DOCSLIB.ORG

Incomplete Versus Complete Myocardial Infarction

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
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). These observations have also called our attention to the not they have spontaneous reperfusion or receive thrombolytic fact that early spontaneous reperfusion may occur in patients therapy, into those who have a completed versus incomplete MI. who experience a non-Q wave MI (2). These two clinical pre­ In determining the incompleteness of MI, a number of factors sentations of incomplete infarction identify patients with initial­ come into play. The presence of Q waves, the location of the ST ly small Mis who are at risk of early recurrence of myocardial and T-wave changes (5), and the degree of ST depression (17, ischemia involving a relatively large area of viable but jeopar­ 18) all are important. Peak serum creatine phosphokinase eleva­ dized myocardium in the infarct-related artery (3). tion may have significance in differentiation of the event. Small Patients recovering from a large but completed Ml have a elevations of creatine phosphokinase suggest an incompleted well-defined increased mortality related to the extent of myocar­ event (16,19). The magnitude of wall motion abnormality in the dium lost (4). In contrast, patients with an incomplete ischemic area of the infarct-related artery, evaluated either by echocardi­ event, despite an initial modest insult, are prone to reinfarction ography or angiography, provides important information as to shortly after their event, leading to a significant increase in mor­ the completeness of the MI. However, early reperfusion of the tality related to further tissue loss and recurrent ischemia (5). occluded artery is not always accompanied by immediate recov­ Patients who experienced early thrombolytic or spontaneous re­ ery of the contractile function in the infarct-related artery seg­ perfusion comprise the patient population of incomplete infarc­ ments (stunned myocardium). This condition in which the myo­ tion. Both groups of patients with incomplete infarction are cardium is viable but not contractile may persist much longer if bound together by the patent but diseased vessel, the high rate of the infarct-related artery is occluded or has a tight stenosis (hi­ early reinfarction, and a limited initial insult. bernating myocardium) (20,21). Identification of areas of viable Given the heterogeneity of the non-Q wave infarction group but not contractile myocardium (stunned or hibernating) may be (6) that includes patients with prior Q waves, different electro­ possible by observing functional recovery by two-dimensional cardiographic locations, and even normal ECGs (7), and the fact echocardiography during infusion of a small dose of dobuta­ that in patients receiving thrombolytic therapy the presence of Q mine (22,23). In addition, residual ischemia, spontaneous or pro­ waves does not always predict a completed event or transmural- voked in the area of the infarct-related artery, plays a pivotal role ity (8-10), it is not surprising that the ECG alone will not prop­ in identifying patients with an incomplete infarction (24). erly identify patients with an incomplete infarction (11-13). The In order to create a framework to describe the features of in­ frequent presence of a Q wave in the incomplete thrombolytic completeness of infarction, we propose the following: infarct is partially related to the duration of symptoms and the protocol demand for significant ST and T-wave changes before administering thrombolytic therapy (14,15). In addition, the ab­ sence of Q waves is not always correlated with a small or suben­ Submitted for publication: August 15. 1991, docardial MI, particularly if the myocardial segments are sup­ Accepled for publication: August 28, 1991, plied by the right or the circumflex coronary artery (16). In this *Heart and Vascular Institute, Division of Cardiovascular Medicine, Henry Ford Hospital, Address correspondence to Dr, Gheorghiade, Hean and Vascular Institute, Division of era of thrombolytic therapy, the absence or presence ofQ waves Cardiovascular Medicine, Henry Ford Hospilal, 2799 W Grand Blvd, Detroit, Ml 48202, Henry Ford Hosp Med J—Vol 39, Nos 3 & 4, 1991 Incomplete Versus Complete MI—Gheorghiade & Goldstein 263 I. Suspect incomplete infarction when: 6, Gibson RS, Non-Q-wave myocardial infarction: Diagnosis, prognosis, and 1. A. Non-Q wave without thrombolytic therapy, or management. Curt ProbI Cardiol 1988;13:8-72. 7, Boden WE, Kleiger RE, Gibson RS, et al. Favourable long term prognosis B. Q or non-Q wave with thrombolytic therapy. in patients with non-Q wave acute myocardial infarction not associated with spe­ 2. Small elevation usually less than 500 lU/L of the cre­ cific electrocardiographic changes, Br HeartJ 1989:61:396-402, atine phosphokinase. 8, Rogers WJ. Bourge RC, Papapietro SE. et al. Variables predictive of good 3. A. Angiographic or echocardiographic evidence of pre­ functional outcome following thrombolytic therapy in the Thrombolysis in served function in the infarct-related area, or Myocardial Infarction phase II (TIMI II) pilot study. Am J Cardiol 1989:63:503- 12, B. Angiographic or echocardiographic evidence of a 9, Califf RM. O'Neil W. Stack RS. et al. Failure of simple clinical measure­ large area of viable but noncontractile myocardium (stunned or ments to predict perfusion status after intravenous tftromtxjiysis, Ann Intem Med hibernating myocardium) identified by low-dose dobutamine 1988:108:658-62, infusion. 10, Jaffe AS. Sobel BE. Thrombolysis with tissue-type plasminogen activator 4. Residual ischemia present (postinfarction angina or ex­ in acute myocardial infarction: Potentials and pitfalls, JAMA 1986:255:237-9, ercise-induced ischemia). 11, Stone PH. Raabe DS. Jaffe AS. et al. Prognostic significance of location and type of myocardial infarction: Independent adverse outcome associated with II. Complete infarction: anterior location, J Am Coll Cardiol 1988:11:453-63, 1. Persistent Q waves. 12, Ross J Jr, Gilpin EA, Madsen EB. et al, A decision scheme for coronary 2. Major elevation of serum creatine phosphokinase. angiography after acute myocardial infarction. Circulation 1989;79:292-303, 3. No evidence of residual ischemia. 13, Benhorin J, Moss AJ. Oakes D. et al. The prognostic significance of first myocardial infarction type (Q wave versus non-Q wave) and Q wave location, J 4. Large area of ventricular akinesis in infarct-related ar­ Am Coll Cardiol 1990:15:1201-7, tery resulting from irreversibly damaged myocardium. 14, Mikell FL, Petrovich J. Snyder MC. etal. Reliability of Q-wave formation The criteria proposed are not rigid but require physician inter­ and QRS score in predicting regional and global left ventricular performance in pretation. A definition of the completeness of the infarction, tak­ acute myocardial infarction and successful reperfusion. Am J Cardiol 1986:57: ing these factors into consideration, is more complex than the 923-6, simple presence or absence of a Q wave. For example, the pa­ 15, Schweitzer P, The electrocardiographic diagnosis of acute myocardial in­ farction in the thrombolytic era. Am Heart J 1990:119:642-54. tient with a Q wave MI with small elevation of the creatine ki­ 16, Gib.son RS. Beiler GA, Gheorghiade M. et al. The prevalence and clinical nase serum level and preserved wall motion in the infarct-re­ significance of residual myocardial ischemia 2 weeks after uncomplicated non- lated area by echocardiography will be assigned to the incom­ Q wave infarction: A praspective natural history study. Circulation 1986:73: plete MI group. On the other hand, the patient with a non-Q 1186-98, wave infarct who
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.
    [Show full text]
  • 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.
    [Show full text]
  • 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.
    [Show full text]
  • Clinical Consequences of Stroke
    EBRSR [Evidence-Based Review of Stroke Rehabilitation] 2 Clinical Consequences of Stroke Robert Teasell MD, Norhayati Hussein MBBS Last updated: March 2018 Abstract Cerebrovascular disorders represent the third leading cause of mortality and the second major cause of long-term disability in North America (Delaney and Potter 1993). The impairments associated with a stroke exhibit a wide diversity of clinical signs and symptoms. Disability, which is multifactorial in its determination, varies according to the degree of neurological recovery, the site of the lesion, the patient's premorbid status and the environmental support systems. Clinical evidence is reviewed as it pertains to stroke lesion location (cerebral, right & left hemispheres; lacunar and brain stem), related disorders (emotional, visual spatial perceptual, communication, fatigue, etc.) and artery(s) affected. 2. Clinical Consequences of Stroke pg. 1 of 29 www.ebrsr.com Table of Contents Abstract .............................................................................................................................................1 Table of Contents ...............................................................................................................................2 Introduction ......................................................................................................................................3 2.1 Localization of the Stroke ...........................................................................................................3 2.2 Cerebral
    [Show full text]
  • Assessment and Management of Patients with Hypertension
    Chapter 32 G Assessment and Management of Patients With Hypertension LEARNING OBJECTIVES G On completion of this chapter, the learner will be able to: 1. Define blood pressure and identify risk factors for hypertension. 2. Explain the difference between normal blood pressure and hyper- tension and discuss the significance of hypertension. 3. Describe the treatment approach for hypertension, including lifestyle changes and medication therapy. 4. Use the nursing process as a framework for care of the patient with hypertension. 5. Describe the necessity for immediate treatment of hypertensive crisis. 854 Chapter 32 Assessment and Management of Patients With Hypertension 855 B lood pressure is the product of cardiac output multiplied by Primary Hypertension peripheral resistance. Cardiac output is the product of the heart rate multiplied by the stroke volume. In normal circulation, pres- Between 21% and 36% of the adult population in the United States sure is exerted by the flow of blood through the heart and blood has hypertension (Hajjar & Kotchen, 2003). Of this population, be- vessels. High blood pressure, known as hypertension, can result tween 90% and 95% have primary hypertension, meaning that from a change in cardiac output, a change in peripheral resis- the reason for the elevation in blood pressure cannot be identified. tance, or both. The medications used for treating hypertension The remaining 5% to 10% of this group have high blood pressure decrease peripheral resistance, blood volume, or the strength and related to specific causes, such as narrowing of the renal arteries, rate of myocardial contraction. renal parenchymal disease, hyperaldosteronism (mineralocorticoid hypertension) certain medications, pregnancy, and coarctation of the aorta (Kaplan, 2001).
    [Show full text]
  • Complication Prevention for Patients with Hypertension a Noncommunicable Disease Education Manual for Primary Health Care Professionals and Patients
    Complication prevention for patients with hypertension A noncommunicable disease education manual for primary health care professionals and patients Complication prevention for patients with hypertension A noncommunicable disease education manual for primary health care professionals and patients The Noncommunicable Disease Education Manual for Primary Health Care Professionals and Patients results from the contributions and hard work of many people. Its development was led by Dr Hai-Rim Shin, Coordinator, and Dr Warrick Junsuk Kim, Medical Officer, of the Noncommunicable Diseases and Health Promotion unit at the WHO Regional Office for the Western Pacific (WHO/WPRO/NCD) in Manila, Philippines. WHO graciously acknowledges the intellectual contributions of Dr Jung-jin Cho, Co-director, Community-based Primary Care Project Committee and Professor, Department of Family Medicine, Hallym University Sacred Heart Dongtan Hospital, Republic of Korea; Dr Hyejin Lee, Volunteer, WHO/WPRO/NCD (currently PhD candidate, Department of Family Medicine, Seoul National University, Republic of Korea); Ms Saki Narita, Volunteer, WHO/WPRO/NCD (currently PhD candidate, Department of Global Health Policy, Graduate School of Medicine, University of Tokyo, Japan); and Mr Byung Ki Kwon, Technical Officer, WHO/WPRO/NCD (currently Director, Division of Health Promotion, Ministry of Health and Welfare, Republic of Korea). Many thanks to Dr Albert Domingo, Dr Sonia McCarthy, Ms Marie Clem Carlos, Dr Katrin Engelhardt, Mr Kelvin Khow Chuan Heng and Dr Roberto Andres Ruiz from the WHO Regional Office for the Western Pacific and Dr Ma. Charina Benedicto, Physician-in-Charge, Bagong Barangay Health Center & Lying-in Clinic, Pandacan, Manila, Philippines for reviewing the draft publication. Financial support for this publication was received from the Korea Centers for Disease Control and Prevention, Republic of Korea.
    [Show full text]
  • Myocardial Infarction
    February 2021 www.nursingcenter.com Myocardial Infarction Myocardial infarction (MI) is defined as a clinical (or pathologic) event in the setting of myocardial ischemia in which there is evidence of myocardial injury (Anderson, Morrow, 2017; Thygesen, Alpert & Jaffe, 2018). The diagnosis is made with cardiac biomarkers (high sensitivity troponin or troponin-I) in association with cardiac symptoms, suggestive electrocardiographic changes, and/or imaging with echocardiography or nuclear studies indicating loss of viable myocardium or new regional wall motion abnormality. Classification of Acute Coronary Syndrome (ACS) ACS is classified based on the presence or absence of ST segment elevation. There are three major classifications of ACS: • Non-ST Segment Elevation Acute Coronary Syndrome (NSTE-ACS): Unstable Angina (UA) Clinical symptoms suggestive of ACS with the absence of persistent ST elevation and no elevation in cardiac biomarkers (troponin) [which are elevated with myocardial tissue damage]; with or without electrocardiogram (ECG) changes indicative of ischemia (Aroesty, Simons, & Breall, 2017). Diagnosis may be made by clinical history alone. • Non-ST Segment Elevation Acute Coronary Syndrome (NSTE-ACS): Non-ST Segment Elevation Myocardial Infarction (NSTEMI) Clinical symptoms suggestive of ACS with elevated cardiac biomarkers (troponin); with or without ECG changes indicative of cardiac ischemia (Anderson et al, 2013). Note: ECG changes suggestive of cardiac ischemia include ST depression, transient ST elevation or prominent T wave inversions. • ST-Segment Elevation Myocardial Infarction (STEMI) ACS symptoms with elevated cardiac biomarkers (troponin); ECG shows persistent ST elevation or new left bundle branch block (LBBB) (O’Gara et al, 2013). These patients should be considered for immediate reperfusion therapy (fibrinolysis or percutaneous coronary intervention [PCI]) (Anderson et al, 2013).
    [Show full text]
  • Symmetrical and Peripheral Gangrene Complicating a Third-Degree Atrioventricular Block: a New Presentation of a Known Disease
    Open Access Case Report DOI: 10.7759/cureus.10477 Symmetrical and Peripheral Gangrene Complicating a Third-Degree Atrioventricular Block: A New Presentation of a Known Disease Hanane Aissaoui 1 , Karima Benbouchta 1 , Noha Elouafi 1 , Brahim Housni 2 , Nabila Ismaili 1 1. Cardiology, Mohammed I University/Mohammed VI University Hospital/Epidemiological Laboratory of Clinical Research and Public Health, Oujda, MAR 2. Intensive Care and Anesthesiology, Mohammed I University/Mohammed VI University Hospital/Epidemiological Laboratory of Clinical Research and Public Health, Oujda, MAR Corresponding author: Hanane Aissaoui, [email protected] Abstract Symmetrical peripheral gangrene (SPG) is a rare, serious entity characterized by ischemic changes of the distal extremities with no vessel occlusion, leading to fatal complications. It is related to numerous causes, and the treatment is not yet consensual. We present the first case of SPG related to low cardiac output secondary to a third-degree atrioventricular block. Physicians should be aware of this entity, as early recognition and adequate management can help in reducing morbidity and mortality and prevent fatal complications. Categories: Anesthesiology, Cardiology, Dermatology Keywords: case report, symmetrical and peripheral gangrene, low cardiac flow, third degree atrioventricular block Introduction Symmetrical and peripheral gangrene (SPG) is a rare entity. It was first illustrated by Hutchinson in 1891 [1]. It is defined by a sudden onset of symmetrical ischemia of two or more extremities, leading to gangrene in the absence of large vessel obstruction or vasculitis, increasing the risk of limb amputation and affecting the quality of life [2-3]. The etiology is multifactorial. Several infective and non-infective etiologies were related to SPG [4].
    [Show full text]
  • Posttraumatic Cerebral Infarction Diagnosed by CT: Prevalence, Origin, and Outcome
    355 Posttraumatic Cerebral Infarction Diagnosed by CT: Prevalence, Origin, and Outcome Stuart E. Mirvis1 Posttraumatic cerebral infarction is a recognized complication of craniocerebral Aizik L. Wolf 2 trauma, but its frequency, cause, and influence on mortality are not well defined. To Yuji Numaguchi1 ascertain this information, all cranial CT studies demonstrating posttraumatic cerebral Gregory Corradino2 infarction and performed during a 40-month period at our trauma center were reviewed. John N. Joslyn1 Posttraumatic cerebral infarction was diagnosed by CT within 24 hr of admission (10 patients) and up to 14 days after admission (mean, 3 days) in 25 (1.9%) of 1332 patients who required cranial CT for trauma during the period. Infarcts, in well-defined arterial distributions, were diagnosed either uni- or bilaterally in the posterior cerebral (17), proximal andjor distal anterior cerebral (11), middle cerebral (11), lenticulostriate/ thalamoperforating (nine), anterior choroidal (three), andjor vertebrobasilar (two) terri­ tories in 23 patients. Two other patients displayed atypical infarction patterns with sharply marginated cortical and subcortical low densities crossing typical vascular territories. CT findings suggested direct vascular compression due to mass effects from edema, contusion, and intra- or extraaxial hematoma as the cause of infarction in 24 patients; there was postmortem verification in five. In one patient, a skull-base fracture crossing the precavernous carotid canal led to occlusion of the internal carotid artery and ipsilateral cerebral infarction. Mortality in craniocerebral trauma with complicating posttraumatic cerebral infarction, 68% in this series, did not differ significantly from that in craniocerebral trauma patients without posttraumatic cerebral infarction when matched for admission Glasgow Coma Score results.
    [Show full text]
  • ICD-10: Clinical Concepts for Cardiology
    ICD-10 Clinical Concepts for Cardiology ICD-10 Clinical Concepts Series Common Codes Clinical Documentation Tips Clinical Scenarios ICD-10 Clinical Concepts for Cardiology is a feature of Road to 10, a CMS online tool built with physician input. With Road to 10, you can: l Build an ICD-10 action plan customized l Access quick references from CMS and for your practice medical and trade associations l Use interactive case studies to see how l View in-depth webcasts for and by your coding selections compare with your medical professionals peers’ coding To get on the Road to 10 and find out more about ICD-10, visit: cms.gov/ICD10 roadto10.org ICD-10 Compliance Date: October 1, 2015 Official CMS Industry Resources for the ICD-10 Transition www.cms.gov/ICD10 1 Table Of Contents Common Codes • Abnormalities of • Hypertension Heart Rhythm • Nonrheumatic • Atrial Fibrillation and Flutter Valve Disorders • Cardiac Arrhythmias (Other) • Selected Atherosclerosis, • Chest Pain Ischemia, and Infarction • Heart Failure • Syncope and Collapse Clinical Documentation Tips • Acute Myocardial • Atheroclerotic Heart Disease Infraction (AMI) with Angina Pectoris • Hypertension • Cardiomyopathy • Congestive Heart Failure • Heart Valve Disease • Underdosing • Arrythmias/Dysrhythmia Clinical Scenarios • Scenario 1: Hypertension/ • Scenario 4: Subsequent AMI Cardiac Clearance • Scenario: CHF and • Scenario 2: Syncope Pulmonary Embolism Example • Scenario 3: Chest Pain Common Codes ICD-10 Compliance Date: October 1, 2015 Abnormalities of Heart Rhythm (ICD-9-CM 427.81, 427.89, 785.0, 785.1, 785.3) R00.0 Tachycardia, unspecified R00.1 Bradycardia, unspecified R00.2 Palpitations R00.8 Other abnormalities of heart beat R00.9* Unspecified abnormalities of heart beat *Codes with a greater degree of specificity should be considered first.
    [Show full text]
  • 7. MINERAL ELEMENTS RELATED to CARDIOVASCULAR HEALTH Leslie M
    7. MINERAL ELEMENTS RELATED TO CARDIOVASCULAR HEALTH Leslie M. Klevay Gerald F. Combs, Jr. USDA Agricultural Research Service Grand Forks Human Nutrition Research Service Grand Forks ND, USA ______________________________________________________________________________ I. INTRODUCTION Consideration of the characteristics of water as determinants of disease risk is not a new idea. Hippocrates is quoted: "We must also consider the qualities of the waters, for as they differ from one to another in taste in weight, so also do they differ much in their qualities" (1). Indeed, the science of epidemiology traces its origin to the 19th century work of Snow who mapped the incidence of cholera in London, showing it to be much higher in areas supplied with a particular water source (2). II. NUTRITIONAL DETERMINANTS OF HEART DISEASE RISK Keys (3) was among the first to notice the great variation in heart disease death rates among various nations. The death rate for men in Finland was 16 times that in Taiwan. Times change and methods vary, but differences still are substantial (4). For example, the male death rate for ischemic heart disease in Scotland is nearly nine times as great as that in Japan which, in turn, is more than five times that in Guatemala. Ischemic heart disease (IHD) is often thought of as a hereditary illness because some families have several affected members and other families have none. It seems unlikely, however, that most ischemic heart disease is hereditary for two reasons. First, in the wealthier nations, ischemic heart disease is far too common to be explained on the basis of heredity; nearly one- fourth of all deaths in the US are from IHD (5) (hereditary illnesses typically occur at prevalences <5 per 1000 live births (6).
    [Show full text]
  • Aka “Heart Attack”)
    AT-A-GLANCE Myocardial Infarction (aka “Heart Attack”) ABOUT THE DISORDER SIGNS AND SYMPTOMS Acute myocardial infarction, commonly known as The outward signs and symptoms of a heart attack heart attack, occurs when the heart is starved of can vary widely from person to person. Many people oxygen because blood flow through one or more of do not experience the crushing chest pain that has the coronary arteries — a group of vessels that been dramatized on television and in movies. surround and supply the heart — is blocked. The lack The most common symptoms include: of oxygen causes chest pain and results in irreversible • CHEST PAIN OR DISCOMFORT damage, eventually leading to the death of heart Most heart attacks involve discomfort in the center muscle (called myocardium). or left side of the chest. It usually lasts for more Atherosclerosis, the progressive accumulation of fat, than a few minutes or goes away and comes back. cholesterol, and other substances within the walls of The discomfort can feel like pressure, squeezing, the coronary arteries, is largely to blame. These waxy fullness, or pain. It also can feel like heartburn or substances, together known as plaque, build up over indigestion, and can be mild or severe. time, narrowing the opening of the blood vessels. • UPPER BODY DISCOMFORT When a piece of plaque ruptures, a blood clot forms, Patients experiencing a heart attack may feel pain completely obstructing blood flow and resulting in a or discomfort in one or both arms, the back, heart attack. (This NHLBI video illustrates the biology shoulders, neck, jaw, or upper part of the stomach behind a heart attack.) (above the belly button).
    [Show full text]