<病史>
This 69-year-old gentleman was a
businessman. He could walk up-stair to 4-floor without
exercise intolerance before. Two months ago, he suffered from
rhinorhea, sorethroat, and productive cough with whitish
sputum initially. He visited a local medical doctor where
upper respiratory tract infection was informed. His symptoms
improved a little after some medicine was taken. However,
sudden onset of dyspnea attacked while working one week later.
He denied either chest tightness, cough, palpitation or leg
edema at that time. Rest or postural change did not relieve
the dyspnea. Nocturnal dyspnea and orthopnea progressed in one
month. Therefore, he was sent to our emergency room for
help.
According to his statement, he
denied hypertension, DM or hyperlipidemia. He denied any cardiac
or pulmonary disease. No smoking or drinking was complained
of. He also denied any traumatic history.
On arrival of the emergency
room, the body temperature was 35.3℃, pulse rate was 100 per
minute, and blood pressure 163/100 mmHg. Throat was not
injected. Jugular vein engorgement was noted. Bilateral basal
crackles were heard and the accessory muscle respiration was
disclosed. PMI was located at 5th intercostal space. There was
no RV heave. Heartbeats were regular but a grade IV/VI
pansystolic murmur with thrill was noticed at the cardiac apex
radiating to the neck, spine and top of the head. Abdomen was
flat and soft, and liver and spleen were not palpable. He was
admitted for further evaluation and treatment.
<Course and Treatment
>
Chest X-ray revealed normal
cardiac size and bilateral pleural effusion. The
pleurocentesis was performed and the biochemistry results of
pleural effusion were listed as below. The cytology was
negative of malignant cells. He was referred to undertake the
echocardiography, which disclosed normal chamber size, severe
eccentric mitral regurgitation, and chordae tendinae rupture
of anterior leaflet. The left ventricular ejection fraction
was 68%, and no regional wall motion abnormality was noticed.
There was also no evidence of infective endocarditis and
degenerative valvular disease was impressed. His dyspnea
subsided gradually after pleurocentesis and diuretics given.
The diagnostic cardiac catheterization was done after his
condition stabilized. The coronary artery was patent.
Cardiovascular surgeon was consulted for surgical
intervention.
<Lab>
CBC + Differential count
WBC |
Seg |
Lym |
RBC |
Hb |
MCV |
Hct |
Plt |
9310 |
63.8% |
25.1% |
4.46 |
13.3 |
89.7 |
40.6 |
192000 |
BCS
Na |
K |
Cl |
Ca |
Glucose |
GOT |
BUN |
Cre |
141 mM/l |
4.0 mM/l |
110 mM/l |
2.17 mM/l |
94 mg/dl |
49 mg/dl |
20 mg/dl |
1.2 mg/dl |
Total Protein |
Albumin |
Globulin |
LDH |
Sugar |
6.9 g/l |
3.9 g/l |
3.0 g/l |
371 U/l |
94 mg/dl |
Pleural effusion
Total Protein |
Albumin |
Globulin |
LDH |
Sugar |
2.5 g/l |
1.5 g/l |
1.0 g/l |
156U/l |
126mg/dl
|
<病案討論>
1. Pathophysiology of acute MR:
(1) Acute MR→ LV volume overloading→ increased LV preload→
increased LV total stroke volume. (2) The unprepared left
atrium and left ventricle cannot accommodate the regurgitant volume→ pulmonary congestion.
2. Pathophysiology of chronic MR:
(1) Chronic MR→ development of eccentric cardiac
hypertrophy→ increase in LV end-diastolic volume
(2) The increase in LV and LA size allows
accommodation of the regurgitant volume at a lower filling
pressure
3. Etiology of acute MR: (1) Disorders of the mitral
valve leaflets (2) Disorders of the chordae tendinae: such
as infective endocarditis, rheumatic valvular heart diseases,
trauma, acute rheumatic fever, spontaneous rupture (ex.
degeneration). (3) Disorders of the papillary muscles
(including myocardial ischemia)
4. Medical treatment: in order to diminish the amount of
MR, increasing forward output, reducing pulmonary congestion;
medication including after-loading reducing agents, diuretics,
nitrates, ventricular rate-controlling agents and
antiarrhythmics.
5. The indications of surgical intervention: severe MR and
symptoms limiting lifestyle; evidence of increasing myocardial
dysfunction; atrial fibrillation (chronic MR); ischemic MR
(should be managed aggressive). The goal of surgical treatment
is to improve symptoms and preserve LV function.
6. Prognosis: (1) Acute vs. chronic; symptom severity;
etiology. (2) Ejection fraction (3) Chronic MR:
end-systolic diameter (ESD) < 2.6 cm/m2, end-systolic
volume (ESV) < 50ml/m2, exercise with peak oxygen
consumption <=
18 ml/kg/min (4)
Early mortality: Degenerative MR: 0-2% Ischemic MR:
7-26%
Valve repair is
better than valve replacement due to preservation of
subvalvular apparatus (5) Late mortality: (A) 95% NYHA Fc I-II in earlier surgical
intervention:
Survival rate |
5y |
10y |
15y |
Degenerative |
85-90% |
80% |
70% |
Rheumatic |
90-96% |
84-93% |
78% (partly due to younger age)
|
(B) Ischemic MR: poorer
prognosis than non-ischemic MR, better survival in aggressive
management.
|