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British Heart J'ournal, I970, 32, 675-682.

Value of reference tracings in diagnosis andassessment of constrictive epi- and pericarditis

H. Kesteloot and B. DenefFrom Department of Cardiology, St. Raphaels University Clinic,Kapucijnen voer, 35, Leuven, Belgium

Reference tracings are of great value in the diagnosis and assessment of constrictive pericarditis.The Q-h interval in the jugular venous pulse tracing is strongly correlated with the mean rightatrialpressure (r= o09I). The left ventricular ejection time, the Q-A2 interval, and the Q-h intervalare independent during atrialfibrillation from the preceding diastolic filling interval. This diff-erentiates constrictive pericarditis from valvular heart disease. Cases with haemodynamicallysignificant constrictive epicarditis are characterized by a rapid evolution, absence of peri-cardial calcification and absence of an early diastolic filling sound, a dominant a wave in thejugular venous pulse tracing, and a high early diastolic ventricular pressure. The haemodynamicbehaviour is similar to thatfound in cases with myocardial fibrosis.

As a disease of the heart, constrictive peri-carditis possesses several unique features. Inmost cases these are due to the presence of anearly normal contractibility of the myocar-dium in the presence of a highly raised fillingpressure.

In the more severe cases, however, contrac-tibility of the myocardium is also impaired.Moreover, though the clinical signs of peri-carditis constrictiva are well known (Kuss-maul, I873; Pick, I896; White, I944; Wood,I956), its differential diagnosis from otherfibrotic myocardial disease is often difficult(Gunnar et al., I955; Nye, Lovejoy, and Yu,I957; Soulie, Chiche, and Acar, I958; Acarand Godeau, I960; Shillingford and Somers,I96I; Somers et al., I968). In constrictivepericarditis the epicardium can also bethickened and this complicates surgical treat-ment of the disease. The purpose of our studyhas been to evaluate the severity of constric-tive pericarditis by means of indirect referencetracings. The possibility of diagnosing aneventual participation of the epicardium inthe disease and the differential diagnosis withother forms of heart disease have also beenexamined.

Subjects and methodsDuring the period from I960 to I968, 26 cases ofconstrictive pericarditis have been studied. Therewere i8 men and 8 women. The mean age of thegroup studied was 27 years (range i6-68). In i6Received I2 November I969.

cases the pericardium was calcified and in I0 casesno calcification was present. Of the I0 cases with-out calcification, 7 had a subacute and 2 had achronic evolution towards constriction, while in icase the beginning of the disease could not beestablished with certainty. In the patients with asubacute evolution, the time interval between thebeginning of the pericardial disease and the find-ing of constrictive pericarditis was less than iyear. In 25 cases a complete clinical and haemo-dynamic evaluation has been performed, includinga right heart catheterization in 24 cases and a rightand left heart catheterization in i case. A level5 cm. below the angle of Louis has been con-sidered as the zero level for the pressure measure-ments. Twenty cases have undergone operation,including all cases with a non-calcified constrictivepericarditis. In 7 cases during operation constric-tive epicarditis was found to coexist with thepericardial disease. This epicardial thickeningcould be partially removed during operation in 5cases, and was verified at necropsy in 2 cases. Inall 7 cases the constrictive epicarditis was thoughtto be the major factor in the disease. Sinus rhythmwas present in 2I cases, and 3 were seen duringatrial fibrillation and 2 during fibrillo flutter.

Post-operative observation included a rightheart catheterization in 4 patients. Phono-mechanocardiographic reference tracings wererecorded before operation in 25 cases, and inseveral cases after operation. This included a jugu-lar venous pulse tracing, an indirect carotid arterytracing, and a phonocardiogram. The left ven-tricular ejection time was measured from theindirect carotid artery tracing. In some cases itwas also possible to obtain an apex cardiogram.The reference tracings were obtained by meansof a piezoelectric transducer with a time constant

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676 Kesteloot and Denef

of I-2 sec. or with a strain gauge transducer EMT32 Elema with a DC output. It has been shownpreviously that a time constant of i 2 sec. causesonly an insignificant time shift when comparedto a DC recording (Kesteloot, Willems, and vanVollenhoven, I969).The method of recording has been described

elsewhere (Kesteloot, I963). For the referencetracings the standard nomenclature was used(Hartman, I960). The upstroke of the y troughhas accordingly been referred to as the h wave.This corresponds to the z wave in the terminologyused by Wood (I956).

For comparative purposes a certain number ofcases of rheumatic valvular heart disease werealso studied with the same methods as the casesof constrictive pericarditis.

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FIG. ia The three types ofjugular venouspulse tracing (see text). A great similarityexists between the morphology of type A and C.

ResultsJugular venous pulse tracingMorphologyIn the cases with sinus rhythm three types ofjugular venous pulse tracing were encoun-tered. Type A had a normal morphology, withthe a wave as the dominant wave and an xtrough or systolic descent larger than the ytrough or diastolic descent. This type wasfound in cases with a normal or only slightlyraised mean right atrial pressure. Type B wasthe form of jugular venous pulse tracingmost commonly encountered in constrictivepericarditis. It had either a W or an M form,but the y trough was always deeper than the xtrough. Type C was very similar to type Abut the a wave tended to be higher and the ytrough to be nearly absent. This type wasfound in the presence of a very high meanright atrial pressure (Fig. i). The haemo-dynamic findings are summarized in Fig. 2.Type C was only found in cases where animportant constrictive epicarditis was alsopresent, and the disease was the most severein this group. The pressure difference betweenthe summit of the v wave in the right atrium

FIG. 2 Haemodynamic findings in the threesubgroups, divided according to the morphologyof the jugular venous pulse tracing and theheight of the mean right atrial pressure. CO -cardiac output (in litres per minute). mRAP -mean right atrial pressure. inmEDPRV - meanearly diastolic pressure in the right ventricle.minPvRA - mean pressure of the summit of thev wave in the right atrium. inmDPRV - meanend diastolic pressure in the right ventricle.inPAP - mean pressure in the pulmonaryartery. miPCP - mean pulmonary capillarypressure. The pressures are given in mm. Hg.

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FIG. ib Another example of type B. Thenadir of the y trough coincides with the earlydiastolic sound.

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Constrictive epi- and pericarditis 677

and the nadir of the early diastolic pressurein the right ventricle was measured in all cases.This mean pressure difference was only about3 mm. Hgin cases oftypeA and C, and 13 mm.Hg in cases of type B.

Haemodynamic correlationsThe relation that exists between different timeintervals measured between electrocardiogra-phic, phonocardiographic, and mechano-cardiographic events derived from the jugularvenous pulse tracing and the mean right atrialpressure was examined. Only the cases with amean right atrial pressure of 4 mm. Hg ormore were used for the calculations, as incases with a lower pressure the constrictivepericarditis could not be considered as clinic-ally important. The best correlation was foundbetween the mean right atrial pressure andthe Q-h interval, i.e. the interval between thebeginning of the depolarization measuredfrom the electrocardiogram and the h wavemeasured on the jugular venous pulse tracing(Fig. 3). The h wave signals the end of theventricular filling during diastole. As an hwave cannot always be identified on the ven-ous pulse tracing in cases with a rapidheart rhythm, other intervals were also mea-sured. The second best correlation was foundbetween the mean right atrial pressure andthe nadir of the y trough of the jugular venouspulse tracing (Fig. 4). The regression equa-tions relating mean right atrial pressure to thedifferent measured time intervals are given inTable I.We also examined the relation between the

mean right atrial pressure and the time inter-val between the beginning of the pulmonarycomponent of the second sound (P2) and the

FIG .3 Relation between Q-h interval mea-sured on the jugular venous pulse tracing andthe mean right atrial pressure.28 -

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FIG. 4 Relation between Q-y interval mea-sured on the jugular venous pulse tracing andthe mean right atrial pressure.

sumnmit of the v wave of the jugular venouspulse tracing. A shortening of this intervalhas been previously described in constrictivepericarditis (Kesteloot, I963). In ii out of i2cases with an interval P2-sumMit v less thanor equal to 003 sec., the mean right atrialpressure was higher than 12 mm. Hg, andthe reverse was true in 6 out of 7 cases with aP2-summit v interval >003 sec. (X2 I 1.9,p <oooi).A remarkable constancy was found in the

Q-h wave interval during atrial fibrillation,making it independent from variations in theduration of the preceding diastole (Fig. 5).The same conclusion can be drawn from themultiple regression equation between themean right atrial pressure and the Q-h inter-val and heart rate. Only the regression co-efficient of the Q-h interval is statisticallysignificant (Table 2).

Left ventricular ejection time The re-gression line relating left ventricular ejectiontime to heart rate in cases of constrictive peri-carditis was about 22 msec. lower than the

TABLE i Regression equation between themean right atrial pressure in mm. Hg (Y) andthe different time intervals in sec. (X), mea-sured on the jugular venous pulse tracing

y x Regression equation r p

mRA pressure Q-h Y=4599- 48-75 X -09I <OOOIQ-nadir y Y=5879- 86&i8 X -o*88 <OOOIsummit v-h wave Y= 29-62- 60o35 X - o-84 <o*ooIP2-nadir y Y=29-06-Il2-62 X -o-83 < OOOIsummit v-nadir y Y=3000-12414 X _o-64 <0 010.4 0.5 06

0-h distance of JVP (sec.)0-7 0 8 04



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TABLE 2 Multiple regression line and mul-tiple and partial correlation coefficients betweenthe mean right atrial pressure in mm. Hg, theQ-h distance in sec., and the RR interval insec.

PRAm =46-07-49-67(q-h)+0-2I RR(I2.-I6) (I2-45)

R =0-9I5 (p<O-OOI)rol-2 =-0-77rO2-1 = °°005

regression line obtained in normal subjects(Fig. 6). In patients successfully operatedupon, the left ventricular ejection time returnsto normal. The regression line obtained innormal subjects has been published previ-ously (Willems and Kesteloot, I967). The leftventricular ejection time also is largely inde-pendent of the length of the preceding RRinterval in subjects with constrictive peri-carditis during atrial fibrillation (Fig. 7). Thiscontrasts with the behaviour of the left ven-tricular ejection time during atrial fibrillationin cases with mitral disease and predominantmitral stenosis (Fig. 8). In 8 such cases thefollowing linear regression equation was cal-culated between the left ventricular ejectiontime in msec. (Y) and the natural logarithm ofthe preceding RR interval in sec./Ioo (X):Y= -I57-68+93-96 ln X (r=o845, n=65).

Q-A2 interval The behaviour of the Q-A2interval was very similar to that of the leftventricular ejection time interval. In patientswith constrictive pericarditis the value of theQ-A2 interval related to heart rate was usuallysmaller than in normal subjects, especially athigher heart rates. It also tended to return tonormal values in patients who had been suc-cessfully operated upon (Fig. 9). The regres-sion line obtained in normal subjects ismentioned in Fig. 9 and has been publishedelswhere (Kesteloot, Willems, and Joossens,i968). In patients with atrial fibrillation theQ-A2 interval showed little variation withheart rate (Fig. io), whereas this was not the

FIG. 7 Relation between left ventricularejection time (LVET) and RR interval duringatrial fibrillation in constrictive pericarditis.The left ventricular ejection time remains con-stant or shows only little variation over a widerange of preceding RR intervals. Each pointrepresents the mean of s measurements duringclosely related RR intervals. The differentsymbols used in Fig. 7, 8, IO, and iI refer todifferent patients.

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FIG. 5 The Q-h distance is nearly indepen-dent of the duration of the preceding RR inter-val during atrial fibrillation.

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FIG. 6 Relation between left ventricular ejec-tion time and heart rate in patients with con-strictive pericarditis. The ejection time returnsto normal in the patients who have beensuccessfully operated on.

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Constrictive epi- and pericarditis 679

case in patients with mitral disease and pre-dominant mitral stenosis (Fig. ii). In 7patients with mitral disease and atrial fibrilla-tion the following relation was found betweenthe Q-A2 interval in msec. (Y) and the naturallogarithm of the preceding RR interval incsec. (X): Y = -26 93 + 84605 ln X (r =o-857, n= 85).

Apex cardiogram The apex cardiogram isusually negative in cases with constrictivepericarditis (Hartman, i964) and this was alsotrue in our cases. The end of the rapid proto-diastolic upstroke of the apex cardiogramcoincides with the loud third heart sound (T3)and marks the end of the rapid protodiastolicfilling of the heart. In cases with atrial fibrilla-tion, the Q-T3 interval was independent ofthe preceding RR interval (Fig. I2).

Findings in constrictive peri-epicarditisIn 7 of the 26 patients a haemodynamicallyimportant constrictive epicarditis coexistedwith the constrictive pericarditis. As men-tioned before, in 4 cases the jugular venouspulse tracing was of type C. In 3 cases, I ofwhich was in atrial fibrillation, it was of typeB. In all 7 cases the evolution to constrictionhad occurred in less than I year after the acuteepisode during which a pericardial effusionwas often present. In none of the 7 cases wasthe pericardium calcified. In the cases with acalcified constrictive pericarditis, a proto-diastolic dip was always present in the pres-sure curve of the right ventricle, and the earlydiastolic pressure in the right ventricle at thenadir of the dip was always less than I0 mm.Hg. In cases with coexisting constrictive epi-carditis, however, the dip was either absentor the early diastolic pressure was more thanio mm. Hg (p < o-ooi).

DiscussionA dominant y trough in the jugular venouspulse tracing, known as the diastolic collapseof Friedreich (i855), is the most common find-ing in constrictive pericarditis, and this wasconfirmed in I0 out of 20 cases in sinusrhythm. During atrial fibrillation a dominanty trough is an obligatory finding. As could beexpected, a nearly normal jugular venouspulse tracing was found in cases with only asmall degree of constriction.An interesting finding in our series was the

existence of a dominant a wave with an xtrough deeper than the y trough (type C) invery severe cases of constrictive pericarditis(Fig. i). In these cases a third heart soundwas constantly absent. As the third heart

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F I G. 8 Relation between left ventricularejection time (LVET) and RR interval duringatrial fibrillation in mitral disease. In mitraldisease the left ventricular ejection time variesdirectly with the length of the preceding RRinterval.

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Heart rate (beats/min.)

FIG. 9 Relation between the Q-A2 intervaland heart rate in subjects with constrictivepericarditis. The Q-A2 interval returns tonormal in successfully operated cases.

sound in constrictive pericarditis is normallythought to signal the end of the rapid fillingof the ventricle by putting the pericardiumunder tension, the absence of such a soundwould point to the absence of a rapid fillingin protodiastole. This is confirmed by theabsence of a deep y trough or the presence ofa less steep y descent in the jugular venouspressure trace in cases with an absent thirdheart sound, as mentioned by Mounsey(I955). The presence of a dominant a wavecan be explained by a low compliance of theright ventricle in diastole, and the same factor



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could also explain the absence of a deep ytrough (Kesteloot, I963).

Constrictive epicarditis has been suggestedas a possible explanation for this abnormalbehaviour of the jugular venous pulsetracing in certain cases of constrictive peri-carditis (Kesteloot, I963), and could be thefactor causing the reduced compliance of theright ventricle. The thickening of the epicar-dium would not permit a rapid dilatation ofthe myocardium in the early diastole. This wasconfirmed by the finding of either an absentdip-plateau wave form in the pressure tracingof the right ventricle or by finding a highearly diastolic pressure in the right ventricle.The existence in these cases of only a smallpressure difference between the summit ofthe v wave in the right atrium and the nadir ofthe early diastolic right ventricular pressure isalso compatible with this explanation. More-over, in all the cases where a jugular venouspulse tracing of type C was present, a haemo-dynamically important constrictive epicarditiswas found during operation to coexist with thepericardial thickening. Similar cases where thex trough was deeper than the ytrough have alsobeen described by Gibson (i959) and Wood(I96I). They point out that the x trough isvery sharp in these cases, a fact that we areable to confirm. It is not easy, however, toformulate this sharpness in a quantitativeway. Furthermore, it is not known whetherconstrictive epicarditis was also present intheir cases. A dominant a wave with an xtrough deeper than the y trough was alsopresent in a case of constrictive peri-epicar-ditis published by Gibbons, Goldbloom, andDobell (I965).The presence of a dominant a wave in the

jugular venous pulse or right atrial pressuretracing and of a high early diastolic pressurein the right ventricle is found in different formsof myocardial fibrosis. These features havebeen described as the best means to differen-tiate between this disease and constrictivepericarditis (Wood, I96I; Storstein, I966;Somers et al., I968). Higher early diastolicpressures in constrictive pericarditis than inmyocardial fibrosis have, however, also beendescribed (Nye et al., I957). The presentstudy shows that these signs are unreliablefor the differential diagnosis between thesedifferent conditions when constrictive epi-carditis is also present. This can be explainedby the similar behaviour of the myocardiumduring diastole in myocardial fibrosis andconstrictive epicarditis.The Q-h interval in the jugular venous pulse

tracing is shortened in constrictive peri-carditis, due to the abrupt early end of ven-

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FIG. IO Relation between Q-A2 and RRinterval during atrial fibrillation in constrictivepericarditis. The Q-A2 interval remains con-stant over a wide range of preceding RR inter-vals. Each point represents the mean of 5measurements during closely related RRintervals.

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FIG. II Relation between Q-A2 and RRinterval during atrial fibrillation in mitraldisease. In cases with mitral disease and pre-dominant mitral stenosis the Q-A2 intervalvaries directly with the length of the precedingRR interval.

tricular filling (Hartman, I960; Kesteloot,I963). In normal subjects its duration is about740 msec., and it is constantly less than 6oomsec. in severe cases of constrictive peri-carditis.Our study has shown that a strong correla-

tion exists between the Q-h interval and themean right atrial pressure in this disease. Thesame is true of various other reference pointsof the jugular venous pulse tracing but to a

lesser degree (Table i). These other referencepoints, however, can be of interest in cases

where the h wave cannot be distinguished, as

sometimes happens with a rapid heart rate.

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Constrictive epi- and pericarditis 68i

The correlation between the mean right atrialpressure and the Q-h wave is not due to theheart rate alone, as multiple regression analy-sis has shown (Table 2).

Moreover, the Q-h interval, the Q-A2 inter-val, and the left ventricular ejection time areremarkably independent of heart rate and re-main nearly constant during atrial fibrillationin each individual case of constrictive peri-carditis (Fig. 5, 7, io). This could be expectedbecause the filling of the heart is only possibleto a constant end-diastolic volume, indepen-dent from the duration of diastole. The highvenous pressure, moreover, permits a com-plete filling of the constricted ventricle evenduring a short diastole. This behaviour differ-entiates constrictive pericarditis from heartinsufficiency due to valvular heart disease(Fig. 8, ii). In these cases a steep decrease inthe mentioned time intervals occurs during ashort diastolic interval. A further study of thisproblem in other cases of heart disease andespecially of myocardial fibrosis will be ofinterest. Preliminary results show that incases of congestive cardiomyopathy, the q-A2interval and the left ventricular ejection timeduring atrial fibrillation vary with the lengthof the preceding RR interval in a similarmanner as the cases of valvular heart diseasestudied above. Both the left ventricular ejec-tion time and the Q-A2 interval are shortenedin cases ofconstrictive pericarditis. This canbeexplained by a smaller stroke volume in thisdisease. The values return to normal in caseswhich have been successfully operated (Fig. 6,9). The Q-h interval also returns to normalvalues in these subjects.A negative apex cardiogram was found

whenever it could be recorded, and this hasalso been found by Hartman (I964). In ouropinion this is due to the negative pressurein the pericardial sac during systole, whichcauses the atmospheric pressure to push thethoracic wall inward at the place of the apexbeat. During early diastole a pronouncedrapid filling wave occurs, the end of whichcoincides with the third heart sound. Theinterval Q-end of the early diastolic ascent isalso independent of the preceding diastolicinterval (Fig. I2).

In I95I, Gonin, Froment, and Gravierdescribed a peculiar form of pericarditis witha rapid evolution toward constriction andwith haemodynamically important epicardialinvolvement. This has been confirmed byothers (Soulie et al., I958; Gibbons et al.,I965). and by the present study. In all ourcases of coexisting constrictive epicarditis theinterval between the acute episode and thediagnosis ofconstriction was less than one year.

R-R:q -T3:

VOD.D 57.956 t

FIG. 12 Relation between Q-EDS and RRinterval during atrial fibrillation in constrictivepericarditis. Negative apex cardiogram inconstrictive pericarditis. The protodiastolicrapid upstroke ends at the time of occurrenceof the early diastolic sound, signalling the endof the rapid ventricular filling.

From the study of our material it appearsthat the presence of a constrictive epicarditisis strongly suggested by: (i) a rapid evolutiontoward constriction of the disease in theabsence of pericardial calcification; (2) adominant a wave and a deep x trough in thejugular venous pressure trace; (3) an absentthird heart sound; and (4) a high early dias-tolic right ventricular pressure.A clinical differentiation between the two

forms of constrictive heart disease with andwithout constrictive epicarditis thus becomespossible. This differentiation is importantbecause the mortality at operation was muchhigher and the operation more difficult in thecases with constrictive epicarditis.

ReferencesAcar, J., and Godeau, P. (i960). Des difficultes du

diagnostic dans les pericardites constrictives.Revue du Praticien, IO, I423.

Friedreich, N. (I855). Ueber den diastolischen Venen-kollaps. In Handbuch der speciellen Pathologie undTherapie. Ed. by R. Virchow.

Gibbons, J. E., Goldbloom, R. B., and Dobell, A. R. C.(I965). Rapidly developing pericardial constrictionin childhood following acute nonspecific pericar-ditis. American Journal of Cardiology, I5, 863.

Gibson, R. (i959). Atypical constrictive pericarditis.In Proceedings of The British Cardiac Society.British Heart Journal, 21, 583.

Gonin, A., Froment, R., and Gravier, J. (ig5i). Lesepicardo-pericardites tuberculeuses a evolutionconstrictive subaigue. J'ournal de Medecine de Lyon,32, I049.

Gunnar, R. M., Dillon, R. F., Wallyn, R. J., andElisberg, E. I. (i955). The physiologic and clinicalsimilarity between primary amyloid disease of theheart and constrictive pericarditis. Circulation, 12,827.

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68z Kesteloot and Denef

Hartman, H. (I960). The jugular venous tracing.American Heart Journal, 59, 698.

- (I964). Phonocardiography and pulse tracings.(In Dutch.) Thesis. De Kempenaer, Leiden.

Kesteloot, H. (1963). Study of the right ventricularhaemodynamics through the jugular venous pulsetracings and the right apexcardiogram. (In Dutch.)Thesis. Arscia ed., Brussels.

- , Willems, J., and Joossens, J. V. (I968). A studyof some determinantts of the q-A2 and q-upstrokeinterval. In Proceedings of the 5th European Congressof Cardiology, Athens, pp. 305-3I2.

- , -, and van Vollenhoven, E. (I969). On thephysical principles and methodology of mechano-cardiography. Acta Cardiologica, 24, 147.

Kussmaul, A. (I873). Ueber schwielige Mediastino-Pericarditis und den paradoxen Puls. BerlinerKlinische Wochenschrift, I0, 433, 445, and 46I.

Mounsey, P. (1955). The early diastolic sound of con-strictive pericarditis. British Heart Journal, 17, 143.

Nye, R. E., Lovejoy, F. W., and Yu, P. N. (I957).Clinical and hemodynamic studies of myocardialfibrosis. Circulation, I6, 332.

Pick, F. (I896). Ueber chronische, unter dem Bildeder Lebercirrhose verlaufende Pericarditis. Zeit-schriftfiir Klinische Medizin, 29, 385.

Shillingford, J. P., and Somers, K. (I96I). Clinical andhaemodynamic patterns in endomyocardial fibrosis.British Heart Journal, 23, 433.

Somers, K., Brenton, D. P., D'Arbela, P. G., Fowler,J. M., Kanyerezi, B. R., and Sood, N. K. (I968).Haemodynamic features of severe endomyocardialfibrosis of right ventricle, including comparisonwith constrictive pericarditis. British Heart_Journal,30, 322.

Soulie, P., Chiche, P., and Acar, J. (I958). Pericarditeschroniques et constriction pericardique. PresseMidicale, 66, 579.

Storstein, 0. (i966). Hemodynamic studies in primarymyocardial disease. Acta Medica Scandinavica,Suppl. 472, p. 113.

White, P. D. (i944). Heart Disease, 3rd ed., pp. 655-668. Macmillan, New York.

Willems, J., and Kesteloot, H. (I967). The left ven-tricular ejection time. Its relation to heart rate,mechanical systole and some anthropometric data.Acta Cardiologica, 22, 401.

Wood, P. (I956). Diseases of the Heart and Circulation,2nd ed., pp. 665-673. Eyre and Spottiswoode,London.

- (I96I). Chronic constrictive pericarditis. Ameri-can Journal of Cardiology, 7, 48.



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