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Valvular disease

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Aortic regurgitation Aortic stenosis
Mitral regurgitation Mitral stenosis

Aortic regurgitation

Aetiology

  • rheumatic heart disease
  • infective endocarditis
  • trauma: surgical or blunt chest trauma
  • bicuspid aortic valve
  • VSD
  • dilatation of aortic ring: syphilis, seronegative arthritides eg ankylosing spondylitis, Marfan’s, aortic dissection
  • Coexisting aortic stenosis essentially limits possible aetiologies to congenital and rheumatic. Aortic valve disease without mitral valve disease less likely to be rheumatic

Haemodynamics

  • associated with increased LV compliance and raised LVEDP (± > 40 mmHg)
  • avoid bradycardia and increased SVR as both increase regurgitant flow and may precipitate cardiac failure
  • tachycardia and low aortic diastolic pressure result in decreased coronary blood flow. Therefore the combination of ischaemic heart disease and AR problematic
  • impaired contractility with chronic volume overload and increased sensitivity to myocardial depressants
  • in severe cases relative inability to increase cardiac output resulting intolerance of sepsis, arrythmias

Symptoms

  • tend to occur late
  • dyspnoea on exertion due to decreased forward flow
  • orthopnoea, PND due to LVF
  • angina, even without ischaemic heart disease

Signs

  • Pulse: collapsing, Corrigan’s, Quinke’s

  • BP: wide pulse pressure

  • JVP: usually normal

  • Thrills: ± diastolic +/or systolic. Latter does not necessarily indicate AS

  • Apex beat: displaced, heaving

  • Heart sounds:

    • A2 usually diminished or absent in severe AR

    • Murmur:

      • early diastolic

      • loudest at LSE or in aortic area (cases due to aortic dilatation).

      • longer murmurs associated with more severe AR

      • accentuated by isometric exercise.

    • ± aortic ejection flow murmur

    • ± Austin-Flint murmur due to displacement of anterior cusp of mitral valve by regurgitant jet. Soft, low pitched mid-diastolic or presystolic. Can be differentiated from MS by absence of presystolic accentuation, loud HS1 and opening snap

    • ± functional MR due to LV dilatation

Investigations

  • ECG. Severe cases: LV strain pattern. LAD and/or QRS prolongation suggest diffuse myocardial disease, generally associated with patchy fibrosis, and usually indicate a poor prognosis
  • CXR: LV dilatation, pulmonary venous hypertension. In cases due to primary valve disease may be dilatation of ascending aorta and knuckle. May be aneurysmal dilatation of aorta in cases due to aortic dilatation
  • Echo
  • Angio

Treatment

Medical

  • treat LVF along conventional lines. ACE inhibitors particularly useful. 
  • nitrates can be used to treat angina but are less effective than in ischaemic heart disease

Surgical

  • aim to replace/repair valve when LV dysfunction occurs but before patient becomes symptomatic
  • AVR does not restore LV function to normal
  • in patients with marked LV dysfunction surgical risk is higher but these patients should still be offered AVR as the prognosis with medical treatment alone is poor.

Aortic stenosis

Epidemiology

  • tends to present in fith to seventh decades

  • 80% of patients with severe aortic stenosis are men

Aetiology

  • congenital: may lead to stenosis as birth or aortic stenosis may develop in later life due to haemodynamic stresses on congenital bicuspid valve

  • rheumatic heart disease

  • idiopathic valve calcification: rarely leads to significant aortic stenosis

Pathophysiology

  • outflow obstruction results in relatively fixed stroke volume
  • obstruction leads initially to LV hypertrophy and, if not relieved, to LV failure and dilatation
  • LV hypertrophy increases transmural pressure and decreases coronary perfusion pressure
  • LVH reduces compliance and therefore high LVEDP (and LAP) required. Atrial contraction very important. Loss can lead to fall in CO of up to 40%. Vigourous atrial contraction reflected in prominent ‘a’ wave in LAP

Haemodynamic problems

  • LV hypertrophy and difficulty in oxygenating the subendocardium. The vicious cycle that must be avoided is:
    • high LV filling pressure
    • decreased subendocardial perfusion pressure
    • decreased subendocardial oxygen delivery
    • subendocardial dysfunction
    • decreased cardiac output
    • decreased aortic and therefore coronary perfusion pressure
    • further ischaemia
    • dysrhythmias
    • VF Once in VF these patients are very difficult to resuscitate.
  • LV dysfunction
  • stroke volume relatively fixed: falls in heart rate and in SVR believed to be poorly tolerated. In the case of the latter, a fall also reduces coronary perfusion pressure which may result in a reduction of cardiac output. Small increase in SVR can usually be tolerated provided LV function has not deteriorated.
    • More recent data from small series of patients suggests that patients may benefit from vasodilatation.
  • tachycardia is also poorly tolerated because of the reduction in duration of diastole
  • important to maintain sinus rhythm

Symptoms

  • exertional dyspnoea: result of raised pulmonary capillary pressure due to raised LVEDP
  • angina
  • syncope: results from inability to raise cardiac output in the face of peripheral vasodilatation or from arrhythmia

Signs

  • Pulse:
    • slow rising small volume pulse is characteristic
    • in severe cases slow rising character may be difficult to determine because of small volume
    • bisferiens pulse virtually excludes pure aortic stenosis
  • BP: usually normal but pulse pressure may be reduced in severe cases. Marked systolic hypertension (eg >200) makes severe AS unlikely
  • JVP: may be prominent ‘a" wave - LV hypertrophy results in limited expansion of RV
  • Thrills: may be present in aortic area and in neck
    • In patients who do not have obstructive airways disease, thick chest walls, thoracic deformity or heart failure the absence of a thrill suggests that AS is mild
  • Apex beat: not displaced until LV decompensation occurs
    • Double impulse may be palpable, especially with patient in left lateral position: atrial contraction followed by ventricular contraction
  • Auscultation:
    • HS1 normal
    • HS2 initially normal progressing through single to reversed splitting due to delayed aortic valve closure
    • ejection systolic murmu radiating to neck and occasionally to apex
    • HS4 in severe AS due to LVH and high LVEDP
    • HS3 usually occurs with LVF

Investigations

  • ECG: LVH and strain
  • CXR: usually normal until late stages. LVH may result in rounding of apex. On fluoroscopy (& echo) calcification of valve may be seen. In adults absence of calcification excludes severe AS
    Echo: thickening and calcification of cusps. Severity can be assessed from estimated transvalvular gradient. In presence of normal cardiac output gradient of ³ 50 mm Hg indicative of severe AS
  • Cardiac catheter

Assessment

Clinical features of severe disease

  • syncope
  • angina
  • low pulse pressure
  • thrill
  • LV dilatation
  • delayed aortic valve closure

Investigations

  • absence of valve calcification in adults suggests disease is not severe
  • valve cross-sectional area < 0.5 cm2/m2 BSA
  • transvalvular gradient. Important to take LV function into account

Management

Medical

  • angina responds to nitrates
  • previously thought that vasodilators are of little benefit in the treatment of heart failure but recent evidence suggests that nitroprusside infusion results in a rapid and marked improvement in cardiac function in patients with severe aortic stenosis and severe LV systolic dysfunction
    • dose was titrated to reduce MAP to 60-70 mmHg
    • patients in study had ejection fraction of 35% or less and aortic valve cross sectional area of 1 cm2 or less
    • resulted in increased stroke volume and cardiac index, decreased pulmonary capillary wedge pressure, pulmonary and systemic vascular resistance
  • diuretics can be used cautiously in the treatment of heart failure but care should be taken to avoid hypovolaemia
  • regular follow-up to detect development of LV failure and dilatation

Surgical

  • children and adolescents with severe non-calcific congenital AS benefit from simple commissural incision even in absence of symptoms
  • adults with severe AS and evidence of LV dysfunction or symptoms. Ideally valve should be replaced before severe LV dysfunction occurs but the prognosis of patients with the latter is so poor that valve replacement is still indicated despite the high operative mortality (15%) and the risk of persistent myocardial dysfunction

Further reading

Khot UN, Novaro GM, Popovic ZB et al. Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis. N Engl J Med 2003; 348:1756-63. A commentary on this paper can be found in Intensive Care Monitor, 2003; 10(4):62-3

Mitral regurgitation

Aetiology

May be caused by disease of cusps, chordae tendinae, papillary muscles or valve ring

  • rheumatic fever
  • subacute bacterial endocarditis
  • trauma: blunt or penetrating injury or inaccurate mitral valvotomy
  • LVF with resulting valve ring dilatation and functional MR
  • MI resulting in papillary muscle rupture or dysfunction
  • congenital
  • ruptured chordae tendinae

Haemodynamics

  • To and fro movement across valve
    • regurgitant jet throughout systole
    • forward flow through aorta decreased
    • increased flow during diastole. LV rapidly distended until downward movement of apex abruptly checked as valve cusps, chordae and papillary muscles drawn tight. This sets up vibrations causing 3rd heart sound (there is some evidence that this is not the mechanism by which 3rd HS produced) and as blood continues to flow rapidly across taut cusps, a flow murmur
  • Increased LA and pulmonary venous pressures
    • large V wave during ventricular systole
    • LAEDP similar to LVEDP as valve not obstructed. Mean LAP usually <LAP in mitral stenosis
  • LV dilatation and LVH

Acute MR

  • acutely impaired LV function, pulmonary oedema and shock: insufficient time for compensation by LV hypertrophy/dilatation and LA dilatation

Symptoms

  • dyspnoea, orthopnoea, PND, haemoptysis, "bronchitis" (due to pulmonary venous congestion)
  • fatigue (low cardiac output)
  • ankle oedema, hepatic pain, anorexia (secondary to RVF)

Examination

  • mitral facies less common than in mitral stenosis because lower mean LAP results in lower incidence of increased PVR and consequently low cardiac output
  • pulse
    • AF usual with severe MR
    • Waveform normal or sharp (powerful LV contraction)
  • JVP: slightly increased. Considerable increase suggests RVF
  • cardiac impulse: heave at apex beat
  • apex beat: displaced
  • auscultation

Investigations

ECG

  • P mitrale (if in sinus rhythm)
  • usually AF
  • LVH

CXR

  • LA and LV dilatation
  • +/- LVF

Echo

  • LV dilatation and hypertrophy
  • LA dilatation
  • failure of closure of valve

Cardiac catheter

  • LV venticulogram allows approximate quantification of regurgitation into mild (jet of contrast seen entering LA) and severe (marked opacification of LA)
  • measurement of LAP not a guide to severity because of damping effect of LA dilatation

Images

Complications

Treatment

Medical

Surgical

  • indications: moderately disabled patients (ie dyspnoeic on normal activity), particularly if cardiomegaly and increased LVEDV persist despite medical treatment
  • valve replacement associated with good immediate results. Complications include: perioperative death, systemic emboli, SBE, peri-prosthetic regurgitation. In patient with high SVR, valve replacement may precipitate LV failure

Mitral stenosis

Images

Epidemiology

  • 4 times more common in females
  • fully developed cases usually present >20 yrs

Aetiology

  • 99% of cases due to rheumatic heart disease
  • congenital: frequently associated with other lesions causing LV outflow obstruction including AS, subaortic stenosis, coarctation
  • other rare causes: calcified mitral valve ring, infective endocarditis (bulky vegetations may cause obstruction to flow), granulomatous infiltration in association with eosinophilia, SLE (treatment of Libman-Sachs endocarditis with steroids may lead to significant fibrosis with development of MS

Haemodynamics

  • raised LAP and hence PCP results in decreased pulmonary compliance, pulmonary oedema and haemoptysis
  • persistently raised LAP leads to reactive pulmonary hypertension. in late stages RVF occurs. Further reduces forward flow. Also LV distorted by bulging RV
  • raised LAP results in LA dilatation and AF. Development of AF and loss of atrial contraction results in a marked deterioration of haemodynamic function and may lead to an exacerbation of pulmonary oedema. Pregnancy and infection may also precipitate decompensation
  • LV dysfunction occurs in 1/4 of patients with severe MS. May be result of extension of scarring into myocardium and chronic reduction of preload
  • low cardiac output in severe cases

Symptoms

  • Due to pulmonary venous hypertension
  • dyspnoea on exertion
  • orthopnoea and paroxysmal nocturnal dyspnoea
  • bronchitis
  • haemoptysis

Signs

  • General: malar flush, pinched and blue facies
  • Pulse: normal/small amplitude, ± AF
  • JVP: NAD
  • Cardiac impulses: tapping impulse at apex, diastolic thrill at apex frequent
  • Auscultation:
    • loud HS1
    • ± loud P2
    • opening snap (best heard at apex or between apex and LSE, absent if valve calcified)
    • low pitched diastolic murmur starting immediately after the OS. Duration directly related to severity of MS. Pre-systolic accentuation (except in AF).
    • ± Graham Steele murmur (pulmonary regurgitation 2° to pulmonary hypertension)

Investigations

ECG

  • p mitrale (notched and > 0.12 sec)
  • ± RVH 2° to pulmonary hypertension

CXR

  • enlarged LA and LA appendage
  • upper lobe blood diversion
  • ± pulmonary oedema

Echo

Severity can be assessed on basis of valve cross-sectional area:
< 1 cm2 = severe
1 - 1.5 cm2 = moderate
1.5-2.5 cm2 = mild

Cardiac catheterization

Only necessary if diagnosis is in doubt or if patient thought to have co-existent coronary artery disease

Complications

  • AF in 40%. ­ incidence with ­ age and size of LA
  • systemic emboli: commonly recurrent, associated with AF and large LA appendage. Occur in 20% of patients with MS at some time. 80% of these patients are in AF at the time
  • reactive pulmonary hypertension in 25% of patients with severe MS
  • acute pulmonary oedema
  • infective endocarditis
  • bronchitis
  • recurrent PE: important cause of morbidity and mortality in late stages. Occur most frequently in patients with RVF

Management

Avoid:

  • bradycardia: relatively fixed stroke volume
  • tachycardia: reduces diastolic filling time and causes large increase in LAP - may precipitate pulmonary oedema and reduce cardiac output
  • hypovolaemia: reduces LAP and therefore ventricular filling (effect magnified by stenosed valve)
  • vasodilatation, for the same reasons

Medical

  • prophylaxis against further attacks of rheumatic fever
  • digoxin for AF
  • diuretics for fluid retention (note that CXR and other changes due to ­ LAP do not respond to diuretics)
  • prompt treatment of chest infections: often precipitate fluid retention so diuretic should be considered at the same time
  • prophylaxis against SBE

Surgical

Indications for surgery
  • significant symptoms which limit normal activity
  • pulmonary oedema without precipitating cause
  • recurrent emboli
  • pulmonary oedema in pregnancy (emergency valvotomy)
  • deterioration due to AF which does not respond to medical treatment
  • valve cross-sectional area <1.3 cm2 (valvotomy) or <1 cm2 if there is a possibility that valve replacement may be required
Surgical procedure

Valvotomy or replacement. Valve replacement leads to greatly increased LV filling ± distension, with ensuing increase in LV afterload



©Charles Gomersall, January, 2018 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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