Presentation on theme: "Valvular Heart Disease J.B. Handler, M.D. Physician Assistant Program University of New England."— Presentation transcript:
Valvular Heart Disease J.B. Handler, M.D. Physician Assistant Program University of New England
Abbreviations n VHD- valvular heart disease n RF- rheumatic fever n MR- mitral regurgitation n AR- aortic regurgitation n HF- congestive heart failure n MS- mitral stenosis n LAP- left atrial pressure n PuVR- pulmonary vascular resistance n RV- right ventricle n CO- cardiac output n TR- tricuspid regurgitation n PI- pulmonic insufficiency n NSST-T- non specific ST-T n PAH- pulmonary artery hypertension n SV- stroke volume n RVH- right ventricular hypertrophy n AoV- aortic valve n MVA- mitral valve area n PSVT- paroxysmal supraventricular tachycardia n MVR- mitral valve replacement n MVP- mitral valve prolapse n AS- aortic stenosis n SEM- systolic ejection murmur n LVEDP- left ventricular end diastolic pressure n PND- paroxysmal nocturnal dyspnea n LSB- left sternal border n ACE- angiotensin converting enzyme n BE- bacterial endocarditis n RF- rheumatic fever
Etiologies of VHD n Rheumatic valve disease n Congenital, including bicuspid aortic valve. n Coronary heart disease: MI, papillary muscles n Dilation of the aorta: Aortic root disease n Chronic “wear and tear”: aortic sclerosis/stenosis n Dilation of the LV- from any cause: MR n Endocarditis n MV prolapse n Others
Acute Rheumatic Fever: IO n 2/3 all cases - developing countries n Episodes of RF are quite uncommon in U.S., except in immigrants. n Epidemiology - Identical to that of Group A Streptococcus; children 5-15 n Pathogenesis- oropharyngeal infection; RF follows the sore throat; usually within 2-3 wks. n Mechanism - systemic immune process involving Group A strep. antigens; abnormal immune response. Preventable with adequate Rx of streptococcal pharyngitis. IO – Interest Only
Diagnosis - Jones Criterion n Carditis - Pancarditis involving valves, endocardium, myocardium and pericardium –Healing of Rheumatic valvulitis - fibrous thickening resulting in valvular stenosis or insufficiency n Migratory polyarthritis n Sydenham’s Chorea n Subcutaneous nodules n Erythema marginatum
Treatment n Antistreptoccal Rx until regimen finished; Penicillin IM or oral (10 day course) Erythromycin and others are alternatives n Arthritis/fever - Salicylates n Severe carditis- Glucocorticoids n HF, MR, AI - specific Rx. n Secondary prophylaxis to prevent recurrences- PCN or alternative until adult.
Cardiac Pressures Images.google.com
Mitral Regurgitation-Etiology n Chronic Rheumatic heart disease- ing frequency n LV dilatation from any cause n Coronary Heart Disease: Papillary muscle dysfunction with ischemia/infarction n Mitral Valve Prolapse n Infective endocarditis
Mitral Regurgitation Images.google.com
Pathophysiology of MR n Blood regurgitates from LV into LA. n LV volume increases progressively as severity of MR increases. –Increased blood return to LA: pulmonary veins + regurgitant volume from previous beat. n LV function- well preserved initially; often deteriorates in later stages as does cardiac output (CO). LV compensates for volume overload via the Starling mechanism. n Left atrium (and LV) dilates over time - LAP and LVEDP gradually rise pulmonary congestion –Afib. common.
Symptoms n Often asymptomatic for years n Fatigue, DOE, orthopnea- symptoms of left sided heart failure (detailed discussion later in CV system). n With chronic severe MR –Elevation of pulmonary venous pressure leads to PuVR PAH and subsequent Rt Heart failure: hepatic congestion, peripheral edema, etc.
Physical Exam n Palpation: Systolic thrill may be present at apex depending on turbulence. n Auscultation: S 1 soft or absent; S 3 gallop if significant MR; Systolic Murmur is hallmark - Gr. II-IV/VI holosystolic in most cases -radiates to axilla (exception is MVP); murmur is high pitched and blowing.
Additional Findings n ECG: LAE; Atrial arrhythmias (Afib). n Echo/Doppler: LA & LV size; LV function. Can estimate severity of MR; LV often dilates with progressive MR. n CxR: Late findings - Progressive LVE; HF; pulmonary edema. LVE- left ventricular enlargement CxR- chest x-ray
Treatment of MR n Medical - Treatment depends on severity. Once symptomatic: Decreased physical activity and Na restriction. Drug therapy often significantly improves symptoms and patients may do well for many years. –ACE inhibitors or other vasodilators: decrease afterload and preload. –Diuretics: decrease preload, Na and volume overload –Inotropic agents: digoxin- limited role
Treatment of MR n Surgical- Indications: –Severe MR with Sx –Dilating LV with progressive dysfunction EF (even with mild symptoms). –Timing of surgery is important; needs to be done before significant deterioration of LV function/EF. n Surgical result dependent on pre-existing LV function. Mitral valve repair is preferred to MV replacement.
Mitral Valve Prolapse n Very common (3-5% adults) - Excessive redundant MV tissue from abnormal connective tissue: – MVP - most common form involves MV without major connective tissue disease elsewhere in body. Familial form also exists- autosomal dominant. –MVP as part of major CT disease (Marfan’s, Ehler’s- Danlos) or variations; these disorders are uncommon. n Pathology- myxomatous degeneration of MV leaflet tissue. n Associated deformities: high arched palate; pectus excavatum.
Mitral Valve Prolapse Images.google.com
MVP: Pathology n Mitral regurgitation can develop due to redundant floppy valve leaflets and/or involvement of the MV supporting structures – chordae tendineae. n Stress on Papillary muscles or chordae is presumed reason for localized and atypical chest pain. n Abnormal valve structure and MR can predispose to infective endocarditis but incidence is very low antibiotic prophylaxis no longer indicated.
Clinical Features n Female > male; Sx, when present, commonly occur at ages n Most are asymptomatic; often detected on PE- characteristic murmur. n Most common symptoms when present: chest pain (*atypical) and palpitations. n Arrhythmias common: PAC’s, PVC’s, PSVT, non-sustained VTach. n Sudden death – exceedingly rare arrhythmias *Atypical – CP unlike the pain/discomfort that is present with coronary heart disease
Physical Findings n Auscultation: Mid to late systolic click (tensing of chordal structures). n High pitched late systolic murmur best heard at apex.- click and murmur occur earlier and get louder with maneuvers that decrease LV volume: standing after squatting, valsalva. Maneuvers that increase LV volume delay the click and soften the murmur: isometric hand grip, squatting.
Additional Findings/Treatment n ECG: NST-TW changes. Usually in leads II, III, aVF. n Echo/Doppler: Diagnostic; shows MVP and identifies MR when present. n Treatment: Reassurance; ß-Blockers for chest pain or arrhythmias; additional anti-arrhythmics usually not necessary. n Infrequently, severe MR develops requiring MV repair (more common in men than women).
Mitral Stenosis n 2/3 females, 1/3 males- only cause is RF. n About 40% of all cases of RF develop MS. n Valve leaflets thicken and calcify, commisures fuse; valve orifice narrows; subvalvular supporting apparatus involved. n Least common rheumatic valvular lesion.
Mitral Stenosis Images.google.com
Pathophysiology n Normal MVA cm 2. Valve leaflets fuse, decreasing valve area. Severe MS < 1 cm 2. n LA pressure rises in order to propel blood across the stenotic valve- pressure gradient compared to LVEDP. n LAP reflected backwards into the pulmonary circulation results in pulmonary venous congestion pulm capillary congestion interstitial fluid dyspnea. Pulmonary arterioles subsequently constrict.
n LV function usually normal. LVEDP normal. n Chronic severe MS - Elevation of pulmonary vascular resistance (PVR) and subsequent development of Pulmonary Artery Hypertension (PAH). n Chronic PAH RVH RV dysfunction and failure. n CO at rest- usually normal but does not rise adequately with exercise. With severe MS and PAH, CO eventually falls.
Symptoms/Complications n DOE, orthopnea, PND pulmonary edema n Findings of Rt Ht failure - late n Atrial arrhythmias: PAC’s, Atrial Fibrillation and Flutter n Hemoptysis ruptured pulmonary capillaries n Atrial Thrombi and embolization - (AFib)
Physical Exam n Palpation: prominent RV impulse n Auscultation: S 1 loud/accentuated; S 2 loud if PAH present Opening Snap of MV-apex, follows S 2. Diastolic Rumble- Follows OS; low pitched/apex; length correlates with severity; MR murmur often audible.
Additional Findings n ECG: LAE/LAA; RAD, RVH (over time) n Echo/Doppler: diagnostic-shows abnormal valve motion, estimates the gradient and MVA, defines LA size and LV function. n CxR: Pulmonary congestion; RVE. n Cardiac Cath: Documents gradient, MVA, presence or absence of MR and more.
MS - Treatment n Sodium restriction, diuretics. n Rate control of Afib or cardioversion. n Surgery -Mitral valvulotomy - marked symptomatic improvement. MVR only when repair cannot be done (mortality 3-5 %). n Percutaneous balloon valvuloplasty- alternative to surgery; if successful, avoids or delays need for surgery.
Aortic Stenosis-Etiologies n Common: 20% all valvular disease; 80% males n Bicuspid valve leaflets thicken, fuse Rheumatic valvulitis leaflets thicken, fuse Idiopathic – Sclerocalcific: chronic wear and tear- develops in the elderly leaflets thicken, fuse n Note: Thickening/calcification (without fusing) of the AoV often occurs with aging (Aortic Sclerosis) without progressing to significant aortic stenosis Gr II/III murmur. Important to differentiate using history (asymptomatic), PE and echocardiogram if needed.
Aortic Stenosis Images.google.com
Pathophysiology n Obstruction to LV outflow- pressure overload. n Systolic gradient between LV and Ao. n Obstruction gradual - initially well tolerated; LV hypertrophy is compensatory. n Cardiac Output often normal at rest - does not adequately rise with activity. n Late in course- LV failure, LVEDP rises, CO falls.
n Myocardial oxygen consumption (MVO 2 ) increases from LVH and high LV pressures. n Coronary blood flow is impaired from high LV pressures. n Myocardial ischemia can occur in the absence of *CHD severe LVH/ high pressures outstrips coronary blood flow –Associated CHD may be present. n Normal AoV area: cm 2 Critical AS: valve area <0.75 cm 2 *CHD- coronary heart disease
AS Hemodynamics Images.google.com
Symptoms of AS n Exertional dyspnea - elevation of LVEDP transmitted backward into pulmonary circuit. n Angina Pectoris-Increased MVO 2 (pressure overload and hypertrophy) and decreased coronary reserve. *CHD may co-exist but does not have to be present for angina to develop. n Syncope - Peripheral vasodilation with inadequate forward CO with activity or from arrhythmia. n HF occurs late - very poor prognosis. CHD – coronary heart disease
Physical Exam n Carotid pulse rises slowly; sustained peak. n Apex displaced laterally; +/- systolic thrill; systolic ejection sound (click ) variable. n Aortic valve closure is delayed - fixed or paradoxical splitting of S 2. n S 4 gallop common. n Murmur - SEM (crescendo-decrescendo)- peaks in mid to late systole depending on severity; harsh, low pitched, best heard at base and radiates to carotids – Grade II-IV/VI.
Additional Findings n ECG: LVH common; LAA. n Echo/Doppler: Diagnostic- identifies LVH, valve calcification and restriction; estimates gradient and aortic valve area. n CxR: LV prominence, displaced apex. n Cardiac Cath: Usually necessary prior to surgery; identifies gradient, valve area, LV function and presence or absence of CAD.
Natural History: Untreated n Angina Pectoris -death within 3 years n Syncope - death within 3 years n Dyspnea - death within 2 years n CHF - death within 1.5 years
Treatment n Medical - Mild to moderate AS without symptoms: Careful F/U; serial echo/doppler studies. Limited role for meds once symptoms begin. n Surgical- severe or symptomatic AS. Valve replacement with tissue or mechanical valve - Op risk 4%; 60-70% 10 yr. survival; marked symptomatic improvement. –Ross procedure an option for young patients with AS. n Ballon valvuloplasty- palliative
Aortic Regurgitation- Etiology n 75% male n Rheumatic Heart Disease n Infective endocarditis on previously deformed valve n Aortic Root disease and dilatation n Bicuspic Aortic Valve (AS more common than AR)
AR: Pathophysiology n Increase in LVEDV (preload): blood returning from LA + regurgitant blood. n LV dilates- allows increased SV (stroke volume) and adequate effective forward SV (Starling’s law). n Over time (years) LV function gradually declines and EF (ejection fraction) deteriorates.
Pathophysiology n LV deterioration often precedes symptoms (reason for serial echo/doppler exams). n As AR progresses, CO fails to rise adequately with exercise, LV dysfunction worsens Increased LVEDP pulmonary congestion HF.
AR: History n Sometimes familial - Connective tissue disease. n History of RF or infective endocarditis. n Patient often asymptomatic for yrs. with significant AI. n Symptoms: Palpitations, exertional dyspnea, orthopnea; PND and HF occur later. n Atypical chest pain common.
AR: Physical Exam n Arterial Pulse - Rapid rising “water-hammer pulse” and collapsing pulse. “Quinke’s pulse” - alternate flushing and palling of the skin at the nail root. n “Pistol shot” sound over femoral artery in systole. n Derosiez’ sign - to and fro murmur over femoral artery. n Arterial pulse pressure widened- elevated systolic pressure (often greater than 200mm) and lowered diastolic pressure.
Physical Exam n Palpation - apex displaced laterally/inferiorly. n Diastolic Thrill may be present along LSB. n Auscultation: S2 soft; S3 common; high pitched blowing diastolic decreshendo murmur (LSB). n Best heard with diaphragm – patient sitting upright/leaning forward. n Systolic ejection (increased flow across AoV) murmur.
Additional Findings n ECG - Increased voltage/LVH develops over time. n Echo/Doppler: early on LV contractility normal or increased - later, LV dysfunction; AI jet detectable and semi quantitated by Doppler. n Cardiac Cath: Identifies severity of AI, degree of LV dysfunction and intra-cardiac pressures. Needed to assess coronary arteries in older adults. Cath may not be needed in younger patients.
Treatment of AR n Medical - very close follow-up; serial Echo/Doppler studies. Same Rx as for CHF: Afterload reduction with vasodilators (ACEI, hydralazine). Preload reduction with diuretics; digoxin may be useful in selected individuals. n Surgical - Timing of surgery is difficult as pts. with AI do not develop symptoms until after the development of LV dysfunction. Surgery indicated for progressive LV dilatation and dysfunction +/- symptoms.
Surgery n Aortic Valve Replacement with bioprosthesis (tissue valve) or mechanical valve. Ross procedure an option if young. n Op mortality dependent on pre-op LV function (5% or greater mortality).