A Handbook Of Aortic Valve Disease - Brossura

Ranjan, Alok

Brossura

ISBN 10: 146854666X ISBN 13: 9781468546668

Casa editrice: AuthorHouse, 2012

Riassunto

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.

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A HANDBOOK OF AORTIC VALVE DISEASE

By Alok Ranjan

AuthorHouse

Copyright © 2012 Alok Ranjan
All right reserved.
ISBN: 978-1-4685-4666-8

Contents

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

Development of symptoms of pulmonary congestion due to raised LAP

This entity (diastolic dysfunction) must be distinguished from dyspnea due to CHF, which carries a grave prognosis.

Rare symptoms:

Systemic emboli Usually silent

Due to Thrombus: Very rare Hence long term anticoagulation is not indicated in AS Vegetation Calcium emboli

IE

Risk of IE decreases as the extent of calcification increases

Unrelated to severity of AS but is related to severity of AS in post AVR cases

GI bleeding: (mainly with degenerative AS): Hayde syndrome

Rare

The high shear stress of stenotic valves makes multimeric Von Willebrand's factor more susceptible to cleavage by a plasma metalloprotease and may increase platelet clearance

May also be due to arteriovenous malformations (angiodysplasia) involving Right colon Small bowel Stomach

Bleeding usually ceases with AVR

Signs

1. Pulse:

Always examine 'Carotid' pulse if AS is suspected Classical finding:

Pulsus parvus et tardus (Slow rising and small volume pulse)

More common in decompensated AS; usually associated with other signs of LV failure.

Other features: Slow rising (pulsus parvus) Delayed peak (pulsus tardus) Reduced amplitude Sustained contour With or without thrill in 'carotid'

* A normal carotid pulse in an adult with clinically normal LV function excludes moderate to severe AS.

Factors that 'mask' the typical quality of AS pulse Associated AR Associated systemic hypertension High cardiac output states Young patients (elastic arterial walls) Elderly patients (arteriosclerosis) CCF

Atrial Fibrillation: Always rule out co-existent MV disease Symptoms may appear as atrial contraction contributes up to 40 % of the ventricular filling during diastole in AS (atrial contraction contributes nearly 20 % in a normal heart)

AF may cause rapid deterioration of clinical features of AS

2. Blood pressure:

Normal in most cases Abnormal if associated with systemic hypertension or with associated AR.

May have narrow pulse pressure in severe AS (not a rule)

High systolic BP does not rule out significant AS unless more than 250 mm Hg

3. Apical impulse

LV type Heaving in character, At normal site (5th ICS, inside mid clavicular line: suggestive of absence of cardiomegaly) Cardiomegaly in case of pure AS indicates CHF and grave prognosis. Palpable S4 Usually indicates AV gradient more than 70 mm Hg May be present even if S4 is not 'audible'

4. Systolic thrill Is a rule if significant AS is present.

Most commonly felt in 'aortic' area; radiates to neck, right supraclavicular or shoulder

Does not always indicate 'severe' AS

5. Jugular Venous Pulse in AS

Feature Findings Mechanism / significance

Level Normal or elevated Elevated with RV failure secondary to LV failure Associated MS with PAH Associated organic TS

Waves

A Normal or prominent Prominent A wave with Severe AS; Severe IVS hypertrophy leads to reduced RV compliance If associated with MS and PH / TS HOCM V/X/Y; Normal Abnormal with RV failure or TV disease

6. Auscultation Ascultation: Sounds

• S1: Normal and unremarkable Loud S1 Associated MS Think of Aortic EC !! A 'loud and discrete' S1 at aortic or pulmonary area is usually EC rather than S1 in a case suspected to be of AS

Soft S1: LV dysfunction Raised LVEDP

• S2: Intensity: A2: Soft; P2: Normal

Soft A2 Indicates fibrotic and calcific valve Usual in rheumatic or degenerative AS Hence, Classically, A2 is diminished to absent (seen in 20% cases);

Normal A2: Rare; seen in 10 % cases; According to Paul Wood, normal A2 is present only in 5% cases of acquired AS

Normal or increased A2 *Indicates pliable and relatively thin leaflet Usual in 'Congenital' AS

Splitting of S2

Normal split: Rules out significant AS. Seen in Mild AS Congenital AS

* Hemodynamically significant AS has abnormal splitting of S2

Single S2 (seen in 70 % cases) Due to A2 'moving into' P2 Can also be due to 'soft' A2 because of fibrocalfic valve

Decreased intensity of A2 and hence only P2 is heard

Reverse split of S2 (seen in 20% cases);

Always indicates severe AS; Reverse A2 P2 split does not indicate severe AS if associated with AR.

• S3: Never heard except in CHF (late stage of AS) and in young patient.

• S4: Always present.

A palpable S4 indicates severe AS; although unreliable sign of severe AS if patient is more than 45 yrs of age

Palpable S4 indicates an LVEDP > 15 mm Hg.

Palpable S4 rules out associated MS

• Aortic EC:

Intensity of EC mirrors that of A2

It confirms the diagnosis of structural heart disease in a case of ejection systolic murmur

Localizes the disease to valve; in absence of dilated aorta or chronic hypertension

Usually it is due to 'congenital' deformity of valve; almost a rule in congenital AS but present in less than 1/3rd patients with AS with more than 50 yrs of age

Uncommon in tricuspid AV with acquired stenosis

More common in less severe AS

Mild to moderate AS (75%) & severe AS (25 %) Hence presence of EC does not predict severity of AS

* A 'loud and discrete' S1 at aortic or pulmonary area is usually EC rather than S1 in a case suspected to be of AS

Auscultation: Murmur

• ESM

Best heard in 'aortic' area

Radiates to carotids and to apex (Gallavardin phenomenon)

Late peaking murmur indicates severe AS

More reliable than length of murmur in assessing severity

Length of murmur is proportional to severity of AS in absence of AR and LVF

Thrill (seen in 80% cases):

Thrill does not indicate severe AS; loudness does NOT correlate with severity.

Loudness does not correlate severity except in congenital AS (Ref.: Abrams)

* Characteristics of murmur do not differentiate congenital vs. acquired or valvular vs. either sub or supravalvular AS

Criteria for Severe AS

Symptomatic patient

Low volume & slow rising pulse with decreased carotid pulsation

Palpable S4

Paradoxical A2 – P2 split

Long and late peaking ESM with absent EC

Criteria for CRITICAL AS

• Valve Area <0.7cm2

• Increase LVEDP

• Decreased LVEF

• Decreased Stroke Volume

Investigations

1. ECG

Almost always abnormal (except in 10 % cases) if AS is severe.

In pure AS, the total 12 lead QRS amplitude in millimeters is equal to LV systolic pressure in mm Hg. More reliable in congenital AS

Presence of Left ventricular hypertrophy (LVH)

Presence of left atrial enlargement (LAE):

Should raise suspicion of coexisting MV disease but LAE may be present in severe AS without MV disease

LAE is present in > 80 % cases with severe isolated AS

Conduction blocks:

More common in AS than any other valve lesions: 5 % cases Bundle Branch Block 1st degree heart block Complete Heart Block Due to Septal trauma due to high intra-myocardial tension Hypoxic damage to conducting fibers Extension of valvular calcification AF: Seen in only 10 – 15 % cases Its presence should raise a suspicion of coexisting MVD

2. CXR

Normal Heart size with increased convexity of the left ventricular silhouette due to ventricular hypertrophy

Calcification of the Aortic Valve:

Usually with valvular AS

Better seen on fluoroscopy and in lateral or oblique views on CXR

Absence of calcification in a patient more than 40 yrs. (not valid for younger patients) rules out significant AS.

Absence of calcification can not be concluded on CXR only.

Fluoroscopy or CT scan are more diagnostic

Ascending aorta dilation: Present;

Usually only with valvular AS (seen in 80 % cases)

Absent in nonvalvular stenosis or coexisting mitral valve disease

Magnitude of dilation does not correlate with severity

Cardiomegaly in end stage disease

* A normal CXR does not rule out severe AS

3. Stress Test

Role of Treadmill stress testing

Dangerous in symptomatic patients

Not useful for diagnosis of CAD

May be used to assess functional significance of severe AS in patients who deny symptoms (e.g., hypotensive response to exercise)

4. ECHOCARDIOGRAPHY

Very useful in diagnosis and management of AS.

Confirms diagnosis of AS and its severity

Defines etiology of AS

Differentiates valvular with non valvular AS

Points to remember in echocardiographic evaluation of AS

Motility of the Leaflet; calcification of valve Gradient across the valve Measurement of the valve areas LVEF Regional Ventricular Motion Ventricular Hypertrophy Left Atrial Enlargement To rule out other congenital heart disease (specially in children)

(Continues...)

Excerpted from A HANDBOOK OF AORTIC VALVE DISEASEby Alok Ranjan Copyright © 2012 by Alok Ranjan. Excerpted by permission of AuthorHouse. All rights reserved. No part of this excerpt may be reproduced or reprinted without permission in writing from the publisher.
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Dettagli dell'edizione

• Editore: AuthorHouse
• Data di pubblicazione: 2012
• Lingua: Inglese
• ISBN 10: 146854666X
• ISBN 13: 9781468546668
• Rilegatura: Copertina flessibile
• Numero di pagine: 108
• Contatto del produttore: non disponibile
• Persona responsabile: gpsr@libri.de; gpsr@libri.de; ; Europaallee 1; Bad Hersfeld; 36244; Germania