Aka “Heart Attack”)
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Effect of Captopril on Post-Infarction Remodelling Visualized by Light
www.nature.com/scientificreports OPEN Efect of captopril on post‑infarction remodelling visualized by light sheet microscopy and echocardiography Urmas Roostalu1*, Louise Thisted1, Jacob Lercke Skytte1, Casper Gravesen Salinas1, Philip Juhl Pedersen1, Jacob Hecksher‑Sørensen1, Bidda Rolin1,3, Henrik H. Hansen1, James G. MacKrell2, Robert M. Christie2, Niels Vrang1, Jacob Jelsing1 & Nora Elisabeth Zois1 Angiotensin converting enzyme inhibitors, among them captopril, improve survival following myocardial infarction (MI). The mechanisms of captopril action remain inadequately understood due to its diverse efects on multiple signalling pathways at diferent time periods following MI. Here we aimed to establish the role of captopril in late‑stage post‑MI remodelling. Left anterior descending artery (LAD) ligation or sham surgery was carried out in male C57BL/6J mice. Seven days post‑surgery LAD ligated mice were allocated to daily vehicle or captopril treatment continued over four weeks. To provide comprehensive characterization of the changes in mouse heart following MI a 3D light sheet imaging method was established together with automated image analysis workfow. The combination of echocardiography and light sheet imaging enabled to assess cardiac function and the underlying morphological changes. We show that delayed captopril treatment does not afect infarct size but prevents left ventricle dilation and hypertrophy, resulting in improved ejection fraction. Quantifcation of lectin perfused blood vessels showed improved vascular density in the infarct border zone in captopril treated mice in comparison to vehicle dosed control mice. These results validate the applicability of combined echocardiographic and light sheet assessment of drug mode of action in preclinical cardiovascular research. Although timely primary coronary percutaneous intervention has substantially improved patient survival post myocardial infarction (MI), the ofen-concomitant cardiac dysfunction and heart failure afect a signifcant num- ber of patients. -
J Wave Syndromes
Review Article http://dx.doi.org/10.4070/kcj.2016.46.5.601 Print ISSN 1738-5520 • On-line ISSN 1738-5555 Korean Circulation Journal J Wave Syndromes: History and Current Controversies Tong Liu, MD1, Jifeng Zheng, MD2, and Gan-Xin Yan, MD3,4 1Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular disease, Department of Cardiology, Tianjin Institute of Cardiology, The Second Hospital of Tianjin Medical University, Tianjin, 2Department of cardiology, The Second Hospital of Jiaxing, Jiaxing, China, 3Lankenau Institute for Medical Research and Lankenau Medical Center, Wynnewood, Pennsylvania, USA, 4The First Affiliated Hospital, Medical School of Xi'an Jiaotong University, Xi'an, China The concept of J wave syndromes was first proposed in 2004 by Yan et al for a spectrum of electrocardiographic (ECG) manifestations of prominent J waves that are associated with a potential to predispose affected individuals to ventricular fibrillation (VF). Although the concept of J wave syndromes is widely used and accepted, there has been tremendous debate over the definition of J wave, its ionic and cellular basis and arrhythmogenic mechanism. In this review article, we attempted to discuss the history from which the concept of J wave syndromes (JWS) is evolved and current controversies in JWS. (Korean Circ J 2016;46(5):601-609) KEY WORDS: Brugada syndrome; Sudden cardiac death; Ventricular fibrillation. Introduction History of J wave and J wave syndromes The concept of J wave syndromes was first proposed in 2004 The J wave is a positive deflection seen at the end of the QRS by Yan et al.1) for a spectrum of electrocardiographic (ECG) complex; it may stand as a distinct “delta” wave following the QRS, manifestations of prominent J waves that are associated with a or be partially buried inside the QRS as QRS notching or slurring. -
Screening for Peripheral Artery Disease and Cardiovascular Disease Risk Assessment with Ankle Brachial Index in Adults the U.S
Understanding Task Force Recommendations Screening for Peripheral Artery Disease and Cardiovascular Disease Risk Assessment with Ankle Brachial Index in Adults The U.S. Preventive Services Task Force (Task The Task Force reviewed the use of ABI to screen for Force) has issued a final recommendation statement PAD and to predict a person’s risk of heart attacks on Screening for Peripheral Artery Disease (PAD) and stroke. The final recommendation statement and Cardiovascular Disease (CVD) Risk Assessment summarizes what the Task Force learned about with Ankle Brachial Index (ABI) in Adults. the potential benefits and harms of this screening: There is not enough evidence to judge the benefits This final recommendation statement applies to and harms of using ABI for this purpose. adults who do not have signs or symptoms of PAD and who have not been diagnosed with PAD, CVD, This fact sheet explains the recommendation and severe chronic kidney disease, or diabetes. what it might mean for you. PAD is a disease in which fatty deposits called plaque build up in What is peripheral the arteries, especially those in the legs. Over time, the plaque can block the flow of blood to the legs often artery disease? leading to pain with walking. What is Cardiovascular disease affects the heart and blood vessels. It is caused by a build up of plaque in arteries that supply the heart, brain, and cardiovascular other parts of the body. When the build up is in the legs it is called disease? PAD. Heart attacks and strokes are other common types of CVD. Facts About CVD and PAD Cardiovascular disease is the leading killer of both men and women in the United States. -
Cardiovascular Disease and Rehab
EXERCISE AND CARDIOVASCULAR ! CARDIOVASCULAR DISEASE Exercise plays a significant role in the prevention and rehabilitation of cardiovascular diseases. High blood pressure, high cholesterol, diabetes and obesity can all be positively affected by an appropriate and regular exercise program which in turn benefits cardiovascular health. Cardiovascular disease can come in many forms including: Acute coronary syndromes (coronary artery disease), myocardial ischemia, myocardial infarction (MI), Peripheral artery disease and more. Exercise can improve cardiovascular endurance and can improve overall quality of life. If you have had a cardiac event and are ready to start an appropriate exercise plan, Cardiac Rehabilitation may be the best option for you. Please call 317-745-3580 (Danville Hospital campus), 317-718-2454 (YMCA Avon campus) or 317-456-9058 (Brownsburg Hospital campus) for more information. SAFETY PRECAUTIONS • Ask your healthcare team which activities are most appropriate for you. • If prescribed nitroglycerine, always carry it with you especially during exercise and take all other medications as prescribed. • Start slow and gradually progress. If active before event, fitness levels may be significantly lower – listen to your body. A longer cool down may reduce complications. • Stop exercising immediately if you experience chest pain, fatigue, or labored breathing. • Avoid exercising in extreme weather conditions. • Drink plenty of water before, during, and after exercise. • Wear a medical identification bracelet, necklace, or ID tag in case of emergency. • Wear proper fitting shoes and socks, and check feet after exercise. STANDARD GUIDELINES F – 3-5 days a week. Include low weight resistance training 2 days/week I – 40-80% of exercise capacity using the heart rate reserve (HRR) (220-age=HRmax; HRmax-HRrest = HRR) T – 20-60mins/session, may start with sessions of 5-15 mins if necessary T – Large rhythmic muscle group activities that are low impact (walking, swimming, biking) Get wellness tips to keep YOU healthy at HENDRICKS.ORG/SOCIAL.. -
Myocardial Infarction (Heart Attack)
Sacramento Heart & Vascular Medical Associates February 19, 2012 500 University Ave. Sacramento, CA 95825 Page 1 916-830-2000 Fax: 916-830-2001 Patient Information For: Only A Test Myocardial Infarction (Heart Attack) What is a myocardial infarction (MI)? Myocardial infarction (MI) is a heart attack. It happens when blood flow to a part of the heart is suddenly blocked. How does it occur? Myocardial infarction may occur at any time and often occurs without warning. As we grow older, our coronary arteries may become narrowed by the buildup of cholesterol plaque. When the arteries narrow, less blood can go through them, and less oxygen gets to the heart muscle. The process of narrowing is called atherosclerosis. The narrower the artery becomes, the more likely it is that a blood clot may form and block the artery completely, causing a heart attack. Sometimes sudden blockages can occur even in places where the artery was not narrow before. A heart attack may also occur when the heart muscle needs more oxygen than the blood vessels can provide. This might happen, for example, during hard exercise such as shoveling snow, or with a sudden increase in blood pressure. Less commonly, a heart attack can occur due to coronary spasm. Coronary spasm is a sudden and temporary narrowing of a small part of an artery that supplies blood to the heart. It may be caused by smoking or drugs such as cocaine. Risk factors for heart disease include: - cigarette smoking - a family history of heart attack - diabetes - overweight - high blood pressure - high blood cholesterol - low HDL cholesterol (that is, too little "good" cholesterol) - stress - a lifestyle that does not include much physical activity. -
Cardiovascular Disease Session Guidelines
Cardiovascular Disease Session Guidelines This is a 15 minute webinar session for CNC physicians and staff CNC holds webinars on the 3rd Wednesday of each month to address topics related to risk adjustment documentation and coding Next scheduled webinar: • Wednesday, February 28th • Topic: Respiratory Disease CNC does not accept responsibility or liability for any adverse outcome from this training for any reason including undetected inaccuracy, opinion, and analysis that might prove erroneous or amended, or the coder/physician’s misunderstanding or misapplication of topics. Application of the information in this training does not imply or guarantee claims payment. Agenda • Statistics • Amputation Status & Atherosclerosis • Angina Pectoris • Acute Myocardial Infarction • Specified Heart Arrhythmias • Congestive Heart Failure • Pulmonary Hypertension • Cardiomyopathy • Hypertensive Heart disease Statistics • Nearly 35 percent of Tarrant County and Dallas area deaths each year are attributed to cardiovascular disease. • About 610,000 people die of heart disease in the United States every year–that’s 1 in every 4 deaths • Heart disease is the leading cause of death for both men and women • Every year about 735,000 Americans have a heart attack. Of these, (approximately 70%) 525,000 are a first heart attack and (approximately 30%)210,000 happen in people who have already had a heart attack Amputations There are nearly 2 million people living with limb loss in the United States Approximately 185,000 amputations occur in the United States each -
The Management of Acute Coronary Syndromes in Patients Presenting
CONCISE GUIDANCE Clinical Medicine 2021 Vol 21, No 2: e206–11 The management of acute coronary syndromes in patients presenting without persistent ST-segment elevation: key points from the ESC 2020 Clinical Practice Guidelines for the general and emergency physician Authors: Ramesh NadarajahA and Chris GaleB There have been significant advances in the diagnosis and international decline in mortality rates.2,3 In September 2020, management of non-ST-segment elevation myocardial the European Society of Cardiology (ESC) published updated infarction over recent years, which has been reflected in an Clinical Practice Guidelines for the management of ACS in patients international decline in mortality rates. This article provides an presenting without persistent ST-segment elevation,4 5 years after overview of the 2020 European Society of Cardiology Clinical the last iteration. ABSTRACT Practice Guidelines for the topic, concentrating on areas relevant The guidelines stipulate a number of updated recommendations to the general or emergency physician. The recommendations (supplementary material S1). The strength of a recommendation and underlying evidence basis are analysed in three key and level of evidence used to justify it are weighted and graded areas: diagnosis (the recommendation to use high sensitivity according to predefined scales (Table 1). This focused review troponin and how to apply it), pathways (the recommendation provides learning points derived from the guidelines in areas to facilitate early invasive coronary angiography to improve relevant to general and emergency physicians, including diagnosis outcomes and shorten hospital stays) and treatment (a (recommendation to use high sensitivity troponin), pathways paradigm shift in the use of early intensive platelet inhibition). -
Incomplete Versus Complete Myocardial Infarction
Henry Ford Hospital Medical Journal Volume 39 Number 3 Article 20 9-1991 Incomplete Versus Complete Myocardial Infarction Mihai Gheorghiade Sidney Goldstein Follow this and additional works at: https://scholarlycommons.henryford.com/hfhmedjournal Part of the Life Sciences Commons, Medical Specialties Commons, and the Public Health Commons Recommended Citation Gheorghiade, Mihai and Goldstein, Sidney (1991) "Incomplete Versus Complete Myocardial Infarction," Henry Ford Hospital Medical Journal : Vol. 39 : No. 3 , 263-264. Available at: https://scholarlycommons.henryford.com/hfhmedjournal/vol39/iss3/20 This Article is brought to you for free and open access by Henry Ford Health System Scholarly Commons. It has been accepted for inclusion in Henry Ford Hospital Medical Journal by an authorized editor of Henry Ford Health System Scholarly Commons. Incomplete Versus Complete Myocardial Infarction Mihai Gheorghiade, MD,* and Sidney Goldstein, MD* Incomplete myocardial infarction (MI), when compared with a complete Ml. is characterized by a small infarct size and a large mass of viable hut jeopardized myocardium within the perfusion zone of the infarct-related vessel that is manifested ctinicalty hy early recurrent infarction. The pathophysiology involves earty spontaneous or thrombolytic reperfusion. Clinical (i.e., residual ischemia), electrocardiographic, and echocardiographic findings and magnitude of serum cardiac enzyme elevatitms should be taken into account in diagnosing an incomplete Ml. (Heniy Ford Hosp MedJ 1991;39:263-4) he observation that the ischemic event associated with on the ECG may not properly identify patients with incomplete Tthrombotic occlusion of the coronary artery can be inter infarction. rupted with thrombolytic therapy has led to the recognition of a When applied to the individual patient, it is therefore more new ischemic syndrome, the incomplete myocardial infarction useful to divide postinfarction patients, regardless of whether or (MI) (1). -
Treatment of Acute Coronary Syndrome
Acute Coronary Syndrome: Current Treatment TIMOTHY L. SWITAJ, MD, U.S. Army Medical Department Center and School, Fort Sam Houston, Texas SCOTT R. CHRISTENSEN, MD, Martin Army Community Hospital Family Medicine Residency Program, Fort Benning, Georgia DEAN M. BREWER, DO, Guthrie Ambulatory Health Care Clinic, Fort Drum, New York Acute coronary syndrome continues to be a significant cause of morbidity and mortality in the United States. Family physicians need to identify and mitigate risk factors early, as well as recognize and respond to acute coronary syn- drome events quickly in any clinical setting. Diagnosis can be made based on patient history, symptoms, electrocardi- ography findings, and cardiac biomarkers, which delineate between ST elevation myocardial infarction and non–ST elevation acute coronary syndrome. Rapid reperfusion with primary percutaneous coronary intervention is the goal with either clinical presentation. Coupled with appropriate medical management, percutaneous coronary interven- tion can improve short- and long-term outcomes following myocardial infarction. If percutaneous coronary interven- tion cannot be performed rapidly, patients with ST elevation myocardial infarction can be treated with fibrinolytic therapy. Fibrinolysis is not recommended in patients with non–ST elevation acute coronary syndrome; therefore, these patients should be treated with medical management if they are at low risk of coronary events or if percutaneous coronary intervention cannot be performed. Post–myocardial infarction care should -
ST-Elevation Myocardial Infarction Due to Acute Thrombosis in an Adolescent with COVID-19
Prepublication Release ST-Elevation Myocardial Infarction Due to Acute Thrombosis in an Adolescent With COVID-19 Jessica Persson, MD, Michael Shorofsky, MD, Ryan Leahy, MD, MS, Richard Friesen, MD, Amber Khanna, MD, MS, Lyndsey Cole, MD, John S. Kim, MD, MS DOI: 10.1542/peds.2020-049793 Journal: Pediatrics Article Type: Case Report Citation: Persson J, Shorofsky M, Leahy R, et al. ST-elevation myocardial infarction due to acute thrombosis in an adolescent with COVID-19. Pediatrics. 2021; doi: 10.1542/peds.2020- 049793 This is a prepublication version of an article that has undergone peer review and been accepted for publication but is not the final version of record. This paper may be cited using the DOI and date of access. This paper may contain information that has errors in facts, figures, and statements, and will be corrected in the final published version. The journal is providing an early version of this article to expedite access to this information. The American Academy of Pediatrics, the editors, and authors are not responsible for inaccurate information and data described in this version. Downloaded from©202 www.aappublications.org/news1 American Academy by of guest Pediatrics on September 27, 2021 Prepublication Release ST-Elevation Myocardial Infarction Due to Acute Thrombosis in an Adolescent With COVID-19 Jessica Persson, MD1, Michael Shorofsky, MD1, Ryan Leahy, MD, MS1, Richard Friesen, MD1, Amber Khanna, MD, MS1,2, Lyndsey Cole, MD3, John S. Kim, MD, MS1 1Division of Cardiology, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado 2Division of Cardiology, Department of Medicine, University of Colorado School of Medicine, Aurora, Colorado 3Section of Infectious Diseases, Department of Pediatrics, University of Colorado School of Medicine, Aurora, Colorado Corresponding Author: John S. -
2015 ESC Guidelines for the Diagnosis and Management Of
European Heart Journal Advance Access published August 29, 2015 European Heart Journal ESC GUIDELINES doi:10.1093/eurheartj/ehv318 2015 ESC Guidelines for the diagnosis and management of pericardial diseases The Task Force for the Diagnosis and Management of Pericardial Diseases of the European Society of Cardiology (ESC) Endorsed by: The European Association for Cardio-Thoracic Surgery (EACTS) Downloaded from Authors/Task Force Members: Yehuda Adler* (Chairperson) (Israel), Philippe Charron* (Chairperson) (France), Massimo Imazio† (Italy), Luigi Badano (Italy), Gonzalo Baro´ n-Esquivias (Spain), Jan Bogaert (Belgium), Antonio Brucato http://eurheartj.oxfordjournals.org/ (Italy), Pascal Gueret (France), Karin Klingel (Germany), Christos Lionis (Greece), Bernhard Maisch (Germany), Bongani Mayosi (South Africa), Alain Pavie (France), Arsen D. Ristic´ (Serbia), Manel Sabate´ Tenas (Spain), Petar Seferovic (Serbia), Karl Swedberg (Sweden), and Witold Tomkowski (Poland) Document Reviewers: Stephan Achenbach (CPG Review Coordinator) (Germany), Stefan Agewall (CPG Review Coordinator) (Norway), Nawwar Al-Attar (UK), Juan Angel Ferrer (Spain), Michael Arad (Israel), Riccardo Asteggiano (Italy), He´ctor Bueno (Spain), Alida L. P. Caforio (Italy), Scipione Carerj (Italy), Claudio Ceconi (Italy), Arturo Evangelista (Spain), Frank Flachskampf (Sweden), George Giannakoulas (Greece), Stephan Gielen by guest on October 21, 2015 (Germany), Gilbert Habib (France), Philippe Kolh (Belgium), Ekaterini Lambrinou (Cyprus), Patrizio Lancellotti (Belgium), George Lazaros (Greece), Ales Linhart (Czech Republic), Philippe Meurin (France), Koen Nieman (The Netherlands), Massimo F. Piepoli (Italy), Susanna Price (UK), Jolien Roos-Hesselink (The Netherlands), * Corresponding authors: Yehuda Adler, Management, Sheba Medical Center, Tel Hashomer Hospital, City of Ramat-Gan, 5265601, Israel. Affiliated with Sackler Medical School, Tel Aviv University, Tel Aviv, Israel, Tel: +972 03 530 44 67, Fax: +972 03 530 5118, Email: [email protected]. -
Myocardial Infarction Does Not Accelerate Atherosclerosis in a Mouse Model of Type 1 Diabetes
Diabetes Volume 69, October 2020 2133 Myocardial Infarction Does Not Accelerate Atherosclerosis in a Mouse Model of Type 1 Diabetes Farah Kramer,1 Amy M. Martinson,2 Thalia Papayannopoulou,3 and Jenny E. Kanter1 Diabetes 2020;69:2133–2143 | https://doi.org/10.2337/db20-0152 In addition to increasing the risk of an initial myocardial observed in response to the acute ischemic event was pos- infarction (MI), diabetes increases the risk of a recur- tulated to be driven by enhanced extramedullary hemato- rent MI. Previous work suggests that an experimental poiesis resulting in increased levels of circulating monocytes MI can accelerate atherosclerosis via monocytosis. To available for recruitment into the nascent atherosclerotic test whether diabetes and experimental MI synergize to lesion, thereby accelerating atherosclerosis (9). accelerate atherosclerosis, we performed ligation of Diabetes accelerates atherosclerosis lesion initiation and the left anterior descending coronary artery to induce progression and hinders lesion regression in response to experimental MI or sham surgery in nondiabetic and dramatic lipid lowering (10–13). Changes in monocyte and diabetic mice with preexisting atherosclerosis. All mice macrophage phenotype are believed to contribute to the COMPLICATIONS fi subjected to experimental MI had signi cantly reduced acceleration of atherosclerosis in diabetes. In both mouse left ventricular function. In our model, in comparisons and human studies, diabetes results in increased macro- with nondiabetic sham mice, neither diabetes nor MI phage accumulation within the artery wall (10,14,15). For resulted in monocytosis. Neither diabetes nor MI led to example, autopsy and atherectomy samples from humans increased atherosclerotic lesion size, but diabetes ac- celerated lesion progression, exemplified by necrotic have shown that lesions from subjects with diabetes have core expansion.