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Valvular heart disease Aortic Valve Diseases Dr. Hussam Al-Faleh Med 341 course Lecture outline General principles : Pressure overload and volume overload Heart murmurs Aortic valve disease Mitral valve disease VALVULAR STENOSIS Pressure in upstream chamber IS HIGHER than Pressure in downstream chamber during time of flow (when valve is normally open). Hemodynamic abnormality = "PRESSURE GRADIENT" Upstream Down stream High pressure low pressure VALVULAR REGURGITATION Retrograde flow of blood "upstream" during time when valve is normally closed. Hemodynamic abnormality = "VOLUME OVERLOAD" Upstream Volume overload Down stream Left Ventricular Hypertrophy “Pressure and Volume overload” Vena Cava RA Pulm Vein LA LV RV Pulm Artery Aorta Aortic stenosis Normal RA RA LV RV LV Vena Cava RA Pulm Vein LA LV RV Pulm Artery Aorta Aortic Insufficiency Example: Aortic regurgitation RA RA ↑↑LV RV LV AI AS Heart murmurs Produced by turbulent blood flow Turbulence is mainly determined by velocity of blood flow across a structure Timing of murmurs (either systolic, or diastolic) can give helpful information regarding the valve lesion Common Murmurs and Timing Systolic Murmurs Aortic stenosis Mitral insufficiency Mitral valve prolapse Tricuspid insufficiency Diastolic Murmurs Aortic insufficiency Mitral stenosis S1 S2 S1 Outline for every valve lesion Etiology Pathphysiology Symptoms and signs Natural history Investigations Management Aortic stenosis Etiology Supra-Valvular Valvular - Congenital - Acquired Sub-Valvular - Discreet - Tubular Etiology Valvular Congenital 1. Uni-cusped - Rare - Ages affected 2-30yrs 2. Bi-cusped - 2% of the population - More common in males - Associated with coarctation in 6% of patients - Ages affected 40-50yrs Etiology Acquired 1. Rheumatic - Adhesion and fusion of valve commissures leads to stiffening of the free borders as well as calcification 2. Degenerative (senile) - Results from mechanical stress - Associated with traditional risk factors for CAD such as HTN, Dyslipidemia and smoking A. Normal Trileaflet AV B. Congenital AS C. Rheumatic AS D. Calcific AS E. Degenerative AS Pathphysiology Symptoms Cardinal symptoms: 1. Chest pain - Occurs due to ↑ O2 demand (LV hypertrophy) and ↓ O2 delivery - Is often related to concomitant CAD. 2. Presyncope/Syncope - Caused by transient ↓ cerebral blood flow - May also be related transients VF or AF 3. Dyspnea - Late manifestation of severe AS Signs Central Pulse : - Slow rising , low volume ( Pulsus Parvus et tardus) - Coarse systolic vibrations at Carotid artery (Carotid Shudder) JVP: - Prominent a wave Apex: - Sustained - Systolic thrill - Displaced (late with LV failure) Aortic pulse Slow rising pulse Signs ( Auscultation) S2 may be soft and single Paradoxical splitting of S2 in severe AS S1 S2 Inspiration Expiration Signs (Auscultation) Aortic ejection sound with Bicuspid AV S4 Ejection S1 Click S4 S1 S2 S2 Auscultation S1 S2 Mild-Moderate S1 S2 Severe Natural history Investigations ECG - LAD - LVH Investigations CXR - Aortic Calcification - Post stenotic dilation of Ascending Aorta Echocardiography - Routinely used to diagnose and estimate the severity of AS - Peak and mean gradients are measured - Valve area is measured Mild AS (area >1.5 cm2) Moderate (area >1.0 to 1.5 cm2) Severe (area <1.0 cm2) Management No place for medical therapy if severe AS is associated with symptoms. Surgery is the treatment of choice. Generally speaking ,if the patient has symptoms with severe AS Surgery is indicated. Aortic Regurgitation Etiology Etiology (chronic AR) Two major causes: A. Intrinsic structural valve problem 1. Congenital : Bicuspid valve 2. Acquired : - Inflammatory (Rheumatic, Connective tissue diseases) - Infectious (IE) - Degenerative Etiology( chronic AR) B. Abnormality of the Ascending Aorta 1. Congenital : Marfans disease 2. Infectious : Syphilis (15-25yr after infection) 3. Inflammatory : Connective tissue diseases (RA, AS, GCA) 4. Idiopathic : progressive dilation (cystic medial necrosis) Etiology (Acute AR) Trauma Aortic dissection Infective endocarditis Aortic regurgitation ↓ effective Stroke volume Excess volume to the LV ↑LV end diastolic pressure ↓ Myocardial O2 supply Stretching of Myocardium LV failure ↑ wall stress Eccentric LV hypertrophy (Ischemia) ↑ Myocardial O2 demand (Ischemia) Symptoms Gradual development of Dyspnea , Orthopnea, and PND Angina Palpitations With Acute AR , abrupt development of dyspnea. Signs of Chronic AR Peripheral signs - De Musset sign (head movment with pulse) - Water hammer pulse (abrupt distention and quick collapse) - Duroziez sign - Muller’s sign (systolic pulsation of Uvula) - Pistol shot/ Traube sign - Quincke sign - Hill’s sign (Popliteal pressure at least 20 mmHg higher than brachial pressure Signs of chronic AR Wide pulse pressure Central pulse: - Large volume pulse - Bisferines pulse - Corrigan pulse JVP may be normal or elevated Displaced and hyperdynamic apex Auscultation S2 may be soft or accentuated S3 indicates severe AI Ejection click High pitched, blowing, decrescendo diastolic murmur at LSB, best heard at end-expiration & leaning forward Auscultation S1 S2 S1 Length of murmur correlates with severity. In Acute AR diastolic murmur is low pitched and short. Austin-Flint murmur indicates severity (mid to late diastolic murmur) Systolic murmur related to high flow state Investigations – LVH, LAD CXR- may show ↑cardiothoracic ratio, and dilated aorta ECG Investigations Angiography: - Would aid in diagnosis and grading of severity Echocardiography: - The easiest and fastest way of diagnosing and grading the severity of AR. - Detection of the underlying mechanism of AR. Natural history Asymptomatic %/Y Normal LV function (~good prognosis) Progression to symptoms or LV dysfunction Progression to asymptomatic LV dysfunction Sudden death <6 < 3.5 < 0.2 Abnormal LV function Progression to cardiac symptoms > 25 Symptomatic (Poor prognosis) Mortality > 10 Management Any patient with severe AR and any of the following should have aortic valve replacement: 1. Symptomatic patients 2. Patients without symptoms, but with LV systolic dysfunction (EF<50%), or marked dilation of the LV. Management Vasodilator therapy ( ACE I, or CCB’s) for: 1. Patients not candidates for surgery 2. Short term to Improve hemodynamics 3. Treatment of hypertension