Left Clinical echocardiographic - Heart · patients the degree of mitral stenosis was judged to be severe enough to warrant mitral commis-surotomy. ECHOCARDIOGRAPHIC FINDINGS Mitralvalve

British Heart journal, 1979, 42, 514-520

Left ventricular function in rheumatic mitral stenosisClinical echocardiographic studyM. MOHSEN IBRAHIMFrom the Cardiac Department and Ultrasonic Laboratory, Cairo University, Egypt

SUMMARY Echocardiography was used to examine the extent and significance of impairment in leftventricular function in 20 patients with rheumatic mitral stenosis. Indices of left ventricular performance-normalised mean rate of circumferential fibre shortening (Vcf), ejection fraction, normalised posteriorwall velocity, and stroke volume were reduced. The impairment in left ventricular function was relatedto the degree of functional disability (NYHA), right ventricular dilatation, and left atrial enlargement.Vcf was inversely related to both the internal right ventricular diameter (r= -0-767, P <0.001) and thedegree of left atrial enlargement (r=-0.554; P <0.05). The normalised velocity of the interventricularseptum and the maximum systolic and diastolic endocardial velocities were also reduced.

These results suggest that abnormalities in contractility of left ventricular myocardium are re-sponsible for the impaired myocardial function in patients with mitral stenosis and that such impairmentis clinically significant.

Rheumatic mitral stenosis is one of the commonestvalvular heart lesions in Egypt and other developingcountries. The only effective treatment is surgical.However, the results of operation, morbidity, andmortality are governed not only by the mechanicaldefect but also by the state of the myocardium. Thepresence of such a myocardial factor in rheumaticmitral stenosis (Harvey et al., 1955; Fleming andWood, 1959) has remained speculative until recently(Feigenbaum et al., 1966; Curry et al., 1970;Heller and Carleton, 1970; Holzer et al., 1973).Since rheumatic heart affection is more severe andthe degree ofvalvular damage is greater in developingcountries than in industrialised Western communi-ties (El-Sherif, 1975), it seems appropriate toexamine the incidence and extent of left ventriculardysfunction in Egyptian patients. Left ventriculardimensions and function were therefore investigatedin a group of patients with rheumatic mitral stenosiswho were referred for mitral commissurotomy. Inaddition, the clinical correlates and the changes inright ventricular and left atrial dimensions wereexamined. Echocardiography had been used in thisstudy for measurements of cardiac chamberdimensions and for the assessment of left ventricularperformance. Good correlation between angio-cardiographic and echocardiographic measurements

Received for publication 18 December 1978

of left ventricular dimensions has already beenshown (Pombo et al., 1971; Feigenbaum et al., 1972).

Methods

Twenty patients with isolated rheumatic mitralstenosis were investigated. All patients wereevaluated clinically and mitral commissurotomywas found necessary. Symptoms, that is degree ofdyspnoea and effort intolerance, were classifiedaccording to New York Heart Association (NYHA).Patients with hypertension (systolic blood pressure> 170 mmHg or diastolic > 100 mmHg), ischaemicheart disease, or other possible causes for leftventricular enlargement or impairment were ex-cluded. The severity of mitral stenosis was deter-mined from history, physical examination, chestradiograph to assess the size of the left atrium andpulmonary venous congestion, and the electro-cardiogram to detect right ventricular hypertrophyand left atrial enlargement. The E-F slope of themitral valve in the echocardiogram was also de-termined to assess the severity of mitral stenosis.

ECHOCARDIOGRAPHYRecording techniqueThe echocardiograms were recorded with a Uniradultrasonoscope model 849 Sono III-GZD using a2*25 MHz transducer with an active diameter of

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Left ventricular function in rheumatic mitral stenosis

13 mm and internal focus 4 to 7 cm, with a repeti-tion rate of 10-0 impulses/s. The ultrasonoscopewas coupled to a strip chart recorder. Recordingswere obtained at a paper speed of 50 mm/s andwhen necessary 100 mm/s. Each patient had anelectrocardiogram recorded simultaneously with theechocardiogram. All patients were examined in thesupine position. The transducer was placed on thethird, fourth, or fifth intercostal space, just to theleft of the sternum, and the ultrasonic beam wasdirected posteriorly and slightly medially until theechogram of the anterior leaflet of the mitral valvewas identified. The transducer was then rotatedinferolaterally until the echoes from the endocardialsurface of the interventricular septum and theposterior left ventricular wall were clearly visualised.Measurements of left ventricular dimensions weremade at an angle in which fragmented echoes of themitral valve together with the interventricularseptal and posterior wall endocardial echoes couldbe recorded (Fig. 1). Particular care was taken tostandardise the pathway of the ultrasonic beamthrough the left ventricle, to identify correctly theinternal and external surfaces of the left ventricularwalls. The transducer was then directed in a pos-terior cephalad and medial manner to record theaorta and left atrium. The transducer was thenrocked inferolaterally to the point at which theaortic valve cusps could be visualised. Echocardio-graphic measurements were made only on record-ings of good quality.

Measurements and calculationsThe left ventricular echocardiographic dimensionswere measured from the endocardial echo of theposterior wall to the endocardial echo of the left sideof the interventricular septum. Measurements atend-diastole (EDD) were made at the peak of the Rwave of the QRS, and measurements at end-systole(ESD) were made at the point of the smallestdistance separating the septum from the posteriorwall (Fig. 1). The left ventricular ejection time(LVET) was measured from the aortic valve echo-gram or from a simultaneously recorded carotidpulse. Septal (IVST), posterior left ventricularthickness (LVT), and right ventricular internaldiameter (RVD) were measured at the peak of the Rof the QRS (Fig. 1). Posterior left ventricular wallexcursion (PWE) was measured from the mostposterior point of the left ventricular endocardialtracing to the most anterior point in systole (Fig. 1).Similar points at the beginning and peak of theseptal systolic excursion were selected to measureseptal excursion (IVSE). The maximal systolicendocardial velocity (MSEV) was measured fromthe slope of the tangent to the steepest part of the

Fig. 1 Echocardiographic measurements. Thetransducer was directed towards the cavity of the leftventricle immediately below the mitral valve leaflets.Fragmentary echoes of the mitral valve (MV) are seen.EDD, end-diastolic diameter of left ventricle; ESD,end-systolic diameter of left ventricle; IVS,interventricular septum; LVPW, left ventricularposterior wall. The slope of the tangent to the steepestpart of the endocardium of the left ventricular posteriorwall was measured in systole (A) and diastole (B) todetermine the maximal systolic endocardial velocity andthe maximal diastolic endocardial velocity. (C)Interventricular septal excursion. (D) Posterior wallexcursion. RVID, right ventricular internal diameter;En, endocardium; Ep, epicardium; CT, chordaetendineae; RV, right ventricle.

endocardium of the left ventricular posterior wallin systole as previously described (Kovick et al.,1975) (Fig. 1). The maximal diastolic endocardialvelocity (MDEV) was measured similarly in diastole.

Other measurements made from the echocardio-gram were the left atrial (LAD) and aortic root(AoRD) dimensions at end-systole (Brown et al.,1974) (Fig. 2). Mitral valve diastolic excursion wasmeasured as the vertical line from the lowest pointof the mitral echogram (C) to the E point. Themitral diastolic closure slope (E-F) was measured.

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Fig. 2 Echocardiographic measurements. The transducerwas directed towards the aortic root (AoR). A, aorticroot diameter; B, left atrial diameter; LA, left atrialcavity.

Left ventricular volumes were derived by cubingEDD and ESD. The difference between end-diastolic volume (EDV) and end-systolic volume(ESV) was the left ventricular stroke volume (SV).These volumes were also used to calculate theejection fraction (EF):

EDV - ESVEF=

EDV

The normalised mean rate of circumferentialfibre shortening (Vcf) was calculated as:

EDD - ESDVcf (circ/s) =

LVET x EDDThe normalised mean posterior wall velocity

(Vpw) was calculated as:

PWEVpw (s-1) = LVET x EDD

Similarly a normalised mean interventricularseptal velocity (Vivs) was calculated as:

IVSE

Vivs (s-1) = LVET x EDD

The ratio of left atrial to aortic root diameters

(LA/Ao) was calculated for improved detection ofleft atrial enlargement (Brown et al., 1974).

All the calculations were made using the averageobtained from five cardiac cycles, excluding fourpatients who were in atrial fibrillation. In thesepatients an average of 10 cycles was used.Normal values for these echocardiographic

measurements were those obtained from a group of14 closely matched healthy subjects with no clinical,radiological, or electrocardiographic evidence ofcardiovascular abnormality.

Results

CLINICAL CHARACTERISTICSEleven male subjects and nine female subjects werestudied, their ages ranged from 16 to 54 years, witha mean age of 31 years. Five patients were in class II(HYHA), 11 were in class III, and four were inclass IV. The electrocardiogram was normal in onlythree patients. Four patients had atrial fibrillation,seven had left atrial enlargement, and eight patientshad electrocardiographic evidence of right ventri-cular hypertrophy. None of the patients had clinicalor laboratory evidence of rheumatic activity. In allpatients the degree of mitral stenosis was judgedto be severe enough to warrant mitral commis-surotomy.

ECHOCARDIOGRAPHIC FINDINGS

Mitral valve echogramAll patients showed the classic findings of mitralstenosis (Feigenbaum, 1976). The E-F slope wasflat in six patients, 10 mm/s or less in eight, andbetween 11 and 18 mm/s in six. The mitral valveexcursion (C-E) ranged from 13 to 30 mm. It wasless than 20 mm in nine patients and the meanvalue for the whole group was 22 mm.

MeasurementsTable 1 shows the measured internal diameters ofthe right and the left ventricles, aortic root, andleft atrium. The thickness and excursion of theseptum and left ventricular posterior wall are shownin Table 2. Though the right ventricular internaldiameter was greater and end-diastole was less inpatients with mitral stenosis than in normal subjects,the changes were not statistically significant.However, the thickness of the left ventricularposterior wall was significantly reduced (P <0-05).In addition, the increase in left atrial dimensionand decrease in aortic root dimension were signifi-cant (P <0-001). The extent of excursion of theposterior wall and interventricular septum was notvery different from that in normal subjects.

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Table 1 Echocardiographic measurements

Case RVD EDD AoRD LADno. (cm) (cm) (cm) (cm)

1 13 4-8 2-9 3-82 0 9 4-4 2-6 4-83 1.0 4-4 2-6 4-84 1-7 4.9 3-3 5 05 1-6 5 0 2-5 3-86 3-1 4-5 1.9 4-57 1.1 4-4 2-9 4-48 - - 19 3-89 - - 2-5 4-1

10 2-5 39 2-3 3-611 2-1 4-1 - 3-812 - 5-0 3-1 3-113 1.9 4-4 1.9 4-414 4-0 3-8 1.9 3-815 2-0 - 2-5 4-416 2-8 4-4 2-5 -17 19 40 19 5018 - 4-5 2-4 4-819 1.9 4-4 2-1 4-420 2-1 5 0 2-4 4-8

Mean 2-0 5-4 2-4 4-3SE 0-19 0 09 0-098 0-125

Normals (mean) 1-5 4-7 3-27 3-23SE 0-12 0-102 0-064 0-062P < 001 NS 0 001 0 001

RVD, right ventricular intemal diameter; EDD, end-diastolicdiameter of left ventricle; AoRD, aortic root diameter; LAD,left atrial diameter.

Table 2 Echocardiographic measurements

Case IVST IVSE LVT PWEno. (cm) (cm) (cm) (cm)

1 0-8 - 0-6 0-82 0-8 0-6 0-6 1.13 10 05 0-6 094 07 - 0-6 1.15 1.1 0-6 05 096 0-6 0 4 0-6 0-87 1.0 0-8 0-6 1-28 1-3 0-6 0 5 0-89 - - 05 0910 0-6 0 5 0-6 0-811 1-3 05 0-8 0912 - 0-4 0-5 0-613 1-3 0-6 0 9 0 914 09 04 0-8 0715 - - 05 1.116 0-8 - 1.0 0-617 10 0-6 0-8 1-218 09 10 09 0-819 0-6 0 4 0-8 0-820 1.1 0-8 0-7 0-6

Mean 09 0-6 0 7 0 9SE 0-058 0-045 0-036 0-042

Normals (mean) 0-8 0-6 0-8 1-2SE 0-040 0.10 0 040 0.10P < NS NS 0 05 0.1

IVST, interventricular septal thickness; IVSE, interventricularseptal excursion; LVT, left ventricular posterior wall thickness;PWE, posterior wall excursion.

Indices of left ventricular performanceThe cardiac output, stroke volume, ejection fraction,and normalised mean rate of circumferential fibreshortening (Vcf) were all reduced in patients withmitral stenosis, and the changes were significant(Table 3). Vcf was reduced by more than twostandard errors (less than 110 circ/s) in 14 out of17 patients, while the ejection fraction was reducedto less than 055 in about 50 per cent of patients.The mean values for the normalised velocities ofthe posterior wall (Vpw), interventricular septum(Vivs), and the maximum systolic and diastolicendocardial velocities were significantly lower inpatients than in normal subjects (Table 4).The changes in myocardial contractility ex-

pressed as Vcf were inversely related to both theinternal right ventricular diameter (r=-0'767,P < 0001) (Fig. 3) and the degree of left atrial en-largement expressed as LA/Ao ratio (r=-0{554,P < 0.05) (Fig. 4). The latter relation did not includecase 12. A positive correlation was present betweenVcf and the extent of posterior wall excursion(r =0-635, P < 0 01) (Fig. 5) and the ejection fraction(r =0-847, P < 0 001).

Clinical echocardiographic correlatesFig. 6 and 7 show the extent of impairment of left

Table 3 Indices of left ventricular function

Case SV CO EF Vcfno. (MI) (i/min) (circls)

1 54 5-18 0-51 0.992 57 570 0-68 1-403 53 4-24 0-63 1-064 83 5-83 0-71 1-405 67 5 09 054 1 006 33 2-71 0-36 0-527 53 3-71 0-63 1-2289 - - - -

10 37 2-15 0-63 0-7711 27 2-38 0 39 0 5012 56 4-48 0 45 0-5813 50 3-10 0-60 0 9314 22 2-33 0-42 0-6115 - - - -

16 36 2-88 0 43 0-8317 37 4 07 0-58 0-8318 60 3-48 0-66 0-9819 47 3-76 0-56 0-8320 61 3 90 0 49 0-72

Mean 49 3-82 0 55 0-89SE 3-76 0-197 0 030 0-067

Normals (mean) 72 5-02 0 74 1-26SE 6-2 0-23 0-013 0-08p < 0-001 0.001 0.001 0.001

SV, stroke volume; CO, cardiac output; EF, ejection fraction;Vcf, normalised mean rate of circumferential fibre shortening.

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Table 4 Indices of myocardial contractility

Case Vpu Vivs MSEV MDEVno. (S-i) (S4) (cm/s) (cm/s)

1 1-27 - 2-5 3-22 109 0-60 2-5 503 0-72 0 40 4-6 6-94 095 - - -5 0-81 054 - -6 0-71 035 50 4-17 1 11 0 74 6-1 3-28 - - 1-8 5-39 - - 2-8 6-910 0-56 0 35 3-1 0-311 0 73 0-41 5-3 6-012 0 39 0-26 - -13 0-71 0-51 2-9 2-214 0-62 0*35 4 0 3-715 - - 5 0 6-916 0-63 - 4-2 2-917 100 050 5-2 6-018 0-56 0-71 4-3 10119 0-65 0 33 4 0 7-620 0 43 0-58 - -Mean 0-76 0-47 4 0 5-6SE 0-056 0 039 0-308 0579

Normals (mean) 0 95 0-61 6-2 18-0SE 0-02 0-02 0-256 0-548P < 0 005 0 005 0 001 0 001

Vpw, normalised velocity of the posterior wall; Vivs, normalisedvelocity of the interventricular septum; MSEV, maximum systolicendocardial velocity; MDEV, maximum diastolic endocardialvelocity.

ventricular function expressed as changes in Vcf,EF, and Vpw in relation to the clinical severity ofmitral stenosis (NYHA classification). Deteriorationin left ventricular performance was greater inpatients of class IV than in those of class II.Increase in right ventricular internal diameter pro-gressed from patients in class II to patients in classIV (Fig. 7). Patients in class IV had the largest rightventricles.

Discussion

The high incidence of impairment in left ventricularfunction in our patients with mitral stenosis was atvariance with previous reported incidences in otherstudies. Harvey et al. (1955) found an incidence of13 per cent in their patients, while Kennedy et al.(1970) found that 37 per cent of patients withmitral stenosis had evidence of impaired myocardialcontraction. In a recent echocardiographic study,McDonald (1976) found an incidence of30 per cent.The very high incidence in our patients was notcompletely unexpected. Two factors might havebeen responsible; first, patients in our study hadmitral stenosis necessitating cardiac surgery. Insuch a selected group of patients the degree ofmitral stenosis and functional disability would begreater than in a random selection of patientspresent in other studies. Secondly, the severe and

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Fig. 3 Relation between Vcf and right ventricularinternal diameter. r=-0 767; P<0001.

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Fig. 4 Relation between Vcf and the degree of leftatrial enlargement expressed as LA/Ao ratio.r=-0554; P<O005. Case 12 is not included in thecorrelation.

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Fig. 5 Relation between Vcf and the extent ofposteriorwall excursion. r=O0635; P<001.

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Fig. 6 Clinical-echocardiographic correlates. Clinicalseverity of mitral stenosis (NYHA classification) andchanges in Vcf and Vpw. The hatched area representsthe mean values for the normals ±2 standard errors.

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Fig. 7 Clinical-echocardiographic correlates. Clinicalseverity of mitral stenosis (NYHA classification) andchanges in ejection fraction (EF) and right ventricularinternal diameter (RVD). The hatched area representsthe normals +42 standard errors.

florid nature of rheumatic fever, its early age ofonset, and the significant haemodynamic burdenin Egyptian patients is different from that in westerncountries (El-Sherif, 1975). Botros and Sabaa(1976) in a haemodynamic study of 32 youngEgyptian patients with mitral stenosis have shownthat the pulmonary arterial pressure approachedsystemic level in 50 per cent of their patients. Thisfigure was 13 per cent in Wood's series (Wood,1954). The cardiac index was reduced in all patientsin the Egyptian series, ranging between 2 and 2-51/min per M2.

Indices of left ventricular performance, viz. Vcf,ejection fraction, Vpw, and stroke volume werereduced in patients with mitral stenosis. The im-pairment in left ventricular function was related tothe degree of functional disability (NYHA), rightventricular dilatation, and left atrial enlargement.

In a disease like mitral stenosis where the haemo-dynamic burden of the mechanical obstruction ison the pulmonary circulation and right ventricle

it was unusual to find a relation between leftventricular dysfunction and clinical disability. Thissuggests that some of the symptoms experienced bypatients with mitral stenosis may be the result ofimpairment in left ventricular function. The in-verse relation between Vcf and right ventricularintemal diameter (r=-0-767; P < 0-001) (Fig. 3)and the degree of left atrial enlargement (LA/Aoratio) (r=-0-554, P <0 05) favours the assumptionthat the impairment of left ventricular contractilitywas also related to the severity of mitral stenosisreflected in left atrial and right ventricular dilatation.On the other hand, hypokinesis of the left ventri-cular wall was found by Curry et al. (1970) not onlyin patients with mitral stenosis but also in patientswith right ventricular enlargement not secondaryto mitral valve disease.

Subtle changes in left ventricular contraction havebeen reported in mitral stenosis by Heller andCarleton (1970). Of their 25 patients, 20 showeddistortion, immobility, and regidity of the postero-basal area of the left ventricle. Similarly, localisedabnormalities in the wall of the left ventricle havebeen described by Horwitz et al. (1973). Fibrosis inor near the papillary muscles was postulated as apossible cause. However, the reduction in ourpatients of the mean values for the normalisedvelocities ofthe posterior wall (Vpw), interventricularseptum (Vivs), and the maximum systolic (MSEV)and diastolic (MDEV) endocardial velocities areconsistent with the view that a generalised abnor-mality of myocardial mechanical performance isresponsible for the occurrence of left ventriculardysfunction in some patients with mitral stenosis.Holzer et al. (1973) found abnormalities of ven-tricular contraction in 10 patients with rheumaticmitral stenosis.The present study suggests that abnormalities in

contractility of the left ventricular myocardium canbe responsible for the impaired myocardial functionin patients with mitral stenosis and that such im-pairment is clinically significant. It may be a con-tributing factor in some patients who have an un-satisfactory clinical response to mitral commis-surotomy. Histopathological studies in patients withmitral stenosis showed that the failure of improve-ment after mitral commissurotomy was related tothe extent of myocardial involvement by therheumatic process (Selim, 1976).

References

Botros, F. E., and Sabaa, H. (1976). Rheumatic mitralstenosis below the age of 20-A hemodynamic andoperative study. Bulletin of the Egyptian Society ofCardiology, 14, 75-81.

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Brown, 0. R., Harrison, D. C., and Popp, R. L. (1974).An improved method for echographic detection of leftatrial enlargement. Circulation, 50, 58-64.

Curry, G. C., Elliot, L. P., and Ramsey, H. W. (1970).Quantitative left ventricular angiographic findings inmitral stenosis: detailed analysis of the anterolateralwall of the left ventricle. American Journal of Cardio-logy, 29, 621-627.

El-Sherif, A. (1975). The epidemiologic features ofrheumatic fever and rheumatic heart disease in Egypt.Bulletin of the Egyptian Society of Cardiology, 14,65-70.

Feigenbaum, H. (1976). Echocardiography, 2nd edn,p. 107. Lea and Febiger, Philadelphia.

Feigenbaum, H., Campbell, R. W., Wunsch, C. M., andSteinmetz, E. F. (1966). Evaluation of the left ven-tricle in patients with mitral stenosis. Circulation,34, 462-472.

Feigenbaum, H., Popp, R. L., Wolfe, S. B., Troy, B. L.,Pombo, J. F., Haine, C. L., and Dodge, H. T. (1972).Ultrasound measurements of the left ventricle. Acorrelative study with angiocardiography. Archives ofInternational Medicine, 129, 461-467.

Fleming, H. A., and Wood, P. (1959). The myocardialfactor in mitral valve disease. British Heart Journal,21, 117-122.

Harvey, R. M., Ferrer, M. I., Samet, P., Bader, R. A.,Bader, M. E., Cournard, A., and Richards, D. W.(1955). Mechanical and myocardial factors in rheu-matic heart disease with mitral stenosis. Circulation,11, 531-551.

Heller, S. J., and Carleton, R. A. (1970). Abnormal leftventricular contraction in patients with mitralstenosis. Circulation, 42, 1099-1110.

Holzer, J. A., Karliner, J. S., O'Rouke, R. A., andPeterson, K. L. (1973). Quantitative angiographicanalysis of the left ventricle in patients with mitralstenosis. British Heart Journal, 35, 497-502.

Horwitz, L. D., Mullins, C. B., Payne, R. M., andCurry, G. C. (1973). Left ventricular function inmitral stenosis. Chest, 64, 609-614.

Kennedy, J. W., Yarnall, S. R., Murray, J. A., andFigley, M. M. (1970). Quantitative angiocardiography.IV. Relationships of left atrial and ventricular pressureand volume in mitral valve disease. Circulation, 41,817-824.

Kovick, R. B., Fogelman, A. M., Abbasi, A. S., Peter,J. B., and Pearce, M. L. (1975). Echocardiographicevaluation of posterior left ventricular wall motion inmuscular dystrophy. Circulation, 52, 447-454.

McDonald, I. J. (1976). Echocardiographic assessmentof left ventricular function in mitral disease. Circula-tion, 53, 865-871.

Pombo, J. F., Troy, B. L., and Russell, R. O., jun(1971). Left ventricular volumes and ejection fractionby echocardiography. Circulation, 43, 480-490.

Selim, N. M. (1976). Studies on rheumatic mitral valvedisease with special emphasis on the myocardialfactor. M.D. Thesis, Assiut University, Egypt.

Wood, P. (1954). An appreciation of mitral stenosis.Part I. Clinical features. Part II. Investigations andresults. British Medical Journal, 1, 1051-1063;113-1124.

Requests for reprints to Dr M. Mohsen Ibrahim,1 El-Sherifein Street, Cairo, Egypt.

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Left Clinical echocardiographic - Heart · patients the degree of mitral stenosis was judged to be severe enough to warrant mitral commis-surotomy. ECHOCARDIOGRAPHIC FINDINGS Mitralvalve