Circulating immune complexes containing IgG, IgA and IgM in patients with myocardial infarction: detection with C1qSP and anti C3SP

Immunological reactions have been recognized in cardiac disease and immune complexes (ICs) have been suggested to be of pathogenetic significance in the occurrence of post-myocardial infarction syndromes. ICs of IgA, IgG, IgM class have been detected in myocardial infarction utilizing a C1qSP and an anti C3 assay. A poor concordance was found between the two methods. Early pericarditis was found to be associated with the presence of ICs, suggesting that ICs may play a role in developing pericarditis or that they may be considered a marker of pericarditis by an immunological mechanism.     

Acute myopericarditis with focal ECG findings mimicking acute myocardial infarction

Background: Although history, physical examination, laboratory data points, and electrocardiogram (ECG) are helpful, distinguishing among pericarditis, myopericarditis, and myocardial infarction can be difficult. Objectives: This case, which presents as pericarditis with concomitant myocarditis (myopericarditis), illustrates the four evolving ECG stages of pericarditis and highlights some of the potential difficulties in differentiating between myopericarditis and acute myocardial infarction. Case Report: We present the case of a previously healthy 15-year-old boy who presented to the Emergency Department (ED) from his family physician's office for chest pain and presumed pericarditis. The patient's initial ECG showed infero-lateral ST-segment elevation, and his troponin T was elevated at 1.54 ng/mL (ref. < 0.03). Several hours after presentation to the ED, the patient experienced “10/10” chest pain, and a repeat ECG showed ST elevation increased from the prior ECG. After an emergent echocardiogram revealed no regional wall abnormalities, he was transferred to a pediatric cardiac intensive care unit, where a heart catheterization revealed no coronary irregularities. He was discharged 4 days later with the diagnosis of myopericarditis. Conclusion: This case report illustrates some of the difficulties in differentiating among myopericarditis and myocardial infarction in a 15-year-old patient presenting with chest pain.     

Pericarditis: inflammation or infarction?

Pericarditis occurs when there is inflammation of the pericardium, a 2-layer sac that surrounds the myocardium. These layers are separated by 15 to 20 mL of thin serous fluid. The accumulation of serous fluid along with the presence of inflammatory cells and fibrin can compromise cardiac function. The cause of pericarditis can be related to many disorders and often mimics signs of myocardial ischemia or acute myocardial infarction (AMI). Complications such as cardiac tamponade can occur with a large effusion and can be life threatening. It is essential to differentiate pericarditis from AMI. Preservation of heart muscle in AMI is essential as is proper treatment and prevention of complications such as cardiac tamponade, which can occur as a result of pericarditis. This article discusses the common causes, clinical manifestations, diagnostic procedures, and treatment associated with pericarditis.     

Left ventricular pseudoaneurysm after myocardial infarction

As is evident from our case and others, post-myocardial infarction pericarditis with the formation of pericardial adhesions creates a suitable milieu for left ventricular pseudoaneurysm. Although the conditions for pseudoaneurysm formation are rarely met, the clinician should be aware of this diagnosis, even long after myocardial infarction, because of its associated mortality and also because it is surgically curable.     

Pleurisy

Pleuritic chest pain is a common presenting symptom and has many causes, which range from life-threatening to benign, self-limited conditions. Pulmonary embolism is the most common potentially life-threatening cause, found in 5 to 20 percent of patients who present to the emergency department with pleuritic pain. Other clinically significant conditions that may cause pleuritic pain include pericarditis, pneumonia, myocardial infarction, and pneumothorax. Patients should be evaluated appropriately for these conditions before an alternative diagnosis is made. History, physical examination, and chest radiography are recommended for all patients with pleuritic chest pain. Electrocardiography is helpful, especially if there is clinical suspicion of myocardial infarction, pulmonary embolism, or pericarditis. When these other significant causes of pleuritic pain have been excluded, the diagnosis of pleurisy can be made. There are numerous causes of pleurisy, with viral pleurisy among the most common. Other etiologies may be evaluated through additional diagnostic testing in selected patients. Treatment of pleurisy typically consists of pain management with nonsteroidal anti-inflammatory drugs, as well as specific treatments targeted at the underlying cause.     

Spontaneous pneumomediastinum mimicking acute pericarditis

ST elevations on electrocardiogram (ECG) have a broad differential diagnosis that can vary from benign to more ominous pathologies. These include early repolarization, coronary vasospasm, acute pericarditis, ST‐elevation myocardial infarction, ventricular aneurysms, and dissecting aneurysm of the aorta reaching the pericardium. ST‐segment changes may also provide a clue to the presence of spontaneous pneumomediastinum (SPM). These ECG changes are seldom reported in literature. We describe two SPM cases with concomitant pneumopericardium that closely mimicked acute pericarditis with a deceptive clinical spectrum.     

Exacerbation of associated bronchial asthma in patients with myocardial infarct

During follow-up of 27 patients with previous long-term history of bronchial asthma it has been established that in 7 of them there was aggravation of broncho-pulmonary illness in the late terms of setting in of myocardial infarction (on the 3rd-6th week, or in 30 days, on the average). Typical features in these patients were blood hypereosinophilia reaching 16-24 per cent and parallel development in some of them of clinical manifestations of the postinfarction syndrome such as pericarditis, pleurisy and transitory lung infiltration. It is believed that this spontaneous aggravation of bronchial asthma in late terms of myocardial infarction can be regarded as one of the manifestations of the postinfarction syndrome typical for this clinical condition. Long-action glucocorticoids (metipred) should be prescribed prior to the development of the clinical symptoms of bronchial asthma to this category of patients taking into consideration only the dynamics of blood eosinophil count.     

Complications associated with myocardial infarction

The incidence of complications after acute myocardial infarction (MI) has been estimated to range from 14-95 per cent, with an overall one-month mortality of 30 per cent. Early treatment, as advocated by the National Service Framework for Heart Disease, has brought about some reduction in associated morbidity and mortality after MI. This article reviews the common complications associated with an acute MI, such as cardiogenic shock, pericarditis and heart failure. Nurses who are knowledgeable about potential complications should be able to detect early signs and symptoms, initiate emergency treatment, and prevent profound haemodynamic compromise occurring.     

A minimally invasive method for induction of myocardial infarction in an animal model using tungsten spirals

Most animal models use surgical thoracotomy with ligation of a coronary artery to induce myocardial infarction. Incision of the chest wall and myocardium affect remodeling after myocardial infarction. The aim of our study was to evaluate a new minimally invasive technique for inducing acute myocardial infarction in pigs. To this end, coronary angiography using a 6-F cardiac catheter was performed in 20 pigs. The cardiac catheter was advanced into the left circumflex artery (LCX) under electrocardiographic monitoring and small tungsten spirals were deployed in the vessel. LCX occlusion was verified by coronary angiography. Two days later, magnetic resonance imaging (MRI) was performed to estimate the extent of infarction. Thereafter, all animals were euthanized and the hearts stained with 2,3,5-triphenyltetrazolium chloride for histologic measurement of infarct size. Tungsten spirals were successfully placed in the LCX in all 20 pigs. About 13 of the 20 animals survived until the end of the experiment. The mean infarct size in the area supplied by the LCX was 4.4 ± 2.3 cm³ at MRI and 4.3 ± 2.2 cm³ at histology (r = 0.99, P < 0.001). No other myocardial regions showed infarction in any of the 13 pigs. Five of nine pigs requiring defibrillation due to ventricular fibrillation died because defibrillation was unsuccessful. One animal each died from pericarditis and pneumonia. Our results show that the minimally invasive method presented here enables reliable induction of myocardial infarction in a fairly straightforward manner. The 25% mortality rate associated with induction of myocardial infarction in our study is comparable to that reported by other investigators.     

Myocardial perfusion scintigraphy (SPECT) during adenosine stress can be performed safely early on after thrombolytic therapy in acute myocardial infarction

The objective of this study was to evaluate the safety of myocardial perfusion scintigraphy with Tc-99 m sestamibi during adenosine stress in patients with recent thrombolytically treated myocardial infarction. Eighty-four patients with thrombolytically treated myocardial infarction, 59 males and 25 females, aged 62·9 ± 8·4, were eligible for myocardial perfusion scintigraphy during adenosine provocation. Exclusion criteria for adenosine stress were hypotension, unstable angina pectoris, cardiac failure, pericarditis and atrioventricular block (AV block) II–III. Adenosine-stress and resting myocardial perfusion scintigraphy was performed 2–5 days after thrombolysis. Scintigraphy at rest was done 24 h after the stress study. Sixty patients (71%) experienced some kind of side-effects during adenosine infusion. The most frequent side-effects were dyspnoea in 43/84 patients (51%) and unspecific chest discomfort in 26/84 patients (31%). During infusion, ST depressions or elevations on ECG were seen in 9 patients (11%), 5 of whom experienced atypical chest discomfort. Five patients (6%) described typical angina but none of them showed electrographic signs of myocardial ischaemia during infusion. Six patients (7%) developed transient AV block I–II. Reversible scintigraphic perfusion defects were seen in 67 patients (79%). No serious complications, such as death, reinfarction or severe arrhythmias, occurred during adenosine infusion or during a 3-day clinical follow-up period. In conclusion, MIBI-SPECT during adenosine stress is a safe diagnostic method that can be performed in most patients early on after thrombolytically treated acute myocardial infarction. Side-effects are common but benign, and not different from those seen in patients with chronic coronary artery disease.     

Early pericarditis after acute myocardial infarction: a clinical echocardiographic study

Clinical and echocardiographic data were evaluated in 46 patients after acute myocardial infarction (AMI). M-mode echocardiogram was performed 24 and 72 h and 5 days after AMI. Early acute pericarditis (EAP) was clinically recognized in 19 (41%) patients. Pericardial effusion (PE) was detected in 29 (63%) patients. In 23 (50%) patients both anterior and posterior PE was observed, while in six (13%) patients PE was only posterior. An echocardiographic pattern consistent with localized fibrinous pericarditis was detected in 11 (24%) patients. Eighteen (95%) of 19 patients with EAP had PE, and only 11 (40%) of the patients without EAP had PE (p less than .001). We conclude that PE is observed frequently after AMI and that the echocardiographic study can help in the diagnosis of EAP after AMI.     

ECG manifestations: noncoronary heart disease

The electrocardiogram reflects changes to the heart beyond those seen in acute myocardial infarction and acute coronary syndromes.Diseases of the pericardium and heart muscle such as pericarditis,myocarditis, and pericardial effusion have characteristic manifestations. Hypertensive heart disease is associated with a variety of changes on the electrocardiogram, as is valvular heart disease. Cardiac rhythm disturbances have been associated with the Brugada syndrome and the long QT syndrome, both of which have telltale findings on the electrocardiogram. The manifestations of dextrocardia, although rare, should be familiar to those who interpret electro-cardiograms. Transplanted hearts also feature classic changes, both in health and in stages of rejection. The various electrocardiographic manifestations of these noncoronary heart diseases are reviewed here.     

Persistent ST segment elevation: a new ECG finding in hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy is a primary disease of myocardium resulting in myocardial hypertrophy without any inciting pressure or volume overload. The typical triad of symptoms includes exertional angina, syncope, and shortness of breath. Sudden cardiac death, the most dreadful complication of this disorder, can be the first manifestation of the disease and is more common in young patients. Elderly patients, on the other hand, may have a relatively benign course with normal or near-normal life span. The electrocardiogram (ECG) and echocardiography are the two most useful measures to diagnose hypertrophic cardiomyopathy. The electrocardiographic features of hypertrophic cardiomyopathy are numerous, including ST segment elevation that may simulate other ST segment elevation syndromes, including acute myocardial infarction, variant angina pectoria, acute pericarditis, bundle branch blocks, ventricular paced rhythm, dyskinetic ventricular segment, ventricular aneurysm, left ventricular hypertrophy, Wolff-Parkinson-White syndrome, and early repolarization syndrome. This report describes a case of an asymptomatic patient who presented with ST segment elevation of acute injury type and, therefore, was admitted to rule out silent myocardial infarction. Myocardial infarction was ruled out by cardiac enzyme levels, but ST segment elevation remained persistent in all of the subsequent ECGs. Echocardiography was performed, which clearly showed hypertrophic cardiomyopathy with left ventricular outflow tract obstruction and a high intracavity pressure gradient. Subsequently, retrieval of old ECGs showed a similar type of ST segment elevation in the patient's previous ECGs.     

Acute post-MI pericarditis.

The diagnosis of acute pericarditis may be difficult to establish in patients with recent transmural infarcts as the symptomatology frequently mimics the clinical presentation associated with recurrent ischemia. A careful assessment of the postmyocardial infarction patient may reveal the clinical and electrocardiographic features associated with developing pericarditis. Prompt and accurate recognition of this complication is critical in order to institute definitive therapy, minimize the risk of hemodynamic compromise, and provide psychological support.     

Experimental needle biopsy of the myocardium of dogs with particular reference to histologic study by electron microscopy

Our experience with needle biopsy of the heart in dogs indicates that myocardial tissue can be sampled one or more times in each animal with comparative safety. Tamponade, pericarditis, serious arrhythmias, or myocardial infarction due to the interruption of coronary vessels was not observed. Excellent specimens were obtained for critical study by light and electron microscopy. Casten and Marsh (1) have used biochemical techniques to study myocardial tissue obtained in similar fashion. Histochemical methods would also be applicable. Although limited to animal studies at present, the technique may conceivably be adapted to the study of human disease. Myocardial puncture has been carried out (20–22) in patients for the recording of intracardiac pressures and for other diagnostic purposes without apparent harm. Our study of the myocardium of dogs by electron microscopy generally confirms the observations of other workers, except that presence of significant numbers of red blood cells in the extravascular spaces of the heart had not been previously described (and is possibly an artifact). Nevertheless, it is notable that the tissue cells, cellular membranes, and intracellular structures appeared to be intact and undistorted in the tissue specimens which were obtained, fixed, and examined by these methods.     

Evaluation of Spodick's Sign and Other Electrocardiographic Findings as Indicators of STEMI and Pericarditis

BackgroundPatients with ST elevation on electrocardiogram (ECG) could have ST elevation myocardial infarction (STEMI) or pericarditis. Spodick's sign, a downsloping of the ECG baseline (the T-P segment), has been described, but not validated, as a sign of pericarditis.ObjectiveThis study estimates the frequency of Spodick's sign and other findings in patients diagnosed with STEMI and those with pericarditis.MethodsIn this retrospective review, we selected charts that met prospective definitions of STEMI (cases) and pericarditis (controls). We excluded patients whose ECGs lacked ST elevation. An authority on electrocardiography reviewed all ECGs, noting the presence or absence of Spodick's sign, ST depression (in leads besides V₁ and aVR), PR depression, greater ST elevation in lead III than in lead II (III > II), abrupt take-off of ST segment (the RT checkmark sign), and upward or horizontal ST convexity. We quantified strength of association using odds ratio (OR) with 95% confidence interval (CI).ResultsOne hundred and sixty-five patients met criteria for STEMI and 42 met those for pericarditis. Spodick's sign occurred in 5% of patients with STEMI (95% CI 3–10%) and 29% of patients with pericarditis (95% CI 16–45%). All other findings statistically distinguished STEMI from pericarditis, but ST depression (OR 31), III > II (OR 21), and absence of PR depression (OR 12) had the greatest OR values.ConclusionsSpodick's sign is statistically associated with pericarditis, but it is seen in 5% of patients with STEMI. Among other findings, ST depression, III > II, and absence of PR depression were the most discriminating.     

Acute rheumatic fever mimicking an acute coronary syndrome

An elevated troponin measurement does not always reflect myocardial ischaemia secondary to obstructive coronary artery disease. Troponin levels can also be elevated in other disease states including pulmonary emboli, myo‐pericarditis, acute rheumatic fever, and in the critically ill. Thus, patients presenting with chest pain and electrocardiological and biochemical evidence of myocardial necrosis are not always suffering from an acute coronary syndrome.     

Case of cholesterol xanthomatous pericarditis with an unusual pathogenesis

Exudative cholesterol xanthomatous pericarditis was found at autopsy of a patient aged 57 who had suffered from the edematous form of thrombophlebitis of the deep crural veins complicated by thromboses of the iliac veins, vena cava inferior, recurring thromboembolism of the pulmonary artery, and pulmonary infarctions. The clinical picture of the main disease was interpreted as cardiac failure; numerous thromboembolic episodes were regarded as myocardial infarctions. The presence of cholesterol crystals in the exudate indicated a prolonged course of pericarditis. Laboratory findings confirmed the aseptic allergic genesis of pericarditis.     

Does atrioventricular ring motion always distinguish constriction from restriction? A Doppler myocardial imaging study.

Constrictive pericarditis and restrictive cardiomyopathy can be difficult to differentiate on clinical examination. Cardiac ultrasonography is increasingly being used as the noninvasive method of choice for confirming the specific morphologic and hemodynamic abnormalities associated with either condition. Interrogation of atrioventricular valve plane motion by Doppler myocardial imaging (DMI) has been suggested as a valuable new approach that can help differentiate one from the other. We report the color DMI, pulsed DMI, and strain rate findings in 2 cases of constrictive pericarditis in which consideration of the annular motion pattern alone would not have allowed such differentiation.     

Traumatic coronary artery fistula

Objective: To present a case of traumatic coronary artery fistula caused by blunt injury. Clinical features: A previously healthy 20-year-old motor cyclist was involved in a motor vehicle accident. He suffered acute myocardial infarction secondary to a traumatic coronary artery fistula (CAF). His other injuries included a fractured left clavicle, bilateral small pulmonary contusions and pneumothoraces, pneum-omediastinum and a small subcapsular haematoma of the liver. Intervention and outcome: He was managed conservatively. Recovery was complicated only by pericarditis and he was well one year after the injury. Conclusion: Traumatic CAF may result from blunt chest trauma and may be diagnosed from history, physical examination, and ECG changes. An echocardiogram should be performed in patients with positive ECG findings or the development of a new continuous murmur. Coronary angiography remains the gold standard but is rarely indicated in the acute situation. Regular follow up is required as traumatic CAF has a high incidence of late complications. With symptomatic CAF, the recommended treatment of surgical repair has a high success rate with few complications.