Evidence Of Acute Myocardial Infarction Research Articles

Implantable Defibrillator Therapy in Cardiac Arrest Survivors With a Reversible Cause.

Current guidelines recommend implantable cardioverter-defibrillator (ICD) therapy in survivors of sudden cardiac arrest (SCA), except in those with completely reversible causes. We sought to examine the impact of ICD therapy on mortality in survivors of SCA associated with reversible causes. We evaluated the records of 1433 patients managed at our institution between 2000 and 2012 who were discharged alive after SCA. A reversible and correctable cause was identified in 792 (55%) patients. Reversible SCA cause was defined as significant electrolyte or metabolic abnormality, evidence of acute myocardial infarction or ischemia, recent initiation of antiarrhythmic drug or illicit drug use, or other reversible circumstances. Of the 792 SCA survivors because of a reversible and correctable cause (age 61±15 years, 40% women), 207 (26%) patients received an ICD after their index SCA. During a mean follow-up of 3.8±3.1 years, 319 (40%) patients died. ICD implantation was highly associated with lower all-cause mortality (P<0.001) even after correcting for unbalanced baseline characteristics (P<0.001). In subgroup analyses, only patients whose SCA was not associated with myocardial infarction extracted benefit from ICD (P<0.001). In survivors of SCA because of a reversible and correctable cause, ICD therapy is associated with lower all-cause mortality except if the SCA was because of myocardial infarction. These data deserve further investigation in a prospective multicenter randomized controlled trial, as they may have important and immediate clinical implications.

High-Sensitivity Troponin I Levels and Coronary Artery Disease Severity, Progression, and Long-Term Outcomes.

BackgroundThe associations between high‐sensitivity troponin I (hsTnI) levels and coronary artery disease (CAD) severity and progression remain unclear. We investigated whether there is an association between hsTnI and angiographic severity and progression of CAD and whether the predictive value of hsTnI level for incident cardiovascular outcomes is independent of CAD severity.Methods and ResultsIn 3087 patients (aged 63±12 years, 64% men) undergoing cardiac catheterization without evidence of acute myocardial infarction, the severity of CAD was calculated by the number of major coronary arteries with ≥50% stenosis and the Gensini score. CAD progression was assessed in a subset of 717 patients who had undergone ≥2 coronary angiograms >3 months before enrollment. Patients were followed up for incident all‐cause mortality and incident cardiovascular events. Of the total population, 11% had normal angiograms, 23% had nonobstructive CAD, 20% had 1‐vessel CAD, 20% had 2‐vessel CAD, and 26% had 3‐vessel CAD. After adjusting for age, sex, race, body mass index, smoking, hypertension, diabetes mellitus history, and renal function, hsTnI levels were independently associated with the severity of CAD measured by the Gensini score (log 2 ß=0.31; 95% confidence interval, 0.18–0.44; P<0.001) and with CAD progression (log 2 ß=0.36; 95% confidence interval, 0.14–0.58; P=0.001). hsTnI level was also a significant predictor of incident death, cardiovascular death, myocardial infarction, revascularization, and cardiac hospitalizations, independent of the aforementioned covariates and CAD severity.ConclusionsHigher hsTnI levels are associated with the underlying burden of coronary atherosclerosis, more rapid progression of CAD, and higher risk of all‐cause mortality and incident cardiovascular events. Whether more aggressive treatment aimed at reducing hsTnI levels can modulate disease progression requires further investigation.

Beta-blockers, and real clinical practice in Russia: the gap between the understanding of the doses of beta-blockers and subsequent prognosis in patients with cardiovascular disease

Presents an analysis of the reception beta-blockers in three epidemiological studies sections of the EPOKhA. Respondents in each slice (2002, 2007, 2017) were stratified into 5 subgroups: only suffering from hypertension - AH (subgroup AH), patients with stable angina pectoris, but in history and clinically has no evidence of acute myocardial infarction (AMI) and chronic heart failure (subgroup of coronary heart disease); after myocardial infarction, but do not have clinical manifestations of chronic heart failure (subgroup myocardial infarction); patients with acute myocardial infarction formed for any reason, but with no previous history of AMI (subgroup chronic heart failure), and patients with clinical manifestations of chronic heart failure after suffering AMI in anamnesis (subgroup myocardial infarction + chronic heart failure). During 15 years in the Russian Federation the frequency of administration of beta-blockers increased from 20% in the section of cardiovascular pathology to 30%. The most sensitive to the use of beta-blockers were patients with a history of AMI and chronic heart failure. Prolonged beta-blockers have been used at the population level only in 2007, but the frequency with any cardiovascular pathology does not exceed the 50% threshold, and the achievement of goals (control heart rate) does not exceed 10% of the level at any pathology. This dependence is associated with low-dose beta-blockers. In any case, the dose of beta-blockers did not exceed 50% of recommended that can be a separate cause of cardiovascular mortality at the population level in Russia.

Effect of Erythropoietin Stimulating Agents on Cardiovascular Events in Chronic Kidney Disease Patients on Hemodialysis

Objectives: Patients with chronic kidney disease (CKD) develop anemia which is treated with erythropoietin-stimulating agents (ESAs). However, ESAs do not reduce the risk of cardiovascular mortality. Furthermore, this is unclear whether ESAs therapy has any association with adverse cardiovascular events.Methods: After an informed consent 275 male and female patients, between ages 35 to 75 years, with CKD stage V on ESAs undergoing twice weekly hemodialysis were enrolled. The dose of ESAs was calculated according to weight as 50mg/kg with target hemoglobin being 11 – 12 g/dl. Dose adjustments were made in the patients who failed to achieve target hemoglobin. The patients were followed for a year with the primary end point being new evidence of acute myocardial infarction (MI) diagnosed through ECG or echocardiography. Safety outcomes included stroke or death.Results: The data was entered and analyzed in Statistical Package for Social Sciences (SPSS) version 18Out of 275 patients, 164 (59.6%) patients were males and 111 (40.4%) were females. Mean age of the patients was 51.52 with standard deviation of ± 5.73. According to the results, 52 (18.9%) patients reported with MI and 223 (81.1%) patients had no evidence of MI. Out of 52 patients who had MI, 37 (71.1%) were males and 15 (28.8%) patients were female.Conclusion: ESAs are associated with an increased risk of MI in CKD patients on hemodialysis. Whether there is a direct association or there are other factors involved remains to be seen.

Left ventricular mural thrombus and dual coronary embolization associated with hyperthyroid cardiomyopathy and atrial fibrillation: a case report

BackgroundThe majority of acute myocardial infarction (AMI) events are caused by thrombotic occlusion of the coronary artery, secondary to atherosclerotic plaque erosion or rupture. However, coronary embolism (CE), while rare, is being increasingly recognized as an important cause of AMI. We present the case of a patient with multi-site coronary artery embolization associated with hyperthyroid-related cardiomyopathy and atrial fibrillation.Case presentationA 49-year-old female with a history of hyperthyroidism and atrial fibrillation (AF) was admitted to our hospital presenting with right upper limb pain and swelling. Initial transthoracic echocardiography demonstrated left ventricular apical mural thrombi and hyperthyroidism-induced cardiomyopathy. On the eighth day after admission, the patient developed sudden onset of severe chest pain and evidence of acute myocardial infarction (AMI). Emergency coronary angiography revealed multi-site coronary embolization of the left anterior descending artery and a large diagonal branch. Despite emergency thrombo-aspiration and balloon angioplasty, the patient went into ventricular fibrillation, from which she did not recover.ConclusionAlthough rare, a fatal case of left ventricular thrombus and dual-vessel coronary embolism associated with hyperthyroid cardiomyopathy and atrial fibrillation is reported.

Association Between Depressive Disorders and Incident Acute Myocardial Infarction in Human Immunodeficiency Virus–Infected Adults

With the advent of highly effective antiretroviral therapy and improved survival, human immunodeficiency virus (HIV)-infected people are living longer and are now at an increased risk for cardiovascular disease (CVD). There is an urgent need to identify novel risk factors and primary prevention approaches for CVD in HIV. Although depression is prevalent in HIV-infected adults and is associated with future CVD in the general population, its association with CVD events has not been examined in the HIV-infected population. To examine whether depressive disorders are prospectively associated with incident acute myocardial infarction (AMI) in a large cohort of adults with HIV. Included in this cohort study were 26 144 HIV-infected veterans without CVD at baseline (1998-2003) participating in the US Department of Veterans Affairs Veterans Aging Cohort Study from April 1, 2003, through December 31, 2009. At baseline, 4853 veterans (19%) with major depressive disorder (MDD; International Classification of Diseases, Ninth Revision [ICD-9] codes 296.2 and 296.3) and 2296 (9%) with dysthymic disorder (ICD-9 code 300.4) were identified. The current analysis was conducted from January 2015 to November 2015. Incident AMI (defined by discharge summary documentation, enzyme/electrocardiography evidence of AMI, inpatient ICD-9 code for AMI (410), or AMI as underlying cause of death [International Statistical Classification of Diseases and Related Health Problems, Tenth Revision code 121]) between the enrollment date and December 31, 2009. The mean (SD) age of those with MDD was 47.3 (7.9) years and for those without MDD was 48.2 (9.7) years. During 5.8 years of follow-up, 490 AMI events (1.9%) occurred. Baseline MDD was associated with incident AMI after adjusting for demographics (hazard ratio [HR], 1.31; 95% CI, 1.05-1.62), CVD risk factors (HR, 1.29; 95% CI, 1.04-1.60), and HIV-specific factors (HR, 1.30; 95% CI, 1.05-1.62). Further adjustment for hepatitis C, renal disease, substance abuse, and hemoglobin level (HR, 1.25; 95% CI, 1.00-1.56) and antidepressant use (HR, 1.12; 95% CI, 0.87-1.42) attenuated associations. Baseline dysthymic disorder was not associated with incident AMI. We report novel evidence that HIV-infected adults with MDD have a 30% increased risk for AMI than HIV-infected adults without MDD after adjustment for many potential confounders. Our findings raise the possibility that MDD may be independently associated with incident atherosclerotic CVD in the HIV-infected population.

Dabigatran Effect on Left Ventricular Thrombus in a Patient with Acute Ischemic Stroke.

Dabigatran Effect on Left Ventricular Thrombus in a Patient with Acute Ischemic Stroke.

Abstract 215: Fatal Arrhythmia In The Adult Patient Of Kawasaki Disease

We herein report the two adult patients hardly predictable sudden cardiac arrest caused by presumed Kawasaki disease (KD). Case 1: A 29- year-old man who had a history of KD at 10 months of his age complicated with bilateral giant coronary aneurysms, and was received a surgery of coronary artery bypass grafting (CABG) when he was 17 years old. He was transferred to emergency center because of sudden cardiac arrest during live concert and revived by automated external defibrillator (AED). Case 2: A 26-year-old man with a history of KD at 1year old of his age, complicated with bilateral giant coronary aneurysms, and was received a catheter intervention of rotational atherectomy (ROTA) to left anterior descending (LAD) artery at 16 years old of his age. He suddenly fell with ventricular fibrillation (VF) on playing futsal, and was hospitalized after revival by AED. Both of them had past history of myocardial infarction (MI) in their youths, however, did not have left ventricular dysfunction, symptomatic arrhythmia, and evidence of acute MI at admission. Therefore, it was difficult to strongly predict possibility of fatal arrhythmia in these cases. Finally, they received the second CABG’s for each after stabilizing and returned to their daily lives. It had been rarely reported a fatal arrhythmia in asymptomatic KD patients with normal left ventricular function with revival with recent spread of life support with public access of defibrillator. Our experiences may suggest one style with a paradigm shift in management of patients with coronary artery complications at the remote period of KD.

Evidence of myocardial scarring and microvascular obstruction on cardiac magnetic resonance imaging in a series of patients presenting with myocardial infarction without obstructed coronary arteries.

Patients with acute chest pain, electrocardiographic ST-elevation and significant elevation of cardiac troponin but without obstructive coronary artery disease represent a diagnostic and therapeutic dilemma. Cardiac magnetic resonance imaging (CMR) can elucidate underlying alternative causes of troponin elevation including detection of (minor) myocardial infarction (MI) by identifying myocardial scarring as delayed enhancement. Of 77 patients, who were admitted between March 2009 and December 2012 with electrocardiographic (ECG) and biochemical evidence of acute MI without obstructive coronary artery disease, 45 patients underwent CMR that showed in 11/77 (14%) late gadolinium enhancement (LGE), compatible with myocardial scarring. We analyzed clinical, echocardiographic, and CMR data of these patients. Elevated troponin I levels were observed in all patients (median 1.3 ng/l, IQR 0.44-187) with median peak creatinine phosphokinase of 485 U/l (IQR 234-618). Echocardiographic wall motion abnormalities were detected in 8/11 (73%) patients; in 75% of these segments, ECG abnormalities were observed in corresponding leads. CMR detected LGE in the inferior (4/11), the inferolateral (5/11), the inferoseptal (2/11), the anterior (3/11), apical (3/11) and in the lateral segments (2/11). In addition, in all but two patients, these segments matched ECG abnormalities in corresponding leads. CMR identified microvascular obstruction in 4/11 (36%) patients. Patients with clinical, ECG, and biochemical signs of acute MI but unobstructed coronary arteries may have CMR-detectable myocardial scars. Information on myocardial scarring may help to make the diagnosis and draw therapeutic consequences. This case series underlines the value of contrast-enhanced CMR for myocardial tissue characterization.

Simultaneously Presented Acute Ischemic Stroke and Non-ST Elevation Myocardial Infarction in a Patient with Paroxysmal Atrial Fibrillation

Although atrial fibrillation is the most frequent cause of embolic stroke, coronary embolism from atrial fibrillation is a very rare cause of acute myocardial infarction. Therefore, simultaneously presented acute ischemic stroke and acute myocardial infarction due to atrial fibrillation in the same patient has not been documented. The present report describes the case of a 58-year-old man with paroxysmal atrial fibrillation who initially presented with a large cerebral infarction due to embolic occlusion of the left middle cerebral artery. Four hours after the diagnosis of cerebral embolism, he was subsequently diagnosed with acute myocardial infarction due to concurrent coronary embolism. He underwent successful coronary revascularization with a drug-eluting stent. The possibility of combined coronary embolism as a rare etiology should be kept in mind when a patient with acute embolic stroke presents, especially when there is evidence of acute myocardial infarction.

Recrudescent Digoxin Toxicity Treated with Plasma Exchange: A Case Report and Review of Literature

A 53-year-old woman presented with digitalis toxicity caused by acute overdose that manifested as atrial tachycardia with block, sinus pauses, and competing AV junctional rhythm with atrial fibrillation. Patient admitted to overdosing with digoxin 15-20 h before presentation with intent to commit suicide. Serum digoxin level was 35.6 ng/ml and renal function was normal. Patient was treated with 1,040 mg of digoxin-specific antibody Fab fragment with prompt resolution of arrhythmias and restoration of sinus rhythm. Four hours after digoxin antibody administration, serum digoxin level declined to 0.2 ng/ml. Eighteen hours after treatment with Fab fragment, patient developed premature ventricular complexes, atrial tachycardia with and without atrioventricular block, and non-sustained ventricular tachycardia followed by ventricular fibrillation from which she was successfully resuscitated. Electrocardiogram showed no evidence of acute myocardial infarction, and emergent coronary angiogram did not reveal significant coronary artery disease. Repeat digoxin level was 20.4 ng/ml. A diagnosis of recrudescent digoxin toxicity was made and the patient was treated with one session of plasma exchange with resolution of arrhythmias. Immediately after plasma exchange, digoxin level decreased to 10.4 ng/ml, and after 10 h, the level further decreased to 6.6 ng/ml. The following day, digoxin level had decreased to 2.9 ng/ml. Our experience with this case would suggest that plasma exchange should be considered as a treatment modality for recrudescent digoxin toxicity.

The prognostic value of early repolarization with ST-segment elevation in African Americans

Increased prevalence of classic early repolarization, defined as ST-segment elevation (STE) in the absence of acute myocardial injury, in African Americans is well established. The prognostic value of this pattern in different ethnicities remains controversial. Measure association between early repolarization and cardiovascular mortality in African Americans. The resting electrocardiograms of 45,829 patients were evaluated at the Palo Alto Veterans Affairs Hospital. Subjects with inpatient status or electrocardiographic evidence of acute myocardial infarction were excluded, leaving 29,281 subjects. ST-segment elevation, defined as an elevation of >0.1 mV at the end of the QRS, was electronically flagged and visually adjudicated by 3 observers blinded to outcomes. An association between ethnicity and early repolarization was measured by using multivariate logistic regression. We analyzed associations between early repolarization and cardiovascular mortality by using the Cox proportional hazards regression analysis. Subjects were 13% women and 13.3% African Americans, with an average age of 55 years and followed for an average of 7.6 years, resulting in 1995 cardiovascular deaths. There were 479 subjects with lateral STE and 185 with inferior STE. After adjustment for age, sex, heart rate, and coronary artery disease, African American ethnicity was associated with lateral or inferior STE (odds ratio 3.1; P = .0001). While lateral or inferior STE in non-African Americans was independently associated with cardiovascular death (hazard ratio 1.6; P = .02), it was not associated with cardiovascular death in African Americans (hazard ratio 0.75; P = .50). Although early repolarization is more prevalent in African Americans, it is not predictive of cardiovascular death in this population and may represent a distinct electrophysiologic phenomenon.

In vitro and in vivo characterisation of biodegradable polymer-based drug-eluting stent

The objective of this study was to investigate the structural integrity and early vascular response of a polylactic acid-coated (i.e., biodegradable polymer) coronary drug-eluting stent (DES) (BioMatrix™; Biosensors International, Singapore) to three currently marketed FDA/CE- mark approved non-erodible polymer-coated DES in a porcine model. BioMatrix™, XIENCE V™ (Abbott Vascular, Santa Clara, CA, USA), TAXUS® Liberté™ (Boston Scientific, Natick, MA, USA), and Cypher SELECT™ (Cordis, Johnson & Johnson, Miami, FL, USA) stents were implanted in pig coronaries for seven days. Polymer integrity was assessed by scanning electron microscopy (SEM) following tissue digestion. In vitro expansion of the BioMatrix™ was also performed. SEM analysis of in vivo stents demonstrated polymer defects on the abluminal surface of all DES including polymer cracking (BioMatrix™), bridging (TAXUS Liberté™), round-small defects (Cypher SELECT™), and flaking (XIENCE V™). Histologically, the myocardium revealed no evidence of acute myocardial infarction or microscopic scarring, moreover all intramyocardial vessels were found to be patent with no evidence of emboli. In vitro results demonstrated greater BioMatrix™ polymer cracking and lifting. These results illustrate the presence of polymer defects in all DES (TAXUS Liberté™, Cypher SELECT™, XIENCE V™, BioMatrix™) implanted seven-days in pigs, with absence of myocardial damage in this small number of samples. Polymer coating irregularity was greater in BioMatrix™ stent expanded in vitro as compared to in vivo, suggesting simulated benchtop deployment induces greater damage to the biodegradable polymer coating than in vivo deployment in healthy porcine coronary arteries.

Risk of Coronary Heart Disease Events Over 15 Years Among Older Adults With Depressive Symptoms

To determine whether depression status is associated with an increased risk of coronary heart disease (CHD) events, defined as CHD death or nonfatal acute myocardial infarction (MI). Prospective cohort study. An urban primary care practice. Two thousand seven hundred twenty-eight adults (71.4% women, 65.5% black), age 60 years and older, who were screened for depression between 1991 and 1993. Depressive symptom severity at baseline was assessed by the Center for Epidemiologic Studies Depression Scale (CES-D). Data regarding baseline demographic and clinical variables, as well as laboratory evidence of acute MI, were obtained from an electronic medical record system. All-cause mortality and CHD death were determined from the National Death Index through 2006. A total of 423 (15.5%) participants reported elevated symptoms of depression (CES-D score ≥16). During the 13 to 16 years of follow-up, 1,646 (60.3%) individuals died from any cause, and 727 (26.6%) died from CHD or suffered an acute MI. Cox proportional hazards models revealed that individuals with elevated depressive symptoms were more likely to experience a CHD event, even after adjustment for demographics and comorbid health conditions (relative risk = 1.46, 95% confidence interval: 1.20-1.77). Depression status was also a significant predictor of all-cause mortality in adjusted models. We report the longest prospective study to date to examine depression status as an independent risk factor for CHD among a cohort of older adults including large numbers of women and underrepresented minorities. The present findings underscore the need to consider depression as a common and modifiable risk factor for CHD events among older adults.

Health Care Insurance, Financial Concerns in Accessing Care, and Delays to Hospital Presentation in Acute Myocardial Infarction

This was a prospective observational study that examined the associations between health insurance status and financial concerns related to accessing health care with delayed presentation to the hospital in patients with acute myocardial infarction. Participants were consecutively enrolled from the TRIUMPH study patient population from 24 urban hospitals within the United States. Patients older than 18 years who had elevated cardiac enzymes within 24h of admission and other supporting evidence of acute myocardial infarction were considered for inclusion.

Severe chest pain during stress dobutamine echocardiogram in patient with patent epicardial coronary arteries

Dobutamine induced ST-segment elevation in the absence of obstructive coronary artery disease is a rare condition. We report a case of a 37-year-old man, a smoker, who developed severe chest pain associated with transient ST-segment elevation in anterolateral leads and significant segmental wall motion abnormalities during dobutamine stress echocardiography that was immediately relieved by sublingual nitrates without evidence of acute myocardial infarction. Coronary angiogram showed patent epicardial coronary arteries.

Can We Prevent Sudden Cardiac Death in Athletes? In Search of Evidence-Based, Cost-Effective Screening

Purpose of a New Project: To develop a novel screening strategy to prospectively establish predictors and to prevent sudden cardiac death (SCD) in athletes. Most cases of SCD are related to preexisting high-risk cardiovascular conditions (hr-CVC) - predominantly coronary artery anomalies (CAAs) and cardiomyopathies that are readily diagnosed with advanced imaging. Currently, there is considerable debate about the need and extent for cardiovascular preparticipation screening of physical training and athletes. At Texas Heart Institute, we recently founded a Center for Coronary Artery Anomalies (CCAA) with a purpose to investigate hr-CVCs and prevent SCD. METHODS: We are currently conducting two coordinated projects: 1) The MRI study - involving cardiac magnetic resonance imaging (cMRI) screening for hr-CVC in 10,000 middle-school children to identify carriers of hr-CVC. This is the first prospective MRI imaging screening study ever performed in a general population, aimed at establishing the prevalence of hr-CVC, while including a large and representative population, from various subgroups. Such program will use a simple clinical information form for cardiovascular symptoms, a modified screening protocol cMRI (no contrast/intravenous access, 5-7 min acquisition time) and a resting electrocardiogram. The subjects with hr-CVC will be referred to specialized centers, for final evaluation and disposition, according to agreed protocols, at 3 local institutions. 2) The Necropsy study - continuous series of 6,000 autopsies carried out over a 2-years period at the Harris County Forensic Center, referral center for the 4 million inhabitants in the Houston, Texas area. This project will be used to collect information about the incidence of the same hr-CVC and all different causes and modes of death in such population. This study will combine clinical data at the time of death (ECG, type of physical activity, previous participation in sports activities) and specific anatomic markers of severity of the hr-CVC. Initial rhythm at time of SCD (ventricular fibrillation, asystole or pulseless electrical activity) will be correlated with anatomical findings and evidence of acute myocardial infarction or previous myocardial scarring. Mortality at 5 years follow-up, in the screened general population and hr-CVC students, will be evaluated and compared to historical mortality databases. CONCLUSIONS: The ultimate purposes of the 2 studies are to establish: 1) prevalence of hr-CVC in different subgroups; 2) cost/efficiency of such screening, in the different subgroups; and 3) effect of instituting such pre-certification screening and work-up for prevention of SCD.

Novel application of black-blood echo-planar imaging to the assessment of myocardial infarction

The purpose of this study was to clarify the characteristics of black-blood echo-planar imaging (BB-EPI) in the assessment of infarct-related myocardial edema (IRME), compared with T2-weighted imaging (T2WI). Thirteen acute myocardial infarction (MI) patients after reperfusion and 11 old MI patients underwent BB-EPI and T2WI, excluding those with posterior MI. In acute MI patients, signal intensity ratio (SI ratio) of edema to normal myocardium was measured. Black-blood echo-planar imaging revealed hyperintensity in the same region identified as IRME on T2WI in all acute MI patients, and SI ratio was significantly higher in BB-EPI (2.66 +/- 1.58) than in T2WI (1.44 +/- 0.22) (P < 0.05). However, BB-EPI showed hyperintensity in posterior wall, where there is no clinical evidence of acute MI, in 2 out of 13 acute MI patients. Both T2WI and BB-EPI detected no IRME in known old infarct area of all old MI patients, but BB-EPI showed hyperintensity in the posterior wall of 4 out of 11 old MI patients. Black-blood echo-planar imaging can depict IRME with sufficient suppression of background and blood flow signals, and with excellent edema-to-normal myocardium contrast resolution. However, BB-EPI sometimes shows an inconsistent signal area with T2WI specifically in posterior wall. The wide practical use of BB-EPI requires the solution to this serious problem.

False positive or true positive troponin in patients presenting with chest pain but 'normal' coronary arteries: lessons from cardiac MRI

Cardiac magnetic resonance imaging (MRI), particularly when enhanced with commonly available gadolinium-based contrast agents, is a powerful clinical tool for characterizing myocardial abnormalities. One of the best-known applications of this relatively new technology has been the detection of myocardial infarction. It is also possible to image myocardial scarring or fibrosis in other disease states such as myocarditis and infiltrative cardiomyopathies. Assomull et al. 1 from the Royal Brompton Hospital document the adjunctive diagnostic value of late gadolinium enhancement imaging in patients who present with chest pain, elevated troponin but unexpectedly ‘normal’ appearing coronary angiograms. The introduction of troponin assays revolutionized the diagnosis of acute myocardial infarction. This was largely based on the high sensitivity and specificity for acute myocardial injury. Elevated troponin was associated with adverse prognosis before we came to a consensus that it must be a marker of cardiac necrosis. On the basis of this work and a much wider range of literature than can be quoted in this brief article, the very definition of myocardial infarction was revised in 2000.2 The revised definition of myocardial infarction required either pathological evidence of acute myocardial infarction or a new set of clinical criteria based largely on serum markers of myocardial necrosis. Acute myocardial infarction can be diagnosed by a typical rise and gradual fall (troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following: (i) ischaemic symptoms, (ii) development of pathological q-waves on ECG, (iii) ECG changes indicative of ischaemia (ST-elevation or ST-depression), or (iv) percutaneous coronary intervention.2 Although overall a substantial advance in our understanding … Corresponding author. Tel: +1 301 496 3658; fax: +1 301 402 2389. E-mail address : araia{at}nih.gov

Sarcoidal Pericardial Effusion Masquerading As Acute Myocardial Infarction

Sarcoidosis is a multisystemic granulomatous disease, with varying modes of presentation. Pericardial sarcoidosis is rare and cardiac tamponade secondary topericardial sarcoidosis is very uncommon. We present a case of a young man who presented with signs and symptoms suggestive of acute myocardial infarction who was thrombolysed but subsequently died. The cause of his death was made apparent on the post mortem examination which revealed a massive pericardial effusion and a necrotic mature mediastinal teratoma. INTRODUCTION We discuss one case of a young man with symptoms and electrocardiographic evidence of acute myocardial infarction who was thrombolysed but later died. Postmortem findings were suggestive of widespread sarcoidosis with a massive pericardial effusion and a necrotic mature mediastinal teratoma. CASE REPORT A 43-year-old obese man with type 2 diabetes mellitus was brought with a 2 hour history of central crushing chest pain and shortness of breath. On initial assessment his blood pressure was 150/90 mm Hg, equal in both arms with a pulse of 90 per minute, sinus rhythm and respiratory rate of 24/min. Cardiovascular examination was normal. An ECG performed in the ambulance showed 1-2 mm ST elevation in the inferior leads -II, III, aVF. (Figure1). He was transferred to the coronary care unit where he was thrombolysed with reteplase. Subsequent ECG's performed in the CCU showed near normalization of the ST segments. AP view of the chest radiograph showed a prominent right hilum and patchy consolidation of the left upper and lower lobes. After remaining stable and pain free for 4-5 hours, his condition deteriorated and he became hypotensive, tachypnoeic and acidotic. An ECG at this stage showed a sinus tachycardia of 120 per minute. He developed extensive haemorrhagic mottling of his back and rapidly succumbed to the cardiogenic shock despite attempt at resuscitation. Post mortem study of the gross specimen of the heart showed a 650 ml, blood stained pericardial effusion. Extensive loose pericardial adhesions were also seen. There wasminimal (20%) coronary atherosclerosis and no evidence of scarring or acute myocardial infarction. The ascending and descending aorta were unremarkable without evidence of dissection. In the upper mediastinum, a 7 cm cystic, necrotic tumour containing blood adherent to the left lung and superior pericardium was seen. Extensive hilar lymphadenopathy was also seen. On histopathological examination, non caseating granulomas and inflammation of the lungs, mediastinal lymph nodes, myocardium, epicardium (Figure 2a) and liver were seen suggestive of extensive multisystem sarcoidosis. The mediastinal mass showed an extensively necrotic and inflamed teratoma with cartilage.(Figure 2b). Figure 1 Electrocardiogram on admission showing ST segment elevation in inferior leads, II, III, aVF Sarcoidal Pericardial Effusion Masquerading As Acute Myocardial Infarction 2 of 4 Figure 2 Histopathological section showing epicardium and outer layer of myocardium. There is a well defined granuloma consistent with sarcoidosis in the epicardial fat. Section of the mediastinal tumour showing a necrotic mass. Preserved areas of the tumour show mature elements including cartilage. These features are those of mature mediastinal teratoma. (Haematoxylin and eosin x 40).