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ACQUIRED VALVULAR HEART DISEASE. Iwona Świątkiewicz Katedra i Klinika Kardiologii i Chorób Wewnętrznych Collegium Medicum w Bydgoszczy. AVHD – acquired valvular heart disease LV – left ventricle LA – left atrium RV – right ventricle RA – right atrium HF – heart failure
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ACQUIRED VALVULAR HEART DISEASE Iwona Świątkiewicz Katedra i Klinika Kardiologii i Chorób Wewnętrznych Collegium Medicum w Bydgoszczy
AVHD – acquired valvular heart disease • LV – left ventricle • LA – left atrium • RV – right ventricle • RA – right atrium • HF – heart failure • AF – atrial fibrillation • AV – aortic valve • MV – mitral valve • EF – ejection fraction • MR - mitral regurgitation • TR – tricuspid regurgitation • LVEDP – LV end-diastolic pressure • LVED(S)V(D) – LV end-diastolic (systolic)volume (diameter) • SV – stroke volume • CO – cardiac output
Left ventricular end-diastolic volume (LVEDV): 110-120 ml • Left ventricular end-systolic volume (LVESV): 40-50 ml • Left ventricular stroke volume (LVSV): 70-80 ml • Left ventricular ejection fraction (LVEF): 58-73% • Cardiac output (CO): at rest about 5 l (on exertion 20-25 l)
Left ventricular end-diastolic pressure (LVEDP): 6-12 mm Hg • Left ventricular end-systolic pressure (LVESP): 90-140 mm Hg • Left atrial pressure (mean): 6-11 mm Hg • Right atrial pressure (mean): 1-5 mm Hg • Right ventricular end-diastolic/end-systolic pressure : 2-7/20-30 mm Hg • Pressure in pulmonary artery (diastolic/peak systolic/mean): 4-13/16-30/9-18 mm Hg • Pulmonary wedge pressure: 5-12 mmHg • Aortic pressure (diastolic/peak systolic/mean): 70-90/90-140/70-110 mmHg • Pulmonary load: 0,8-1,1 (0,3-1,6) acc. Wood’s
Acquired valvular heart disease - definition The dysfunction of heart due to the presence of acquired abnormal structure and/or function of the valve
Acquired valvular heart disease – primary (structural) - due to the changes in the structure of valve
Acquired valvular heart disease – secondary (functional) - due to the changes in the function of valve caused by abnormalities in the structure of other elements of the heart
Causes of death in acquired valvular heart disease • Congestive heart failure • Sudden cardiac death • Arrythmia • Stroke • Infective endocarditis • Death in the periintervention period (because of the complications of interventional/surgical treatment)
Left ventricle in acquired valvular heart diseases • Volume and/or pressure overload • Remodelling • Dysfunction – decides about prognosis
Remodelling of left ventricle • Left ventricular hypertrophy (LVH) • Left ventricular enlargement • Spheric shape of left ventricle • Increased wall stress of left ventricle
Left ventricular hypertrophy • Left ventricular eccentric hypertrophy (volume overload) • Left ventricular concentric hypertrophy (pressure overload)
T = p X R² / ThT – LV wall stressp – LV pressureR – LV radiusTh – LV wall thickness
Aortic stenosis • the third most frequent cardiovascular disease • Aortic valve replacement • – the second most frequent cardiosurgical procedure
Aortic valve - physiology Aortic valve area (AVA): 2–4 cm2 Peak velocity of aortic flow: 1,0–1,7 m/s Left ventricular pressure: end-systolic (140-90 mm Hg) end-diastolic (do 12 mm Hg) Peak pressure gradient across aortic valve < 20 mmHg
Bicuspid aortic valve Most frequent congenital defect in adults More frequent in male (4x) Positive family history With other cardiovascular defects (CoA, PDA) 30% patients – cardiovascular complications (valvular and/or vascular)
Bicuspid aortic valve Valvular complications Aortic stenosis Aortic regurgitation Infective endocarditis – prevention !!! Vascular complications Dilatation/aneurysma Dissecting aneurysm
Aortic stenosis - patophysiology Aortic valve area < 1 cm2 Left ventricular outflow obstruction during systole • LV systolic pressure LV pressure overload ↓ LV concentric hypertrophy → normalisation of LV wall stress
Aortic stenosis - patophysiology Compensation preventing cardiac output decrease: • LV systolic pressure , • antegrade velocity across the narrowed valve, • systolic pressure gradient across aortic valve (between LV and aorta), • LV concentric hypertrophy , • LV contractility, • LV ejection time. Unchanged cardiac output at rest Decreased cardiac output on exertion symptoms (angina, syncope) LV end-diastolic pressure caused by LVH symptoms on exertion (dyspnea, fatigue)
Aortic stenosis - patophysiology • LV contractility (caused by increased wall stress) ↓ LV cardiac output symptoms (syncope, angina) • LV end- systolic volume • LV end-diastolic pressure symptoms (dyspnea, fatigue) LV heart failure symptoms (dyspnea in rest)
Aortic stenosis - history • Asymptomatic for many years • First symptoms in calcified bicuspid valve at age of 50-60 years, and in degenerative tricuspid valve at age of 70-80 years • First symptoms associated with exertion, • Angina (5 years to death), • Syncope (3 years), • Dyspnea (2 years).
Aortic stenosis Symptoms: - angina - exertional lightheadedness - syncope - heart failure - sudden cardiac death
Aortic stenosis - angina • Reasons: • - Coronary artery disease • Inadequate oxygen supply/demand • LV hypertrophy • coronary microciculation not increased • increase of vascular thickness and load • perivascular fibrosis • LV EDP increase • subendocardial ischaemia
Aortic stenosis - syncope • Reasons: • Inadequate brain perfusion: • - acute drop in blood pressure due to an inappropriate LV baroreceptor response • - ventricular arrhythmias
Aortic stenosis – reasons of death Heart failure 50-60% Infective endocarditis 15-20% SUDDEN DEATH 5-34% 65-80% pt - symptomatic 3-5% pt - asymptomatic
Aortic stenosis – physical examination (key features) • Apex beat displaced laterally and down • Loud single second heart sound (severe AS) or reverse splitting of second heart sound (moderate AS) • S4 gallop • Systolic murmur: timing - crescendo-decrescendo during systole; location - the loudest at the base (over the right second intercostal space); systolic thrill (in severe AS); radiation - to the carotides; typically AS first diagnosed based on the finding on a murmur on auscultation • Palpation of the carotid pulse contour and amplitude: pulsus tardus (peak aortic pressure later in systole) and parvus (decreased pulse amplitude) • Typical signs of heart failure (if hemodynamic decompensation occured)
Aortic stenosis –diagnostic approaches • - ECG (LVH) • Chest radiograph (poststenotic dilatation • of ascending aorta, calcifications of • aortic valve) • - Echocardiography
Aortic stenosis – echocardiography - morphology and mobility of AV leaflets - calcifications of AV - maximum velocity of aortic jet (vmax) - peak pressure gradient - meanpressure gradient - AV area (AVA) - contractility and LV ejection fraction - LV hypertrophy - assessment of other valves!!!
Severe aortic stenosis – echocardiographic criteria v maxMeanPG AVA >4,0 m/s >40 mmHg <1,0 cm2AVAI <0,6cm2/m2 ESC, 2012
Predictors of survival in adult patients with symptomatic aortic stenosis are stenosis severity expressed as jet velocity or transaortic gradient, functional status and LV systolic function.
Aortic stenosis -prognosis 50% increase of cardiovascular risk 5-year survival in symptomatic patients15-50%
Mitral valve - physiology Mitral valve area 4 – 6 cm2 Diastolic pressure gradient between LA and LV 1 – 3 mmHg Maximal velocity of mitral flow 0,6 – 1,3 m/s
Mitral stenosis - ethiology • - rheumatic • (fibrosis and thickening of leaflets; fusion of leaflet edges along commissures; fusion, thickening and shortening of chordae; superimposed calcific changes) • - myxoma in LA • massive calcifications in mitral annulus poreumatyczna
Mitral stenosis - pathophysiology Presence of mechanical obstruction at MV level (significant if MVA < 2,0 cm²) diastolic transmitral pressure gradient between LA and LV LA pressure • normal LV filling but LA pressure
Mitral stenosis - pathophysiology MVA 1–1,5 cm² transmitral gradient and LA pressure LA enlargement • Pulmonary venous pressure dyspnea • Pulmonary arterial pressure RV pressure overload RV hypertrophy RV dilation + tricuspid functional regurgitation Right heart failure
Mitral stenosis – clinical history • Acute rheumatic fever episode in past medical history (rare finding) • Slow but progressive decline in exercise capacity, fatigue • Symptoms of pulmonary congestion: dyspnea on exertion, shortness of breath, paroxysmal nocturnal dyspnea, pulmonary oedema • Symptoms of right heart failure: peripheral oedema, abdominal distention, decreased appetite • Hoarseness (Ortners’ s. – due to compression of the left recurrent laryngeal nerve by the enlarged LA) • Recurrent pulmonary infections, hemoptysis