relation arterial blood pressure to transverse diameter...

Relation of Arterial Blood Pressure to theTransverse Diameter of the Heart in

C-ompensated Hypertensive Heart DiseaseBy ELI A. RAMIREZ, M.D., F.A.C.P., AND PEDRO H. GARcGA PONT, M.D.

T HE CURRENT concept regarding theclinical manifestations and complications

of hypertensive heart disease is that they aredue to a high diastolic pressure rather than toa high systolic pressure.' It is well known,however, that hypertensive patients usuallyexhibit elevation of both the systolic and thediastolic pressures. In fact, the systolic pres-sure is frequently more elevated than thediastolic pressure and the pulse pressure isincreased.A recent actuarial study has shown that at

any level of diastolic pressure mortality in-creases progressively with increases in systol-ic pressure.2 Within the blood pressure rangestudied it was shown that the adverse effectsof a high systolic pressure are greater thanthose of a high diastolic pressure. These ob-servations indicate that systolic pressure ele-vation, which has been generally regarded as

an innocent bystander of diastolic hyperten-sion, may have adverse clinical significanceof its own.3The object of the present study is to deter-

mine the association of systolic and diastolicpressures with the size of the heart in a largegroup of hypertensive patients. This wouldenable a distinction between the separate ef-fects of both pressures upon a manifestationof hypertensive heart disease which is associ-ated with significant morbidity and mortality.

Materials and Methods

The data were collected in nine Veterans Ad-

From the Medical Service, Veterans AdministrationHospital and the Department of Medicine, Universityof Puerto Rico School of Medicine, San Juan, PuertoRico.

Presented in part at the Fourth World Congress ofCardiology, Mexico City, October, 1962.

542

ministration's hospitals* which are collaboratingin a study of antihypertensive drugs. All patientswere hospitalized male veterans who satisfied thecriteria of the original protocol as published pre-

viously.4 No selection was made except for theexclusion of patients with surgically curable hy-pertension, malignancy, uremia, or other condi-tions that would interfere with adequate follow-up observations.The blood pressures were taken four times

daily in the sitting position. Only patients whosediastolic blood pressure averaged 90 mm. Hg or

above from the fourth through the sixth hospitalday were included in the study. The diastolicpressure was read at the point of disappearanceof all sounds.The transverse diameter of the heart was meas-

ured in the conventional teleroentgenogram andcorrected according to the Ungerleider table.5Cardiac volume was calculated according to themethod of Musshoff and Reindell.6The analysis of the data was done with an

automatic IBM computing system. The statisticalformulas to calculate correlation coefficients, sig-nificance of correlation coefficients, significance ofdifferences, and exclusion of partial effects were

taken from standard reference sources.7 8 Differ-ences of probability greater than p = 0.05 were

not considered significant.

ResultsThe correlation coefficients ("r") between

systolic pressure, diastolic pressure, and cor-

rected transverse diameter in 535 compensat-

ed hypertensive patients are shown in table1. Although, as shown by the p values, thecorrelation coefficients between the pressures

and the transverse diameter are highly sig-nificant, the degree of association they express

is relatively small.

* Brooklyn; Chicago, West Side; Iowa City; Okla-homa City; Richmond, Virginia; San Juan, PuertoRico; Seattle; Washington, D. C.; West Roxbury,Massachusetts.

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TRANSVERSE DIAMETER OF HEART

Table 1

Correlation Coefficients ("r"') between Systolic Pressure, Diastolic Pressure, and Cor-rected Transverse Diameter in 535 Compensated Hypertensive Patients

Systolic vs. corrected transverse diameter + 0.310 (p < 0.001) = r13Diastolic vs. corrected transverse diameter + 0.209 (p < 0.001) = r12Systolic vs. diastolic + 0.764 (p <0.001) =r23

The calculated lines of regression and thestandard errors of the estimates for the rela-tion between the transverse diameter andboth pressures are shown in figures 1 and 2.The slopes of the lines are small, showingthat both pressures are poor predictive in-dices of transverse diameter. The slightlysmaller standard error of the estimate givenby the systolic pressure is consistent withrelatively less scatter of heart size for thesystolic than for the diastolic pressure.

In order to determine if the degree of asso-

ciation between the systolic pressure and thetransverse diameter ("r" = + 0.310) is signifi-cantly greater than that between the diastolicpressure and the transverse diameter ("r"+ 0.209), the data were analyzed with use of

Kt

KR

(14

130

120

110

100

90

80

(146) 0 0

0(44) (14)

(100)

..

.-1... N 535

0-00" r = .310

Y' 81.45 + .1588X

S.E.- 11 82

120 140 160 180 200 220 240

SYSTOLIC PRESSURE (mm.Hg)Figure 1

The relationship of the corrected transverse diameterwith the systolic blood pressure. Corrected transversediameter is expressed as percentage of normal. Thesolid line is the calculated line of regression and theinterrupted lines are the boundaries of the standarderror of the estimate. The dots are the distributioncenters of each class interval and the numbers inparentheses are the patients in each interval.


L(J

130

120

110

100

9 0

80

_9s- ~~~~~~~~~(5'

........ 1((35)

(158) (113) (62)

(151)

N = 535r .209

Y 87.62 + .1874 X

S.E. X 1 2.16

90 100 110 120 130 140 150

DIASTOLIC PRESSURE (mm.Hg)Figure 2

The relationship of the corrected transverse diameterwith the diastolic blood pressure. Corrected transversediameter is expressed as percentage of normal. Thesolid line is the calculated line of regression and theinterrupted lines are the boundaries of the standarderror of the estimate. The dots are the distributioncenters of each class interval and the numbers inparentheses are the patients in each interval.

a formula suggested by McNemar.9 This for-mula can be applied to correlated data as inthe present instance.* Calculation of the dataof table 1 gives a "t" value of 3.56, which indi-cates that the difference between both correla-tion coefficients is significant at a p <0.001level.The data were also analyzed by comparing

the mean transverse diameters of groups seg-

regated according to the medians of systolicand diastolic pressure. The results are shownin table 2. The differences in mean transverse

*The formula is

(rI2- r13) /(N-3) (l+r23)t=/2 ( 1-r122-r132-r232 + 2 r12 r13 r23

543

O.-

o.0--loO..0000"

-.0-0010


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RAMIREZ, GARCIA PONT

Table 2

Differences between Mean Corrected Tranverse Diameters of 535 HypertensivePatients When Grouped According to the Medians of the Systolic and Diastolic Pressures

Number of paticntsMean corrected transverse diameterDifference

S.E.p

Difference between differencesS.E.p

The median diastolic pressure was 107 mm.mm. Hg.

diameters are very significant regardless of thepressure used. However, the difference is sig-nificantly greater for the systolic than for thediastolic pressure (p < 0.01). This evidencealso points to a significantly greater associa-tion of the transverse diameter with the sys-tolic than with the diastolic pressure.

Because of the strong correlation betweensystolic and diastolic pressure ("r" - + 0.764),an attempt was made to determine the inde-pendent association of each pressure with thetransverse diameter. The formula excludesmathematically the partial effect of each pres-sure.* When the calculation is done with thedata of table 1, the correlation coefficientwhich remains after the exclusion of the partialeffect of diastolic pressure is + 0.238, which issignificant at a p < 0.001 level. However, afterthe exclusion of the partial effect of systolicpressure, the correlation coefficient which re-mains for the association between diastolicpressure and transverse diameter is -0.045,which is not significant.The combined correlation of both the sys-

tolic and diastolic pressures with the trans-verse diameter was also determined by cal-culating the multiple correlation coefficient"R." The multiple correlation coefficient forour data is +0.313. It will be noted that this

*The formula is

r12.3 =r12- (rI3 r23)

Diastolic pressureMedian I > Median

280 255106.48% 109.63%

3.15%1.083

< 0.005

Systolic pressureMedian t > Median

275 260104.54% 111.62%

7.08%1.036

<0.0013.93%1.499

<0.01

Hg and the median systolic pressure was 164

coefficient is practically the same as the cor-relation coefficient of the systolic pressurealone with the transverse diameter.The results suggest that the diastolic pres-

sure is not truly associated with the transversediameter. In other words, the correlation be-tween diastolic pressure and transverse diam-eter may be significant only because mostindividuals who have diastolic hypertensionalso have systolic hypertension, and it is thelatter pressure that carries the correlation withthe transverse diameter.

If systolic pressure correlates better thandiastolic pressure with the transverse diam-eter, pulse pressure should also correlate posi-tively with the transverse diameter. To testthis point the correlation coefficient betweenpulse pressure and transverse diameter wvascalculated in the 535 patients. The coefficientobtained was +0.269, which is highly signifi-cant (p < 0.001).The correlation coefficient was also calculat-

ed between the transverse diameter and amean pressure estimated according to theformula: mean pressure - diastolic pressure+ pulse pressure. The value obtained was

3+ 0.277, which falls between the values fordiastolic pressure and systolic pressure.The relationship of age to the correlation

between systolic pressure and transverse di-ameter is shown in table 3. As shown by the pvalues, these correlation factors are highly

Circulation, Volume XXXI. April 1965

/(I -rI32) (1-r232)

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Table 3

Correlation Coefficients ("r") between Systolic Pressure, Corrected Transverse Diameterand Age in 535 Compensated Hypertensive Patients

Systolic vs. corrected transverse diameterAge vs. corrected transverse diameterSystolic vs. age

significant although the degree of associationthey express is relatively small. The resultsadmit the possibility that age might be theunderlying reason for the relationship be-tween systolic pressure and transverse diam-eter.

Correlation coefficients are inaccurate whenthe distribution of one of the variables is ab-normal. The 535 patients exhibit the bimodalage distribution characteristic of the veteranpopulation. There are peaks at 42.0 and 62.26years corresponding to the major armed con-

flicts. These peaks introduce a lack of homo-scedasticity in the age axis of the scattergramand therefore restrict the significance of thecorrelation coefficients obtained.

In order to determine if age is the under-lying reason for the association between sys-

tolic pressure and transverse diameter, the re-

RK.-l115

110

105

100

95

5 %

I M T S

30 -40 60 -70

AGE (yrs.)

Figure 3

The mean transverse diameter in 99 patients of 30to 40 years of age and in 155 patients of 60 to 70years of age when each group is divided into thosewith a systolic pressure either above or below 160mm. Hg. Corrected transverse diameter is expressedas percentage of normal.


lationship was studied in two different age

groups selected arbitrarily (fig. 3). The firstgroup consisted of 99 patients of 30 to 40years of age and the second of 155 patientsof 60 to 70 years of age. In the first group

there were 43 patients with a systolic pressure

above 160 mm. Hg and 56 patients with a

systolic pressure below 160 mm. Hg. In thesecond group the corresponding figures were

102 and 53 patients. Within each group thosepatients with the higher systolic pressures

had significantly greater transverse diametersthan those patients with the lower systolicpressures. The levels of significance were p

< 0.001 in the 30 to 40 year group and p <0.002 in the 60 to 70 year group.

DiscussionFrom the point of view of the complications

associated with increase in the transverse di-ameter of the heart, the findings of the pres-

ent study are inconsistent with the impor-tance customarily given to diastolic pressure

in the evaluation of the cardiac status ofhypertensive patients. In fact, calculation ofthe index of forecasting efficiency indicatesthat in predicting the transverse diameter, thediastolic pressure increases the efficiency byonly 2.2 per cent. The systolic pressure is alsoquite poor for this purpose. The same calcula-tion indicates that the systolic pressure

increases the efficiency for predicting thetransverse diameter by only 4.37 per cent.Therefore, although the transverse diameter issignificantly better associated with the systolicthan with the diastolic pressure, the differenceis of little practical importance in individualpatients. Nevertheless, if one pressure were

to be chosen to evaluate this particular aspectof the cardiac status of hypertensive patients,it would have to be the systolic rather thanthe diastolic pressure.

+ 0.310+ 0.225+ 0.1708

(p < 0.001)(p < 0.001)(p < 0.001)

= r12= r23= rl3

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The accuracy of the methods used in thepresent investigation needs to be considered.It was already reported4 that in patients ofthe present study treated double blind withplacebos, the baseline blood pressure deter-mined as described previously was almostidentical to the average blood pressure ob-tained daily by the patients in their homes.This observation indicates that the baselinepressure here used represents a fair approx-imation to the usual blood pressure to whichthe patients are exposed.

It has long been known that arterial bloodpressure cannot be measured with precisionby a pneumatic cuff manometer. Nevertheless,because of the convenience and simplicity ofthe auscultatory method, it is generally re-garded as an adequate bedside procedure toestimate blood pressure.There is uniform agreement that the sys-

tolic pressure should be read at the start ofsounds. In practice there is little difficulty inrecognizing this point. In the case of thediastolic pressure, although it is generally ac-cepted that the disappearance of all sounds isthe best index,'0 agreement is not universal."Under certain hemodynamic circumstances,cessation of sounds does not occur and themuffling of sounds must be used as the endpoint. In practice there is no question that attimes it is difficult to determine where thesounds disappear and then it is necessary touse the muffling point.

It is possible that enough such instances mayhave occurred in the large number of observa-tions of the present study to increase signifi-cantly the scatter of the diastolic pressure de-terminations over that of the systolic pressure.It has been shown, however, that the meanerror of determination of clinical blood pres-sure measurement is similar for both systolicand diastolic pressures.10 In our data thestandard error of the estimate to predict pres-sure from heart size is 23.04 mm. Hg for thesystolic pressure and 13.56 mm. Hg for thediastolic pressure. This indicates that the vari-ability of the systolic pressure is considerablylarger than that of the diastolic pressure. Forthese reasons it seems unlikely that error of

determination can account for the significant-ly different association of both pressures withthe transverse diameter.The transverse diameter was used as a

measure of heart size because it was practicaland feasible to standardize its determinationin the participating hospitals. Admittedly, theaccuracy of the method is less than that at-tainable with other methods such as biplaneangiography. On the other hand, other meth-ods do not lend themselves as well to applica-tion in many subjects in different institutions.The large number of observations made pos-sible by the use of the transverse diametercompensates in part for the inaccuracy of themethod by diminishing the statistical standarderrors.An estimate of the relative accuracy of the

transverse diameter may be obtained fromthe following comparisons. In a sample of 101patients of the present study the correlationcoefficient between transverse diameter andcardiac volume was + 0.802 (fig. 4). Thisindicates a rather satisfactory agreement be-tween the transverse diameter and a measureof heart size, which is generally considered tobe more exact. In a sample of 41 unselectedpatients not of the present study who died in

2000

1800

1600

'S

Nj

0t

1400

1200

1000

800

600

400

200

N 101r = .802

Y =- 749.99 +010939) XS.E. 139.6

11 12 13 14 15 16 17 It

TRANSVERSE DIAMETER (cms.)

Figure 4

is 19 20

The scattergram of transverse diameter versus heartvolume in 101 hypertensive patients showing regres-sion line and standard error of the estimate.


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700

S 600-

x 500

400

3:X 001

200

N = 4 1

r- 882

Y'= - 224.48tX (46.

S.E = 61.79

112 13 14 15 16 17 18 19 20

TRANSVERSE DIAMETER (cms.)

Figure 5

The scattergram of the transverse diameter versus

empty heart weight in 41 unselected males showingregression line and standard error of the estimate.

our hospital within 6 months after having a

teleroentgenogram, the transverse diameterwas correlated with the actual weight of theempty heart at autopsy (fig. 5). The correla-tion coefficient obtained was +0.882 and thestandard error of the calculated line of re-

gression was 61.79 Gm. This compares with a

standard error of 23.3 Gm. which Dodge etal.12 obtained for the prediction of left ven-

tricular mass using biplane angiography. Thecomparison is not too unfavorable, since theangiographic studies were done postmortemon hearts under controlled conditions. Biplaneangiography is regarded as the most accurateavailable method to determine left ventricularmass in vivo.

In view of these observations it seems un-

likely that the poor correlations betweenpressures and transverse diameter obtainedin the present study can be explained on thebasis of relative inaccuracy of the measure-

ments. It is worth noting that comparably lowlevels of correlation which barely suggest a

linear relationship have been reported in ana-

tomopathologic studies of mean pressure andleft ventricular weight.'3 The obvious con-

clusion is that the association between cardiacsize and hypertensive disease is in all proba-Circulation, Volume XXXI, April 1965

bility a multifactorial complex in which thelevel of pressure is but one of the importantcomponents.

It is generally believed that, barring thepossibility of intrinsic myocardial changes,heart size increase in hypertension is prob-ably the result of increased cardiac work.Cardiac work may be expressed according tothe formula :14

Work =static + Kinetic

component component

W = QR + M(V) Kg. m./sec.2gWVhereW = work in Kg. m./sec.

Q = cardiac output in liters/sec.R = mean pressure in meters.M = blood mass expelled in Kg./sec.V = blood velocity in meters/sec.g = gravity constant (9.81 m./sec.)

The static component is usually consideredto be the major factor of cardiac work. Theformula shows the reason why an increase inpressure results in an increase in cardiac work.It should be noted, however, that an increasein flow can also result in an increase in cardiacwork.

Sarnoff et al.15 have shown that externalcardiac work is directly proportional to myo-cardial oxygen consumption only when theincrease in work is due to increase in meansystolic pressure. When the increase in ex-ternal wvork is due to increase in flow, theoxygen consumption is not increased and theratio of extrinsic work to oxygen consumptionindicates a high external myocardial efficiency.In contrast, systolic hypertension causes anincrease in oxygen consumption which leadsto relative myocardial hypoxia. The ratio ofextrinsic work to oxygen consumption is de-creased, indicating a low external myocardialefficiency.

After differentiating experiments Sarnoff etal.15 found that the mean systolic pressure isnot the fundamental determinant of myocar-dial oxygen consumption. Myocardial oxygenconsumption actually correlates best with thetension-time index which is defined as theproduct of the mean systolic pressure and the

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duration of the tension state. Nevertheless,these authors observed in their flow experi-ments that whenever there was an incrementin myocardial oxygen consumption, it wasconsistently a function of the associated in-crement in aortic systolic pressure; this wastrue at different ranges of cardiac output,flow, and pressure.Burch et al.'6 have shown that the structure

and mechanisms of the normal heart are suchthat it exerts less force per unit cross sectionat the end of systole than at the isometricphase of contraction. Therefore, at the endof systole the normal heart consumes lessoxygen and economizes effort even thoughthe internal tension is higher. This economyis possible because according to the law ofLaplace, the shortening of the integrated ven-tricular radii of curvature during systole per-mits the development of more internal tensionwith less force and less oxygen consumption.

In the pathologically dilated heart, the in-tegrated ventricular radii of curvature do notshorten enough at the end of systole to permitan economy of energy. The wall is at amechanical disadvantage. The total internalsystolic tension cannot be developed unlessthe force per unit of cross section increasesand more oxygen is consumed. If systolichypertension is present, it adds its own in-creased oxygen consumption to that requiredby the dilatation.

Linzbach17 believes that the ratio of oxygenconsumption to heart mass is one of the mostimportant biologic settings of the body. Heis of the opinion that for any level of oxygenconsumption there is an optimal amount ofheart muscle which yields the maximum en-ergy economy. Therefore, when oxygenconsumption is increased, the stimulus to hy-pertrophy may reside in an adjustment mech-anism which restores the best energy economyratio of heart mass to oxygen consumption byincreasing the heart mass.These concepts are in agreement with the

findings of the present study. They point tothe systolic load rather than the diastolic loadas the one principally responsible for the en-largement of the heart in hypertensive dis-

ease. Unquestionably, there are other factorsinvolved among which may be mentioned met-abolic changes in the myocardium, neuro-hormonal mechanisms, and those factors lead-ing to cardiac dilatation. It is difficult toquantitate their effects, particularly under thechanging circumstances of daily life. Irrespec-tive of other factors, the findings of the pres-ent study suggest that systolic pressure ratherthan diastolic pressure is relatively importantin determining clinical cardiac enlargementin hypertension.

In view of these observations, the questionwhy hypertensive patients exhibit more orless systolic hypertension for any given levelof diastolic pressure may have considerableimportance. A possible explanation is the well-known fact that when the distensibility of thelarge arteries is reduced, systolic pressure in-creases. The reduced distensibility could bedue to the same process that increases theperipheral resistance or to arteriosclerosis. An-other possible explanation is that the level ofsystolic pressure may depend on cardiachemodynamic changes that affect pressureand flow in hypertension.'8 Overfilling of theaorta with blood under increased pressuremay lead to a maximal stretching of the aorticwall, which restricts further distention. Thefindings of the present study do not clarifythis question, although the fact that the as-sociation of the systolic pressure with thetransverse diameter is independent of agemight suggest that a degenerative process isnot involved.

Cardiac enlargement is accepted as a sig-nificant prognostic index in hypertensive dis-ease. In untreated patients, graded degreesof cardiac enlargement have been associatedwith progressively higher mortality rates ir-respective of age and sex.19 In our own ex-perience, hypertensive patients in congestiveheart failure have larger hearts than thosewithout. In addition, those patients who havesignificantly larger hearts tend to go morefrequently into congestive heart failure thanthose who do not. In view of these observa-tions the relationship between systolic pres-sure and cardiac enlargement appears to be of


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clinical importance in the diagnosis, progno-

sis, and therapy of hypertensive patients. Itis considered likely that this relationship may

account in part at least for the actuarial dataquoted at the beginning of this article, whichlink progressive increases of systolic hyper-tension with a higher mortality.

Summary

In 535 male hypertensive patients thecorrelation coefficient between the correctedtransverse diameter of the heart and the sys-

tolic pressure was +0.301. With diastolic pres-

sure the correlation coefficient was +0.209.Both coefficients were significant (p <0.001),but the association between the variables was

quite small in both correlations. The correla-tion between the corrected transverse diam-eter and the systolic pressure was significant-ly better than with the diastolic pressure,

(p < 0.001). The correlation between thecorrected transverse diameter and the systolicpressure was independent of age.

Conclusion

From the point of view of the complicationsassociated with increase in the transverse di-ameter of the heart, the findings presented are

inconsistent with the importance customarilygiven to diastolic pressure in the evaluationof the cardiac status of hypertensive patients.Both systolic and diastolic pressures correlatepoorly with the transverse diameter of theheart. Nevertheless, if one pressure were tobe chosen to evaluate this particular aspectof the cardiac status of hypertensive patients,it would have to be the systolic rather thanthe diastolic pressure.

These findings agree with physiologic con-

cepts that link systolic pressure, oxygen con-

sumption, cardiac mechanics, and the size ofthe heart. If diminished aortic distensibilityor hemodynamic cardiac changes are involvedin the pathogenesis of a high systolic pressure,

they may represent significant adverse factorsin hypertensive disease.

Since cardiac enlargement is a significantprognostic factor in hypertensive disease, thefindings of the present study may explain, at


least in part, the reported association betweenprogressive increases of systolic hypertensionand a higher mortality. By the same token,the relationship between systolic hypertensionand cardiac enlargement appears to be asignificant clinical observation in the diagno-sis, prognosis, and therapy of hypertensivepatients.

AcknowledgmentI am indebted to Dr. Edward Freis for his helpful

criticism and stimulating support, and acknowledgethe help of Mrs. Esther V. Aviles and Mrs. CarmenC. Rivera in the secretarial and statistical work.

References1. FRIEDBERG, C. K.: Diseases of the Heart. Ed. 2.

Philadelphia, W. B. Saunders Company, 1956,p. 921.

2. Build and Blood Pressure Study. Society of Ac-tuaries, Vol. 1, 1959; Vol. 2, 1960.

3. GUBNER, R. S.: Systolic hypertension: A patho-genetic entity. Significance and therapeuticconsideration. Am. J. Cardiol. 9: 773, 1962.

4. Veterans Administration cooperative study on an-tihypertensive agents: A double blind controlstudy of antihypertensive agents. I. Compara-tive effectiveness of reserpine, reserpine andhydralazine, and three ganglionic blockingagents, chlorisondamine, mecamylamine, andpentolinium tartrate. Arch. Int. Med. 106: 81,1960.

5. UNGERLEIDER, H. E., AND CLARK, C. P.: Astudy of the transverse diameter of the heartsilhouette with prediction table based on theteleoroentgenogram. Am. Heart J. 17: 92, 1939.

6. MUSSHOFF, K., AND REINDELL, H.: Radiographicexamination of the heart in the erect andlying position. The influence of the body posi-tion on heart volume. Deutsche medWchnschr. 81: 1001, 1956.

7. BRADFORD, H. A.: Principles of Medical Statis-tics. Ed. 6. New York, Oxford UniversityPress, 1956.

8. DOWNIE, N. M., AND HEATH, R. W.: Basic Statis-tical Methods. New York, Harper, 1959.

9. MCNEMAR, Q.: Psychological Statistics. Ed. 2.New York, John Wiley & Sons, Inc., 1955,p. 148.

10. BoRDLExY, J., III, CONNOR, C. A. R., HAMILTON,W. F., KERR, W. J., AND WIGGERS, C. J.:Recommendations for human blood pressuredetermination by sphygmomanometer. Circu-lation 4: 503, 1951.

11. BURTON, A. C.: Peripheral circulation. Ann. Rev.Physiol. 15: 213, 1953.

12. DODGE, H. T., RACKLEY, C. E., COBLE, Y. D.,

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JOHNSTON, R. R., AND HAY, R. E.: Deter-mination of left ventricular mass in man. Cir-culation 26: 708, 1962.

13. JONES, R. S.: Weight of the heart and its cham-bers in hypertensive cardiovascular diseasewith and without failure. Circulation 7: 357,1953.

14. WIGGERS, C. J.: Physiology in Health and Dis-ease. Ed. 5. Philadelphia, Lea and Febiger,1949.

15. SARNOFF, S. J., BRAUNWALD, E., WELCH, G.H., JR., CASE, C. B., STAINSBY, W. N., ANDMACRUZ, R.: Hemodynamic determinants ofoxygen consumption of the heart with specialreference to the tension time index. Am. J.Physiol. 192: 148, 1958.

16. BuRCH, G. E., RAY, C. T., AND CRONVICH, M. S.:Certain mechanical peculiarities of the hu-man cardiac pump in normal and diseasedstates. Circulation 5: 504, 1952.

17. LINZBACH, A. J.: Heart failure from the point ofview of quantitative anatomy. Am. J. Cardiol.5: 370, 1960.

18. SALANS, A. H., KATZ, E. N., RAHAM, G. R.,GORDON, A., ELISBERG, E. J., AND GERBER, A.:A study of the central and peripheral arterialpressure pulse in man. Correlation with si-multaneously recorded electrokymograms. Cir-culation 4: 510, 1951.

19. SOKOLOW, M., AND PERLOFF, D.: The prog-nosis of essential hypertension treated con-servatively. Circulat on 23: 697, 1961.

Historical Perspective

Some scientists regard an interest in the history of their subject as inere antiquarian-ism, and it may be that the very remote past consists largely of mistakes to be avoided.But it deserves to be remembered that the history of any scientific discipline intimatelydetermines the current-modes of investigation. The frames of reference which appeareligible at any given epoch, the instruments accepted as respectable, and the types of"fact" taken to have evidential value are historically conditioned. To pretend otherwiseis to claim for human reason, as manifested in scientific progress, a universality andfixity it has never manifested.-MAx BLACK. The Definition of Scientific Method, Sci-ence and Civilization, Edited by ROBERT C. STAUFFER, The University of WisconsinPress, Madison, 1949.


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ELI A. RAMIREZ and PEDRO H. GARCIA PONTCompensated Hypertensive Heart Disease

Relation of Arterial Blood Pressure to the Transverse Diameter of the Heart in

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1965 American Heart Association, Inc. All rights reserved.

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