VALVULAR HEART DISEASE

Overview
Aortic Stenosis
Mitral Stenosis
Aortic Regurgitation
Acute and Chronic
Mitral Regurgitation
Acute and Chronic

Etiology
Pathophysiology
Physical Exam
Natural History
Testing
Treatment

Aortic Stenosis

Aortic Stenosis Overview:
Normal Aortic Valve Area: 3-4 cm2
Symptoms: Occur when valve area is 1/4th of normal area.
Types:
Supravalvular
Subvalvular
Valvular

Etiology of Aortic Stenosis
Congenital
Rheumatic
Degenerative/Calcific
Patients under 70: >50% have a congenital cause
Patients over 70: 50% due to degenerative

Pathophysiology of Aortic Stenosis
A pressure gradient develops between the left ventricle and the aorta. (increased afterload)
LV function initially maintained by compensatory pressure hypertrophy
When compensatory mechanisms exhausted, LV function declines.

Presentation of Aortic Stenosis
Syncope: (exertional)
Angina: (increased myocardial oxygen demand; demand/supply mismatch)
Dyspnea: on exertion due to heart failure (systolic and diastolic)
Sudden death

Physical Findings in Aortic Stenosis
Slow rising carotid pulse (pulsus tardus) & decreased pulse amplitude (pulsus parvus)
Heart sounds- soft and split second heart sound, S4 gallop due to LVH.
Systolic ejection murmur- cresendo-decrescendo character. This peaks later as the severity of the stenosis increases.
Loudness does NOT tell you anything about severity

Natural History
Mild AS to Severe AS:
8% in 10 years
22% in 22 years
38% in 25 years
The onset of symptoms is a poor prognostic indicator.

Evaluation of AS
Echocardiography is the most valuable test for diagnosis, quantification and follow-up of patients with AS.
Two measurements obtained are:
Left ventricular size and function: LVH, Dilation, and EF
Doppler derived gradient and valve area (AVA)

Evaluation of AS
Cardiac catheterization: Should only be done for a direct measurement if symptom severity and echo severity don’t match OR prior to replacement when replacement is planned.

Management of AS
General- IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis.
Medical - limited role since AS is a mechanical problem. Vasodilators are relatively contraindicated in severe AS
Aortic Balloon Valvotomy- shows little benefit.
Surgical Replacement: Definitive treatment

Echo Surveillance
Mild: Every 5 years
Moderate: Every 2 years
Severe: Every 6 months to 1 year

Simplified Indications for Surgery in Aortic Stenosis
Any SYMPTOMATIC patient with severe AS (includes symptoms with exercise)
Any patient with decreasing EF
Any patient undergoing CABG with moderate or severe AS

Summary
Disease of aging
Look for the signs on physical exam
Echocardiogram to assess severity
Asymptomatic: Medical management and surveillance
Symptomatic: AoV replacement (even in elderly and CHF)

Mitral Stenosis

Mitral Stenosis Overview
Definition: Obstruction of LV inflow that prevents proper filling during diastole
Normal MV Area: 4-6 cm2
Transmitral gradients and symptoms begin at areas less than 2 cm2
Rheumatic carditis is the predominant cause
Prevalence and incidence: decreasing due to a reduction of rheumatic heart disease.

Etiology of Mitral Stenosis
Rheumatic heart disease: 77-99% of all cases
Infective endocarditis: 3.3%
Mitral annular calcification: 2.7%

MS Pathophysiology
Progressive Dyspnea (70%): LA dilation ? pulmonary congestion (reduced emptying)
worse with exercise, fever, tachycardia, and pregnancy
Increased Transmitral Pressures: Leads to left atrial enlargement and atrial fibrillation.
Right heart failure symptoms: due to Pulmonary venous HTN
Hemoptysis: due to rupture of bronchial vessels due to elevated pulmonary pressure

Natural History of MS
Disease of plateaus:
Mild MS: 10 years after initial RHD insult
Moderate: 10 years later
Severe: 10 years later
Mortality: Due to progressive pulmonary congestion, infection, and thromboembolism.

Physical Exam Findings of MS
prominent "a" wave in jugular venous pulsations: Due to pulmonary hypertension and right ventricular hypertrophy
Signs of right-sided heart failure: in advanced disease
Mitral facies: When MS is severe and the cardiac output is diminished, there is vasoconstriction, resulting in pinkish-purple patches on the cheeks

Diastolic murmur:
Low-pitched diastolic rumble most prominent at the apex.
Heard best with the patient lying on the left side in held expiration
Intensity of the diastolic murmur does not correlate with the severity of the stenosis
Heart Sounds in MS

Loud Opening S1 snap: heard at the apex when leaflets are still mobile
Due to the abrupt halt in leaflet motion in early diastole, after rapid initial rapid opening, due to fusion at the leaflet tips.
A shorter S2 to opening snap interval indicates more severe disease.
Heart Sounds in MS

Evaluation of MS
ECG: may show atrial fibrillation and LA enlargement
CXR: LA enlargement and pulmonary congestion. Occasionally calcified MV
ECHO: The GOLD STANDARD for diagnosis. Asses mitral valve mobility, gradient and mitral valve area

Management of MS
Serial echocardiography:
Mild: 3-5 years
Moderate:1-2 years
Severe: yearly
Medications: MS like AS is a mechanical problem and medical therapy does not prevent progression
β-blockers, CCBs, Digoxin which control heart rate and hence prolong diastole for improved diastolic filling
Duiretics for fluid overload

Management of MS
Identify patient early who might benefit from percutaneous mitral balloon valvotomy.
IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

Simplified Indications for Mitral valve replacement
ANY SYMPTOMATIC Patient with NYHA Class III or IV Symptoms
Asymptomatic moderate or Severe MS with a pliable valve suitable for PMBV

Aortic Regurgitation

Aortic Regurgitation Overview
Definition: Leakage of blood into LV during diastole due to ineffective coaptation of the aortic cusps

Etiology of Acute AR
Endocarditis
Aortic Dissection
Physical Findings:
Wide pulse pressure
Diastolic murmur
Florid pulmonary edema

Treatment of Acute AR
True Surgical Emergency:
Positive inotrope: (eg, dopamine, dobutamine)
Vasodilators: (eg, nitroprusside)
Avoid beta-blockers
Do not even consider a balloon pump

Etiology of Chronic AR
Bicuspid aortic valve
Rheumatic
Infective endocarditis

Pathophysiology of AR
Combined pressure AND volume overload
Compensatory Mechanisms: LV dilation, LVH. Progressive dilation leads to heart failure

Natural History of AR
Asymptomatic until 4th or 5th decade
Rate of Progression: 4-6% per year
Progressive Symptoms include:
- Dyspnea: exertional, orthopnea, and paroxsymal nocturnal dyspnea
Nocturnal angina: due to slowing of heart rate and reduction of diastolic blood pressure
Palpitations: due to increased force of contraction

Physical Exam findings of AR
Wide pulse pressure: most sensitive
Hyperdynamic and displaced apical impulse
Auscultation-
Diastolic blowing murmur at the left sternal border
Austin flint murmur (apex): Regurgitant jet impinges on anterior MVL causing it to vibrate
Systolic ejection murmur: due to increased flow across the aortic valve

MRI of the Heart Revealing a Central, High-Velocity Jet Projecting into the Left Ventricular Cavity.
The jet clearly strikes the anterior mitral-valve leaflet, causing distortion and premature closure during diastole.

The Evaluation of AR
CXR: enlarged cardiac silhouette and aortic root enlargement
ECHO: Evaluation of the AV and aortic root with measurements of LV dimensions and function (cornerstone for decision making and follow up evaluation)
Aortography: Used to confirm the severity of disease

Management of AR
General: IE prophylaxis in dental procedures with a prosthetic AV or history of endocarditis.
Medical: Vasodilators (ACEI’s), Nifedipine improve stroke volume and reduce regurgitation only if pt symptomatic or HTN.
Serial Echocardiograms: to monitor progression.
Surgical Treatment: Definitive Tx

Simplified Indications for Surgical Treatment of AR
ANY Symptoms at rest or exercise
Asymptomatic treatment if:
EF drops below 50% or LV becomes dilated

Mitral Regurgitation

Definition: Backflow of blood from the LV to the LA during systole
Mild (physiological) MR is seen in 80% of normal individuals.
Chronic Mitral Regurgitation Overview

Acute MR
Endocarditis
Acute MI:
Malfunction or disruption of prosthetic valve

Management of Acute MR
Myocardial infarction: Cardiac cath or thrombolytics
Most other cases of mitral regurgitation is afterload reduction:
Diuretics and nitrates
nitroprusside, even in the setting of a normal blood pressure.

Management of Acute MR
Do not attempt to alleviate tachycardia with beta-blockers. Mild-to-moderate tachycardia is beneficial in these patients because it allows less time for the heart to have backfill, which lowers regurgitant volume.

Treatment of Acute MR
Balloon Pump
Nitroprusside even if hypotensive
Emergent Surgery

Myxomatous degeneration (MVP)
Ischemic MR
Rheumatic heart disease
Infective Endocarditis
Etiologies of Chronic Mitral Regurgitation

Pathophysiology of MR
Pure Volume Overload
Compensatory Mechanisms: Left atrial enlargement, LVH and increased contractility
Progressive left atrial dilation and right ventricular dysfunction due to pulmonary hypertension.
Progressive left ventricular volume overload leads to dilation and progressive heart failure.

Physical Exam findings in MR
Auscultation: soft S1 and a holosystolic murmur at the apex radiating to the axilla
S3 (CHF/LA overload)
In chronic MR, the intensity of the murmur does correlate with the severity.
Exertion Dyspnea: ( exercise intolerance)
Heart Failure: May coincide with increased hemodynamic burden e.g., pregnancy, infection or atrial fibrillation

The Natural History of MR
Compensatory phase: 10-15 years
Patients with asymptomatic severe MR have a 5%/year mortality rate
Once the patient’s EF becomes <60% and/or becomes symptomatic, mortality rises sharply
Mortality: From progressive dyspnea and heart failure

Imaging studies in MR
ECG: May show, LA enlargement, atrial fibrillation and LV hypertrophy with severe MR
CXR: LA enlargement, central pulmonary artery enlargement.
ECHO: Estimation of LA, LV size and function. Valve structure assessment
TEE if transthoracic echo is inconclusive

Management of MR
Medications
Vasodilator such as hydralazine
Rate control for atrial fibrillation with β-blockers, CCB, digoxin
Anticoagulation in atrial fibrillation and flutter
Diuretics for fluid overload

Management of MR
Serial Echocardiography:
Mild: 2-3 years
Moderate: 1-2 years
Severe: 6-12 months
IE prophylaxis: Patients with prosthetic valves or a Hx of IE for dental procedures.

Simplified Indications for MV Replacement in Severe MR
ANY Symptoms at rest or exercise with (repair if feasible)
Asymptomatic:
If EF <60%
If new onset atrial fibrillation