DOCSLIB.ORG

Left Ventricular Hypertrophy

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text

Load more

Evaluation of Subclinical Target Organ Damage for Risk Assessment and Treatment in the Hypertensive Patients: Left Ventricular Hypertrophy Enrico Agabiti-Rosei, Maria Lorenza Muiesan, and Massimo Salvetti Internal Medicine, University of Brescia, Brescia, Italy At some point in the natural history of hypertension, the compensatory increase in left ventricular mass ceases to be beneficial. Left ventricular hypertrophy (LVH) becomes a preclinical disease and an independent risk factor for congestive heart failure, ischemic heart disease, arrhythmia, sudden death, and stroke. In addition to elevated BP, several mechanisms are involved, including body size, age, gender, race, fibrogenic cytokines, and neurohumoral factors, notably angiotensin II, which favor interstitial collagen deposition and perivascular fibrosis. These tissue changes are responsible for the insidious contractile dysfunction that is associated with LVH, consequent to decreased coronary reserve and altered diastolic ventricular filling and relaxation. The cardinal investigations are echocardiography and electrocardiography. All antihypertensive drugs regress LVH, notably those that act on the renin-angiotensin-aldosterone system, which also could target the detrimental tissue changes. Regression enhances systolic midwall performance, normalizes autonomic function, and restores coronary reserve. The resulting improvement in prognosis has enshrined the detection, prevention, and reversal of LVH in the current guidelines of hypertension management. J Am Soc Nephrol 17: S104–S108, 2006. doi: 10.1681/ASN.2005121336 t some point in the natural history of hypertension, hemodynamic load, echocardiographic LVM could be assessed the compensatory increase in left ventricular mass in the individual patient as deviation from the value that is A (LVM) is not beneficial anymore. In fact, it becomes a appropriate for a given cardiac workload, corrected for gender preclinical disease and an independent risk factor for conges- and body size. LVM that overcompensates for hemodynamic tive heart failure, ischemic heart disease, arrhythmia, sudden load tends to cluster with metabolic risk factors and is associ- death, and stroke (1). ated with high cardiovascular risk (6,7). The definition and the clinical evaluation of “inappropriate” LVM require further Determinants of Hypertensive Left study. Ventricular Hypertrophy Among the main nonhemodynamic factors that may contrib- The high prevalence of LV hypertrophy (LVH) in hyperten- ute to the development of LVH, a variety of neurohumoral and sion reflects the increased afterload imposed on the left ventri- growth factors (e.g., catecholamines, angiotensin II [AngII], al- cle, although other important determinants are demographic dosterone, endothelins) are included. The effect of sympathetic characteristics (e.g., age, gender, race), neurohumoral and nervous system activity is evident in experimental models but growth factors, and underlying genetic factors. Hypertension is less clear-cut in humans: in pheochromocytoma LVH preva- the fundamental trigger to the sequence of biologic events that lence is relatively low and LVM seems to increase proportion- lead to the development of LVH. LVM is more closely related ately to BP, then in essential hypertension, LVH is associated to average 24-h BP (2–4). Volume load, inotropy, and arterial with altered autonomic activity and a blunted response to compliance also are important determinants of the develop- ␤-adrenoceptor stimulation (8–10). Experimental studies also ment and the degree of LVH. Other contributing factors include highlighted the role of the renin-angiotensin-aldosterone sys- stage of hypertensive disease, genetics, demographic factors, tem (RAAS) in mediating LVH (11,12). AngII induces hyper- comorbid diseases (e.g., diabetes, obesity, coronary artery dis- trophy and hyperplasia in myocytes and vascular smooth mus- ease), possibly mediated via cardiac load. Obesity, which com- cle cells and may regulate collagen synthesis. Excess AngII pounds hemodynamic load independent of a clear-cut increase production may regulate the expression of fibrogenic cytokine in BP, is a major determinant of LVM, because it is associated TGF-␤1 and favor perivascular and interstitial fibrosis. In ad- with increased plasma volume and cardiac output (5). It has dition, AngII may interfere with the process of collagen degra- been suggested that considering these measurable factors and dation, modulating the activity of metalloproteinases (a family of zinc-containing proteins that include stromelysins, collag- enases, and gelatinases) and their inhibitors (12). Aldosterone Address correspondence to: Prof. Enrico Agabiti-Rosei, Internal Medicine, Med- also may stimulate extracellular collagen deposition and myo- ical and Surgical Sciences, University of Brescia, c/o 2a Medicina Spedali Civili di Brescia, Piazza Spedali Civili 1, 25100 Brescia, Italy. Phone: ϩ30-396044; Fax: cardial fibrosis. ϩ30-3388147; E-mail: [email protected] The pathogenic role of the RAAS in the development of Copyright © 2006 by the American Society of Nephrology ISSN: 1046-6673/1704-0104 J Am Soc Nephrol 17: S104–S108, 2006 Pathophysiology and Treatment of Hypertensive LVH S105 hypertensive LVH requires confirmation, although LVM is sig- more expensive or time-consuming and are still of limited nificantly increased in renovascular hypertension and primary availability. aldosteronism compared with essential hypertension (13,14). Methods have been developed to quantify tissue composi- Increased activity of the RAAS and sympathetic nervous sys- tion. Studies in animals and humans have shown that LV tem, hypervolemia, and anemia all may influence the increase acoustic properties under physiologic and pathologic condi- of LVM in patients with renal disease. tions are influenced by several tissue components (myocar- Hypertensive LVH often is associated with insulin resistance dium, contractile and elastic tissue, collagen and inelastic tis- and high insulin levels (15). The involvement of IGF- I could sue, arteries, veins, myocytes, and sarcomeres). Results with clarify the link among obesity, BP elevation, LVH, and the videodensitometry and integrated backscatter to characterize metabolic syndrome. Leptin is another possible neuroendocrine tissue in several diseases that are associated with abnormal determinant. LVH in an animal model of leptin deficiency (the myocardial tissue, including hypertensive LVH and diabetes, ob/ob mouse) reversed rapidly in response to exogenous leptin, indicate that these techniques can complement clinical evalua- therefore indicating the involvement of myocardial leptin re- tion by revealing preclinical end-organ damage (25,26). Further ceptors in cardiac remodeling (16). Other major metabolic car- reproducibility and feasibility studies are required to assess the diovascular risk factors, notably hypercholesterolemia and hy- clinical applications of these techniques. perglycemia, also may have an influence on LVM and the prevalence of LVH (17). Prognostic Significance of LVH Several studies have suggested that approximately 30% of Whether assessed by ECG or echocardiography, LVH is a LVM variance is genetically determined (18). Studies of genetic well-documented harbinger of morbidity and mortality. In sev- influence on LVM have focused mainly and are ongoing on the eral studies, the adjusted risk for cardiovascular morbidity role of candidate genes, including those that are related to the associated with baseline LVH ranges from 1.5 to 3.5 with a RAAS, ␣- and ␤-adrenoceptors, and components of the signal weighted risk ratio of 2.3 for all studies combined (27). Con- transduction mechanisms involved in cardiac hypertrophy. centric hypertrophy seems to carry the highest risk and eccen- tric hypertrophy an intermediate risk, whereas concentric re- modeling is probably associated with a smaller, albeit Methods of Assessing LVH noteworthy, risk. As recommended by the European Society of Hypertension The structural remodeling of cardiomyocytes, nonmyocytes, and European Society of Cardiology (19), LVH is diagnosed and fibroblasts that occurs in cardiac hypertrophy contributes most commonly using electrocardiography (ECG) and M-mode to perivascular fibrosis, initially around intramural coronary and two-dimensional echocardiography. New ECG criteria in arteries and thereafter in the interstitial space, leading to pro- addition to repolarization abnormalities and increased voltage gressive abnormalities of diastolic ventricular filling and relax- have been proposed, the Cornell method probably being the ation, systolic dysfunction, arrhythmias, and conduction dis- most sensitive (20). The ECG also can be used to detect patterns turbances, thereby greatly compounding the risk that is of ventricular overload (“strain”) or ischemia, which indicate associated with LVH (1). higher cardiovascular risk. ECG and echocardiographic LVH The resulting pathophysiologic and clinical changes that ac- both predict mortality independent of each other and other count for increased risk in hypertensive LVH include both cardiovascular risk factors, thus conveying, at least in part, diastolic and systolic dysfunction. LVH and failure are fre- different prognostic information (21,22). Echocardiography has quently associated with coronary artery disease, and hyperten- some advantages because it provides comprehensive wall, sion is a major risk factor for coronary atherosclerosis. In ECG chamber, and LVM measures, together
Recommended publications
  • Life-Threatening Events in Patients with Pheochromocytoma

    Life-Threatening Events in Patients with Pheochromocytoma

    A Riester and others Life-threatening events in 173:6 757–764 Clinical Study pheochromocytoma Life-threatening events in patients with pheochromocytoma Anna Riester, Dirk Weismann1, Marcus Quinkler2, Urs D Lichtenauer3, Sandra Sommerey4, Roland Halbritter5, Randolph Penning6, Christine Spitzweg7, Jochen Schopohl, Felix Beuschlein and Martin Reincke Medizinische Klinik und Poliklinik IV, Klinikum der Universita¨ tMu¨ nchen, Ludwig-Maximilians-Universita¨ t, Ziemssenstr. 1, D-80336 Munich, Germany, 1Medizinische Klinik und Poliklinik I, Universita¨ tsklinikum Wu¨ rzburg, Correspondence Wu¨ rzburg, Germany, 2Endokrinologie in Charlottenburg, Berlin, Germany, 3Helios Klinik Schwerin, Schwerin, should be addressed Germany, 4Chirurgische Klinik und Poliklinik – Innenstadt, Klinikum der Universita¨ tMu¨ nchen, Ludwig-Maximilians- to M Reincke Universita¨ tMu¨ nchen, Munich, Germany, 5Facharztpraxis, Pfaffenhofen, Germany, 6Institut fu¨ r Rechtsmedizin and Email 7Medizinische Klinik und Poliklinik II, Klinikum der Universita¨ tMu¨ nchen, Ludwig-Maximilians-Universita¨ t, Munich, martin.reincke@ Germany med.uni-muenchen.de Abstract Objective: Pheochromocytomas are rare chromaffin cell-derived tumors causing paroxysmal episodes of headache, palpitation, sweating and hypertension. Life-threatening complications have been described in case reports and small series. Systematic analyses are not available. We took an opportunity of a large series to make a survey. Design and methods: We analyzed records of patients diagnosed with pheochromocytomas in three geographically spread German referral centers between 2003 and 2012 (nZ135). Results: Eleven percent of the patients (ten women, five men) required in-hospital treatment on intensive care units (ICUs) due to complications caused by unsuspected pheochromocytomas. The main reasons for ICU admission were acute catecholamine induced Tako-Tsubo cardiomyopathy (nZ4), myocardial infarction (nZ2), acute pulmonary edema (nZ2), cerebrovascular stroke (nZ2), ischemic ileus (nZ1), acute renal failure (nZ2), and multi organ failure (nZ1).
  • Study of Essential Hypertension with Special Reference to End Organ Damage in Adults

    Study of Essential Hypertension with Special Reference to End Organ Damage in Adults

    International Journal of Advances in Medicine Rukmini RM et al. Int J Adv Med. 2018 Oct;5(5):1227-1233 http://www.ijmedicine.com pISSN 2349-3925 | eISSN 2349-3933 DOI: http://dx.doi.org/10.18203/2349-3933.ijam20183899 Original Research Article Study of essential hypertension with special reference to end organ damage in adults Rukmini Ramya M.*, Rajya Lakshmi M. Department of General Medicine, Rangaraya Medical College, Kakinada, Andhra Pradesh, India Received: 30 June 2018 Revised: 10 July 2018 Accepted: 27 July 2018 *Correspondence: Dr. Rajya Lakshmi M., E-mail: [email protected] Copyright: © the author(s), publisher and licensee Medip Academy. This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License, which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. ABSTRACT Background: Hypertension, a major public health concern, affecting 20-25% of the adult population. It is the major risk factor for diseases involving Cardio Vascular (CV) and renal system. The World Health Organization (WHO) has estimated that high Blood Pressure (BP) causes 1 in every 8 deaths, making hypertension the third leading killer in the world. The recent emerging trend in the treatment of hypertension is not only based on the pragmatic need to lower BP levels, but also on lowering the CV risk profile, which is largely linked to the presence of the end organ damage. Methods: One hundred patients with hypertension are recruited in this study. The ethics committee of Rangaraya Medical College, Kakinada approved this study and all the participants provided informed consent for all the procedures in the study protocol.
  • Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management

    Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management

    Journal of Clinical Medicine Review Thrombotic Thrombocytopenic Purpura: Pathophysiology, Diagnosis, and Management Senthil Sukumar 1 , Bernhard Lämmle 2,3,4 and Spero R. Cataland 1,* 1 Division of Hematology, Department of Medicine, The Ohio State University, Columbus, OH 43210, USA; [email protected] 2 Department of Hematology and Central Hematology Laboratory, Inselspital, Bern University Hospital, University of Bern, CH 3010 Bern, Switzerland; [email protected] 3 Center for Thrombosis and Hemostasis, University Medical Center, Johannes Gutenberg University, 55131 Mainz, Germany 4 Haemostasis Research Unit, University College London, London WC1E 6BT, UK * Correspondence: [email protected] Abstract: Thrombotic thrombocytopenic purpura (TTP) is a rare thrombotic microangiopathy charac- terized by microangiopathic hemolytic anemia, severe thrombocytopenia, and ischemic end organ injury due to microvascular platelet-rich thrombi. TTP results from a severe deficiency of the specific von Willebrand factor (VWF)-cleaving protease, ADAMTS13 (a disintegrin and metalloprotease with thrombospondin type 1 repeats, member 13). ADAMTS13 deficiency is most commonly acquired due to anti-ADAMTS13 autoantibodies. It can also be inherited in the congenital form as a result of biallelic mutations in the ADAMTS13 gene. In adults, the condition is most often immune-mediated (iTTP) whereas congenital TTP (cTTP) is often detected in childhood or during pregnancy. iTTP occurs more often in women and is potentially lethal without prompt recognition and treatment. Front-line therapy includes daily plasma exchange with fresh frozen plasma replacement and im- munosuppression with corticosteroids. Immunosuppression targeting ADAMTS13 autoantibodies Citation: Sukumar, S.; Lämmle, B.; with the humanized anti-CD20 monoclonal antibody rituximab is frequently added to the initial ther- Cataland, S.R.
  • Stroke Prevention in Atrial Fibrillation

    Stroke Prevention in Atrial Fibrillation

    STROKE PREVENTION IN ATRIAL FIBRILLATION OBJECTIVE: To guide clinicians in the selection of antithrombotic therapy for the prevention of ischemic stroke and arterial thromboembolism in patients with atrial fibrillation. BACKGROUND: Atrial fibrillation (AF) is the most common pathologic arrhythmia and increases in prevalence with increasing age (prevalence of 10-15% in patients who are ≥80 years). The most devastating complication of AF is arterial embolism of a left atrial thrombus resulting in ischemic stroke, peripheral limb ischemia, or other end organ damage. AF is associated with a 3- to 6-fold increased risk of stroke or non-central nervous system (CNS) systemic embolism. Furthermore, ischemic strokes in patients with AF are larger and more frequently associated with death and disability than strokes that occur in the absence of AF. Therefore, stroke prevention is a critical part of AF treatment. The risk of arterial thromboembolism can be significantly reduced with anticoagulant therapy (warfarin, apixaban, dabigatran, edoxaban or rivaroxaban) and, to a much lesser extent, with antiplatelet therapy. Selection of antithrombotic therapy should be guided by assessment of presumed thrombotic risk, assessment of presumed bleeding risk on antithrombotic therapy and patient preference. Thrombotic Risk: Prognostic models incorporating patient age and co-morbidities provide validated estimates of the annual risk for thromboembolism without anticoagulant therapy. These models were developed for patients with non-valvular AF, which refers
  • Assessment of Preclinical Organ Damage in Hypertension

    Assessment of Preclinical Organ Damage in Hypertension

    Assessment of Preclinical Organ Damage in Hypertension Enrico Agabiti Rosei Giuseppe Mancia Editors 123 Assessment of Preclinical Organ Damage in Hypertension Enrico Agabiti Rosei • Giuseppe Mancia Editors Assessment of Preclinical Organ Damage in Hypertension Editors Enrico Agabiti Rosei Giuseppe Mancia Department of Clinical IRCCS Istituto Auxologico Italiano and Experimental Sciences University of Milano-Bicocca University of Brescia Milano Brescia Italy Italy This book is endorsed by the European Society of Hypertension ISBN 978-3-319-15602-6 ISBN 978-3-319-15603-3 (eBook) DOI 10.1007/978-3-319-15603-3 Library of Congress Control Number: 2015940816 Springer Cham Heidelberg New York Dordrecht London © Springer International Publishing Switzerland 2015 This work is subject to copyright. All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifi cally the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfi lms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed. The use of general descriptive names, registered names, trademarks, service marks, etc. in this publication does not imply, even in the absence of a specifi c statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use. The publisher, the authors and the editors are safe to assume that the advice and information in this book are believed to be true and accurate at the date of publication. Neither the publisher nor the authors or the editors give a warranty, express or implied, with respect to the material contained herein or for any errors or omissions that may have been made.
  • The Treatment of Adults with Essential Hypertension

    The Treatment of Adults with Essential Hypertension

    APPLIED EVIDENCE The Treatment of Adults with Essential Hypertension STEVEN A. DOSH, MD, MS Escanaba, Michigan ypertension is arbitrarily defined as diastolic KEY POINTS FOR CLINICIANS Hblood pressure (DBP) of 90 mm Hg or higher, ● Only 53% of hypertensive patients are being systolic blood pressure (SBP) of 140 mm Hg or high- treated, and only 24% have their hypertension er, or both, on 3 separate occasions. Essential hyper- under control. tension is hypertension without an identifiable ● The first step in planning the treatment of a cause. Essential hypertension, also known as pri- patient with essential hypertension is to catego- mary or idiopathic hypertension, accounts for at least rize the patient's risk status. 95% of all cases of hypertension. ● The target blood pressure of patients who have According to the third National Health and diabetes or renal failure should be less than Nutrition Examination Survey (NHANES III), approx- 130/85. imately 60% of the 50 million Americans with hyper- ● Diuretics are safe, well tolerated, effective, rela- tension are at increased risk for cardiovascular dis- tively inexpensive, and convenient for initial ease resulting from uncontrolled hypertension. This drug treatment of hypertension in patients who is because only 53% of hypertensive patients are do not have concomitant illness. being treated and only 24% have their hypertension ● Alpha-adrenergic blockers should be used with under control.1 Physicians must play an active role in caution in the treatment of hypertension. identifying and treating hypertension. ● Ambulatory blood pressure measurements pre- In an earlier Applied Evidence article2 an dict cardiovascular events more closely than clin- approach to the diagnosis of hypertension was pre- ic blood pressure measurements.
  • Brain Vs. Bone: Does Fracture Fixation Technique Influence Outcomes in Patients with Traumatic Brain Injury (TBI)?

    Brain Vs. Bone: Does Fracture Fixation Technique Influence Outcomes in Patients with Traumatic Brain Injury (TBI)?

    EAST MULTICENTER STUDY DATA COLLECTION TOOL Brain vs. Bone: Does fracture fixation technique influence outcomes in patients with traumatic brain injury (TBI)? 1.Patient Number: The following sheets are for annotation. All data will be entered electronically at each site into the AAST data collection tool for secure/encrypted electronic sharing with the coordinating site. Facility Characteristics (2-6): 2. Name: 3. Location: 4. Yearly trauma volume: 5. Urban Environment: YES NO 6. Academic Affiliation: Teaching Non-teaching Demographics and Injury Characteristics (7-35): Age_____ Sex_____ Race: White Black Asian Hispanic or Latino Native Hawaiian Other 10-24. Past Medical History (Circle all that apply) Diabetes Mellitus Liver disease AIDS Chronic Kidney Disease Atrial Fibrillation Congestive Heart Failure Myocardial Infarction Chronic Pulmonary Peripheral Vascular disease Disease Stroke Dementia Hemiplegia Rheumatic or Connective Peptic Ulcer Disease Cancer/Chemotherapy tissue disorder 25. Mechanism of injury: Blunt Penetrating Crush Other 26. Mechanism of injury description: MVC MCC Peds Struck GSW Stab Assault Found down Sports Injury Industrial Injury Fall <10 ft Fall >10 ft Other 27. Injury Severity Score (ISS): 28-35: AIS Values HEAD FACE NECK SPINE THORAX ABDOME LOWER UPPER EXTREMITY EXTREMITY Initial Evaluation in the Trauma Bay (36-63): 36-41. Vitals and GCS: Heart Rate Systolic Blood Diastolic Respiratory Temperature C Pressure Blood Rate Pressure GCS E-Score V-Score M-Score 42. Intubated Prior to Admission: YES NO 42. Intubated
  • Section 1: Cardiology Chapter 2: Hypertension

    Section 1: Cardiology Chapter 2: Hypertension

    SECTION 1: CARDIOLOGY CHAPTER 2: HYPERTENSION Q.1. A 47-year-old male with diabetes presents as a new patient to your clinic. He does not recall any abnormal blood pressure readings. You find his blood pressure to be 138/86 on two readings during this visit. You should A. Start HCTZ 12.5 mg every day B. Provide lifestyle counseling and start HCTZ 12.5 mg every day C. Provide lifestyle counseling and recheck blood pressure within a few months D. Do nothing now and recheck blood pressure within one year E. Do nothing now and recheck blood pressure within a few months Answer: C. Although drug therapy is indicated for diabetics with high normal blood pressure (i.e., 130–139/85–89), it is first necessary to establish the diagnosis of hypertension, which requires elevated readings on at least two office visits, not just two readings during one office visit. Lifestyle counseling, however, should begin immediately. Q.2. A 48-year-old woman presents to the emergency room with headache and a blood pressure of 192/104. She has a long history of hypertension, for which she has been treated in the past with benazepril, hydrochlorothiazide, and metoprolol. She does not have a history of coronary artery disease. After careful interviewing, you determine that she stopped taking her antihypertensive medications approximately two months ago because she was feeling well and “did not want to be dependent on medications.” She reports no other symptoms. On examination, she appears comfortable and is fully alert and oriented. Funduscopic examination reveals arteriovenous crossing changes but no papilledema.