Johnstone Kayandabila, MDFeb, 2017.

Department of Internal MedicineKilimanjaro Christian Medical Center

KCMC

Contents

1. Aortic Stenosis (AS)2. Aortic Insufficiency (AI)3. Mitral Regurgitation (MR)4. Mitral Stenosis (MS)5. Mitral Valve Prolapse (MVP)6. Tricuspid Regurgitation7. Prosthetic Heart Valves

Introduction

Distribution of VHD in the Euro Heart Survey

ESC, 2007

Approach to the cardiac patient

InspectionBody habitus - marfansFace + neck - mitral

facies, cyanosis, JVP, carotid pulse

Chest wall – scars, apex beat.

Hands – cyanosis, stigmata of endocarditis

EtiologyPhysical ExamAssessing SeverityNatural History PrognosisTiming of Surgery

PalpationPulse - rate, rhythm ,character, volume, equalityThrills - Aortic + pulmonary areas, apex, LSE Heaves - with right ventricular hypertrophy (left

sternal edge)Apex - hypertrophied, dilated.Palpable sounds

1st (mitral stenosis, tapping apex), 2nd – pulmonary or systemic hypertension

AuscultationSplit up the cardiac cycle

○ first and second sounds○ Added sounds○ Systole○ Diastole

List with breath held in expiration (most murmurs are left sided)

Track murmurs across the chest wallAlways listen for an early diastolic murmur in

expiration at the left sternal edge

Investigations for murmurs FBC, TFT’s – flow murmurs. CXR ECG Echocardiogram Angiography (prior to surgery) If endocarditis suspected:

Blood cultures, CRP, urine dipstick and microscopy, trans oesophageal echocardiogram

SYSTOLIC AND DIASTOLIC MURMURS SYSTOLIC

Flow murmurs Aortic stenosis Hypertrophic obstructive

cardiomyopathy Mitral regurgitation Ventricular septal defect Pulmonary stenosis Coarctation Tricuspid regurgitation

DIASTOLIC Aortic regurgitation Mitral stenosis Pulmonary regurgitation

MURMURS AND THECARDIAC CYCLE

Aortic stenosis

Mitral Regurgitation

1 2

1 2

Mitral valve prolapse withlate regurgitation

1 2

Evaluation of cardiac patient

Epidemiology Primary VHD ranks below Coronary HD, HTN,

obesity, & DM as major threat to the public health Has significant morbidity & mortality rates.

Rheumatic fever – dominant cause of VHD in LIC. Prevalence of RF 1/100,000 school-age children in

Costa Rica, 150/100,000 in China. RHD; 12-65% of hosp admissions due to CV-d’se. (Harrison, 2015)

RHD incidence at Muhimbili by Echo 5.4% btn 10-19 yo; Females>Males (Luggajo, 2009)

Cont’ Globally, about 15-20 million people live

with RHD; new cases 300,000, & CFR 233,000/yr

Highest mortality reported in Southeast Asia, 7.6/100,000.

A 71 yo M is evaluated for symptoms of HF. On physical exam, the apical impulse is enlarged and displaced laterally and a grade 2/6 midsystolic murmur is heard at the right upper sternal border that radiates to the carotid arteries.

Echo shows hypokinesis & LVEF of 30%, calcified aortic valve cusp with diminished mobility, and transvalvular mean gradient is 26 mmHg.

The correct answer is;a) Severe AS with cardiomyopathyb) Low transvalvular gradient is due to LV dysfunctionc) Treatment is by cardiac catheterization or valve replacementd) All the abovee) None of the above

A 71 yo M is evaluated for symptoms of HF. On physical exam, the apical impulse is enlarged and displaced laterally and a grade 2/6 midsystolic murmur is heard at the right upper sternal border that radiates to the carotid arteries.

Echo shows hypokinesis & LVEF of 30%, calcified aortic valve cusp with diminished mobility, and transvalvular mean gradient is 26 mmHg.

The correct answer is;a) Severe AS with cardiomyopathyb) Low transvalvular gradient is due to LV dysfunctionc) Treatment is by cardiac catheterization or valve replacementd) All the abovee) None of the above

Aortic Stenosis (AS)Etiology; Calcific: predominant cause in patients > 70y

Risk factors; HTN, ↑chosterolaemia, ESRD

Congenital Bicuspid AoV →premature calcification (40-60yrs) cause in 50% of pts <70 y William syndrome

RHD: AS usually a/c by AI & MV disease DDx: subvalvular- HCMP, membranous subAo

stenosis , supravalvular AS

Pathogeneis of calcific aortic stenosis

Harrison 19th Edition, 2015. pp. 1530.

Major causes of Aortic valve disease

Table 283-1, pp.1529

Valve lesion Etiologies

Aortic stenosis Congenital (bicuspid, unicuspid)Degenerative calcificRheumatic fever, Radiation

Aortic regurgitation

ValvularCongenital (bucuspid)Endocarditis, Rheumatic feverMyxomatous (prolapse), TraumaticSyphilis, Ankylosing spondylitisRoot disease

Aortic dissection, Cystic medial degenerationMarfan’s syndrome, Bicuspid aortic valveNonsyndromic familial aneurysmAortitisHTN

Harrison, pp. 1529

Aortic valves

DEGENERATIVE AORTIC VALVE DISEASE

BICUSPID AORTIC VALVE

Clinical manifestations Usually indicates AVA 1 cm2 or concomitant CAD

Cardinal features Angina: ↑O2 demand (hypertrophy) + ↓O2 supply (↓ cor

perfusion pressure) +/- CAD Syncope (exertional): peripheral vasodil. w/ fixed CO → ↓MAP

→ ↓cerebral perfusion. Heart failure: outflow obstruct + diastolic dysfxn → pulm.

edema; precip. by AF & AV dissociation (↓ LV filling)

Acquired von Willebrand disease ( ̴20% of severe AS): destruction of vWF (NEJM 2003;349:343)

Natural hx: usually slowly progressive (AVA ↓ ̴ 0.1 cm2 per y, but varies; Circ 1997;95:2262), until sx develop

Mean survival based on sx: angina = 5 y; syncope = 3 y; CHF = 2 y

Physical exam Midsystolic crescendo-decrescendo murmur at RUSB,

harsh, high-pitched, radiates to carotids, apex (holosystolic = Gallavardin effect)

↑ w/ passive leg raise, ↓ w/ standing & Valsalva

In contrast, dynamic outflow obstruction (eg, HCMP) ↓ w/ passive leg raise & ↑ w/ standing & Valsalva

Ejection click after S1 sometimes heard with bicuspid AoV Signs of severity:

late-peaking murmur, paradoxically split S2 or inaudible A2, small and delayed carotid pulse (“pulsus parvus

et tardus”), LV heave, S4 (occasionally palpable)

Diagnostic studies ECG: LVH, LAE, LBBB, AF (in late disease) CXR:

cardiomegaly, AoV calcification, post-stenotic dilation of ascending aorta, pulmonary congestion

Echo: valve morphology, estimate pressure gradient & calculate aortic valve area, EF

Cardiac cath: pressure gradient ( ) across AoV, ∇ AVA, r/o CAD (in 50% of calcific AS)

ECG in Aortic Valve disease

LVH LAE LBBBAF (in late

disease)

CXR in Aortic Valve disease

Fig. 283-2: management strategy for patients with aortic stenosis (pp.2101)

Classification of Aortic Stenosis

Stage Mean Gradient (mmHg)

Jet vel. (m/s)

AVA (cm2)

LVEF

Normal 0 1 3-4 Normal

Mild < 25 <3 >1.5 Normal

Moderate 25-40 3-4 1.0 – 1.5 Normal

Severe, compensated

>40 >4 < 1.0* Normal

Severe, decompensate

d

Variable Variable <1.0* ↓

AVA index (AVA relative to BSA) < 0.6 cm2/m2 also qualifies for severe AS.

Treatment Management decisions are based on

symptoms: once sx develop surgery is needed.

If asx wt preserved EF; HTN can be Rx’d; BB, ACE-INitroglycerin: relieves angina sx HMG-CoA reductase inhibitors (statins); lower

progression of leaflet calcification & AVA reduction. The need for endocarditis prophylaxis is restriced to

AS patients with a prior h/o endocarditis

Harrison, 19th Edition, pp. 1532. 2015

Medical therapy: used in sx Pts who are not operative candidates

○ diuresis, ○ control HTN, maintain SR; ○ digoxin if low EF or AF○ avoid venodilators (nitrates) & negative

inotropes (CCB & B-blockers) in severe AS○ avoid vigorous physical exertion once AS

moderate-severe○ ? nitroprusside if p/w CHF w/ sev.AS, EF

35%, CI 2.2, & normal BP

(NEJM 2003;348:1756)

Balloon Ao valvotomy: 50% ↑ AVA & ↓ peak , ∇ but 50% restenosis by 6–12 mo & ↑ risk of

peri-PAV stroke/AI (NEJM 1988;319:125)

∴ bridge to AVR or palliation

Transcatheter AoV implantation (TAVI); bioprosthetic valve mounted on balloon expandable stent (JACC 2009;53:1829); AVA ↑ ̴ 1 cm2 (JACC 2010;55:1080)

Indications for Aortic Valve Replacement AVR is indicated in those with;

Severe AS (AVA < 1 cm2) Or 0.6 cm2/m2 body surface

area with sx LV systolic dysfunction (EF<

50%) with sx BAV disease and an aneurysmal

root or ascending aorta (maximal dimension > 5.5 cm) Aneurysmal disease wt aortic

diameters 4.5 – 5.0 cm in positive FHx of an aortic catastrophe

Rapid aneurysm growth > 0.5 cm/year

Asx moderate or severe AS who are referred for coronary artery bypass grafting surgery.

NOTE: Perioperative risk; 15 – 20%

Relative Indications;

Abnormal response to treadmill

exercise

Rapid progression of AS (in

conditions wt compromised access

to health care)

Very severe AS

Aortic jet velocity > 5 m/s

Mean gradient > 60 mmHg

Low operative risk

Excessive LVH in the absence of

systemic HTN

NOTE: Perioperative risk; 15 – 20%

Aortic Insufficiency (AI) Introduction Confer to Table 283-1

AR may be caused by primary valve disease or by primary aortic root disease.

Introduction:

Isolated AR is rare without association with mitral valve disease.

Patients wt congenital BAV disease may develop predominant AR & about 20% will require aortic valve surgery btn 10 & 40 yrs of age

Etiology Valve disease (43%)

RHD (usually mixed AS/AI and concomitant MV disease) Bicuspid AoV: natural hx: 1/3 → normal, 1/3 → AS, 1/6

→AI, 1/6 → endocarditis →AI Infective endocarditis

○ valvulitis: RA, SLE; anorectics (fen/phen) & other serotoninergics (NEJM 2007;356:29,39)

Root disease (57%) HTN aortic aneurysm or dissection, annuloaortic ectasia,

Marfan syndrome aortic inflammation: giant cell, Takayasu’s, ankylosing

spond., reactive arthritis, syphilis (Circ 2006;114:422)

Pathophysiology Total SV ejected by the LV (effective forward

SV + Volume of Regurgitant flow) ↑ in AR. In severe AR, the volume of regurgitant flow

may equal the effective forward SV. In AR, the entire LV-SV is ejected into a

high-pressure LA, the aorta An ↑ in the LV end-diastolic volume (↑pre-

load) → major hemodynamic compensation of AR→ LVH → ↑ LV systolic tension

All changes reflect the Laplace’s law.

In chronic AR, LV preload & afterload both↑ ↑ failure of adaptive mechanism → ↓LV function → ↑↑ End-diastolic volume & pressure (> 40 mmHg) → ↓forward SV & EF => sx development

The reverse pressure gradient from Aorta to LV, ↓progressively during diastole → decrescendo nature of the diastole murmur.

Early sign of LV dysfunction is ↓EF In advanced stages; LA, PA wedge, PA, & RV pressures all

elevate with lowering of forward CO at rest.

Myocardial ischemia is resulted by; Increased myocardial oxygen requirements by LV dilatation, LVH,

↑ LV systolic tension, & compromised coronary blood flow Subendocardium is more susceptible even in absence of

epicardial CAD. In acute AR; the valve is unprepared;

Clinical manifestations Acute: sudden ↓ forward SV and ↑LVEDP

(noncompliant ventricle) → pulmonary edema +/- hypotension & cardiogenic shock

Chronic: clinically silent while LV dilates (to ↑ compliance to keep LVEDP low) more than it hypertrophies → chronic volume overload → LV decompensation → CHF

Natural hx: variable progression (unlike AS, can be fast or slow); once decompensation begins, prognosis poor w/o AVR (mortality ̴10%/y)

Physical examination Early diastolic decrescendo murmur at LUSB

(RUSB if dilated Ao root); ↑/ sitting forward, expir, handgrip; severity of AI α duration of murmur (except in acute and severe late); Austin Flint murmur: mid-to-late diastolic rumble at apex (AI jet interfering w/ mitral inflow): SOFT MURMUR

Wide pulse pressure due to ↑ stroke volume, hyperdynamic pulse → many of classic signs; pulsepressure narrows in late AI with T LV fxn; bisferiens(twice-beating) arterial pulse

diffuse and laterally displaced point of maximal impulse; soft S1 (early closure of MV); +/- S3 (≠ ↓ EF but rather just volume overload in AI): AT THE 4th interspace

Austin Flint - Murmur

LV

AV

MV

AR

DiastolicFilling

1 2

Anterior leaflet of mitral valve vibrates between AR and filling jets

1

Classic Eponymous Signs in Chronic AI (South Med J. 1981; 74: 459)Sign Description Corrigan’s pulse “water hammer” pulse (ie, rapid rise/fall or

distention/collapse)

Hill’s sign (popliteal SBP – brachial SBP) > 60 mmHg

Duroziez’s sign to-and-fro murmur heard over femoral artery w/ light compression

Pistol shots sounds

Pistol shot sound heard over femoral artery

Trabe’s sound Double sound heard over femoral artery when compressed distally

de Musset’s sign Head-bobbing with each heartbeat (low Se)

Muller’s sign Systolic pulsations of the uvula

Quincke’s pulses Subungual capillary pulsations (low Sp)

Arterial pulse

CXR: In chronic severe AR;

Downward displaced apex to the leftcardiomegaly ascending Ao dilatation in presence of aortic

root aneurysmLateral view; aorta filling the entire

retrosternal space

Diagnostic studies• ECG:

LVH, ST-segment depression, TWI in leads I, aVL, V5, & V6 (‘LV-strain) in pts with chronic severe AR;

LAD +/- QRS prolongation denote diffuse myocardial disease/patchy fibrosis, signify poor prognosis

Echo: (TTE/TEE) severity of AI

o severe = width of regurgitant jet > 65% LV outflow tract, o vena contracta > 0.6 cm, o regurg fraction ≥50%, o regurg orifice ≥ 0.3 cm2, o flow reversal in descending Ao

LV size & functiono LV size ↑in chronic AR, systolic function is normal until

myocardial contractility declineso TEE – provides detailed anatomic assessment of the

valve, root, & portions of aorta.

Cardiac MRI Is indicated in patients whom;

TTE is limited by poor acoustical windows or inadequate semiquantitative assessment of LV

function or severity of the regurgitation. It allows accurate assessment of aortic size &

contour

NOTE: Echo, cardiac MRI, chest CT-angiography are more sensitive than CXR for detecting root & ascending aortic enlargement

Cardiac catheterization & angiography

Treatment

Acute decompensation (consider ischemia and endocarditis as possible precipitants)surgery usually urgently needed for acute severe

AI which is poorly tolerated by LVIV afterload reduction (nitroprusside) and inotropic

support (dobutamine) +/- chronotropic support (↑ HR →↓ diastole →↓ time for regurgitation)

pure vasoconstrictors and IABP contraindicated In chronic AI, management decisions based

on LV size and fxn (and before sx occur) Circ 2008;118:e523

Medical therapy:

vasodilators (nifedipine, ACEI, hydralazine) if severe AI w/ sx or LV dysfxn & Pt not operative can didate or to improve hemodynamics before AVR;

no clear benefit on clinical outcomes or LV fxn when used to try to prolong compensation in asx severe AI w/ mild LV dilation & normal LV fxn

NEJM 2005;353:1342

Indication for Valve Replacement in Aortic Regurgitation ACC/AHA Class I

Symptomatic patients with preserved LVF (LVEF >50%)

Asymptomatic patients with mild to moderate LV dysfunction (EF 25-49%)

Patients undergoing CABG, aortic or other valvular surgery

ACC/AHA Class II aAsymptomatic patients with preserved LVEF but

severe LV dilatation (EDD>75 mm or ESD > 55mm)

Indication for Valve Replacement in Aortic Regurgitation ACC/AHA Class II b

Patients with severe LV dysfunction (EF < 25%)Asymptomatic patients with normal systolic

function at rest (EF >0.50) and progressive LV dilatation when the degree of dilatation is moderately severe (EDD 70 to 75 mm, ESD 50 to 55 mm).

ACC/AHA Class III Asymptomatic patients with normal

systolic function at rest (EF >0.50) and LV dilatation when the degree of dilatation is not severe (EDD <70 mm, ESD <50 mm).

Mitral Regurgitation (MR)

MITRAL VALVE STRUCTURE

ETIOLOGIES OF MR

Harrison pp., 3984

Etiology Leaflet abnormalities:

myxomatous degeneration (MVP),

endocarditis, calcific RHD, valvulitis (collagen-vascular

disease), congenital, anorectic drugs

Functional: infero-apical papillary muscle

displacement due to ischemic LV remodeling or other causes of DCMP;

LV annular dilation due to LV dilation

Ruptured chordae tendinae:myxomatousendocarditisspontaneoustrauma

Acute papillary muscle dysfxn b/c of ischemia or rupture during MI [usu. Posteromedial papillary m. vs. anterolateral]

HCMP

Lancet 2009;373:1382

Clinical manifestations Acute: pulmonary edema,

hypotension, cardiogenic shock

Chronic: typically asx for yrs, then as LV fails → progressive dyspnoea on exertion, fatigue, AF, PHT

Prognosis: 5-y survival w/ medical therapy is 80% if asx, but only 45% if sx

NEJM 2004;351:1627

Physical examination High-pitched, blowing, holosystolic murmur

at apex; radiates to axilla; +/- thrill; ↑ w/ handgrip (Se 68%, Sp

92%), ↓w/ Valsalva (Se 93%) (NEJM 1988;318:1572) ant. leaflet abnormal → post. jet heard at spine post. leaflet abnormal → ant. jet heard at sternum

Lateral displaced hyperdynamic point of maximal impulse, obscured S1, widely split S2 (A2 early b/c T LV afterload, P2 late if PHT); S3

Carotid upstroke brisk (vs. diminished and delayed in AS)

Diagnostic studies ECG: LAE, LVH, +/- AF CXR: dilated LA, dilated LV, +/- pulmonary

congestion Echo:

MV anatomy MR severity: jet area, jet width at origin, or effective

regurgitant orifice (predicts survival, NEJM 2005;352:875);

LV fxn (EF should be supranormal if compensated, ∴EF 60% w/ sev. MR LV dysfxn);TEE if TTE inconclusive or pre/intraop to guide repair vs. replace

Cardiac cath: prominent PCWP cv waves, LVgram for MR severity & EF

Classification of Mitral Regurgitation

Severity Regurgitation fraction

Jet area (% of LA)

Jet width (cm)

ERO (cm2)

Angio (see footnote)

Mild <30% <20 <0.3 <0.2 1+

Moderate 30-49% 20-40 0.3-0.69 0.2-0.39 2+

Severe ≥50% >40 ≥0.70 ≥0.40 3/4+

1+ = LA clears w/ each beat; 2+ = LA does not clear, faintly opac. After several beats; 3+ = LA & LV opac. equal

RADIOLOGICAL FEATURES OF MITRAL REGURGITATION

WHEN TO INTERVENE IN MITRAL REGURGITATION

Treatment Acute decompensation -consider ischemia and

endocarditis as precipitants IV afterload reduction (nitroprusside), +/- inotropes

(dobuta), IABP, avoid vasoconstrictors

Medical: benefit (incl ACEI) in asx pts; indicated if ∅sx but not an operative candidate ↓preload (↓CHF and MR by ↓ MV orifice): diuretics, nitrates (espec if ischemic/fxnal MR) if LV dysfxn: ACEI, βB (carvedilol), +/-biV pacing; maintain

SR

Circ 2008;118:e523; NEJM 2009;361:2261

• Surgery ○ Surgery usually needed for acute severe MR as

prognosis is poor w/o MVR

repair [preferred if feasible] vs. replacement w/ preservation of mitral apparatus)

sx severe MR, asx severe MR and EF 30–60% or LV sys. diam. 40 mm consider MV repair for asx severe MR w/ preserved

EF, esp. if new AF or PHT

Mitral Stenosis (MS)

Mitral Stenosis – Aetiology Rheumatic Fever

Commissural fusion and thickening 30%Cuspal thickening 15%Chordal 10%Remainder combinedPure MS 25%Combined MS/MR 40%

Etiology Rheumatic heart

disease: fusion of commissures →“fish mouth” valve-from autoimmune rxn to strep infxn;

Mitral annular calcification : encroachment upon leaflets → functional MS

Congenital, infectious endocarditis w/ large lesion, myxoma, thrombus

Valvulitis (SLE, amyloid, carcinoid) or infiltration (mucopolysaccharidoses)

Mitral Stenosis - Presentation Dyspnoea

HaemoptysisSudden Haemorrhage (bronchial venous bleed)Blood stained sputum associated with PNDPink frothy sputum with acute pulmonary oedemaPulmonary infarction ( late)Blood stained sputum associated with COPD

Chest pain Thrombo embolism (20% of patients during life)

Directly related to age, cardiac output and size of left atrium

Ortners syndrome – LA compression of RLN

Lancet 2009;374:1271

Physical exam Low-pitched mid-diastolic rumble at apex

w/ presystolic accentuation Best heard in left lateral decubitus position during

expiration ↑ w/ exercise

Opening snap high-pitched early diastolic sound at apex from fused leaflet tips; MVA proportional to S2– OS interval tighter valve →↑ LA pressure → shorter interval

Loud S1 (unless MV calcified)

Diagnostic studies ECG: left atrial enlargement (“P mitrale”), AF, RVH CXR:

dilated LA (straightening of left heart border, double density on right, left mainstem bronchus elevation)

Echo: estimate pressure gradient, RV-systolic pressure, valve area, valve echo score (0–16, based on leaflet mobility &

thickening, subvalvular thickening exercise TTE if discrepancy between sx and severity of MS

at rest; TEE to assess for LA thrombus before percutaneous mitral

valvuplasty Cardiac cath: from simultaneous PCWP & LV pressures, calculated ∇

MVA; LA pressure tall a wave and blunted y descent; ↑ PA pressures

VCXR in Mitral

Stenosis• Double Right Heart border.• Splayed carina• Straight left heart border• Kerley B lines• Kerley A lines

MITRAL STENOSIS – MORPHOLOGY (ECHO)

Classification of Mitral Stenosis

Stage Mean gradient (mmHg)

MV area (cm2)

PA Systolic (mmHg)

Normal 0 4-6 <25

Mild <5 1.5-2 <30

Moderate 5-10 1-1.5 30-50

Severe >10 <1 >50

Treatment Medical:

Na restriction, cautious diuresis, β-blockers, sx-limited physical stress

Anticoagulation if AF, prior embolism, LA thrombus, or large LA

Circ 2008;118:e523

Surgical MV repair if possible, o/w replacement consider in sx Pts wt ≤ MVA 1.5 if percutaneous mitral vulvotomy unavailable or

contraindicated (mod. MR, LA clot), or valve morphology unsuitable

Pregnancy: if NYHA class III/IV → PMV, o/w medical Rx w/ low-

dose diuretic & βB

Indications for mechanical intervention:

heart failure sx wt MVA ≤ 1.5 orheart failure sx wt MVA > 1.5 but ↑

PASP, PCWP, or MV w/ exercise, or ∇asx Pts wt MVA ≤ 1.5 and PHT (PASP

> 50 or 60 mmHg wt exercise) or new-onset AF

Harrison, pp. 2115

Tricuspid Regurgitation

Etiology: Congenital

Ebsteins anomaly Rheumatic Right ventricular dilatation

Secondary to cardiomyopathySecondary to pulmonary hypertension

Intrinsic valve diseaseEndocarditisCarcinoid syndrome

Clinical Features Systolic waves on JVP (time with carotid

pulse) therefore not v waves. RV+ S3 + pasnsystolic murmur in 4th intercostal

space Pulsatile liver Ascites Peripheral oedema

Tricuspid RegurgitationManagement Medical Valve ring

Mitral Valve Prolapse (MVP)

PATHOLOGY OF MITRAL VALVE PROLAPSE

Definition and Etiology Bulging of MV leaflet ≥2 mm above mitral

annulus in parasternal long axis echo view

Leaflet redundancy from myxomatous proliferation of spongiosa of MV apparatus

Prevalence 1–2.5% of gen. population, females > males; and prevalence of 5% (OHCM, 2015)

most common cause of MR

NEJM 1999;341:1

Occurrence

Occurs alone or with; ASD, PDA, Cardiomyopathy, Turner’s syndrome, Marfan’s syndrome, WPW, osteogenesis imperfecta.

Clinical manifestations

usually asymptomatic Or

atypical chest painsPalpitationsSymptoms of autonomic dysfunction;

○ Anxiety, panic attack, syncope

Physical exam

High-pitched, midsystolic click +/- mid-to-late systolic murmur

↓LV volume (standing) → click earlier; ↑ LV volume or afterload → click later, softer

Complications: Mitral regurgitation Cerebral emboli, Arrythmias Sudden death

Diagnostic studies Echo is diagnostic ECG; may show inferior T-wave

inversion

http://content.nejm.org/content/vol345/issue10/images/large/07f2.jpeg

Treatment

Β-blockers for palpitations & chest pains Endocarditis prophylaxis no longer

recommended (Circ 2007:116:1736) Aspirin or anticoagulation if prior neurologic

event or A-fib Surgery in case of severe MR.

Prosthetic Heart Valves Mechanical (60%)

○ Bileaflet (eg, St. Jude Medical); tilting disk; caged-ball

○ Characteristics: very durable (20–30 y), but thrombogenic and require anticoagulation ∴consider if age 65 y or if anticoagulation already indicated (JACC 2010;55:2413)

Bioprosthetic (40%)Bovine pericardial or porcine heterograft (eg,

Carpentier-Edwards), homograftCharacteristics: less durable, but minimally

thrombogenic

consider if age 65 y, lifespan 20 y, or contraindication to anticoagulation

Physical examination

• Normal: crisp sounds, soft murmur during forward flow (normal to have small )∇

• Abnormal: regurgitant murmurs, absent mechanical valve closure sounds

Anticoagulation

Warfarinlow-risk mech AVR: INR 2–3 (consider 2.5–3.5 for 1st

3 mo)mech MVR or high-risk mech AVR: INR 2.5–3.5high-risk bioprosthetic: INR 2–3 (and consider for 1st

3 mo in low-risk)○ high-risk features: prior thromboembolism, AF, ↓EF,

hypercoagulable

ASA (75–100 mg indicated for all Pts with prosthetic valves; avoid adding to warfarin if h/o GIB, uncontrolled HTN,

erratic INR, or 80 y

Circ 2008;118:e523

Correction of overanticoagulation Risk from major bleeding must be weighed

against risk of valve thrombosis Not bleeding & INR 5: withhold warfarin, do

not give vit K, serial INRs✓

Not bleeding & INR 5–10: withhold warfarin, vit K 1–2.5 mg PO, serial INRs✓

Bleeding or INR 10: FFP low-dose (1 mg) vit K IV

Circ 2008;118:e626

Endocarditis prophylaxisIndicated for all prosthetic valves to ↓ risk of

infective endocarditis during transient bacteremia

ComplicationsStructural failureParavalvular leakInfective endocarditisEmbolizationBleeding (from anticoagulants)Hemolysis

What to remember AR & MR cause ventricular dilatation

The duration of diastolic murmurs indicates the severity of AR and MS.

Intervention for AS is based on the combination of severity with symptoms

Intervention in AR & MR is based on symptoms &/or evidence of left ventricular dysfunction

The primary investigation for all valvular heart disease is echocardiography

Systolic Murmurs

MURMURS AND THECARDIAC CYCLE

Aortic stenosis

Mitral Regurgitation

1 2

1 2

Mitral valve prolapse withlate regurgitation

1 2

Aortic stenosis vs Mitral regurgitation

Pulse BP HS Murmur Rad RV Apex

AS Slowrising

Lowpulse

pressureA2 ▼3+, 4+

Ejection Carotid N Hypertrophy

MR Good Volume

Normal P2▲, 3+ Pansystolic Axilla + Dilated

Diastolic murmurs

Aortic regurgitation

1 2

Mitral Stenosis

1 2

OS

Mitral Stenosis vs Aortic Regurgitation

Pulse BP HS Murmur Rad RV Apex

AR Collapsing↑pulse

Pressure

↓diastolic pressure

A2 ▼3+

Early diastolic

LSE N Dilated

MS

Small Volume

(AF)Normal

1st ▲P2 ▲ Mid/late

DiastolicAxilla ++ Tapping

1st sound

Asante