Large Coronary Artery Aneurysm with Thrombotic Coronary Occlusion Resulting in ST-Elevation Myocardial Infarction After Warfarin Interruption
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Best Threshold for Diagnosis of Stenosis Or Thrombosis Within Six Months of Access Flow Measurement in Arteriovenous Fistulae
J Am Soc Nephrol 14: 3264–3269, 2003 Best Threshold for Diagnosis of Stenosis or Thrombosis within Six Months of Access Flow Measurement in Arteriovenous Fistulae MARCELLO TONELLI,*†‡ GIAN S. JHANGRI,§ DAVID J. HIRSCH,ʈ¶ JOANNE MARRYATT,¶ PAULA MOSSOP,¶ COLLEEN WILE,¶ and KAILASH K. JINDAL* *Department of Medicine, University of Alberta, Edmonton, Canada; †Department of Critical Care, University of Alberta, Edmonton, Canada; ‡Institute of Health Economics, Edmonton, Canada; §Department of Public Health Sciences, University of Alberta, Edmonton, Canada; ʈDepartment of Medicine, Dalhousie University, Halifax, Canada; and ¶Queen Elizabeth II Health Sciences Centre, Halifax, Canada Abstract. Canadian clinical practice guidelines recommend within 6 mo, and both seemed superior to Ͻ400 ml/min. performing angiography when access blood flow (Qa) is Ͻ500 However, the frequency of the composite definition of stenosis ml/min in native vessel arteriovenous fistulae (AVF), but data among AVF with Qa between 500 and 600 ml/min was only 6 on the value of Qa that best predicts stenosis are sparse. (25%) of 24, as compared with 58 (76%) of 76 when Qa was Because correction of stenosis in AVF improves patency rates, Ͻ500 ml/min. This suggests that most lesions that would be this issue seems worthy of investigation. Receiver-operating found using a threshold of Ͻ600 ml/min occurred in AVF with characteristic curves were constructed to examine the relation- Qa Ͻ500 ml/min and that the small gain in sensitivity associ- ship between different threshold values of Qa and stenosis in ated with the Ͻ600-ml/min threshold would be outweighed by 340 patients with AVF. -
Everything I Need to Know About Renal Artery Stenosis
Patient Information Renal Services Everything I need to know about renal artery stenosis What is renal artery stenosis? Renal artery stenosis is the narrowing of the main blood vessel running to one or both of your kidneys. Why does renal artery stenosis occur? It is part of the process of arteriosclerosis (hardening of the arteries), that develops in very many of us as we get older. As well as becoming thicker and harder, the arteries develop fatty deposits in their walls which can cause narrowing. If the kidneys are affected there is generally also arterial disease (narrowing of the arteries) in other parts of the body, and often a family history of heart attack or stroke, or poor blood supply to the lower legs. Arteriosclerosis is a consequence of fat in our diet, combined with other factors such as smoking, high blood pressure and genetic factors inherited, it may develop faster if you have diabetes. What are the symptoms? You may have fluid retention, where the body holds too much water and this can cause breathlessness, however often there are no symptoms. The arterial narrowing does not cause pain, and urine is passed normally. As a result this is usually a problem we detect when other tests are done, for example, routine blood test to measure how well your kidneys are working. What are the complications of renal artery stenosis? Kidney failure, if the kidneys have a poor blood supply, they may stop working. This can occur if the artery blocks off suddenly or more gradually if there is serious narrowing. -
Hereditary Hemorrhagic Telangiectasia: Diagnosis and Management From
REVIEW ARTICLE Hereditary hemorrhagic telangiectasia: Ferrata Storti diagnosis and management from Foundation the hematologist’s perspective Athena Kritharis,1 Hanny Al-Samkari2 and David J Kuter2 1Division of Blood Disorders, Rutgers Cancer Institute of New Jersey, New Brunswick, NJ and 2Hematology Division, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA ABSTRACT Haematologica 2018 Volume 103(9):1433-1443 ereditary hemorrhagic telangiectasia (HHT), also known as Osler- Weber-Rendu syndrome, is an autosomal dominant disorder that Hcauses abnormal blood vessel formation. The diagnosis of hered- itary hemorrhagic telangiectasia is clinical, based on the Curaçao criteria. Genetic mutations that have been identified include ENG, ACVRL1/ALK1, and MADH4/SMAD4, among others. Patients with HHT may have telangiectasias and arteriovenous malformations in various organs and suffer from many complications including bleeding, anemia, iron deficiency, and high-output heart failure. Families with the same mutation exhibit considerable phenotypic variation. Optimal treatment is best delivered via a multidisciplinary approach with appropriate diag- nosis, screening and local and/or systemic management of lesions. Antiangiogenic agents such as bevacizumab have emerged as a promis- ing systemic therapy in reducing bleeding complications but are not cur- ative. Other pharmacological agents include iron supplementation, antifibrinolytics and hormonal treatment. This review discusses the biol- ogy of HHT, management issues that face -
A Successful Intra-Pleural Fibrinolytic Therapy with Alteplase in a Patient with Empyematous Multiloculated Chylothorax
CASE REPORT East J Med 24(3): 379-382, 2019 DOI: 10.5505/ejm.2019.72621 A Successful Intra-Pleural Fibrinolytic Therapy With Alteplase in A Patient with Empyematous Multiloculated Chylothorax Mohamed Faisal1*, Rayhan Amiseno1, Nurashikin Mohammad2 1Respiratory Unit, Universiti Kebangsaan Malaysia Medical Centre, Malaysia 2Medical Department, Universiti Sains Malaysia ABSTRACT Chylothorax is a collection of chyle in the pleural cavity resulting from leakage of lymphatic vessels, usually from the thoracic duct. In majority of cases, chylothorax is a bacteriostatic pleural effusion. Incidence of infected or even empyematous chylothorax are not common. Here, we report a case of a 57-year-old man with end stage renal disease and complete central venous stenosis who presented with recurrent right-sided chylothorax. It was complicated with sepsis and multilocated empyema and treated successfully with intra-pleural fibrinolytic therapy using alteplase. Key Words: Chylothorax, empyema, intrapleural fibrinolysis Introduction effusions and empyema in the adult population for the outcomes of treatment failure (surgical Chyle is a non-inflammatory, bacteriostatic fluid intervention or death) and surgical intervention with a variable protein, fat and a lymphocyte alone (4). Our patient had chylothorax which was predominance of the total nucleated cells. (1,2) complicated with empyema and treated with Incidence data are available for only post- combination of intravenous antibiotic and operative chylothorax, which can occur after sequential intra-pleural alteplase (without almost any surgical operation in the chest. It is deoxyribonuclease) administered to different most often observed after esophagectomy (about pleural locules. 3% of cases), or after heart surgery in children (up to about 6% of cases) (1). -
Vascular Disease in the Elderly
Chapter 13: Vascular Disease in the Elderly Nobuyuki Bill Miyawaki* and Paula E. Lester† *Division of Nephrology and †Division of Geriatrics, Winthrop University Hospital, Mineola, New York PHYSIOLOGIC EFFECTS OF AGING ON stiffening of medium and large arteries lined with BLOOD VESSEL ELASTICITY AND atheromatous plaques. The progressive accumula- COMPLIANCE tion of atherosclerotic plaque continues with aging and often remains silent until lesions reach a critical The aging process is commonly associated with in- stenotic threshold or rupture, leading to dimin- creased vascular rigidity and decreased vascular ished organ perfusion. Arterial stiffening also leads compliance. This process reflects the accumulation to an increase in pulse wave velocity and an en- of smooth muscle cells and connective tissue in the hancement in central aortic systolic pressure.3 The walls of major blood vessels. Endothelial cells and increased waveform velocity allows the backward smooth muscle cells constitute most of vessel wall reflective wave to return earlier back to the heart. cellularity and the remainder of the wall is com- The resulting increases of the left ventricular myo- posed of extracellular matrix including collagen cardial load and the loss of coronary perfusion at and elastin. Although aging has minimal effect on the onset of diastole may potentiate myocardial the muscular tunica media layer thickness, aging ischemia.3 leads to profound progressive thickening of the tu- Common ailments in the elderly including dia- nica intima layer comprised -
Coronary Thrombosis
University of Nebraska Medical Center DigitalCommons@UNMC MD Theses Special Collections 5-1-1938 Coronary thrombosis R. W. Karrer University of Nebraska Medical Center This manuscript is historical in nature and may not reflect current medical research and practice. Search PubMed for current research. Follow this and additional works at: https://digitalcommons.unmc.edu/mdtheses Part of the Medical Education Commons Recommended Citation Karrer, R. W., "Coronary thrombosis" (1938). MD Theses. 669. https://digitalcommons.unmc.edu/mdtheses/669 This Thesis is brought to you for free and open access by the Special Collections at DigitalCommons@UNMC. It has been accepted for inclusion in MD Theses by an authorized administrator of DigitalCommons@UNMC. For more information, please contact [email protected]. CORONARY THROMBOSIS by R. w. Karrer Senior Thesis presented to the College of Medicine, University of Nebraska Omaha, 1938. 480947 INTRODUCTION The terms coronary thrombosis, coronary occlusion, and cardiac or myocardial infarction are often em- ployed as synonyms, although there are useful differences in their meanings. In this thesis the author will deal only with that special type of coronary occlusion in which coronary thrombosis is the final event in the process of occlusion. Also, the thesis will be limited, more or less, to that type of thrombosis which is acute thrombosis of a coronary artery, rather than to the chronic type which is neither as spec tacular a disease nor as clean cut in its clinical picture. The definition of coronary thrombosis as given by Dorland {1935} is, "The formation of a clot in a branch of the coronary arteries which supply blood to the heart muscle, resulting in obstruction of the artery and infarction of the area of the heart supplied by the occluded vessel." Cecil (1935) modifies the definition in that he mentions the obstruction is generally acute. -
Relationship Between Cerebrovascular Atherosclerotic Stenosis and Rupture Risk of Unruptured Intracranial Aneurysm a Single-Cen
Clinical Neurology and Neurosurgery 186 (2019) 105543 Contents lists available at ScienceDirect Clinical Neurology and Neurosurgery journal homepage: www.elsevier.com/locate/clineuro Relationship between cerebrovascular atherosclerotic stenosis and rupture risk of unruptured intracranial aneurysm: A single-center retrospective T study Xin Fenga,b, Peng Qia, Lijun Wanga, Jun Lua, Hai Feng Wanga, Junjie Wanga, Shen Hua, Daming Wanga,b,⁎ a Department of Neurosurgery, Beijing Hospital, National Center of Gerontology, No. 1 DaHua Road, Dong Dan, Beijing, 100730, China b Graduate School of Peking Union Medical College, No. 9 Dongdansantiao, Dongcheng District, Beijing, 100730, China ARTICLE INFO ABSTRACT Keywords: Objectives: Cerebrovascular atherosclerotic stenosis (CAS) and intracranial aneurysm (IA) have a common un- Atherosclerotic stenosis derlying arterial pathology and common risk factors, but the clinical significance of CAS in IA rupture (IAR) is Intracranial aneurysm unclear. This study aimed to investigate the effect of CAS on the risk of IAR. Risk factor Patients and methods: A total of 336 patients with 507 sacular IAs admitted at our center were included. Rupture Univariable and multivariable logistic regression analyses were performed to determine the association between IAR and the angiographic variables for CAS. We also explored the differences in CAS in patients aged < 65 and ≥65 years. Results: In all the patient groups, moderate (50%–70%) cerebrovascular stenosis was significantly associated with IAR (odds ratio [OR], 3.4; 95% confidence interval [CI], 1.8–6.5). Single cerebral artery stenosis was also significantly associated with IAR (OR, 2.3; 95% CI, 1.3–3.9), and intracranial stenosis may be a risk factor for IAR (OR, 1.8; 95% CI, 1.0–3.2). -
Rendu-Osler-Weber Syndrome: What Radiologists Should Know
http://dx.doi.org/10.1590/S0100-39842013000300011 Agnollitto PM et al. Rendu-Osler-Weber:ICONOGRAPHIC whatESSAY radiologists should know Rendu-Osler-Weber syndrome: what radiologists should know. Literature review and three cases report* Síndrome de Rendu-Osler-Weber: o que o radiologista precisa saber. Revisão da literatura e apresentação de três casos Paulo Moraes Agnollitto1, André Rodrigues Façanha Barreto1, Raul Fernando Pinsetta Barbieri1, Jorge Elias Junior2, Valdair Francisco Muglia2 Abstract Rendu-Osler-Weber syndrome or hereditary hemorrhagic telangiectasia is an autosomal dominant vascular disease involving multiple systems whose main pathological change is the presence of abnormal arteriovenous communications. Most common symptoms include skin and mucosal telangiectasias, epistaxis, gastrointestinal, pulmonary and intracerebral bleeding. The key imaging finding is the presence of visceral arteriovenous malformations. The diagnosis is based on clinical criteria and can be confirmed by molecular biology techniques. Treatment includes measures for management of epistaxis, as well as surgical excision, radiotherapy and embolization of arteriovenous malformations, with emphasis on endovascular treatment. The present pictorial essay includes a report of three typical cases of this entity and a literature review. Keywords: Rendu-Osler-Weber; Hereditary hemorrhagic telangiectasia; Arteriovenous fistula; Epistaxis. Resumo A síndrome de Rendu-Osler-Weber ou teleangiectasia hemorrágica hereditária é uma doença vascular autossômica do- minante com acometimento de múltiplos sistemas, cujo principal achado patológico é a presença de comunicações arteriovenosas anômalas. Os sintomas mais comuns são teleangiectasias cutaneomucosas e epistaxe, além de sangra- mento pulmonar, gastrintestinal e intracerebral. O principal achado evidenciado nos métodos de diagnóstico por ima- gem é a presença de malformações arteriovenosas viscerais. O diagnóstico é realizado por meio de critérios clínicos e pode ser confirmado por técnicas de biologia celular. -
Spinal Stenosis.Pdf
Spinal Stenosis Overview Spinal stenosis is the narrowing of your spinal canal and nerve root canal along with the enlargement of your facet joints. Most commonly it is caused by osteoarthritis and your body's natural aging process, but it can also develop from injury or previous surgery. As the spinal canal narrows, there is less room for your nerves to branch out and move freely. As a result, they may become swollen and inflamed, which can cause pain, cramping, numbness or weakness in your legs, back, neck, or arms. Mild to moderate symptoms can be relieved with medications, physical therapy and spinal injections. Severe symptoms may require surgery. Anatomy of the spinal canal To understand spinal stenosis, it is helpful to understand how your spine works. Your spine is made of 24 moveable bones called vertebrae. The vertebrae are separated by discs, which act as shock absorbers preventing the vertebrae from rubbing together. Down the middle of each vertebra is a hollow space called the spinal canal that contains the spinal cord, spinal nerves, ligaments, fat, and blood vessels. Spinal nerves exit the spinal canal through the intervertebral foramen (also called the nerve root canal) to branch out to your body. Both the spinal and nerve root canals are surrounded by bone and ligaments. Bony changes can narrow the canals and restrict the spinal cord or nerves (see Anatomy of the Spine). What is spinal stenosis? Spinal stenosis is a degenerative condition that happens gradually over time and refers to: • narrowing of the spinal and nerve root canals • enlargement of the facet joints • stiffening of the ligaments • overgrowth of bone and bone spurs (Figure 1) Figure 1. -
Neonatal Myocardial Infarction a Retrospective Study and Literature
Progress in Pediatric Cardiology 55 (2019) 101171 Contents lists available at ScienceDirect Progress in Pediatric Cardiology journal homepage: www.elsevier.com/locate/ppedcard Review Neonatal myocardial infarction: A retrospective study and literature review T ⁎ Othman A. Aljohania, , James C. Perrya, Hannah R. El-Sabroutb, Sanjeet R. Hegdea, Jose A. Silva Sepulvedaa, Val A. Catanzaritec, Maryam Tarsad, Amy Kimballe, John W. Moorea, Howaida G. El-Saida a Division of Pediatric Cardiology, Department of Pediatrics, Rady Children's Hospital, University of California, San Diego, CA, United States b Department of Molecular, Cell and Developmental Biology, University of California, Los Angeles, CA, United States c Division of Maternal and Fetal Medicine, Rady Children's Specialists of San Diego, University of California, San Diego, CA, United States d Division of Maternal Fetal Medicine, Department of Reproductive Medicine, University of California, San Diego, CA, United States e Division of Neonatology, Department of Pediatrics, Rady Children's Hospital, University of California, San Diego, CA, United States ARTICLE INFO ABSTRACT Keywords: Neonatal myocardial infarction (MI), in the absence of congenital heart disease or cardiac surgery involving the Neonatal myocardial infarction coronaries, is a rare condition with associated high mortality. A cluster of neonatal myocardial infarction cases Neonatal coronary thrombosis was observed, leading to an investigation of causes and contributors. We performed a single-center review of neonates >37 weeks between 2011 and 2017 to identify neonates with myocardial infarction. Neonates with prior cardiac surgery, congenital anomalies of the coronaries, or sepsis were excluded. Diagnosis of MI was based on ECG changes, elevated troponin, decreased function or regional wall abnormality, and abnormal coronary angiography. -
Acute Thrombosis of Double Major Coronary Arteries Associated with Amphetamine Abuse
Case Reports Acta Cardiol Sin 2007;23:268-72 Acute Thrombosis of Double Major Coronary Arteries Associated with Amphetamine Abuse Wei-Ren Lan, Hung-I Yeh, Charles Jia-Yin Hou and Yu-San Chou Drug-induced acute myocardial infarction is not a common phenomenon. The underlying mechanism in the majority of such patients has been related to coronary spasm, including in those with amphetamine abuse, in whom the coronary arteriogram was always found normal. We report a 30-year-old male amphetamine abuser with acute myocardial infarction owing to acute thrombosis of the left anterior descending coronary artery and left circumflex coronary artery. We postulate a relationship between the use of amphetamine and occurrence of acute thrombosis of multiple major coronary arteries. Key Words: Amphetamine · Coronary · Thrombosis INTRODUCTION after intruding into a private apartment when acute chest pain occurred. He was brought by policemen to our emer- Amphetamines have been gaining popularity as a gency unit 2 hours after the onset of acute chest pain, recreational drug worldwide over the past few decades. which radiated to the back and was accompanied by nausea Acute myocardial infarction (AMI) owing to amphe- and vomiting but no shortness of breath. The patient had no tamine abuse often occurs in young adults, in whom coro- history of hypertension, hyperlipidemia, diabetes mellitus, nary spasm is thought to be the underlying mechanism.1 atrial fibrillation, or family history of coronary artery To our knowledge, there is no published registry of am- disease. He had smoked 2 packs of cigarettes daily for more phetamine-induced AMI with multiple coronary thrombo- than 10 years. -
Coronary Heart Disease
CORONARY HEART DISEASE Shalon R. Buchs, MHS, PA-C ■ Outline the diagnostic criteria and management for stable angina ■ Discuss clinical features and diagnostic approach for each of the acute coronary syndromes: unstable angina, STEMI and NSTEMI ■ Recognize causes of MI – – Type 1 (blocked coronary due to atherosclerosis) – Type 2- (ischemia from a non coronary artery disease cause) ■ Develop an understanding of the medical management for each of the acute coronary syndromes ■ Discuss the indications for percutaneous coronary intervention vs. thrombolytics vs. surgical intervention for coronary artery disease Objectives Epidemiology of CHD ■ Heart disease mortality has been declining in the US and areas where economies and health care systems are advanced ■ BUT from a global perspective it is the number one cause of death and disability in the developed world Epidemiology of CAD ■ While recent numbers show an overall decline in mortality; prediction models estimate that mortality from CAD will grow from ~9 million in 1990 to ~19 million in 2020. – Increased life expectancy – Diet and obesity – Sedentary lifestyles – Increased cigarette smoking Epidemiology CAD is the leading cause of death in adults in the US Approximately one third of all deaths in persons over age 35 can be attributed to CAD 18% increase for both sexes by 2030 Incidence Lifetime risk of development of CAD is 49% for men age 40 Lifetime risk of development of CAD is 32 % for women age 40 Prevalence and burden ~18.2 million adults in the US have CAD (CDC) More than 1 million