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    A Handbook of Aortic Valve Disease
    A Handbook of Aortic Valve Disease
    A Handbook of Aortic Valve Disease
    Ebook97 pages1 hour

    A Handbook of Aortic Valve Disease

    By Alok Ranjan

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    About this ebook

    "A Handbook of Aortic Valve Disease" contains a detailed description of the disease. Etiology, pathogenesis and hemodynamics of Aortic Stenosis and Regurgitation have been dealt in simple and comprehensible manner. Special effort has been made to explain the clinical features (Symptoms and signs) of aortic valve disease. Probably the clinical features is the forgotten art in the newer text books. However, the author has taken a special interest to include a detailed description of clinical features. In the investigation section, echocardiography has been written comprehensively. The diagnosis, severity and prognosis of aortic valve disease depends heavily on echocardiography. The natural history of aortic valve disease in another section where readers will find interesting and minute details about the various stages of aortic valve disease. The treatment section includes description about the various interventions (catheter based as well as surgical) and it also includes the ACC / AHA guidelines.

    All in all, the book promises to be a great reference book for Aortic Valve disease and is worth having it on shelf for easy reading. The pointwise and concise writing has made this book specially useful for students and exam going students.

    LanguageEnglish
    PublisherAuthorHouse
    Release dateMar 16, 2012
    ISBN9781468546644
    A Handbook of Aortic Valve Disease

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      Book preview

      A Handbook of Aortic Valve Disease - Alok Ranjan

      Contents

      Disclaimer

      Aortic Stenosis

      Introduction

      Etiology

      Pathophysiology

      Hemodynamics

      Clinical features

      Investigations

      Natural History

      Management

      Aortic Regurgitation

      Introduction

      Etiology

      Pathophysiology

      Hemodynamics

      Chronic AR: Clinical Features

      Investigations

      Natural History

      AR: Management

      Suggested Reading

      Abbreviations

      About the Author

      Disclaimer

      Medicine is a constantly changing science. New research findings necessitate continual changes in disease concept and its management. The author and publisher of this handbook have used reasonable efforts to provide up-to-date, accurate information that is within generally accepted medical standards at the time of publication. However, as medical science is ever evolving, and human error is always possible, the author and publisher (or any other involved parties) do not guarantee total accuracy or comprehensiveness of the information in this handbook, and they are not responsible for omissions, errors, or the results of using this information. The reader should confirm the accuracy of the information in this handbook from other sources. In particular, all drug doses, indications, and contraindications should be confirmed in package inserts.

      The author has made every effort to trace the copyright holders for borrowed material. If he has inadvertently overlooked any, he will be pleased to make necessary arrangement at the first opportunity.

      Dedicated to wife, Puja and kids, Adishree and Anirvan.

      Families are like fudge – mostly sweet with a few nuts

      Thank you for tolerating ‘the nut’.

      Aortic Stenosis

      Introduction

      Aortic stenosis is usually defined by restricted systolic opening of the valve leaflets, with a mean transvalvular pressure gradient of at least 5 - 10 mm Hg.

      LVOTO (Left ventricular outflow tract obstruction) includes obstruction at valve, sub-valvular and supravalvular level.

      The normal aortic valve is 3 to 4 sq. cm. in area when fully open.

      The natural progression of Aortic Stenosis is slow and is from mild to moderate to severe stenosis. Development of symptoms indicates more than moderate Aortic Stenosis

      Thus, AS is an insidious disease with a long latency period followed by rapid progression after the appearance of symptoms, resulting in a high rate of death (approximately 50% in the first 2 years after symptoms appear) among untreated patients.

      Etiology

      Causes of left ventricular outflow tract obstruction (LVOTO)

      Valvular Aortic stenosis

      Acquired

      Post inflammatory (usually rheumatic)

      The most distinctive aortic valve change secondary to valvulitis is commissural fusion, the single most important finding in determining that the cause is rheumatic (or post-inflammatory). Severe AS may be seen after brucellar or rickettsial infection.

      Degenerative

      Bi or tricuspid AV

      It is unusual for a bicuspid or tricuspid valve to be stenotic in absence of significant calcification. Non calcific AS with fibrosis is therefore more likely to be rheumatic in origin.

      Congenital

      Unicuspid valve

      Tricuspid with fusion of commissures

      Hypoplastic annulus

      Rare causes

      SLE (especially after steroid therapy)

      Fabry’s disease and Ochronosis (metabolic products accumulates in cusps)

      Type II hyperlipoprotenemia

      IE

      Secondary to Radiotherapy

      Nonvalvular aortic stenosis

      Rare; as all acquired pathology and more than 70 % of congenital lesions are valvular stenosis

      Subvalvular obstruction

      Discrete fibromembranous

      Diffuse fibromuscular (tunnel)

      Muscular (Hypertrophic subaortic stenosis)

      Supravalvular obstruction

      Hourglass

      Hypoplastic

      Membranous

      Age of presentation of LVOTO

      Infancy to first decade:

      Congenital valvular, subvalvular or supravalvular pathology

      Early childhood to late adulthood

      Rheumatic AS

      Hypertrophic subaortic stenosis

      Early to late adulthood

      Degenerative AV disease

      Degenerative Tricuspid AV disease usually present after 65 yrs of age

      Pathophysiology

      Valvular aortic stenosis results in chronic left ventricular pressure overloading. The AVA has to be reduced by about 50% of normal before a measurable gradient can be demonstrated in humans. Pure aortic valve stenosis results in compensatory ventricular hypertrophy proportional to the degree of obstruction. Mild degrees of obstruction are usually well tolerated, with minimal hypertrophy and normal left ventricular function. As stenosis progresses, hypertrophy increases and reduces wall stress. In most patients with AS, cardiac output

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