Pericarditis after Acute Myocardial Infarction

Fifty-two (6·8%) of 779 patients admitted to a coronary monitoring unit with acute myocardial infarction developed a pericardial friction rub. A diagnosis of postmyocardial infarction syndrome was made in three of these.The course of the 52 patients with pericarditis was compared with that of a consecutive series of 100 patients without pericarditis. As a group those with pericarditis manifested a longer period of pyrexia, a greater rise in serum enzymes, and a higher incidence of major arrhythmias and of radiological pulmonary oedema. The Peel prognostic index, however, did not differ significantly in the two groups. The hospital mortality of the pericarditis group was not significantly different from that of the 727 non-pericarditis patients. No specially adverse features were found in a follow-up of the pericarditis group.Though the presence of a pericardial rub in the first few days after a myocardial infarction may be a sign of extensive myocardial damage and is associated with a relatively high incidence of ventricular fibrillation, it does not appear to influence the hospital mortality of patients treated in a monitoring unit.     

Scintigraphie myocardique et séquelles de myocardite : présentation d’un cas clinique

Acute and subacute myocarditis are well-defined pathological entities but it is often difficult to identify them because their clinical expression is variable and the diagnosis is histological showing myocardial inflammation associated with degeneration and/or necrosis. Often symptoms are similar to those of acute pericarditis with “chest-crushing” pain that mimics myocardial infarction and prompts practitioners to request angiography, especially when there are cardiovascular risk factors. We report the case of a 61-year-old patient with neither cardiac history nor cardiovascular risk factor who consulted for a long and self-limited atypical chest pain with normal clinical examination and electrocardiogram. Myocardial perfusion scintigraphy showed a non-reversible photopenic area suspected of being a nontransmural necrosis or an artifact. The discovery of inferolateral hypokinesis of left ventricle on echocardiography led to perform a coronary angiography which was finally normal. Cardiac MRI allowed to diagnose scars of a previous episode of myocarditis.     

Bacterial pericarditis and tamponade due to nonencapsulated Haemophilus influenzae complicating a case of adult community-acquired pneumonia

We report a case of bacterial pericarditis in an immunologically competent adult female caused by nonencapsulated Haemophilus influenzae (H influenzae) that was complicated by the acute development of life-threatening pericardial tamponade. H influenzae is a gram-negative coccobacillus, a pathogen most frequently associated with childhood exanthema (otitis media, meningitis) and, less frequently, adult pneumonia. Encapsulated, type b, or typable H influenzae is the strain implicated in childhood infections. On the other hand, nonencapsulated or nontypable H influenzae is the specific strain most often associated with exacerbation of chronic obstructive airway disease. Bacterial pericarditis caused by either subtype of H influenzae is exceedingly rare. We have located only 15 previously reported cases of H influenzae pericarditis occurring in adults in the world medical literature, the majority of which date back to the pre-antibiotic era. In 12 of these 15 cases (the only cases in which typing could be accomplished), the encapsulated strain of H influenzae was cultured from the pericardial fluid. Thus, to the best of our knowledge, we are reporting here the first case of bacterial pericarditis caused by nonencapsulated H influenzae in an immunologically competent adult.     

Inflammation and pericarditis: Are neutrophils actors behind the scenes?

The morbidity of acute pericarditis is increasing over time impacting on patient quality of life. Recent clinical trials focused especially on clinical aspects, with a modest interest in pathophysiological mechanisms. This narrative review, based on papers in English language obtained via PubMed up to April 2018, aims at focusing on the role of the innate immunity in pericarditis and discussing future potential therapeutic strategies impacting on disease pathophysiology. In developed countries, most cases of pericarditis are referred to as idiopathic, although etiological causes have been described, with autoreactive/lymphocytic, malignant, and infectious ones as the most frequent causes. Apart the known impairment of the adaptive immunity, recently a large body evidence indicated the central role of the innate immune system in the pathogenesis of recurrent pericarditis, starting from similarities with autoinflammatory diseases. Accordingly, the “inflammasome” has been shown to behave as an important player in pericarditis development. Similarly, the beneficial effect of colchicine in recurrent pericarditis confirms that neutrophils are important effectors as colchicine, which can block neutrophil chemotaxis, interferes with neutrophil adhesion and recruitment to injured tissues and abrogate superoxide production. Anyway, the role of the adaptive immune system in pericarditis cannot be reduced to a black or white issue as mechanisms often overlap. Therefore, we believe that more efficient therapeutic strategies have to be investigated by targeting neutrophil-derived mediators (such as metalloproteinases) and disentangling the strict interplay between neutrophils and platelets. In this view, some progress has been done by using the recombinant human interleukin-1 receptor antagonist anakinra.     

Technetium pyrophosphate scanning in the detection of acute myocardial infarction: clinical experience.

Technetium-99m-stannous pyrophosphate (99mTc-PYP) accumulates in acutely infarcted myocardium and can be detected by scintiscanning. The clinical value of 99mTc-PYP scintiscanning was studied in 83 patients 6 hours to 21 days after the onset of acute chest pain. In 12 patients with normal electrocardiograms and serum enzyme values no uptake of 99mTc-PYP was detected on the scintigrams. Of 44 patients with electrocardiographic or enzyme evidence, or both, of acute myocardial infarction the scintigrams were positive in 31, "questionable" in 2 and negative in 11; no positive scan was obtained within 12 hours of the onset of pain, and the scans generally remained positive for up to 5 days. In 24 patients with evidence of prolonged myocardial ischemia the scans were positive in 2, questionable in 4 and negative in 18. The scans were negative in each of three patients with acute or constrictive pericarditis. Localization by electrocardiography and scintiscanning correlated nearly perfectly for transmural infarcts but subendocardial infarcts could not always be localized precisely by scintiscanning. The infarct area (total area of 99mTc-PYP uptake) correlated well with the peak serum value of creatine phosphokinase.     

Difficulties in diagnosing chronic constrictive pericarditis

This presentation calls attention to the many problems involved in the positive, aetiological and differential diagnosis of chronic constrictive pericarditis. We mention the difficulties in aetiological diagnosis in the absence of an episode of acute pericarditis in the past medical history and the clinical findings similar to vascular decompensated cirrhosis or idiopathic restrictive cardiomyopathy. ECG and two-dimensional echocardiography do not have an important role in diagnosis, and in the absence of computed tomography and magnetic resonance imaging, chest radiography, especially a lateral view, could establish the diagnosis. A delay in diagnosis creates difficulties in the surgical treatment, but this treatment improves the patient''s condition in the long term more than the short term.     

Myocardial abscess complicating healed myocardial infarction.

An isolated myocardial abscess due to Bacteroides fragilis developed in the scar of a myocardial infarction. Fever, chills and signs of pericarditis were the main clinical features. Mild enteritis 1 week prior to the onset of symptoms related to the abscess was the most likely cause of the bacteremia. The diagnosis was established at thoracotomy, performed because of cardiac tamponade. Thirteen other cases of isolated bacterial myocardial abscess accompanying myocardial infarction have been reported, but all the infarctions were recent. Surgical resection for a suspected myocardial abscess should be considered in view of the high mortality, largely from cardiac rupture.     

Influence of involvement of anterior leaflet versus posterior leaflet on residual regurgitation as assessed by transesophageal echocardiography in patients undergoing valve repair for mitral regurgitation due to mitral valve prolapse

Cardiac tamponade is the phenomenon of hemodynamic compromise caused by a pericardial effusion. Following a myocardial infarction, the most common causes of pericardial fluid include early pericarditis, Dressler's syndrome, and hemopericardium secondary to a free wall rupture. On transthoracic echocardiography, pericardial fluid appears as an echo-free space in between the visceral and parietal layers of the pericardium. Pericardial fat has a similar appearance on echocardiography and it may be difficult to discern the two entities. We present a case of a post-MI patient demonstrating pseudo tamponade physiology in the setting of excessive pericardial fat.     

Pericarditis in the course of acute leukemia

Among 140 patients with acute leukemia (AL) diagnosed according to FAB criteria, pericarditis was diagnosed clinically in 5 of them. They were 2 women and 3 men with different types of AL (L2-in one, M2-in one, M3-in one and M4-in two persons). It occurred in one patient at the onset of the disease and was associated with hyperuricemia, in another one--in complete remission, in the third--during partial remission, and in remaining two patients--during induction therapy. In all patients pericarditis was manifested by fever up to 38-40 degrees C, tachycardia and pericardial friction, in 3-heart silhouettes were enlarged. The ECG revealed mainly depression of ST segments. In 1 case only ECG pattern was typical of pericarditis. Clinically the symptoms of right ventricle failure predominated in 3 and of septic shock--in 2 patients. The etiologic factors were: Pseudomonas aeruginosa 2 X, Enterobacter cloacae 1 X, tuberculosis infection 1 X and hyperuricemia and Enterobacter sepsis 1 X. Pericarditis was favourably influenced by treatment with antibiotics, cardiaca and diuretics in 4 patients. One patient died of a sepsis. In no case the patient's death was attributable to pericarditis. The results of postmortem examinations in 79 cases of AL has revealed three additional cases of pericarditis due to tuberculosis infection, Staphylococcus aureus sepsis and aspergillosis.     

Subclinical myocardial infarction presenting as free wall rupture

A 50-year-old man presented twice within a period of two weeks with symptoms and electrocardio-graphic (ECG) findings suggesting postinfarct angina. The ECG showed sinus tachycardia with Q waves, ST-segment elevation and terminally negative T waves in lead II, III and aVF, suggesting remote inferior myocardial infarction. During the first hospitalisation the ECG also showed signs of pericarditis. Troponin I levels were only slightly elevated. Echocardiographic evaluation at the second presentation demonstrated a posterolateral false aneurysm following ischaemic left ventricular rupture (figure 1).     

Initial Heparin Therapy in Acute Myocardial Infarction

The administration of heparin during the first 48 hours following acute myocardial infarction is widely practised. Heparin treatment is also recommended for acute coronary insufficiency on the grounds that it may prevent development of an impending myocardial infarction. These measures had been accepted without support of a controlled clinical trial. By random selection, 101 patients hospitalized with a provisional diagnosis of acute myocardial infarction received heparin (100 mg. intravenously every eight hours for 48 hours) and 105 patients were assigned to a control group. Both groups of patients received bishydroxycoumarin (Dicumarol). The mortality in the heparin series was 30% and in the control group, 28%. A significantly large number of the heparin-treated patients developed clinical and laboratory proof of recent myocardial infarction. It is concluded that early intermittent intravenous heparin treatment does not lower the mortality in patients with acute myocardial infarction nor does it prevent impending myocardial infarction in patients with acute coronary insufficiency.     

ELECTROCARDIOGRAMS AND VECTORELECTROCARDIOGRAMS—An Appraisal of Their Value in Subendocardial and in Transmural Myocardial Infarction

By vector methods quantitative differences can be shown to be present between subendocardial and transmural myocardial infarction. In acute transmural infarction the vector shift occurs later, the degree of shift is greater, the return to normal is later in time and an abnormal vector shift remains more frequently than in subendocardial infarction. In acute anteroseptal transmural infarction the degree of vector shift was closely correlated with the severity of the acute illness.     

Electrocardiograms and vectorelectrocardiograms; an appraisal of their value in subendocardial and in transmural myocardial infarction

By vector methods quantitative differences can be shown to be present between subendocardial and transmural myocardial infarction. In acute transmural infarction the vector shift occurs later, the degree of shift is greater, the return to normal is later in time and an abnormal vector shift remains more frequently than in subendocardial infarction. In acute anteroseptal transmural infarction the degree of vector shift was closely correlated with the severity of the acute illness.     

Changes in Left Ventricular Wall Movement after Acute Myocardial Infarction Measured by Reflected Ultrasound

Serial measurements of left ventricular posterior wall movement were made in eight patients with acute myocardial infarction by an ultrasound technique. Maximum posterior wall velocity and excursion were decreased during the first 36-hour period after infarction. In two patients a reduction in posterior wall velocity was associated with an increased pulmonary artery pressure and as the pressure returned towards normal the posterior wall motion also improved. It is suggested that this method provides a convenient, non-invasive bedside assessment of left ventricular function after acute myocardial infarction.     

Matrix metalloproteinases and membrane damage markers in sera of patients with acute myocardial infarction

Coronary artery disease is a multifunctional disease and represents one of the leading causes of death worldwide. Oxidative stress appears as an etiological factor for myocardial damage during acute myocardial infarction. Some data suggest that acute coronary syndromes may also be influenced by matrix metalloproteinases through degradation of the fibrous cap of vulnerable atherosclerotic lesions. It has been indicated that gelatinases A and B play a key role in acute myocardial infarction and deoxyribonuclease I has been postulated to be a novel early phase marker of disease. The aim was to study activity of gelatinases A and B in acute myocardial infarction and its association with some membrane damage markers. Seventy-five patients with disease and seventy-five healthy controls were enrolled. Activities of lactate dehydrogenase, malate dehydrogenase, and deoxyribonuclease I were estimated using standard spectrophotometric assay and isoforms of lactate and malate dehydrogenases were determined using direct zymography. Activity of dehydrogenases was significantly higher in patients, while deoxyribonuclease I was lower. Isoform 2 of lactate dehydrogenase was significantly higher in the patient group. Gelatinases A and B were detected only in patients group. The results suggest determination of serum malate dehydrogenase activity to be used as an additional parameter for acute myocardial infarction diagnosis. Those findings suggest important role of gelatinases A and B as biomarkers of early stage of acute myocardial infarction together with membrane damage parameters.     

急性心肌梗死患者肠道优势菌群分析

目的探讨急性心肌梗死患者肠道优势菌群的改变及其与疾病严重程度的关系。方法共筛选急性心肌梗死患者71名及正常健康体检者33名,急性心肌梗死患者根据是否心衰分为急性心肌梗死组36名和急性心肌梗死伴泵衰竭组35名,所有入选者收集大便及血清标本,分别采用qPCR及化学发光仪测定肠道优势菌群改变和血清脑钠肽前体及肌钙蛋白水平。结果急性心肌梗死患者肠道优势菌群显著改变,肠道肠杆菌以及肠球菌细菌数量较对照组显著增加,均与脑钠肽前体、肌钙蛋白、Killip分级显著正相关,而双歧杆菌、乳酸杆菌等细菌数量显著降低,与脑钠肽前体、肌钙蛋白、Killip分级显著负相关。结论急性心肌梗死患者呈现典型的肠道菌群紊乱,且与患者疾病严重程度相关。     

Humane medicine

Despite the increasing incidence of acute non-Q-wave myocardial infarction, controversy remains regarding its validity as a distinct pathophysiologic physiologic and clinical entity. Review of the data indicates that the controversy is more apparent than real. The pathophysiologic factor discriminating best between non-Q-wave and Q-wave infarction is the incidence rate of total occlusion of the infarct-related artery, approximately 30% in non-Q-wave infarction and 80% in Q-wave infarction. Patients with non-Q-wave infarction have a higher incidence of pre-existing angina than patients with Q-wave infarction; they also have lower peak creatine kinase levels, higher ejection fractions and lower wall-motion abnormality scores, which suggests a smaller area of acute infarction damage. However, patients with non-Q-wave infarction have a significantly shorter time to peak creatine kinase level and more heterogeneous ventriculographic and electrocardiographic infarct patterns. The in-hospital death rate is lower in non-Q-wave than in Q-wave infarction (approximately 12% v. 19%). The long-term death rates are similar for the two groups (27% and 23%), but the incidence of subsequent coronary events is higher among patients with non-Q-wave infarction; in particular, reinfarction is an important predictor of risk of death. Most of the differences in biologic and clinical variables between the two types of acute infarction can be related to a lower incidence of total occlusion, earlier reperfusion or better collateral supply in non-Q-wave infarction. Further study is needed to better characterize the long-term risk and to define the most appropriate therapies.     

A comparison of the illness beliefs of people with angina and their peers: a questionnaire study

Background

Systolic compression of a coronary artery by overlying myocardial tissue is termed myocardial bridging. Myocardial bridging usually has a benign prognosis, but some cases resulting in myocardial ischemia, infarction and sudden cardiac death have been reported. We are reporting a case of myocardial bridging which was complicated with acute myocardial infarction associated with inappropriate blood donation.

Case presentation

A 33 year-old-man was admitted to our emergency with acute anteroseptal myocardial infarction after a blood donation. The electrocardiography showed sinus rhythm and was consistent with an acute anteroseptal myocardial infarction. We decided to perform primary percutanous intervention (PCI). Myocardial bridging was observed in the mid segment of the left anterior descending coronary artery on coronary angiogram. PCI was canceled and medical follow up was decided. Blood transfusion was made because he had a deep anemia. A normal hemaglobin level and clinical reperfusion was achieved after ten hours by blood transfusion. At the one year follow up visit, our patient was healthy and had no cardiac complaints.

Conclusions

Myocardial bridging may cause acute myocardial infarction in various clinical conditions. Although the condition in this case caused profound anemia related acute myocardial infarction, its treatment and management was unusual.     

灯盏花素治疗脑梗死50例临床观察

目的：观察灯盏花素治疗脑梗死的临床疗效。方法交１００例急性脑死患者随机分为两组,治疗组５０例,应用灯盏花素治疗;对照组５０例,应用脉络宁治疗。结果治疗组总有效率为９２．００％,对照组照组总有效率为７２．００％,两组比较有显著性差异（Ｐ〈０．０５）。结论灯盏花素是治疗急性脑梗死较为理想的药物,值得临床推广。     

A subpopulation of endothelial progenitor cells with low aldehyde dehydrogenase activity attenuates acute ischemic brain injury in rats

Previous studies have examined the therapeutic effect of endothelial progenitor cells (EPCs) during the chronic phase of cerebral infarction in rats; however, few studies have investigated the effects of EPCs during the acute phase of infarction. In this study, we evaluated the therapeutic effect of EPCs with low aldehyde dehydrogenase activity (Alde-Low EPCs) in rats with acute cerebral infarction, and our results provide insight that may help to identify a therapeutic mechanism of EPCs for acute cerebral infarction. The administration of Alde-Low EPCs into rats with acute cerebral infarction results in the accumulation and migration of the Alde-Low EPCs into the infarct area and the subsequent decrease of infarct volume. Moreover, we found that the stromal cell-derived factor-1 (SDF-1) and CXC chemokine receptor 4 (CXCR4) signaling pathway may regulate the accumulation of Alde-Low EPCs. The transplantation of Alde-Low EPCs may represent a potential treatment strategy for acute cerebral infarction.