Angiographic evidence of hemorrhagic myocardial infarction after intracoronary thrombolysis with streptokinase

The reperfusion of acutely ischemic myocardium by intracoronary streptokinase thrombolysis is an exciting new therapy for acute myocardial infarction (MI). It appears that successful thrombolysis and reperfusion in the first few hours after acute coronary occlusion may salvage myocardium and possibly improve prognosis. A potential adverse effect of reperfusion is the production of hemorrhage in the area of myocardial necrosis. We report on a patient with prompt, successful coronary thrombolysis by streptokinase infusion who showed angiographic evidence of a hemorrhagic MI.     

Aortic infarction following dissecting aortic aneurysm

Aortic infarction was observed in 21 of 34 cases of dissecting aortic aneurysm. This lesion occurred as a central zone of necrosis with preserved elastic laminae, sparing media adjacent to the true and false lumens. In cases where the false lumen was occluded, the central infarction extended to this lumen. The infarction followed rather than preceded dissection, took approximately 48 hours to develop, and did not organize with time. The lesion occurred exclusively in the thoracic aorta, and bore no relationship to medial cystic necrosis. Present surgical therapy does not extirpate these areas, and the implication of these lesions in terms of management remains to be determined.     

High-dose intravenous magnesium attenuates complement consumption after acute myocardial infarction treated by streptokinase

OBJECTIVE: This study was designed to detect changes in complement levels following acute myocardial infarction and to test whether magnesium sulphate (MgSO4) administration interferes with the complement response that follows acute myocardial infarction. DESIGN: Twenty-nine patients with acute myocardial infarction treated with streptokinase were included and randomly assigned to three treatment groups. In groups A and B, a bolus of 1 g MgSO4 was infused intravenously followed by 4 g (group A) and 14 g (group B) MgSO4 for 24 h while normal saline was administered in group C (control). Blood samples for C3, C4 and CH-100 were obtained at baseline and repeatedly during the 48 h following the initiation of magnesium infusion. RESULTS: In groups A and C, a remarkable decrease in the levels of C3, C4 and CH-100 was observed when measured 1 h after the end of streptokinase infusion and thereafter for the ensuing 48 h compared to baseline values (P < 0.05). In group B, the decrease in these complement elements was attenuated, and a significant (P < 0.05) delayed decrease of C3 and C4 was observed only at 24 h and later up to 48 h. The mean level of CH-100 in group B was significantly depressed compared to baseline from 3 h and thereafter up to 48 h. Mean C3 values plotted against observation time differed between the three groups (P = 0.021). A similar trend was observed for C4 (P = 0.133) but not for CH-100 (P = 0.46). CONCLUSION: (1) Complement elements are being consumed following acute myocardial infarction treated by streptokinase. (2) High-dose intravenous magnesium attenuates the complement process following acute myocardial infarction. (3) These results might signify that magnesium modulates the inflammatory response that follows infarction.     

Precocious myocardial infarction after radiation treatment for Hodgkin's disease

A 26-year-old man received extensive cardiac radiation in the course of treatment of mediastinal Hodgkin's disease, and six years later, he experienced an acute myocardial infarction. Angiographic studies demonstrated extensive atherosclerotic abnormalities in the coronary arterial system. It is suggested that radiation-induced injury was a provocation of these precocious arterial abnormalities.     

Aortic intimal sarcoma with acute myocardial infarction

An autopsy case of aortic sarcoma who died of acute myocardial infarction caused by coronary involvement is reported. The patient was a 54 year old woman who was admitted because of an undiagnosed fever and general fatigue of 6 months duration. Magnetic resonance imaging (MRI) showed a tumor in the aortic arch. Total aortic arch replacement was performed. It was diagnosed as a malignant mesenchymal tumor of the aorta. The patient died of acute myocardial infarction 10 months after the operation. At autopsy, the tumor had invaded the luminal surface and intima of the proximal anastomosis (the remnant ascending aorta and the graft), the aortic valves, the distal anastomosis (surgical line of the thoracic aorta plus the graft), and the coronary arteries. The left main coronary artery showed complete obstruction by fibrin thrombus with tumor invasion in the intima, which was responsible for acute myocardial infarction. Primitive and bizarre tumor cells proliferated with many slit-like tissue spaces. Most of the tumor except for its luminal surface showed necrosis. Ultrastructurally, there were spaces between tumor cells, suggesting lumen formation, and some of them had microvilli. This sarcoma was considered to be the so-called aortic intimal sarcoma.     

Is prophylactic treatment after myocardial infarction evidence-based?

In Barrett's esophagus, the squamous lining of the lower esophagus is replaced by columnar epithelium. Barrett's esophagus is associated with gastroesophageal reflux and an increased risk of the development of esophageal cancer. Endoscopy shows red columnar epithelium in the lower esophagus. Biopsy is needed to confirm intestinal metaplasia. Some cases progress from dysplasia to invasive adenocarcinoma. Medical or surgical antireflux treatment controls symptoms and esophagitis, but Barrett's esophagus remains. Patients are usually followed up by endoscopy for detection of dysplasia or early cancer. For patients with low-grade dysplasia, follow-up is adequate; however, for those with high-grade dysplasia, esophagectomy or experimental endoscopic mucosal ablation is advised.     

Aortic aneurysm developing after umbilical artery catheterization

A variety of complications of umbilical vessel catheterization in the newborn have been reported by earlier investigators. This paper describes a case in which umbilical artery catheterization probably gave rise to an aortic aneurysm. The histological findings suggested that the hypoxic changes in the aortic wall as well as the mechanical effect of the catheter were involved in the origin of the aneurysm.     

Clinical and angiographic features of patients with an occluded versus a patent infarct vessel after intravenous streptokinase for acute myocardial infarction

Despite early treatment with thrombolytic agents for acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. To study the various factors related to achieving patency in the infarct vessel, 201 patients who received streptokinase within six hours of symptoms were studied. All patients underwent cardiac catheterization during the same hospitalization at 5.40 +/- 3.26 days after admission. Forty-five (22.4%) patients were found to have an occluded infarct artery (group 1) and 156 (77.6%) had a patent infarct vessel (group 2). There was no difference in the time from onset of symptoms to receiving streptokinase between the two groups. The two groups were similar to each other with regard to age, gender, history of myocardial infarction or angina, and major risk factors for coronary disease. Coagulation parameters before and after streptokinase therapy, reflecting the lytic state, were similar in both groups. The left ventricular end diastolic pressure was significantly higher and the left ventricular ejection fraction was significantly lower in group 1 than in group 2. These observations suggest that despite early initiation of thrombolytic therapy in patients with acute myocardial infarction, a significant portion of patients fail to achieve a patent infarct artery. This failure cannot be explained by the observed clinical parameters or the lytic state after streptokinase.     

Randomized trial of direct coronary angioplasty versus intravenous streptokinase in acute myocardial infarction

OBJECTIVES: The objective of this study was to obtain preliminary data on the relative clinical utility of direct coronary angioplasty compared with that of intravenous thrombolytic therapy for patients with acute myocardial infarction. BACKGROUND: The relative merits of intravenous thrombolytic therapy and direct coronary angioplasty as treatment for acute myocardial infarction are incompletely understood, and randomized trials of these treatments have been extremely limited. METHODS: One hundred patients with ST segment elevation presenting to a single high volume interventional center within 6 h of the onset of chest pain were randomized to receive either streptokinase (1.2 million U intravenously over 1 h) or immediate catheterization and direct coronary angioplasty. Patients were excluded for age > or = 75 years, prior bypass surgery, Q wave infarction in the region of ischemia or excessive risk of bleeding. All patients were then treated with aspirin (325 mg orally/day) and heparin (1,000 U intravenously/h) for 48 h until catheterization was performed to determine the primary study end point, namely, infarct-related artery patency at 48 h. Secondary end points were in-hospital death, left ventricular ejection fraction at 48 h and time to treatment. RESULTS: There was no difference in the baseline characteristics of the two treatment groups. Overall patient age was 56 +/- 10 years, 83% of patients were male, 11% had prior infarction, 40% had anterior infarction and 97% were in Killip class I or II. Although time to treatment was delayed in the angioplasty group (238 +/- 112 vs. 179 +/- 98 min, p = 0.005), there was no difference in 48-h infarct-related artery patency or left ventricular ejection fraction (patency 74% vs. 80%; ejection fraction 59 +/- 13% vs. 57 +/- 13%; angioplasty vs. streptokinase, p = NS for both). There were no major bleeding events, and the mortality rate with angioplasty (6%) and streptokinase (2%) did not differ (p = NS). CONCLUSIONS: These results suggest that intravenous thrombolytic therapy might be preferred over coronary angioplasty for most patients because of the often shorter time to treatment.     

Serum paraoxonase after myocardial infarction

A new concept in reproductive endocrinology is that the status of the ovary as a glucocorticoid target organ alters with follicular development. Evidence for a physiological role of glucocorticoids in the regulation of ovarian folliculogenesis has been strengthened by the discovery that 11beta-hydroxysteroid dehydrogenase (11betaHSD) mRNA expression in human granulosa cells is developmentally regulated. In this study, we quantified the pattern of expression and investigated the cellular location of 11betaHSD type 1 (11betaHSD1), 11betaHSD type 2 (11betaHSD2), glucocorticoid receptor (GR), and mineralocorticoid receptor (MR) mRNAs during follicular maturation in rat ovary. Immature female rats received treatment with eCG to induce preovulatory follicular development or eCG followed by hCG to induce luteinization. 11betaHSD1, 11betaHSD2, GR, and MR mRNAs were all detectable by ribonuclease protection assay in ovarian total RNA. Treatment with eCG alone caused an approximately 8-fold increase in the ovarian level of 11betaHSD1 mRNA, which rose to approximately 30-fold after additional treatment with hCG. Equine CG alone did not measurably affect the ovarian 11betaHSD2 mRNA level, but additional treatment with hCG reduced it to 34% of the control level. Expression of GR mRNA was unchanged by any gonadotropin treatment, while MR mRNA was down-regulated. A similar pattern of 11betaHSD1, 11betaHSD2, GR, and MR mRNA expression was observed in isolated granulosa cells. These results provide direct experimental evidence that 11betaHSD genes are gonadotropically regulated in the rat ovary, including granulosa cells, and are consistent with a shift in glucocorticoid metabolism from inactivation (due to oxidation by 11betaHSD2) to activation (reduction by 11betaHSD1) during hCG-induced granulosa cell luteinization.     

'Rescue' after failed thrombolysis for acute myocardial infarction

Prompt restoration of coronary artery patency in acute myocardial infarction is associated with substantial improvements in morbidity and mortality. The pivotal role of thrombolysis and aspirin in achieving these goals is well established. However, despite the success of thrombolytic therapy in large trials, clinical assessment in individual patients often suggests that reperfusion has not occurred after initial therapy. This review considers the validity of such bedside predictions and discusses whether such patients should be managed differently.