Most of the evidences for beneficial effects of beta-blockers in patients with acute myocardial infarction (AMI) were from the clinical studies published in the pre-reperfusion era when anti-platelet drugs, statins or inhibitors of renin-angiotensin-aldosterone system which are known to reduce cardiovascular mortality of patients with AMI were not introduced. In the reperfusion era, beta-blockers’ benefit has not been clearly shown except in patients with reduced ejection fraction (EF; ≤40%). In the era of the early reperfusion therapy for AMI, a number of patients with mildly reduced EF (>40%, <50%) or preserved EF (≥50%) become increasing. However, because no randomized clinical trials are available until now, the benefit and the optimal duration of oral treatment with beta-blockers in patients with mildly reduced or preserved EF are questionable. Registry data have not showed the association of oral beta-blocker therapy with decreased mortality in survivors without heart failure or left ventricular systolic dysfunction after AMI. In the Korea Acute Myocardial Infarction Registry-National Institute of Health of in-hospital survivors after AMI, the benefit of beta-blocker therapy at discharge was shown in patients with reduced or mildly reduced EF, but not in those with preserved EF, which provides new information about beta-blocker therapy in patients without reduced EF. However, clinical practice can be changed when the results of appropriate randomized clinical trials are available. Ongoing clinical trials may help to answer the unresolved issues of beta-blocker therapy in patients with AMI.
Background Coronary atherosclerosis is the leading cause of coronary artery disease. Several investigations have indicated that tear-sensitive plaques contain macrophages and T cells. Neopterin is an essential cellular immune response biomarker. The main goal of this study was to see if there were any changes in biomarkers like unconjugated pteridines, neopterin, and biopterin, as well as kynurenine pathway enzymes like indoleamine 2,3-dioxygenase (IDO), which catalyzes the rate-limiting step in tryptophan degradation, in patients with the acute coronary syndrome (ACS) caused by angiographic atherosclerosis.
Methods High-performance liquid chromatography was used to determine the amounts of neopterin, biopterin, and creatinine in urine samples, as well as tryptophan and kynurenine in serum samples. The enzyme-linked immunosorbent assay was used to assess the amounts of neopterin in serum samples. The measured parameters were evaluated between ACS patients and controls.
Results The measured levels of neopterin, biopterin and the kynurenine to tryptophan ratio reflecting IDO activity, and the specifically known biomarkers such as cardiac troponin, creatine kinase, myoglobin, and natriuretic peptides are statistically higher in ACS patients compared to control subjects. On the other hand, the measured parameters are inadequate to classify the conventional kinds of ACS, ST-elevation- and non-ST-elevation- myocardial infarction.
Conclusions The study found that determining and using neopterin and IDO parameters as biomarkers in individuals with the ACS can support traditional biomarkers. However, it can be concluded that evaluating pteridine biomarkers solely have no privilege to clinical findings in ACS diagnosis and classification.
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Acute cerebral infarctions are rare in children; however they can occur as a complication of a Mycoplasma pneumoniae (MP) infection due to direct invasion, vasculitis, or a hypercoagulable state. We report on the case of a 5-year-old boy who had an extensive stroke in multiple cerebrovascular territories 10 days after the diagnosis of MP infection. Based on the suspicion that the cerebral infarction was associated with a macrolide-resistant MP infection, the patient was treated with levofloxacin, methyl-prednisolone, intravenous immunoglobulin, and enoxaparin. Despite this medical management, cerebral vascular narrowing progressed and a decompressive craniectomy became necessary for the patient’s survival. According to laboratory tests, brain magnetic resonance imaging, and clinical manifestations, the cerebral infarction in this case appeared to be due to the combined effects of hypercoagulability and cytokine-induced vascular inflammation.
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Predisposing factors for venous thrombosis can be identified in the majority of patients with established venous thromboembolism (VTE). However, an obvious precipitant may not be identified during the initial evaluation of such patients. In the present case, a 47-year-old female presented to the emergency department of our hospital after ingesting multiple drugs. She had no VTE-related risk factors or previous episodes, nor any family history of VTE. After admission to the intensive care unit sudden hypoxemia developed, and during the evaluation cerebral, renal, and splenic infarctions with pulmonary embolisms were diagnosed. However, the sources of the emboli could not be identified by transthoracic echocardiography or computed tomography angiography. Protein C deficiency was identified several days later. We recommend that hypercoagulable states be taken into consideration, especially when unexplained thromboembolic events develop in multiple or unusual venous sites.
A 51-year-old male patient was referred for a sudden out-of-hospital cardiac arrest. Upon arrival, he was conscious and had no chest pain complaints. There was no abnormality in initial electrocardiographic and echocardiographic examinations. However, episodes of recurrent ventricular fibrillation (VF) were documented on rhythm monitoring. Each VF episode was triggered by an isolated monomorphic ventricular premature complex (VPC).
Suspecting idiopathic VF, emergency radiofrequency catheter ablation was planned for the VPCs. However, when coronary angiography was performed to exclude silent ischemia, the results showed a total occlusion of the right coronary artery posterolateral branch, which is thought to supply the left ventricular inferior and septal wall. After successful reperfusion, VF episodes and the triggering VPCs disappeared. We are documenting this case to emphasize the potential for silent myocardial infarction to cause out-of-hospital sudden cardiac arrest even in a patient without any symptom or sign of acute coronary syndrome.
Decompressive hemicraniectomy followed by subsequent therapeutic hypothermia can reduce mortality in patients with malignant cerebral infarction without significantly increasing risk. We report three cases of malignant cerebral infarction treated with hemicraniectomy followed by hypothermia. Case 1 received elective decompressive surgery and hypothermia. Case 2 developed subsequent cerebral infarction with uncal herniation. Therefore, emergent decompressive surgery and hypothermia was performed in this case. Despite surgery and hyperosmolar therapy, case 3 received hypothermia treatment for refractory increased intracranial pressure. All patients survived with a score of 4 or 5 on the modified Rankin scale. Therefore, we suggest that application of hypothermia after hemicraniectomy is safe and feasible. Several possible modifications can be made to improve the management strategy in order to increase the benefits of hypothermia treatment.
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Kawasaki disease (KD) is an acute, systemic vasculitis of childhood. The early mortality of KD results from coronary complications, mainly aneurysmal thrombosis with myocardial infarction, and the subacute phase of KD has the highest risk of mortality. Although there have been reports of ischemic heart disease as late cardiologic sequelae of KD in young adults, acute myocardial infarction caused by coronary complications in the subacute phase of KD is rare. We experienced one pediatric patient who developed coronary artery aneurysm and acute myocardiac infarction (AMI) during the subacute phase of incomplete and intravenous immunoglobulin (IVIG)-nonresponsive KD. The patient was given a good prognosis due to close monitoring and early recognition of AMI. Physicians should carefully monitor KD patients who do not respond to initial IVIG therapy and who show progressive coronary artery dilatation. If such a patient complaints of chest pain and the ECG shows hyperacute T waves, the physician should suspect development of AMI.
The common predisposing risk factors for perioperative stroke include: previous stroke, atrial fibrillation, old age (> 75 years), carotid stenosis, and diabetes mellitus.
An endoscopic sinus surgery was performed in a 49-year-old male with chronic paranasal sinusitis and nasal polyps. The vital signs, physical and laboratory examinations, and electrocardiography on admission were within the normal limit. Anesthesia was maintained with nitrous oxide in oxygen and 6% desflurane. The operation and anesthesia were uneventful with the exception of transient intraoperative hypotension. The patient recovered fully from the anesthesia (modified Aldrete score: 10) in the recovery room. However, he developed right arm weakness and dysarthria in the general ward 7 hours after the operation. We report a rare case of multifocal acute cerebral infarctions found on the postoperative magnetic resonance imaging in a noncardiac surgical patient.
Malignant cerebral infarction has a high risk of fatal brain edema and increased intracranial pressure with cerebral herniation causing death. One of the major causes of death is a rebound cerebral edema during rewarming phase. A 66-year-old male patient presented with the right hemiplegia and global aphasia due to malignant cerebral infarction in the whole territory of middle cerebral artery with the occlusion of the proximal internal carotid artery. Being refused decompressive hemicraniectomy, he received the therapeutic hypothermia for 6 days. After rewarming for 6 hours, mentality was suddenly decreased and dilated left pupil. Follow-up CT revealed that midline shifting was more aggravated. We decided on repeated hypothermia for rebound cerebral edema and successfully controlled. We report our experience with repeated hypothermia for rebound cerebral edema following therapeutic hypothermia in malignant cerebral infarction.
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Therapeutic Hypothermia after Decompressive Craniectomy in Malignant Cerebral Infarction Jun Young Chang, Jeong-Ho Hong, Jin-Heon Jeong, Sung-Jin Nam, Ji-Hwan Jang, Jae Seung Bang, Moon-Ku Han Korean Journal of Critical Care Medicine.2014; 29(2): 93. CrossRef
Malignant cerebral infarction as postoperative complication after pulmonary resection occurs rarely, but can be rather serious. We report a case of 81-year-old man who suffered from malignant cerebral infarctions after pulmonary resection for lung cancer. He had a history of well-controlled hypertensions, but no evidences of arrhythmia, and neither stenosis nor atheroma in the carotid arteries and intracranial arteries. There were no specific events during his operation except that an inadvertent left carotid artery puncture occurred during the central line insertion. In intensive care unit (ICU), he had a delayed recovery of consciousness and dysarthria with right hemiplegia. Computed tomography revealed malignant middle cerebral infarctions due to the occlusion of left middle cerebral artery. It could be the thromboembolism due to pulmonary resections or carotid artery punctures in the patient without high risk factors.
BACKGROUND Limited data are available for gender-based differences among patients with acute myocardial infarction (AMI) undergoing coronary revascularization in Korea. The purpose of this study is to identify gender-based differences in clinical characteristics, risk factors and outcomes among Korean patients undergoing percutaneous coronary intervention (PCI). METHODS Patients with AMI undergoing PCI between Jan 2009 and Sep 2011 were included (n = 457) in the study. Clinical characteristics and cardiovascular risk factors as well as major adverse cardiac events (MACE), including death after PCI, were compared between women (n = 134) and men (n = 323). RESULTS Women were older (69.8 +/- 10.7 vs. 60.0 +/- 11.7 years, p < .001) and had more comorbidities, such as diabetes (44.0% vs. 32.8%, p = .025) and hypertension (64.9% vs. 48.9%, p = .002) compared to men. Women were less likely to have a smoking history (p < .001). There were no significant differences in all causes of death and in MACE between women and men. By the multivariate analysis, age, HDL-cholesterol and left ventricle ejection fraction are associated with mortality and MACE. CONCLUSIONS In this study, women did not emerge as an independent predictor for MACE; however, they were older and had a higher incidence of hypertension and diabetes than men.
Woo Seung Shin, Mi Youn Park, You Mi Hwang, Hui Kyung Jeon, Man Young Lee, Jong Min Lee, Byoung Joo Shim, Sung Sik Kim, Seung Jae Lee, Yong Seog Oh, Tai Ho Rho, Ki Bae Seung
BACKGROUND Atrial fibrillation (AF) has been linked to an increased risk for in-hospital and long-term mortality rates in patients with acute myocardial infarction (AMI). Obesity and metabolic syndrome (MS) are known to play an important role in cardiovascular morbidity and mortality. However, it is uncertain whether obesity and MS increase the risk of AF in patients with AMI. Therefore, we investigated independent risk factors for the occurrence of new-onset AF in patients with AMI who received optimal percutaneous coronary intervention (PCI). METHODS We prospectively analyzed the association between MS and the incidence of cardiac arrhythmia in 146 patients with AMI who underwent PCI. Twenty-four-hour Holter monitoring was performed 3 days after AMI. We divided the patients into two different groups based on the development of AF and analysed their obesity based on body mass index (BMI) (kg/m2) and evaluated the existence of MS, as well as visceral obesity with fat computed tomography. RESULTS Seventy-five patients (51.4%) were obese (BMI > or = 25) and 64 (44%) had MS. AF occurred in 33 (22.6%) patients. Age, MS, and visceral obesity were significantly associated with AF (p = 0.001, p = 0.003, and p = 0.03, respectively). There was no difference between obese and non-obese patients in the incidence of AF and VT.
Multivariate analysis revealed that age and MS were independent risk factors of post-AMI AF. CONCLUSIONS MS is an important and modifiable risk factor for new-onset AF especially in patients with AMI who underwent PCI.
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