Project description:A number of vaccines have been developed and deployed globally to restrain the spreading of the coronavirus disease 2019 (COVID-19). The adverse effect following vaccination is an important consideration. Acute myocardial infarction (AMI) is a kind of rare adverse event after COVID-19 vaccination. Herein, we present a case of an 83-year-old male who suffered cold sweat ten minutes after the first inactivated COVID-19 vaccination and AMI one day later. The emergency coronary angiography showed coronary thrombosis and underlying stenosis in his coronary artery. Type II Kounis syndrome might be a potential mechanism, which is manifested as coronary thrombosis secondary to allergic reactions in patients with underlying asymptomatic coronary heart disease. We also summarize the reported AMI cases post COVID-19 vaccination, as well as overview and discuss the proposed mechanisms of AMI after COVID-19 vaccination, thus providing insights for clinicians to be aware of the possibility of AMI following COVID-19 vaccination and potential underlying mechanisms.
Project description:We report a case that presented as acute myocardial infarction (AMI) caused by lymphocytic myocarditis (LM), and explore the relationship between AMI and LM. We also performed a literature search to identify publications that previously reported LM-associated myocardial infarction. Coronary angiography of our patient revealed normal coronary arteries. However, a perfusion-metabolism mismatch in the apex and mid-inferior walls supported the diagnosis of AMI, and right ventricular septal endomyocardial biopsy showed LM. Extensive viral serological tests were negative for an infectious etiology. Immunosuppressive therapy may be beneficial in patients with high-risk myocarditis who are pathologically confirmed to be virus-negative.
Project description:BackgroundGuillain-Barre syndrome after myocardial infarction occurs infrequently, and its occurrence following percutaneous coronary intervention is extremely rare. Due to the high mortality rate of myocardial infarction and the disability of Guillain-Barre syndrome, early identification of Guillain-Barre syndrome after myocardial infarction and early intervention can decrease the mortality rate, lead to early recovery, and provide a better outcome.Case presentationHerein, we reported a rare case of Guillain-Barre syndrome after myocardial infarction treated with percutaneous coronary intervention. The patient was a 75-year-old woman from China who was admitted to hospital due to sudden loss of consciousness. Electrocardiography showed acute myocardial infarction in the right ventricle and inferior and posterior walls. The patient underwent emergency percutaneous intervention of the posterior collateral artery of the right coronary artery. Soon after, her condition worsened resulting in limb weakness and numbness. Unfortunately, she continued to develop respiratory failure, and treated with intravenous immunoglobulin and ventilator-assisted breathing. A physical examination showed hypotonia of all four limbs, complete quadriplegia, bulbar palsy, dysarthria, and tendon areflexia. Serum immunoglobulin (Ig) G anti-ganglioside antibody analysis was positive with anti-GT1a antibodies (+ +), anti-GM1 antibodies ( +), anti-GM2 antibodies ( +), and anti-GM4 antibodies ( +), and he was diagnosed with Guillain-Barre syndrome after myocardial infarction. She was discharged due to poor response to treatment. The patient died two days after being discharged.ConclusionsMyocardial infarction and/or percutaneous coronary intervention may activate immune-mediated response and cause severe complications. Clinician should be alert to Guillain-Barre syndrome after myocardial infarction and/or percutaneous coronary intervention.
Project description:Bullous pemphigoid (BP) is a rare, life-threatening autoimmune blistering disease with pruritus and tension blisters/bullous as the main clinical manifestations. Glucocorticosteroids are the main therapeutic agents for it, but their efficacy is poor in some patients. Tofacitinib, a small molecule agent that inhibits JAK1/3, has shown incredible efficacy in a wide range of autoimmune diseases and maybe a new valuable treatment option for refractory BP. To report a case of refractory BP successfully treated with tofacitinib, then explore the underlying mechanism behind the treatment, and finally review similarities to other cases reported in the literature. Case report and literature review of published cases of successful BP treatment with JAK inhibitors. The case report describes a 73-year-old male with refractory BP that was successfully managed with the combination therapy of tofacitinib and low-dose glucocorticoids for 28 weeks. Immunohistochemistry and RNA sequencing were performed to analyze the underlying mechanism of tofacitinib therapy. A systematic literature search was conducted to identify other cases of treatment with JAK inhibitors. Throughout the 28-week treatment period, the patient experienced clinical, autoantibody and histologic resolution. Immunohistochemical analysis showed tofacitinib significantly decreased the pSTAT3 and pSTAT6 levels in the skin lesions of this patient. RNA sequencing and immunohistochemical testing of lesion samples from other BP patients identified activation of the JAK-STAT signaling pathway. Literature review revealed 17 previously reported cases of BP treated with four kinds of JAK inhibitors successfully, including tofacitinib (10), baricitinib (1), upadacitinib (3) and abrocitinib (3). Our findings support the potential of tofacitinib as a safe and effective treatment option for BP. Larger studies are underway to better understand this efficacy and safety.
Project description:Coronary artery vasospasm (CVS), an uncommon cause of acute chest pain, can be provoked by vasoconstriction-induced medications. Misoprostol, a prostaglandin analog, is a safe medication to terminate a pregnancy. However, misoprostol can cause coronary artery vasospasm due to vasoconstrictor properties, leading to acute myocardial infarction with nonobstructive coronary arteries (MINOCA), especially in patients with a high risk for cardiovascular disease. We report a case of a 42-year-old female with a past medical history of hypertension who presented with ST-elevation myocardial infarction following the administration of a high-dose Misoprostol. The fact that coronary angiogram and intravascular ultrasound revealed normal coronary arteries suggested transient coronary vasospasm. CVS is a severe but rare cardiac adverse effect associated with high-dose misoprostol. This medication should be prescribed with caution and close monitoring, especially in those with pre-existing heart disease or cardiovascular risk factors. Our case raises awareness of severe cardiovascular complications that can be related to using misoprostol in high-risk patients.
Project description:BACKGROUND:Genetic susceptibility to the development of coronary artery disease (CAD) and myocardial infarction (MI) is well established. However, lack of replication, and difficulty in the identification of specific genes that underlie impressive linkage peaks remain challenges at the molecular level due to the heterogeneity of phenotype and their associated genotypes. We present two cases of first-degree family members of acute myocardial infarction (AMI) having similar clinical and angiographic features of obstructive coronary lesions at same anatomic locations. CASE PRESENTATION:The father presented with significant chest discomfort and loss of consciousness. The electrocardiogram (ECG) showed an acute anterior ST-segment-elevation myocardial infarction (STEMI). Coronary angiogram demonstrated a subtotal occlusion in the mid-left anterior descending (LAD) coronary artery. One week later, the son presented after an in-hospital cardiac arrest with pulseless electric activity preceded by significant chest pain and loss of consciousness. His ECG also showed an acute anterior STEMI. Catheterization revealed strikingly similar angiographic characteristics with his father: subtotal occlusion in the proximal to mid-LAD coronary artery. CONCLUSIONS:More considerations should be given to patients with similar phenotypic characterization in genetic studies of CAD/MI in the future.
Project description:Background: One of the most serious complications of cranial radiotherapy is the development of radiation-induced glioma, which is estimated to occur in 1 to 4% of patients who have received cranial irradiation and has a worse prognosis than sporadic glioblastoma. To date, owing to its rarity, no standard of care has been established for radiation-induced glioma. Although comprehensive genetic analysis has recently uncovered the molecular characteristics of radiation-induced glioma, the full picture remains unclear, and the molecular features associated with treatment response and prognosis are poorly understood. Case presentation: A 45-year-old man presented with generalized seizures caused by multiple brain tumors involving the right frontal lobe, thalamus, and brainstem. The patient had a history of whole-brain radiotherapy for the recurrence of Burkitt's lymphoma at the age of 12. He underwent craniotomy, and the histological diagnosis was a high-grade glioma with isocitrate dehydrogenase-wildtype, which was presumed to be a radiation-induced glioma that developed 33 years after whole-brain irradiation. The Heidelberg DNA-methylation brain classifier most closely matched diffuse pediatric-type high-grade glioma, receptor tyrosine kinase-1 subtype, which is a typical methylation class of radiation-induced glioma. Methylation-specific polymerase chain reaction showed that the O6-methylguanine-DNA methyltransferase gene promoter was unmethylated. Next-generation sequencing identified CDKN2A/B deletion as well as co-amplification of several receptor tyrosine kinase-encoding genes including PDGFRA, KIT, and KDR, which are all located on chromosome 4q12. Amplification of this region is present broadly across cancers and is associated with a poor prognosis in sporadic glioblastoma. Nevertheless, the patient received conventional chemoradiotherapy with temozolomide. Subsequent multimodal imaging with magnetic resonance imaging and 11C-methionine positron emission tomography revealed complete remission of all lesions. Two years later, the patient is currently alive with a favorable performance status. Conclusions: Despite radiation-induced glioma with molecular features suggestive of an aggressive phenotype, our patient unexpectedly responded well to conventional chemoradiotherapy, resulting in complete remission that is exceptional in sporadic glioblastoma. Our case indicates that some of the radiation-induced gliomas may have distinct molecular characteristics involved in the therapeutic response that differ from those of sporadic glioblastomas.
Project description:ST-segment elevation in absence of acute coronary syndrome can be seen in multiple conditions, including acute pericarditis and coronary vasospasm, but it is rarely seen with severe hypercalcemia. The authors present a case of an 81-year-old female with a history of stage 4 squamous cell cancer of the lung, who presented to the emergency room with profound fatigue, weakness, anorexia, and drowsiness two weeks after her first chemotherapy cycle. Additionally, she had complaints of right-sided chest pain associated with worsening shortness of breath, as well as right arm numbness. An EKG obtained on arrival to the hospital showed diffuse ST-segment elevation (leads V3-V6, I, II, III, and aVF). Basic lab work found a calcium level of 20.4?mg/dl with elevated parathyroid hormone-related protein (PTHrP) of 135?pg/ml. Troponin I remained within normal limits. Serial EKS obtained during the patient's hospitalization demonstrated resolution of the ST elevation as calcium level normalized. This case emphasizes the importance of hypercalcemia as a differential diagnosis for ST-segment elevation and QT shortening when acute coronary syndrome is not present. Awareness of these EKG changes is critical for early diagnosis, recognition, and appropriate treatment.
Project description:BackgroundInterventricular septal dissection is a critical disease characterized by the separation of the intraventricular septum into two layers, forming an intermediate layer with a cystic cavity that communicates with the root of the aorta or ventricle. It has low morbidity and high mortality rates.Case presentationCase 1: A 58-year-old male with a history of hypertension and smoking presented to a local hospital due to chest tightness and pain for 4 days. Coronary angiography revealed diffuse lesions from the proximal to the middle segment of the left circumflex branch, with 80% stenosis at its most severe point, and complete occlusion of the proximal segment of the right coronary artery. A stent was implanted in the middle of the right coronary artery. Three months later, the patient was misdiagnosed with an aneurysm of the membranous ventricular septum with defect via echocardiography at the local hospital. After the implantation of a stent in the left circumflex branch, the patient came to our hospital for further diagnosis and treatment. The first ultrasound of our hospital misdiagnosed it as ventricular septal rupture, and a senior ultrasound doctor diagnosed the patient with interventricular septal dissection secondary to myocardial infarction. The patient underwent follow-up echocardiography every 1-2 months for 6 months. The patient remains asymptomatic with stable hemodynamics. The original treatment regimen and follow-up continues. Case 2: A 70-year-old male was admitted to a local hospital due to repeated chest distress for more than 20 years that worsened over several hours. Coronary angiography revealed complete occlusion of the right coronary artery. Cardiogenic shock occurred after percutaneous coronary intervention. The initial several echocardiography of the local hospital and our hospital misdiagnosed it as interventricular septal rupture secondary to myocardial infarction. The later echocardiography diagnosed it as interventricular septal dissection with rupture secondary to myocardial infarction. The patient underwent interventricular septal repair and mitral valvuloplasty after 25 days of medical treatment and died of multiple organ failure on the fourth day after the operation.ConclusionsThese two cases illustrate a complication of acute myocardial infarction and highlight the importance of echocardiography in its diagnosis. By exploring the etiology, pathogenesis, and key diagnostic points of IVSD, this study aims to provide valuable insights for clinical practice.