilateral kidneys, right lung, and liver. Laboratory testing also demonstrated disseminated intravascular coagulopathy. She was admitted to the intensive care unit for treatment and subsequently developed ventricular tachycardia, anterolateral ST segment elevation, acute dysarthria, and nonreactive pupils. Pulseless electrical activity developed with unsuccessful resuscitative measures. The patient died secondary to presumed cerebrovascular and coronary thromboses causing stroke and anterolateral infarct complicated by ventricular tachycardia and pulseless electrical activity.ConclusionThis case is notable as a case of acute myeloid leukemia causing acute thrombosis of coronary arteries with anterolateral ST elevation myocardial infarction, ventricular tachycardia, and pulseless electrical activity. Prognosis of concomitant acute myeloid leukemia and acute myocardial infarction is poor. Management is challenging due to thrombocytopenia, platelet dysfunction, and systemic coagulopathy, and administration of thrombolytic agents can be fatal. This is an extreme presentation of a case of acute myocardial infarction with disseminated intravascular coagulopathy causing acute coronary thrombosis and sudden death with dramatic electrocardiogram and telemetry findings recorded with rapid progression from normal sinus rhythm to acute myocardial infarction to terminal rhythm.

ST-elevation myocardial infarction complicated by cardiac arrest in a young patient with familiar dyslipidemia

Coronary heart disease in young patients always poses great challenges for every healthcare system with differences in clinical manifestations, etiology, epidemiology, angiographic characteristics and prognosis. The objective of this study was to describe a case of ST-elevation myocardial infarction complicated by cardiac arrest in a young patient with familial dyslipidemia. A 30-year-old male visited our hospital with typical angina. During the examination, he suffered a sudden loss of consciousness, the monitor showed ventricular fibrillation. After successful resuscitation of cardiac arrest, electrocardiography showed apparent ST-elevation from V2 to V6 leads consistent with the diagnosis of anterolateral infarction. Emergency coronary angiogram showed severe three-vessel lesions including complete occlusion of the LAD artery and 80 - 90% stenosis of the other two coronary branches. Our patient’s coronary arteries were revascularized using drug-eluting stents in LAD artery and subsequently RCA artery, stem cell therapy was applied during the interventional process. Routine laboratory test results showed dyslipidemia and his family records suggested familiar (hereditary) dyslipidemia which affected his mother and sister. 1-month follow-up echocardiography showed a drastic improvement of LVEF by roughly 15%. The combination of revascularization, stem cell therapy, and lipid-lowering therapy has shown a good therapeutic effect.

Assessment of Right Ventricular Function Using Strain and Strain Rate in Patient with Acute Anterior ST Segment Elevation Myocardial Infarction

Introduction: Anterior ST-segment elevation myocardial infarctions (STEMI) are those involving the anterior ECG leads of the heart as a result of transmural ischaemia. They can be subdivided according to their extension into anteroseptal and anterolateral infarctions. Objective: The aim of this study is assessment of right ventricular function using strain and strain rate imaging in patients with anterior ST segment elevated myocardial infarction (STEMI). Methods: This prospective study was conducted on 35 patients with anterior ST segment elevated myocardial infarction (STEMI) who were admitted to ER and CCU department in National Heart Institute from May 2018 to May 2019. Results: Comparison between groups regarding longitudinal strain showed that there is highly statistically significant difference between them in lateral wall (all segments), septum (all segments) and global LS of right ventricle. Comparison between studied groups regarding circumferential strain revealed that there is highly statistically significant difference between them in all segments of right ventricle. Conclusions:Strain and strain rate imaging are feasible and reproducible tools in assessment of right ventricular function in patients with anterior ST segment elevated myocardial infarction (STEMI).

Topographic location of unisolated pontine infarction

BackgroundThe topographic location of acute pontine infarction is associated with clinical syndromes and prognosis. Previous studies focused on isolated pontine infarction, but the topographic location of unisolated pontine infarction has remained unclear.MethodsThis was a prospective, multicenter, longitudinal registry study. Patients with acute pontine infarction confirmed by magnetic resonance imaging (MRI) were enrolled. Based on the territory of the pontine artery, the topographic location was divided into anteromedial, anterolateral, tegmental, bilateral and unilateral multiple infarctions.ResultsFrom May 1, 2003, to Oct 31, 2017, 1003 patients were enrolled, and 330 had unisolated pontine infarction. For isolated pontine infarction, 44.9, 19.8, 16.0, 13.1 and 6.2% of patients had anteromedial, anterolateral, tegmental, bilateral and unilateral multiple pontine infarctions, respectively. For unisolated pontine infarction, 30.3, 19.7, 24.5, 15.2 and 10.3% of patients had anteromedial, anterolateral, tegmental, bilateral and unilateral multiple pontine infarctions, respectively.ConclusionIn this large series study, our data revealed fewer anteromedial infarctions and more tegmental and unilateral multiple infarctions in patients with unisolated pontine infarction than in patients with isolated pontine infarction.

Visualization of Culprit Perforators in Anterolateral Pontine Infarction: High-Resolution Magnetic Resonance Imaging Study

Background: The stroke mechanism for anterolateral pontine infarction (ALPI) is poorly understood. We aimed to investigate the perforator arteries relevant to ALPI using high-resolution MRI (HR-MRI). Methods: Of 62 patients with ALPI who were admitted to the Asan Medical Center, 13 patients agreed to participate in this study. We used HR-MRI with a 3-Tesla scanner and assessed the perforating branches directly connected with the infarcted area. Results: Perforating arteries penetrating ALPI were identified in all 13 patients. Perforators arising from the basilar artery (BA) were involved in the stroke mechanism in 9 patients, the superior cerebellar artery (SCA) perforator in 1 patient, and the anterior inferior cerebellar artery perforator in 1 patient. In 2 patients, both BA and SCA perforators were involved. Conclusions: Using 3-Tesla HR-MRI may allow visualization of the perforating branches presumably related to ALPI. Identification of the relevant cerebral perforating arteries may help us to understand the stroke mechanism in patients with posterior circulation territory infarction.

Demographic profile, clinical characteristics and outcomes of patients undergoing coronary artery bypass grafting—retrospective analysis of 4,024 patients

Large databases give an insight into patient characteristics and outcomes of patients undergoing coronary artery bypass grafting (CABG) in western populations. However, there is paucity of data in Indian population. This study was designed to understand the clinical characteristics and short-term outcomes of patients undergoing CABG at our institute. All the patients who underwent isolated CABG from January of 2001 to December of 2011 were included in the study. Those who underwent re-operative CABG and concomitant valve surgery were excluded. A total of 4,024 patients underwent CABG during the 11-year period. Mean age of patient population was 57 ± 9.6 years. The incidence of female patients undergoing surgery was 12.6 %. Diabetes mellitus was present in 58.4 % of patients. A total of 1,972 (49 %) patients had prior myocardial infarction. Thirty percent of patients had anterior and anterolateral wall infarction. Nineteen percent of patients had inferior wall infarction; 10.6 % had ischemic cardiomyopathy. Incidence of significant left main disease was 10.9 %. Majority of patients (66.4 %) presented with triple vessel disease. Ninety patients (2. 23 %) died in the early post-operative period. Post-operative stroke rate was 0.15 %. Acute renal failure requiring dialysis and mediastinitis occurred in 0.5 and 0.75 % of patients, respectively. Compared to Western population, this cohort of patients who underwent coronary artery bypass grafting had higher incidence of diabetes mellitus and ischemic cardiomyopathy and low incidence of significant left main disease. Post-operative stroke rate was significantly lower compared to 1–2 % stroke rate reported in western population.

Experimental model of transthoracic, vascular-targeted, photodynamically induced myocardial infarction

We describe a novel model of myocardial infarction (MI) in rats induced by percutaneous transthoracic low-energy laser-targeted photodynamic irradiation. The procedure does not require thoracotomy and represents a minimally invasive alternative to existing surgical models. Target cardiac area to be photodynamically irradiated was triangulated from the thoracic X-ray scans. The acute phase of MI was histopathologically characterized by the presence of extensive vascular occlusion, hemorrhage, loss of transversal striations, neutrophilic infiltration, and necrotic changes of cardiomyocytes. Consequently, damaged myocardium was replaced with fibrovascular and granulation tissue. The fibrotic scar in the infarcted area was detected by computer tomography imaging. Cardiac troponin I (cTnI), a specific marker of myocardial injury, was significantly elevated at 6 h (41 ± 6 ng/ml, n = 4, P < 0.05 vs. baseline) and returned to baseline after 72 h. Triphenyltetrazolium chloride staining revealed transmural anterolateral infarcts targeting 25 ± 3% of the left ventricle at day 1 with a decrease to 20 ± 3% at day 40 (n = 6 for each group, P < 0.01 vs. day 1). Electrocardiography (ECG) showed significant ST-segment elevation in the acute phase with subsequent development of a pathological Q wave and premature ventricular contractions in the chronic phase of MI. Vectorcardiogram analysis of spatiotemporal electrical signal transduction revealed changes in inscription direction, QRS loop morphology, and redistribution in quadrant areas. The photodynamically induced MI in n = 51 rats was associated with 12% total mortality. Histological findings, ECG abnormalities, and elevated cTnI levels confirmed the photosensitizer-dependent induction of MI after laser irradiation. This novel rodent model of MI might provide a platform to evaluate new diagnostic or therapeutic interventions.

Effect of Partial Oxygen Supply on Mitochondrial Electron Transport System During Complete Cardiac Ischemia

During complete ischemia we assessed myocardial utilization of the small amount of oxygen available. We also determined whether blood cardioplegia has any advantage over crystalloid cardioplegia in this setting. Patients with preserved left ventricular myocardial function and without anterolateral wall infarct or aneurysm were included to the study. Intermittent cold blood and crystalloid cardioplegia were used in 10 patients (group BC) and 9 patients (group CC), respectively. From myocardial biopsies, obtained before and after ischemia, complete electron transport system (ETS) enzyme activities (NDH, SDH, NCCR, SCCR, and COX) and lactate content were analyzed. Biochemical and hemodynamic analyses also were done. Myocardial and blood temperatures were monitored. Ischemic time was longer in group CC (p < 0.05). There were no important differences in biochemical and hemodynamic variables between the two groups. In addition, there was no difference in NDH and SDH activities as well as COX/SCCR and COX/RS-NCCR ratios between the two groups before and after ischemia. After Ischemia, RS-NCCR in group CC and SCCR and COX activities in both groups were lower than the control. For all enzymes, activity change ratios were not different between groups. Myocardial lactate content was increased in both groups after ischemia. However, the increase in group BC was less (p < 0.01). Based on our findings, we believe that the superiority of blood cardioplegia over crystalloid cardioplegia does not depend on oxygen content, but on other factors such as buffering and free oxygen radical scavenger effects among others. However, with the warm and continuous blood cardioplegia technique, oxygen content might be more important.

Unusual Complication of Aortic Valve Grape-Like Myxoma

A 15-year-old boy was transferred to our hospital because of an acute myocardial infarction and persistent chest pain. His electrocardiogram showed an inferior and anterolateral infarct with persistent ST elevation and Q-wave. Elevations were documented in the levels of troponin I (25.59 ng/mL), creatine phosphokinase (3014 U/L), and creatine kinase-MB subunit (250.6 U/L).

Regional remodeling strain and its association with myocardial apoptosis after myocardial infarction in an ovine model

Progressive left ventricular remodeling after myocardial infarction has been viewed as an important contributor to progressive heart failure. The objective of this study was to investigate the relationship between myocardial apoptosis and strain during progressive cardiac remodeling. Before creation of an anterolateral left ventricular infarction by ligation of diagonal arteries, 16 sonomicrometry transducers were placed in the left ventricular free wall of 8 sheep to assess regional deformation in the infarct, adjacent, and normally perfused remote myocardial regions over 8 weeks' duration. Hemodynamic, echocardiographic and sonomicrometric data were collected before infarction and then 30 minutes and 2, 6, and 8 weeks after infarction. At the end of the study, regional myocardial tissues were collected for apoptotic signaling proteins. At terminal study, an increase in left ventricular end-diastolic pressure of 8.1 +/- 0.1 mm Hg, a decrease in ejection fraction from 54.19% +/- 5.68% to 30.55% +/- 2.72%, and an end-diastolic volume increase of 46.08 +/- 5.02 mL as compared with the preinfarct values were observed. The fractional contraction at terminal study correlated with the relative abundance of apoptotic protein expressions: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.27, P < .05), caspase-3 (r(2) = 0.31, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.30, P < .05). These myocardial apoptotic activities also correlated with remodeling strain: cytochrome c (r(2) = 0.02, P < .05), mitochondrial Bax (r(2) = 0.28, P < .05), caspase-3 (r(2) = 0.43, P < .05), and poly (adenosine diphosphate-ribose) polymerase (r(2) = 0.37, P < .05). Increase in regional remodeling strain led to an increase in myocardial apoptosis and regional contractile dysfunction in heart failure.

Oral treatment with probucol in a pharmacological dose has no beneficial effects on mortality in chronic ischemic heart failure after large myocardial infarction in rats

Cardiac remodeling after myocardial infarction is in part triggered and maintained by reactive oxygen species. Antioxidants such as probucol have shown positive short-term effects on these cardiac interstitial changes in different experimental models after intraperitoneal administration or after per-oral administration with a long pre-treatment period or in high doses. In this study, the long-term effects on mortality and cardiac remodeling were examined after induction of a large myocardial infarction in a clinical daily-life-like setting. Male Lewis rats were randomized to the study groups. Large anterolateral myocardial infarctions were induced or sham operations performed. The oral treatment was started after 48 h either with probucol or placebo after myocardial infarction and with placebo after sham operation. Induction of large myocardial infarctions led to changes of the left ventricular stiffness constants, a dilatation of the left ventricle and an increased interstitial fibrosis in the remote non-infarcted part. These changes were in tendency, but not significantly, reversed after treatment with probucol. The 6-month survival rates were 53.1% in the group probucol-myocardial infarction, 43.2% in the group placebo-myocardial infarction and 100% in the group after sham operation. There were no significant differences at Kaplan–Meier analysis between the groups after myocardial infarctions. Oral treatment with the antioxidant probucol started after myocardial infarction in a pharmacological dose does not have favourable effects on the long-term mortality in the chronic ischemic heart failure model in the rat.

Acute Myocardial Infarction and Status Asthmaticus: A Case Report

A patient with a painless, extensive anterolateral myocardial infarct, which occurred during a prolonged bout of refractory asthma, is presented. Cardiac catheterization revealed a large akinetic area involving the septum and anterolateral walls and completely normal coronary arteries. The etiology of the infarct was believed to be intense coronary vasospasm occurring during the lengthy period of status asthmaticus.

Outcome of Primary Percutaneous Coronary Intervention in Octogenarians with Acute Myocardial Infarction

Acute myocardial infarction (AMI) results in more complications and increased mortality in octogenarians compared to patients in younger age groups. This study investigated the short- and long-term outcomes in octogenarians after primary percutaneous coronary intervention (PCI). During the study period from May 1997 to August 2004, 54 patients > or = 80 years old with ST-elevation myocardial infarction (STEMI) were eligible for primary PCI. Data collected included baseline clinical characteristics and usage of cardiovascular medications. Diagnostic coronary angiography and revascularization procedures were performed using standard practices. During hospitalization, the clinical course including serial changes in cardiac enzymes, adverse events associated with myocardial infarction or treatment, and inhospital or long-term mortality of patients were recorded. The mean age of the 54 patients (35 men, 19 women) was 82.8 +/- 2.5 years (range, 80-89 years). Among them, 27 (50%) had anterior infarction, six (11%) had anterolateral infarction, and 21 (39%) had inferior infarction, inclusive of three patients with accompanying right ventricular infarction. Among them, 20 (37%) patients were in Killip class I, nine (17%) were in class II, two (4%) in class III, and 23 (43%) in class IV. The mean delay from onset of symptoms to arrival in hospital was 220 +/- 167 minutes, and 189 +/- 169 minutes from hospital arrival to reperfusion. Diagnostic coronary angiography revealed that 48 (89%) patients had multivessel disease. Inhospital death occurred in 23 (43%) patients, with the leading causes of death being profound cardiogenic shock (61%), and free wall rupture (26%). Octogenarian patients who developed STEMI tended to have multivessel disease. These patients had a high inhospital mortality rate that was most likely to be due to cardiogenic shock.

Myocardial Infarction, Other Arterial Thrombosis and Invasive Coronary Procedures, in Hemaophilia B: A Critical Evaluation of Reported Cases

Myocardial infarction and other arterial thrombosis are commonly maintained to be rare in hemophilia patients. This, in general, seems true but the occurrence of a thrombotic event in hemophilia B is not exceptional. A thorough search of the literature has yielded 13 patients with myocardial infarction and 1 patient with a cerebrovascular accident. There were three fatalities. In five cases MI occurred after infusion of Prothrombin Complex Concentrates. In three additional patients the event occurred after infusion of plasma, Feiba or cryoprecipitate supernatant. Four patients had an antero-lateral infarction. Two had a non-Q infarction and one each showed a multiple or a posterior-inferior form. Several therapeutic coronary procedures (GABG and PTCA) were carried out in hemophilia B patients without undue complication providing adequate level of FIX were maintained. Heparin prophilaxis was used in all patients but one. The analysis of the literature indicates that (1) MI may occur in hemophilia B patients and (2) that invasive coronary artery therapeutic procedures may be carried out without complications.

Cardiac Imaging Impaired by a Silicone Breast Implant

The authors report a case of a left-sided silicone breast implant interfering with nuclear imaging of the myocardium. Cardiac SPECT imaging of a woman documented widespread infarct in the anterolateral, inferior, and posterolateral walls, as well as mixed ischemia/infarct in the anterior wall. Subsequent cardiac MRI revealed just anterolateral and inferolateral infarct. The anterior wall was completely viable. Also apparent on the MR images was a left breast implant overlying the anterior myocardial wall. This case of a left-sided silicone breast implant interfering with nuclear imaging of the myocardium highlights the importance of understanding the potential interference from silicone breast implants.

How reliable is electrocardiography in differentiating transmural from non-transmural myocardial infarction? A study with contrast magnetic resonance imaging as gold standard

Cardiovascular magnetic resonance (CMR) using contrast enhancement allows exact determination of the site and transmural extent of myocardial infarction (MI). We evaluated whether 12-lead electrocardiography can differentiate transmural from non-transmural MI or determine the site of MI by comparing the findings with those of contrast-enhanced CMR. A total of 27 patients (59.5±12.9 years) with a history of MI (6.4±2.9 months) underwent CMR (Magnetom, Siemens, Erlangen, Germany). Cine images were acquired in the horizontal and vertical long axes and short axis by TrueFISP. Contrast-enhanced CMR images were acquired in the same axes by segmented FLASH 15 min after administration of gadolinium–DTPA (0.15 mmol/kg). This showed the MI to be transmural in 11 patients and non-transmural in 16. An electrocardiogram (ECG) was recorded in all patients before CMR. T-wave alterations, descending ST-depression, pathological Q-waves and absent R waves were more frequent in non-transmural MI than transmural MI, as defined by contrast-enhanced CMR ( p≥0.618). However, none of the differences were statistically significant. R-wave reduction, q waves and horizontal ST-depression were more frequent in transmural than in non-transmural MI ( p≥0.157). Again, the differences were not significant. The sensitivity of the ECG for MI localization was highest in inferior infarctions (85.71%), the specificity was highest in anterior infarctions (100%), the best positive predictive value (80%) was achieved for anterolateral infarctions, and the best negative predictive value for lateral infarctions (95.83%). Transmural and non-transmural MI cannot be differentiated by ECG. The ECG is most accurate in detecting anterolateral MI.

Rápida lisis de gran trombo coronario con abciximab

126 A 47-year-old man with an acute anterolateral myocardial infarct more than 24 hours old and without previous fibrinolitic treatment was admitted with clinical signs of postinfarct angina. Coronary angiography revealed a complete occlusion, with thrombotic material, of the descending anterior proximal artery without visualization of the distal vein by collateral circulation (Figure 1), moderate stenosis of the circumflex artery, and extensive occupational thrombus in the median and distal segments of the right coronary artery (Figure 2A), with decreased coronary flow (TIMI II). Ventricular function was significantly reduced (IVEF=42%), with the presence of a thrombus in the apex. Before the procedure abciximab (bolus and perfusion) and 6000 U of heparin were administered. Permeability of the descending anterior artery was achieved and normal coronary flow was reestablished through implantation of a stent before dilatation with a balloon catheter. At the conclusion of the procedure (40 minutes) a new contrast injection into the right coronary artery was made, showing the complete disappearance of the thrombus on angiography (Figure 2B). The patient s clinical course was satisfactory. We believe that the state of hypercoagulability coupled with the elevated left ventricular telediastolic pressure inherent in extensive anterior infarct contributed to the formation of a large thrombus in the right coronary artery. The administration of heparin and abciximab, together with improvement in left ventricular function after the reperfusion, enabled rapid lysis of the thrombus in the right coronary artery. What is interesting in this case is the angiographic rendering of early lysis of a large thrombus present in an artery that had nothing to do with the infarct, found during a rescue angioplasty of the responsible artery.