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.
A HANDBOOK OF AORTIC VALVE DISEASE
By Alok RanjanAuthorHouse
Copyright © 2012 Alok Ranjan
All right reserved.ISBN: 978-1-4685-4666-8Contents
Introduction......................................3Etiology..........................................5Pathophysiology...................................7Hemodynamics......................................9Clinical features.................................11Investigations....................................21Natural History...................................31Management........................................35Introduction......................................49Etiology..........................................51Pathophysiology...................................53Hemodynamics......................................55Chronic AR: Clinical Features.....................57Investigations....................................67Natural History...................................77AR: Management....................................81Suggested Reading.................................89Abbreviations.....................................91
Chapter One
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 is in the normal range and initially increases normally with exercise. Eventually, however, left ventricular hypertrophy results in either 1) diastolic dysfunction with the onset of congestive symptoms, or 2) myocardial oxygen needs in excess of supply with the onset of angina. Some patients may also experience exertional syncope, because as the severity of AS increases progressively, the cardiac output remains within the normal range at rest, but, on exercise, it no longer increases in proportion to the amount of exercise undertaken or does not increase at all (fixed cardiac output). With the development of heart failure, there is a reduction in the resting cardiac output and tachycardia. As a result, stroke volume may be so lowered that it results in a small gradient across the left ventricular outflow tract in spite of severe AS.
At any stage of life, however, the natural history of aortic stenosis largely reflects the functional integrity of the mitral valve. As long as adequate mitral valve function is maintained, the pulmonary bed is protected from the systolic pressure overloading imposed by aortic stenosis. In contrast to mitral valve disease where the pulmonary circuit is directly involved, compensatory concentric left ventricular hypertrophy allows the pressure overloaded ventricle to maintain stroke volume with modest increases in diastolic pressure, and patients can remain asymptomatic for many years.
Hemodynamics
Reduction in valve size more than 50 % results in increased gradient across AV.
For hemodynamically significant AS, valve area should be reduced by more than 60 %. At this stage compensatory mechanism in form of LV hypertrophy starts.
The hemodynamic characteristics of significant AS are:
Raised LVEDP
High 'a' wave in LA pressure trace
No increase in mean LAP, PAWP or RVSP in asymptomatic patients with normal LV function.
Unlike MS, the AV gradient does not increase with exercise because tachycardia mainly occurs at the expense of diastolic time.
Clinical features
Symptoms
Classical Triad
Angina Syncope Congestive Heart Failure
1. ANGINA (angina pectoris)
Presenting feature in 70 % cases;
Usually indicates severe AS; in only less than 10 % patients AS may not be severe.
Usually the initial symptom
More frequent with AS than any other valve lesions
Life expectancy less than 5 years after onset of angina
Typically exertional angina
Mechanisms: Demand – supply mismatch Subendocardial ischemia Hypertrophied muscles more prone to ischemia Additional CAD
Responds to nitrate but avoid as nitrate induced hypotension can be dangerous
Angina at rest indicates associated coronary artery disease
2. SYNCOPE
Presenting feature in 33 % cases;
Indicates severe AS; only in less than 10% cases, AS may not be severe
Occurs during exercise as a consequence of
Reduction of the systematic vascular resistance (Vasodilation in skeletal muscle)
Failure of forearm vasoconstriction during leg exercise (Ventricular Bazold – Jarisch reflex)
Failure of cardiac output to rise due to severe fixed obstruction
Arrhythmias (Tachy or bradyarrhythmias): Can lead to syncope at rest also.
Syncope in 'mild AS': Causes
Coronary artery disease Hypertrophic cardiomyopathy Unrelated non cardiac cause
3. CONGESTIVE HEART FAILURE (CHF)
Seen in 15 % cases Symptoms include. Dyspnea. Orthopnea. Paroxysmal Noctural Dyspnea. Pulmonary Edema. Pulmonary Hypertension. End Stage: Right Ventricular Failure Dyspnea in AS Causes: Diastolic dysfunction of LV Congestive heart failure
Dyspnea in a case of 'Mild AS'
Associated Mitral valve disease; if in a case of RHD and AS, if the duration of dyspnea is longer than 5 yrs, then associated MV disease should be strongly suspected.
Hypertrophic cardiomyopathy
Coronary artery disease
Unrelated pathology (eg., Pulmonary cause)
Diastolic Dysfunction as cause of dyspnea:
It is a common cause of dyspnea on exertion in AS (seen in 45 % cases).
Mechanism:
AS leads to LV hypertrophy as a compensatory mechanism
Increase LV wall thickness reduces ventricular compliance: Leads to raised LVEDP
The Atrium needs higher pressure to fill the ventricle: Leads to raised LAP
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