DOCSLIB.ORG

11 Valvular Heart Disease and Rheumatic Fever

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
11 Valvular Heart Disease and Rheumatic Fever Chapter 11: Valvular Heart Disease and Rheumatic Fever 375 11 Valvular Heart Disease and Rheumatic Fever CONTENTS AORTIC STENOSIS AORTIC REGURGITATION MITRAL STENOSIS MITRAL REGURGITATION MITRAL VALVE PROLAPSE RHEUMATIC FEVER BIBLIOGRAPHY AORTIC STENOSIS Aortic stenosis is the most common valvular lesion in the United States. This lesion is common because approximately 2% of individuals are born with a bicuspid valve which is prone to stenosis, and the aging population is increasing, and calcific aortic stenosis progresses with advancing years. Rheumatic aortic stenosis is now uncommon, except in Asia, Africa, the Middle East, and Latin America. The patient’s age at the time of diagnosis usually gives a reasonable assessment of the underlying disease. • Diagnosis before age 30 is typical of congenital aortic stenosis. • In patients over age 70, calcific aortic sclerosis owing to degenerative calcification is common, and significant stenosis develops in up to 5% of these individuals. Aortic sclerosis is common in the elderly, and although the lesion is significant, it is hemody- namically not important. Stenosis develops particularly when there is associated hyper- cholesterolemia. Importantly, the progression of stenosis can be significantly retarded by statin therapy. • A bicuspid valve occurs in approximately 2% of the population, with a male to female ratio of 4:1, and is predisposed to degenerative calcification and stenosis. Between ages 30 and 70, calcification of a bicuspid valve is the most common cause of aortic stenosis, and much less frequently, cases of rheumatic valvular disease are encountered. The causes of aortic stenosis can be seen in Table 11.1. From: Contemporary Cardiology: Heart Disease Diagnosis and Therapy: A Practical Approach, Second Edition Edited by: M. Gabriel Khan © Humana Press Inc., Totowa, NJ 375 376 Heart Disease Diagnosis and Therapy: A Practical Approach Table 11.1 Causes of Aortic Valvular Stenosis Biscuspid calcific 60%a Degenerative calcific 15% Rheumatic 20%a Other 5% aReverse in Asia, Africa, Middle East, and Latin America. Physical Signs of Significant Aortic Stenosis Some physical signs of significant aortic stenosis include the following: • A systolic crescendo–decrescendo murmur best heard at the left sternal border, the sec- ond right interspace, or occasionally at the apex, with radiation to the neck. • The timing of the peak intensity of the murmur is a more reliable sign of severity of aortic stenosis than the intensity of the murmur. Severe stenosis is indicated by a murmur that peaks late in systole. • The longer the murmur the greater the gradient. • The intensity of the murmur, in the absence of significant aortic regurgitation, is usually grade 3 or greater, except if cardiac output (CO) is low, as with heart failure (HF); then, even a grade 2 murmur may be in keeping with severe stenosis. Aortic regurgitation (AR) increases flow across the aortic valve and may produce a loud systolic murmur without stenosis. • An absent or very soft aortic component of the second sound (A2). With increased calcification, mobility of the valve leaflets is reduced; thus, the closing sound of the aortic valve becomes soft or even lost; A2 disappears when the valve does not open or closes well. The soft pulmonary second heart sound produces a soft single second heart sound. Paradoxic splitting of the second heart sound may occur, but is uncommon. • An S4 gallop is usually present and is highly significant in patients under age 50. • A thrill is commonly present over the base of the heart or the carotid arteries; this indicates a murmur of grade 4 or louder and may relate to the severity of aortic stenosis if AR is absent. • A thrusting, forceful apex beat of left ventricular hypertrophy (LVH); the apex beat is usually not displaced, except in patients with concomitant AR or with terminal left ventricular (LV) dilatation. • The carotid or brachial pulse in patients under age 65 shows a typical delayed upstroke. In the elderly, loss of elasticity in arteries often masks this important sign. The decreased elasticity increases the rate of rise of the carotid upstroke, and this may mislead the clinician into thinking that the stenosis is mild when it is severe. The average survival of patients are given in Table 11.2. • Approximately 50% of patients present with dyspnea and more than half are expected to die within 2 years. • Approximately 33% of patients with aortic stenosis present with angina and half are expected to die within 5 years. • Approximately 15% of patients present with syncope and half of these die within 3 years. Chapter 11: Valvular Heart Disease and Rheumatic Fever 377 Table 11.2. Average Survival in Patients With Moderate or Severe Aortic Stenosis Clinical parameters Survival (years) Left ventricular failure 1–2 Severe shortness of breath 50% die within 2 Mild shortness of breath 3–5 Syncope 50% die within 3 Angina 50% die within 5 Investigations ELECTROCARDIOGRAM The electrocardiogram (ECG) in patients with moderate to severe stenosis often shows features of LVH: • S-wave in V1, plus R in V5 or V6 greater than 35 mmHg. • S wave-V3, plus R in aVL greater than 20 mmHg. • Left atrial enlargement. • ST-T change typical of LV strain: the ascending limb of the T-wave is steeper than the descending in leads V5 and V6, with a lesser change in V4. • Left bundle branch block. Although some patients with LVH caused by aortic stenosis may not manifest ECG signs of LVH, the ECG remains an important test in those who do show LVH. The presence of LVH on ECG in the absence of significant hypertension is in keeping with severe aortic stenosis. CHEST X-RAY Concentric LVH occurs; thus, the chest X-ray usually shows a normal heart size, with some rounding of the left lower cardiac border and apex, and occasionally some posterior protrusion in the lateral view may suggest LVH. The heart size may be increased if cardiac failure supervenes or with concomitant AR. A common hallmark of valvular aortic stenosis is poststenotic dilatation of the ascending aorta. ECHOCARDIOGRAPHY The severity of aortic stenosis can be determined by continuous-wave Doppler echocardiography. This technique agrees with data obtained from catheterization in up to 85% of cases. Mild aortic stenosis is indicated by a mean aortic valve pressure gradient equal to or less than 20 mmHg. Moderate stenosis is indicated by a mean pressure gradient 21–39 mmHg. A valve area greater than 1.5 cm2 indicates mild aortic stenosis. Moderate to severe aortic stenosis is indicated by the following: • Valve mean pressure gradient greater than 40 (range in several clinical studies, 40–120 mmHg). • Doppler peak systolic pressure gradient is usually greater than 50 mmHg in the presence of a normal CO but in more than 33% of patients the gradient is 40–50 mmHg. • Maximal instantaneous Doppler gradient greater than 60 mmHg (range 55–165 mmHg). • Peak systolic flow velocity greater than 4 m/s (range often observed, 4–7 m/s). 378 Heart Disease Diagnosis and Therapy: A Practical Approach Table 11.3. Hemodynamic Parameters for Severe Aortic Stenosis Aortic valve Aortic valve Peak systolic Mean gradient areaa (cm2) area index (cm2/m2) gradient (mmHg) (mmHg) Severe stenosis <0.75 <0.4 >80 >70 Probable severe 0.75–0.9 0.4–0.6 50–79 40–69 Uncertain >0.9-1.2 >0.6 <50 <40 aIn an average-sized adult. • Valve area less than about 0.75 cm2 in an average-sized adult, 0.4 cm2/m2 of body surface area, severe or critical stenosis (Table 11.3.). • 0. 8 to 1.4 cm2 indicates moderate stenosis. The aortic valve area (AVA) and expected mean gradient is as follows: • 0.5 cm2 mean gradient greater than 100 mmHg • 0.7 cm2 mean gradient greater than 50 mmHg • 0.9 cm2 mean gradient greater than 30 mmHg • 1 .0 cm2 mean gradient greater than 25 mmHg • 3 to 4 cm2 is normal and gradient less than 3 mmHg It must be emphasized that in cardiac catheterization studies, no aortic valve gradient (mean or peak) has been found to be both sensitive and specific for severe aortic stenosis. Eslami et al. points out that AVA should be measured at cardiac catheterization in all patients with suspicion of severe aortic stenosis even when the mean aortic valve gradient is less than 50 mmHg (0% of their study patients) and/or the peak gradient in less than 60 mmHg (present in up to 47% of their patients). These authors believe that the severity of aortic stenosis is best determined by measuring the AVA as follows: • severe aortic stenosis AVA is less than 1.0 cm2, AVA index less than 0.6 cm2. • Moderate stenosis AVA greater than 1.0–1.52. • In patients with congenital aortic stenosis, the peak instantaneous valve pressure gradient is used for determining the severity of stenosis. Therapy Medical therapy plays a small role in management. Because the consequences of valve surgery may be life-threatening, the timing of valve replacement requires accurate knowl- edge of the natural history of significant aortic stenosis, as well as careful attention to details in the patient’s history and the sound appraisal of information gathered from Doppler echocardiography correlated with catheterization data. Sophisticated echo-Doppler techniques are available and can, in over 80% of patients, dispense with catheterization data. However, because valve surgery is a life-saving but hazardous procedure, it is vital to gather information from all sources, including catheter- ization, to allow for sound decision making when surgery is being contemplated. In certain patients, ancillary information about the state of the coronary arteries is of cardi- nal value in reaching a therapeutic decision. In a study comparing echo-Doppler with catheterization data to determine the timing for valve surgery, agreement varied from a 92% level for AR to 90% for mitral stenosis but only 83% and 69% for aortic stenosis and mitral regurgitation, respectively.
Load more

Recommended publications
  • Rheumatic Heart Disease in Children: from Clinical Assessment to Therapeutical Management
    European Review for Medical and Pharmacological Sciences 2006; 10: 107-110 Rheumatic heart disease in children: from clinical assessment to therapeutical management G. DE ROSA, M. PARDEO, A. STABILE*, D. RIGANTE* Section of Pediatric Cardiology, *Department of Pediatric Sciences, Catholic University “Sacro Cuore” – Rome (Italy) Abstract. – Rheumatic heart disease is presence of valve disease or carditis can be still a relevant problem in children, adolescents easily recognized through echocardiographic and young adults. Molecular mimicry between examinations, but the combination of clinical streptococcal and human proteins has been pro- posed as the triggering factor leading to autoim- tools and echocardiography consents the munity and tissue damage in rheumatic heart most accurate assessment of heart involve- disease. Despite the widespread application of ment2. It is well known however that minimal Jones’ criteria, carditis is either underdiagnosed physiological mitral regurgitation can be or overdiagnosed. Endocarditis leading to mitral identified in normal people and might over- and/or aortic regurgitation influences morbidity diagnose the possibility of carditis. Only in and mortality of rheumatic heart disease, whilst myocarditis and pericarditis are less significant 30% patients serial electrocardiogram studies in determining adverse outcomes in the long- are helpful in the diagnosis of acute RF with term. Strategy available for disease control re- non-specific findings including prolonged PR mains mainly secondary prophylaxis with the interval, atrio-ventricular block, diffuse ST-T long-acting penicillin G-benzathine. changes with widening of the QRS-T angle and inversion of T waves. Carditis as an ini- Key Words: tial sign might be mild or even remain unrec- Rheumatic heart disease, Pediatrics.
    [Show full text]
  • CARDIOLOGY Section Editors: Dr
    2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce
    [Show full text]
  • Cardiology 2
    Ch02.qxd 7/5/04 3:06 PM Page 13 Cardiology 2 FETAL CARDIOVASCULAR PHYSIOLOGY The ‘basic science’ nature of this topic – as well as the potential pathological implications in paediatric cardiology – makes it a likely viva question. Oxygenated blood from the placenta returns to the fetus via the umbilical vein (of which there is only one). Fifty per cent traverses the liver and the remaining 50% bypasses the liver via the ductus venosus into the inferior vena cava. In the right atrium blood arriving from the upper body from the superior vena cava (low oxygen saturation) preferentially crosses the tricus- pid valve into the right ventricle and then via the ductus flows into the descending aorta and back to the placenta via the umbilical arteries (two) to reoxygenate. The relatively oxygenated blood from the inferior vena cava, however, preferentially crosses the foramen ovale into the left atrium and left ventricle to be distributed to the upper body (including the brain and coro- nary circulation). Because of this pattern of flow in the right atrium we have highly oxygenated blood reaching the brain and deoxygenated blood reach- ing the placenta. High pulmonary arteriolar pressure ensures that most blood traverses the pulmonary artery via the ductus. Changes at birth 1. Occlusion of the umbilical cord removes the low-resistance capillary bed from the circulation. 2. Breathing results in a marked decrease in pulmonary vascular resistance. 3. In consequence, there is increased pulmonary blood flow returning to the left atrium causing the foramen ovale to close. 4. Well-oxygenated blood from the lungs and the loss of endogenous prostaglandins from the placenta result in closure of the ductus arteriosus.
    [Show full text]
  • Rheumatic Heart Disease
    RHEUMATIC HEART DISEASE Rheumatic fever is an acute immunologically mediated multisystem inflammatory disease that occurs few weeks after an attack of group A beta- hemolytic streptococcal pharyngitis. It is not an infective disease. The most commonly affected age group is children between the ages of 5-15 yearsQ. The disease is a type II hypersensitivity reaction in which antibodies against ‘M’ protein of some streptococcal strains (1, 3, 5, 6, and 18) cross-react with the glycoprotein antigens in the heart, joints and other tissues (molecular mimicry). CLINICAL FEATURES It presents with fever, anorexia, lethargy and joint pain 2-3 WEEKS after an episode of Streptococcal Infection is required for diagnosis Migratory Polyarthritis is the commonest major manifestation. Q Salient feature`s of the major criteria Carditis All the layers of the heart namely pericardium, myocardium and endocardium are involved, so this is called pancarditis. The pericarditis is associated with fibrinous/serofibrinous exudate and is called as ‘bread and butter’ pericarditis. It may manifest as breathlessness (due to heart failure or pericardial effusion), palpitations or chest pain (usually due to pericarditis or pancarditis). Other features include tachycardia, cardiac enlargement and new or changed murmurs. A soft mid-diastolic murmur (the Carey Coombs murmur) is typically due to valvulitis, with nodules forming on the mitral valve leaflets. Aortic regurgitation occurs in 50% of cases but the tricuspid and pulmonary valves are rarely involved. Pericarditis may cause chest pain, a pericardial friction rub and precordial tenderness. Cardiac failure may be due to myocardial dysfunction or valvular regurgitation. Valvular involvement is common in rheumatic heart disease.
    [Show full text]
  • Cardiovascular Pathology the Perfect Preparation for USMLE® Step 1
    Cardiovascular Pathology The Perfect Preparation for USMLE® Step 1 2021 Edition You cannot separate passion from pathology any more than you can separate a person‘s spirit from his body. (Richard Selzer) www.lecturio.com Cardiovascular Pathology eBook Live as if you were to die tomorrow. Learn as if you were to live forever. (Mahatma Gandhi) Pathology is one of the most-tested subjects on the USMLE® Step 1 exam. At the heart of the pathology questions on the USMLE® exam is cardiovascular pathology. The challenge of cardiovascular pathology is that it requires students to be able to not only recall memorized facts about cardiovascular pathology, but also to thoroughly un- derstand the intricate interplay between cardiovascular physiology and pathology. Understanding cardiovascular pathology will not only allow you to do well on the USMLE® Step 1 exam, but it will also serve as the foundation of your future patient care. This eBook... ✓ ...will provide you with everything you need to know about cardiovascular pathology for your USMLE® Step 1 exam. ✓ ...will equip you with knowledge about the most important diseases related to the cardiovascular system, as well as build bridges to the related medical sciences, thus providing you with the deepest understanding of all cardiovascular pathology topics. ✓ ...is specifically for students who already have a strong foundation in the basic sciences, such as anatomy, physiology, biochemistry, microbiology & immunology, and pharmacology. Elements of this eBook High-yield: Murmurs of grade III and above are High-yield-information will help you to focus on the most important facts. usually pathological. (...) A number of descriptive pictures, mnemonics, and overviews, but also a reduction to the essentials, will help you to get the best out of your learning time.
    [Show full text]
  • CHAPTER E13 Approach to the Patient with a Heart Murmur
    S1 S2 CHAPTER e13 A Approach to the Patient With a Heart Murmur B Patrick T. O’Gara C Joseph Loscalzo CHAPTER e13 A2 P2 D Ⅵ INTRODUCTION The differential diagnosis of a heart murmur begins with a careful assessment of its major attributes and response to bedside maneu- vers. The history, clinical context, and associated physical examina- E tion findings provide additional clues by which the significance of a heart murmur is established. Accurate bedside identification of a OS Approach to the Patient With a Heart Murmur heart murmur can inform decisions regarding the indications for F noninvasive testing and the need for referral to a cardiovascular specialist. Preliminary discussions can be held with the patient regarding antibiotic or rheumatic fever prophylaxis, the need to S3 restrict various forms of physical activity, and the potential role for G family screening. Heart murmurs are caused by audible vibrations that are due to increased turbulence from accelerated blood flow through normal or abnormal orifices, flow through a narrowed or irregular orifice H into a dilated vessel or chamber, or backward flow through an incompetent valve, ventricular septal defect, or patent ductus arte- Figure e13-1 Diagram depicting principal heart murmurs. riosus. They traditionally are defined in terms of their timing within A. Presystolic murmur of mitral or tricuspid stenosis. B. Holosystolic (pansystolic) the cardiac cycle ( Fig. e13-1 ) . Systolic murmurs begin with or after murmur of mitral or tricuspid regurgitation or of ventricular septal defect. the first heart sound (S1 ) and terminate at or before the component C. Aortic ejection murmur beginning with an ejection click and fading (A2 or P2 ) of the second heart sound (S2 ) that corresponds to their before the second heart sound.
    [Show full text]
  • Pediatric and Adolescent Care
    CHAPTER 11 – CARDIOVASCULAR SYSTEM First Nations and Inuit Health Branch (FNIHB) Pediatric Clinical Practice Guidelines for Nurses in Primary Care. The section on Rheumatic Fever (Carditis) has been updated as of December 2017. The remaining content of this chapter was reviewed in September 2011. Table of Contents INTRODUCTION ....................................................................................................11–1 ASSESSMENT OF THE CARDIOVASCULAR SYSTEM .......................................11–1 In Infants ..........................................................................................................11–1 In Children ........................................................................................................11–2 Medical History (Specific to Cardiovascular System) ......................................11–2 Physical Findings .............................................................................................11–2 COMMON PROBLEMS OF THE CARDIOVASCULAR SYSTEM ..........................11–3 Heart Murmurs .................................................................................................11–3 Innocent Heart Murmur ....................................................................................11–4 EMERGENCY PROBLEMS OF THE CARDIOVASCULAR SYSTEM ...................11–5 Cardiac Failure .................................................................................................11–5 Cyanosis in the Newborn (Birth to 6 Weeks) ...................................................11–6
    [Show full text]
  • Cardiovascular
    Notes compiled for Pediatrics Cardiovascular (Med I, Block 3, CV) Contents CV 036 Valvular Heart Disease A CV Dr. J Tam CV 042 Valvular Heart Disease II T1 CV Dr. J Tam CV 044 Development of the Heart and Lung L AN Dr. M Torchia CV 045 Valvular Heart Disease III T5 CV Dr. J Tam CV 046 Congenital Heart Disease I A PD Dr. R Soni CV 048 Development of the Heart and Lung A AN Dr. M Torchia CV 049 Congenital Heart Disease II L PD Dr. R Soni CV 050 Congenital Heart Disease III T1 PD Dr. R Soni CV 075 Genetic Aspects of Cardiomyopathy L GN Dr. A Chudley CV 076 Acquired Pediatric Heart Disease L PD Dr. R Soni CARDIOVASCULAR COURSE: MED I BLOCK III Valvular Heart Disease I & II (CV036) OBJECTIVES: Assigned Reading to be completed prior to CV042 University of Manitoba –Faculty of Medicine Instructor: Dr. J. Tam Objectives: At the completion of these sessions, the student will be able to: 1. Describe the common etiology, pathology and pathophysiology of: a) aortic stenosis b) aortic regurgitation c) mitral stenosis d) mitral regurgitation e) tricuspid regurgitation 2. Apply the above knowledge to describe the clinical manifestations and physical findings of the above valvular abnormalities. 3. Describe the laboratory findings (chest x-ray, ECG, echocardiogram) that assist in the diagnosis of the above entities. 4. Relate the pathophysiology to therapeutic approaches (both medical and surgical). 5. Briefly discuss the indications for surgical intervention of valvular heart disease. 6. List the various surgical options – repair, mechanical replacement, bioprosthetic replacement, homograft replacement, autograft replacement.
    [Show full text]
  • Selected References
    Selected references BOOKS Markowitz, M. and Cordis, L. (1972). Rheumatic Fever. 2nd Edn. Philadelphia: W. B. Saunders Co. Stollerman, C. H. (1975). Rheumatic Fever and Streptococcal Irifection. New York: Crune & Stratton, Inc. Wannamaker, L. W. and Matsen, J. M. (Eds.) (1972). Streptococci and Streptococcal Diseases. New York: Academic Press, Inc. ARTICLES Aryanpur, K. et al. (1977). Rheumatic heart disease in the developing countries. In Moss, A. J. (ed.) Heart Disease in Infants, Children and Adolescents. Baltimore: Williams & Wilkins Bhayana, J. N. et al. (1974). Mitral steQ.osis in the young in developing countries.]' Thorac. Cardiovasc. Surg., 68, 126 Bravo, L. C. et a!. (1979). Streptococcal infections and rheumatic recurrences in subjects on secondary prophylaxis. Philipp. ]. Intern. Med., 17, 12 Chamovitz, R. et al. (1954). Prevention of rheumatic fever by treatment of previous infections. 1. Evaluation ofbenzathine penicillin C. N. Eng!. ]. Med., 251,466 Chesler, E. (1966). The pattern of rheumatic heart disease in the urbanized Bantu of Johannesburg. S. Afr. Med.]', 40, 899 DiSciascio, C. and Taranta, A. (1980). Rheumatic fever in children: a review. Am. Heart]., 99, 635 Cordis, L. (1973). Effectiveness of comprehensive care programs in preventing rheumatic fever. N. Eng!.]. Med., 289,331 John, S. et al. (1973). Results of mitral valve replacement in young patients with rheumatic heart disease.]. Thorac. Cardiovasc. Surg., 66, 255 Jones, T. D. (1944). The diagnosis of rheumatic fever.]. Am. Med. Assoc., 126, 481 92 SELECTED REFERENCES Lue, H. C. et al. (1979). The natural history of rheumatic fever and rheumatic heart disease in the Orient. jpn. Heart]., 20, 237 Mori, C.
    [Show full text]
  • Rheumatic Heart Disease
    PLEASE CHECK Editing file BEFORE! ​ ​ ​ ​ Rheumatic Heart Disease ★ Objectives: ​ 1. Know that RHD is prevalent in our region, and economic burden 2. Know how to diagnose the disease and how to approach a patient with RHD 3. Know the principles of management 4. Know how to prevent RHD; Who needs prophylaxis and for how long 5. Recognize complications and how to manage it ★ Resources Used in This lecture: Slides, Kumar, Class notes, 433 teamwork. ​ ​ ​ ​ ​ Done by: Razan Alsubhi & Rasha Bassas Contact us at: [email protected] ​ ​ ​ Epidemiologic Background ● Globally rheumatic heart disease is the commonest CVD in young people 25 yrs old ● The overall incidence of ARF from 5-51 per 100000 population with a mean of 19 per 100000 population ● In children 5-14 yrs old 0.8-5.7 per 1000 children with a median of 1.3 per 1000 ● The incidence of RF and the prevalence of RHD has declined substantially in developed nations. ● This decline has been attributed to: ✓ Improved hygiene. ✓ Reduced household crowding. ✓ Improved medical care. ● A disease of poverty1 and low socioeconomic status ● In underdeveloped countries RHD is the leading cause of CV death during the first five decades of life. Global Burden of RHD ● Total cases with RHD: 20 Millions ● 3 Million have CHF. ​ ​ ● 1 Million require valve surgery. ​ ​ ● Annual incidence of RF: 0.5 Million, nearly half develop carditis ​ ● Estimated deaths from RHD: 230,000 per year. ​ ​ ■ Imposes a substantial burden on healthcare systems with limited budgets VS ARF ​ ​ RHD : ✓ Acute Rheumatic Fever (ARF): Is a systemic inflammatory disorder that occurs in children ​ ​ between 5 and 15 years of age as a result of group A beta hemolytic streptococcal throat infection ​ ​ ​ “Pharynx is the most common site for infection leading to RF”.
    [Show full text]
  • Manual of Cardiology
    MANUAL OF CARDIOLOGY MANUAL OF CARDIOLOGY V Jacob Jose MD DM card, MS Univ of Penn, FCCP, FACC, FIAE Professor of Cardiology Department of Cardiology Christian Medical College Hospital Vellore, Chennai JAYPEE BROTHERS MEDICAL PUBLISHERS (P) LTD New Delhi Published by Jitendar P Vij Jaypee Brothers Medical Publishers (P) Ltd B-3 EMCA House, 23/23B Ansari Road, Daryaganj New Delhi 110 002, India Phones: +91-11-23272143, +91-11-23272703, +91-11-23282021, +91-11-23245672, Rel: 32558559, Fax: +91-11-23276490, +91-11-23245683 e-mail: [email protected], Visit our website: www.jaypeebrothers.com Branches 2/B, Akruti Society, Jodhpur Gam Road Satellite Ahmedabad 380 015, Phones: +91-079-26926233, Rel: +91-079-32988717, Fax: +91-079-26927094, e-mail: [email protected] 202 Batavia Chambers, 8 Kumara Krupa Road Kumara Park East, Bangalore 560 001 Phones: +91-80-22285971, +91-80-22382956, Rel: +91-80-32714073, Fax: +91-80-22281761, e-mail: [email protected] 282 IIIrd Floor, Khaleel Shirazi Estate, Fountain Plaza Pantheon Road, Chennai 600 008, Phones: +91-44-28193265, +91-44-28194897, Rel: +91-44-32972089, Fax: +91-44-28193231, e-mail: [email protected] 4-2-1067/1-3, 1st Floor, Balaji Building, Ramkote Cross Road Hyderabad 500 095, Phones: +91-40-66610020, +91-40-24758498, Rel:+91-40-32940929, Fax:+91-40-24758499, e-mail: [email protected] No. 41/3098, B & B1, Kuruvi Building, St. Vincent Road Kochi 682 018, Kerala, Phones: 0484-4036109, +91-0484-2395739, +91-0484-2395740, e-mail: [email protected] 1-A Indian Mirror Street, Wellington Square Kolkata 700 013, Phones: +91-33-22451926, +91-33-22276404, +91-33-22276415, Rel: +91-33-32901926, Fax: +91-33-22456075, e-mail: [email protected] 106 Amit Industrial Estate, 61 Dr SS Rao Road, Near MGM Hospital, Parel, Mumbai 400 012, Phones: +91-22-24124863, +91-22-24104532, Rel: +91-22-32926896, Fax: +91-22-24160828, e-mail: [email protected] “KAMALPUSHPA” 38, Reshimbag, Opp.
    [Show full text]
  • 186923 3 En Bookfrontmatter 1..20
    2 CARDIOLOGY Section Editors: Dr. Mustafa Toma and Dr. Jason Andrade Aortic Dissection DIFFERENTIAL DIAGNOSIS PATHOPHYSIOLOGY (CONT’D) CARDIAC DEBAKEY—I ¼ ascending and at least aortic arch, MYOCARDIAL—myocardial infarction, angina II ¼ ascending only, III ¼ originates in descending VALVULAR—aortic stenosis, aortic regurgitation and extends proximally or distally PERICARDIAL—pericarditis RISK FACTORS VASCULAR—aortic dissection COMMON—hypertension, age, male RESPIRATORY VASCULITIS—Takayasu arteritis, giant cell arteritis, PARENCHYMAL—pneumonia, cancer rheumatoid arthritis, syphilitic aortitis PLEURAL—pneumothorax, pneumomediasti- COLLAGEN DISORDERS—Marfan syndrome, Ehlers– num, pleural effusion, pleuritis Danlos syndrome, cystic medial necrosis VASCULAR—pulmonary embolism, pulmonary VALVULAR—bicuspid aortic valve, aortic coarcta- hypertension tion, Turner syndrome, aortic valve replacement GI—esophagitis, esophageal cancer, GERD, peptic OTHERS—cocaine, trauma ulcer disease, Boerhaave’s, cholecystitis, pancreatitis CLINICAL FEATURES OTHERS—musculoskeletal, shingles, anxiety RATIONAL CLINICAL EXAMINATION SERIES: DOES THIS PATIENT HAVE AN ACUTE THORACIC PATHOPHYSIOLOGY AORTIC DISSECTION? ANATOMY—layers of aorta include intima, media, LR+ LRÀ and adventitia. Majority of tears found in ascending History aorta right lateral wall where the greatest shear force Hypertension 1.6 0.5 upon the artery wall is produced Sudden chest pain 1.6 0.3 AORTIC TEAR AND EXTENSION—aortic tear may Tearing or ripping pain 1.2–10.8 0.4–0.99 produce
    [Show full text]