2. Duration of Secondary Prophylaxis
CATEGORY DURATION OF PROPHYLAXIS
RF without Carditis 5 years after last attack or until 21 y/o (whichever is longer) RF with Carditis, but no residual
valvular disease
10 years after last attack or until 21 y/o (whichever is longer) RF with persistent valvular disease 10 years after last attack or until 40 y/o (sometimes lifetime)
VALVULAR HEART DISEASE (VHD)
I. STAGES OF PROGRESSION OF VHD CLASS STAGE A
(At Risk)
STAGE B (Progressive)
STAGE C (Asymptomatic Severe)
STAGE D (Symptomatic Severe) General Definition
Risk + + + +
Symptoms - - - +
Severity - Mild-to-Moderate Severe Severe
Individual Valvular Heart Disease Staging
AS At risk Asymptomatic
Progressive
Asymptomatic Severe C1: normal LVEF
C2: low LVEF
Symptomatic Severe D1: high gradient D2: low flow, low gradient, low
LVEF
70 D3: low flow, low gradient, preserved LVEF (paradoxical
low-flow severe AS)
AR At risk Asymptomatic
Progressive
Asymptomatic Severe C1: normal LVEF C2: low LVEF or dilated
LVEF
Symptomatic Severe
MS At risk Asymptomatic
Progressive
Asymptomatic Severe Symptomatic Severe
MR At risk Asymptomatic
Progressive
Asymptomatic Severe C1: normal LVEF C2: low LVEF & dilated
LVEF
Symptomatic Severe
TR At risk Asymptomatic
Progressive
Asymptomatic Severe Symptomatic Severe
II. INDIVIDUAL VALVULAR HEART DISEASES (VHD) A. Aortic Stenosis (AS)
Most common cause: degenerative calcification of aortic cusps in adults
Most common congenital defect: bicuspid aortic valve (BAV)
Symptoms (dyspnea, angina, exertional syncope) are rarely present until valve orifice <1 cm2
Death usually at 7th-8th decades, and may depend on the presence of symptoms:
o If with syncope I angina: death in 3 years o If with dyspnea: death in 2 years
o If with CHF: death in 1.5-2 years
Physical Exam
Pulsus parvus et tardus: weak and late pulse
Low pitched midsystolic ejection murmur at 2nd R ICS
Murmur may be transmitted to the apex, resembling murmur of MR (Gallavardin effect)
Diagnostics CXR / ECG: LVH (with strain pattern on ECG)
2D Echo: calcified aortic valve with restriction in opening
Therapy
Avoidance of strenuous activity and competitive sports
Diuretics for CHF
Caution with the use of nitrates and afterload unloaders (ACEI/ARBs) as these may precipitate hypotension
Statins for slower progression of leaflet calcification
Intervention: Transcatheter Aortic Valve Implantation (TAVI), aortic valve replacement (surgery)
B. Aortic Regurgitation (AR)
Physical Exam
Austin Flint murmur: soft low-pitched rumbling mid-to-late diastolic murmur
De Musset sign: jarring of the body & bobbing of the head with each systole in severe AR
Quincke’s pulse: visible capillary pulsations at the root of the nail with pressure
Traube sign: booming pistol shot sound over femoral arteries
Duroziez sign: to and from murmur when femoral artery is compressed
Water hammer (Corrigan’s) pulse: bounding and forceful pulse, rapidly increasing and subsequently collapsing
Others: widened pulse pressure, absence of A2 in severe AR Diagnostics
ECG: LVH usually with ST depression and T wave inversion in I, aVL, V5-6 (lateral leads)
2D Echo: mosaic color flow across the aortic valve during diastole Therapy Diuretics, ACEI and vasodilators for CHF
Intervention: aortic valve replacement (surgery)
71 C. Mitral Stenosis (MS)
Rheumatic heart disease is the leading cause
Poor prognosis for those >65 y/o, marked cardiac output depression, RV dysfunction and pulmonary hypertension
Physical Exam
Loud S1 and accentuated P2
Apical diastolic rumble and murmur
Opening snap Diagnostics
CXR: LAE, RAE, RVH
ECG: LAE, RAE, RVH; atrial fibrillation in severe cases
2D ECHO: doming motion of the mitral valve (anterior leaflet) during diastole
Therapy
For fluid retention: sodium, restriction, diuretics
For rate control: beta-blockers, non-dihydropyridine calcium channel blockers, digoxin
For secondary prophylaxis of rheumatic heart disease: penicillin
For prevention of stroke: warfarin (target INR 2-3)
Intervention: percutaneous transseptal mitral commisurotomy (PTMC) or mitral valve replacement therapy (surgery)
D. Mitral Regurgitation (MR) Physical Exam
Soft S1; S4 in acute severe MR
Apical holosystolic murmur radiating to axilla (characteristic finding)
Hyperdynamic LV with brisk systolic impulse and laterally displaced apex beat Diagnostics
CXR: LAE, LVH
ECG: LAE, LVH; atrial fibrillation in severe cases
2D ECHO: mosaic color flow across the mitral valve during systole Therapy
For fluid retention: sodium, restriction, diuretics
For acute MR:vasodilators (decreases afterload and helps reduce severity of MR)
Intervention:mitral valve repair or replacement (surgery) E. Mitral Valve Prolapse (MVP, Floppy Valve Syndrome, Barlow’s Syndrome)
More common in women 15-30 years old
More severe in men and >50 years old
Most patients are asymptomatic
Frequent finding in heritable connective tissue disease Physical Exam
Apical mid- or late non-ejection systolic click (characteristic finding)
High pitched late crescendo-decrescendo murmur after systolic click
Murmur is accentuated by standing and strain phase of Valsalva, diminished by squatting and isometric exercises
Diagnostics
CXR / ECG: usually normal; but may have biphasic or inverted T in II, III, aVF (inferior leads) on ECG
2D ECHO: systolic displacement of MV leaflets (prolapse) at least 2 mm into LA superior to mitral plane
Therapy
IE prophylaxis for patients with prior endocarditis
Symptoms: beat-blockers for palpitations; warfarin if with AF
Intervention: mitral valve repair or replacement (surgery) if with severe MR F. Tricuspid Stenosis (TS)
Generally rheumatic in origin; does not occur in isolation and usually associated with MS
Almost always accompanied by severe TR Physical Exam
Symptoms of right-sided CHF (ascites, edema, hepatosplenomegaly)
Opening snap of TV ~0.06 sec after PV closure
Diastolic murmur at LLSB, augmented during inspiration and reduced during expiration & strain phase of Valsalva
Diagnostics ECG: RAE, RVH
2D ECHO: restriction in opening of the TV Therapy Salt restriction, bed rest and diuretics
Interventions: surgery
72 G. Tricuspid Regurgitation (TR)
Physical Exam
Distended neck veins, hepatomegaly, ascites, (+) hepatojugular reflux
Prominent RV pulsation along left parasternal region
Carvallo sign: blowing holosystolic murmur at LPSB intensified by inspiration Diagnostics ECG: RAE, RVH
2D ECHO: mosaic color flow across tricuspid valve during systole Therapy
Isolated TR is usually tolerated and does not require surgery
Intervention: valve annuloplasty or replacement for severe cases H. Pulmonic Regurgitation (PR)
Most common acquired abnormality is regurgitation from severe pulmonary arterial HPN
Graham Steell murmur: high-pitched, decrescendo, diastolic blowing murmur along left sternal border
Intervention: percutaneous pulmonic valve replacement for severe PR
PERICARDITIS
I. ETIOPATHOGENESIS
Most common pathology affecting the pericardium and classified clinically and etiologically
May be infectious, non-infectious (MI, uremia, neoplasia, myxedema, cholesterol, chylopericardium, trauma, aortic dissection, post-irradiation, acute idiopathic, sarcoidosis) or presumably related to hypersensitivity or autoimmunity (rheumatic fever, collagen valvular disease, drug-induced, post-cardiac injury)
II. CLINICAL MANIFESTATIONS A. Acute Pericarditis (< 6 weeks)
Pain resembles that of acute MI
Chest pain: severe, pleuritic, may be retrosternal or left pericordial and may be referred to neck and, arms or left shoulder
Pericardial pain may be relieved by sitting up and leaning forward and is intensified by lying supine
PE may reveal pericardial friction rub (85%): high-pitched and is described as rasping, scratching or grating and heard most frequently at end-expiration with patient upright and leaning forward
B. Chronic (Constrictive) Pericarditis (> 6 months)
Results when the healing of an acute fibrinous or serofibrinous pericarditis or the resorption of a chronic pericardial effusion is followed by obliteration of the pericardial cavity with formation of granulation tissue
Weakness, weight gain, fatigue, increased abdominal girth / ascites and edema
Common in the Philippines: tuberculosis, malignancy and radiation-induced
Kussmaul’s sign: increase in systemic venous pressure with inspiration (in normal conditions, there should be a decrease in pressure with inspiration)
Pericardial knock: early diastolic sound in the left sternal border
III. DIAGNOSIS AND MANAGEMENT
DIAGNOSTICS ACUTE PERICARDITIS CHRONIC (CONSTRICTIVE PERICARDITIS)
Cardiac biomarkers Modest increase May be normal-minimally
increased
ECG
Subepicardial inflammation displays:
Stage 1: Diffuse SST-elevation with upward concavity and PR segment depression
Stage 2: ST segments normalize
Stage 3: T-wave inversions
Stage 4: ECG returns to
Low voltage QRS complexes
Diffuse flattening or inversion of T-waves
Atrial fibrillation in 1/3 of patients
73 normal (weeks or months)
This is in contrast with ECG findings in AMI wherein ST-elevations are convex, QRS changes occur and T-wave inversion is seen within hours before the ST-segments become isoelectric
Echocardiography
Pericardial fluid or thickening
Differentiate pericarditis from MI: assessment of wall motion
Pericardial thickening
Septal bounce
Dilation of the IVC and hepatic veins
Normal ventricular systolic function
Flattening of the LV posterior wall
CT/MRI Pericardial fluid collection
Pericardial thickening
Pericardial thickening (more accurate)
Management
Bed rest
NSAIDs, colchicine
Pericardiocentesis if with tamponade
Pericardial resection / pericardectomy
Sodium restriction & diuretics
Anti-Koch’s for TB patients
Steroids (uncertain benefi)