notes by dr. Claudio Italiano
It is a very frequent and highly disabling valvulopathy, 1/3 of mitral
defects are insufficiencies; the mitral valve, so called because it has 2 cusps
and recalls the miter, ie the headgear used by the bishops, (see anatomy of the
heart) is located between the left atrium and the left ventricle and has the
task of allowing the passage of the blood flow to the left ventricle and closes
at the time of systole; the blood is pushed into the aorta, through the other
important valve that is the aortic valve. In severe forms of mitral
insufficiency it happens that a considerable amount of blood is regurgitated in
the left atrium and, consequently, creates an obstacle to the outflow of
arterial blood from the lung to the heart.
Mitral insufficiency can be:
a) rarely congenital
b) or almost always acquired, depending on:
- rheumatic endocarditis
- bacterial endocarditis
- mitral valve prolapse syndrome
- myocardial infarction with papillary muscle necrosis after commissurotomy.
Inability of the mitral valve to close, resulting in blood regurgitation during
systole (ie the contraction of the left ventricle) with passage of regurgitated
blood into the left atrium. This causes an overload of the volume in the left
atrium and left ventricle. The left atrium dilates and the left ventricle
undergoes left ventricular hypertrophy. Contrary to mitral stenosis, the
pressure in the left atrium increases only when the left ventricle is overloaded
by the volume of regurgitation, thus becoming insufficient, ie in the left
ventricle decompensation. This condition causes a pressure increase in the left
atrium to be determined, so that the pulmonary circulation meets resistance to
its outflow and causes pulmonary hypertension which in its turn, again, affects
upstream, ie on the atrium and right ventricle, causing pressure overload in the
right ventricle. Finally also the right ventricle becomes insufficient and we
talk about "terminal right heart failure".
The pictures may be those of chronic mitral insufficiency, when the pathological process is slow and gradual over time, or of acute mitral insufficiency, if it is established quickly, for example due to a structural failure in myocardial infarction
This condition for the most favorable volume overload life expectancy with mild
mitral insufficiency may be almost normal. However the symptoms may be missing
or insignificant for a long time even in the case of significant mitral
insufficiency. Only with the left ventricular insufficiency more serious
disorders are quickly established such as dyspnoea, palpitations, nocturnal
cough attacks, etc. The clinical picture is similar to that of mitral stenosis.
As mentioned before, in acute mitral insufficiency (eg from papillary muscular
necrosis in the infarction) the time for cardiac adaptation is lacking and a
left ventricular decompensation with pulmonary edema and evtl is rapidly
established. cardiogenic shock.
Auscultation: 1st light tone
-
3rd tone strong (filling tone)
murmur systolic in reduction or continuous directly after the 1st tone,
p.m. above the cardiac tip with irradiation in the axillary region
evtl. low frequency diastolic murmur (after the 3rd tone) in case of severe
mitral insufficiency with large volume of regurgitation (relative mitral
stenosis)
ECG: in case of more pronounced mitral insufficiency, signs of overload of the
left heart: P mitral (P in DII> 0.11 sec. and bifida) evtl.
atrial fibrillation
with total arrhythmia, evtl. signs of
left ventricle hypertrophy. Signs of a subsequent
overload of the right heart (with pulmonary hypertension) are often not present
at the ECG.
Radiology
enlargement of the left atrium and (in contrast to mitral stenosis) also of the
left ventricle: projection p.a .: enlarged heart with protruding contour mitral
configuration. Lateral projection: narrowing of retrocardial space at the atrial
and ventricular level (after barium intake) with final signs of pulmonary stasis:
hilar venous congestion in interstitial pulmonary edema, Kerley B lines in
alveolar pulmonary edema, "emery glass" appearance.
Echocardiography: indirect signs: enlargement of left atrium and left ventricle,
direct documentation of insufficient range to color doppler, evtl. documentation
of mitral valve prolapse, rupture of the mitral flap.
I <15
II 15-30
III 30-50
IV> 50
Pressure measurement: typical left atrial pressure curve in mitral insufficiency
with systolic pressure increase (normal: decrease in systolic pressure in the
left atrium) injection of the contrast medium in the left ventricle:
quantification of insufficiency by evaluation of the regurgitation fraction;
evaluation of the speed of passage and of the valvular mobility. It is also
necessary to document a possible secondary mitral stenosis, exclusion of other
cardiac defects, diagnosis of function of the left ventricle and evaluation of
the coronary arteries:
It is based among:
- relative insufficiency of the tricuspid in the right heart failure: this
systolic murmur is more accentuated with the inhalation, it is not transmitted
to the axillary area and disappears after compensation
- aortic stenosis (systolic murmur above the aorta with irradiation to the
carotid arteries)
- ventricular septal defect (echocardiogram)
- functional systolic murmur (diagnosis by exclusion).
- Diagnosis: auscultation / phonocardiogram - radiography - echocardiogram.
treatment of heart failure (see decompensation therapy)
thromboembolic prophylaxis with anticoagulants, in case of atrial fibrillation
or unstable sinus rhythm
prophylaxis of endocarditis
reconstruction (if possible) of the mitral valve, otherwise valve replacement
Indications:
acute mitral insufficiency in urgency
chronic mitral insufficiency only in evidently symptomatic patients progressing
from stage II to III.
Synonyms: Barlow syndrome or systolic click.
Definition: systolic protrusion of the posterior cusp of the mitral valve or of
both cusps in the left atrium. Often it does not involve any haemodynamic or
clinical impairment, more rarely it results a mitral insufficiency with clinical
consequences.
Epidemiology
more frequent form of valvular alteration in adulthood. Prevalence 4-10%, F> M,
familiarity.
Etiology
often congenital anomaly in connective tissue disorders (in 90% of patients with
Marfan syndrome: leptosomal conformation, slender, abnormally long extremities,
arachnodactyly, joint hyperextensibility)
acquired: myxomatosis proliferation of unclear etiology of the mitral flaps,
post-infarct dysfunction of the papillary muscle, etc.
The majority of those affected are asymptomatic. In a small part of the patients
there are:
rhythm disorders (ventricular ventricles, paroxysmal supraventricular
tachycardias) with palpitations, vertigo, evtl. syncopations
atypical, similar to endangered disorders or rarely mitral-type disorders.
They are rare: in mitral insufficiency evtl. We have bacterial endocarditis and
arterial embolisms, evtl. Ventricular tachyarrhythmias with sudden cardiac death
(very rare).
Auscultation: mesosisteric click, in case of mitral systolic murmur immediately
after the 1st tone.
ECG: in most cases normal, evtl. disturbances in stimulus genesis and rhythm
(ECG sec. Holter).
Echocardiography
systolic prolapse in the left atrium of one or both of the mitral flaps (in the
form of a "hammock"); documentation of a possible regurgitation jet in the color
doppler
- systolic murmates of other genesis
- coronary heart disease.
auscultation - echocardiogram.
only in case of disturbances, eg:
- treatment of rhythm disorders and angina-like symptoms with beta-blockers
- treatment of hemodynamically significant mitral insufficiency.
- prophylaxis of endocarditis in hemodynamically significant mitral
insufficiency
Prognosis: most patients have a prognosis