The effect of chronic pulmonary hypertension on left ventricular size, function, and interventricular septal motion

The effect of chromic pukmnwy on left wen&icular size, function, inter ventricular s8pQal motion

hypertension and

The effect of right ventricular pressure overload secondary to chronic pulmonary arterial hypertension on left ventricular size and function and on kterventrkular septal motion was studied in 13 patients in whom coronary artery disease, hypertension, and hypoxemia were excluded. Regional and global left ventricular function were assessed by computer-assisted analysis of two-dimensional directed M-mode echocardiograms obtained within 24 hours of a hemodynamlc study. Septal position and motion were further analyzed by delineating seven points along the right and left sldes of the septum during a single cardiac cycle. All echocardlographk data were compared to those of 10 normal subjects. Mean values for right ventricular systolic, mean pulmonary artery and pulmonary capiltary wedge pressures were: 71 + 26 mm Hg, 46 _+ 16 mm Hg, and 7 f 1 mm Hg, respective& Septel motion was interpreted from the M-mode echocardlograms as normal In seven patients (group I) and abnormal in the remaining six patients (group II). The only hemodynamic parameter which distinguished these two patterns was AP, the transseptal systolic pressure gradlent across the interventricular septum, which was significantly different (p < 0.02) in group I (AP = 66 f 16 mm Hg) from that of group II (AP = 21 + 24 mm Hg). As a result of abnormal septal position, the septal-free wall dimensions of the left ventricle were reduced, but there was no evidence of depressed left ventricular performance in these patients. We conclude that resting left ventricular function Is well preserved in patients with pulmonary hypertension, despite significant alterations in septal posltion and left ventricular size. Abnormal septal motion In patients with right ventricular pressure overload is related to changes in the pressure gradlent across the Interventricular septum. (AM HEART J lg67;113:1114.)

Marie11 Jessup, M.D., Martin St. John Sutton, M.B., M.R.C.P., Karl T. Weber, M.D., and Joseph S. Janicki, Ph.D. Philadelphia, Pa., Boston, Mass., and Chicago, Ill.

In 1910, Bernheim’ suggested that left ventricular hypertrophy or dilatation might compromise the performance of the right ventricle by a displacement of the interventricular septum to the right, interfering with right ventricular outflow. More recently, Dexter2 postulated that the development of abnormal left ventricular function in patients with atria1 septal defect could be accounted for by an abnormal septal position and a concomitant decrease in the septal contribution to, as well as interference with, left ventricular ejection! the so-called “reverse Bernheim effect”. Subsequently, several investigators reported that approximately 30% of patients with car puhnonale had either clinical or postmortem evidence of left ventricular hypertrophy unexFrom Hahnemann University Hospital, and Michael Reese Received

for publication

Reprint University,

requests: Broad

1114

June

Hospital, Hospital, 26, 1966;

Peter Bent Brigham and University of Chicago. accepted

Sept.

Womens

18, 1986.

Marie11 Jessup, M.D., Cardiology Section, and Ontario St., Philadelphia, PA 19140.

Temple

plained by concomitant systemic hypertension.3-5 These early observations initiated a host of inquiries into the effects of chronic pulmonary hypertension and subsequent right ventricular pressure overload on the otherwise disease-free left ventricle. Experimental studies6 and animal models of acute and chronic right ventricular pressure overload have shown that the shape of both ventricles is altered as a result of a leftward displacement of the septum from its normal position. 7-*oIn addition, a number of echoc~diopraphic sMieis hiye Qovua$u@d @at 1 wide variety of patients with right ventricular pressure or volume overload are frequently found to have distinctly abnormal septal motion.11-16 In these studies, however, the echocardiographic observations were not correlated with any hemodynamic parameters. Nevertheless, these findings have served to focus attention on the interventricular septum and its role in mediating ventricular interaction. The purpose of the present study was to examine left ventricular size and function in a

Volume Number

Table

113 5

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hypertension

and LV function

1115

I. Patient population with right ventricular pressureoverload and pulmonary hypertension

Patient No.

Age

Sex

2

16 48

M

3 4 5

71 28 61

M F

6 7 8

24 47 51

F F M

9 10 11 12 13

36 52 54 47 30

F M F

1

F

M

F M

Mean PAP (mm W

Etiology

Systolic BP (mm Hd

(mm

AP Hd

Septal motion

IdiopathicPH Idiopathic pulmonary fibrosis* ASD, asthma IdiopathicPH* Interstitial lung disease*

60 28

80 48

110 120

+30 +72

N N

36 38 26

62 52 30

136 120 110

+74 +68 +80

N N N

Chronic

26 40 44

34 68 66

100 135 120

+66 +67 +54

64 47 50 74 70 46 f 16

104 83 85 104 110 71 f 26

105 105 120 90 136 117 + 14

+1 +22 +35 -14 +26 +45 + 30

PE*

Scleroderma* Allergic pneumonitis* IdiopathicPH* IdiopathicPH Chronic

PE

Scleroderma IdiopathicPH

Abbreviations: A = abnormal septal motion as interpreted N = normal septal motion as interpreted by M-mode PAP = pulmonary artery pressure; RV = right ventricular *Results confirmed by open lung biopsy.

by M-mode echocardiography; ASD = atria1 echocardiography; PE = multiple emboli pressure; AP = BP systolic - RV systolic.

population of patients with chronic right ventricular pressure overload secondary to pulmonary arterial hypertension. Additionally, an objective characterization of septal motion with respect to the relative position of the interventricular septum throughout the cardiac cycle was delineated for a range of hemodynamic abnormalities in this population. METHODS Study population.

Systolic RV (mm W

Thirteen patients with chronic pulmonary arterial hypertension of diverse etiology gave informed written consent to undergo catheterization and pharmacologicintervention for the potential treatment of their pulmonary hypertension. The 13 were from a larger group of 17 patients referred for further evaluation and possibletreatment of their pulmonary hypertension and in whom the presenceof coronary artery disease,aortic or mitral valvular disease,systemic hypertension, and other causes of left heart diseasewere excluded by history, physical examination, echocardiography, and/or cardiac catheterization, and in whom high-quality two-dimensional and M-mode echocardiograms were obtained. All patients presented with symptoms of exertional dyspnea for at least 6 months prior to referral, and the majority also had exertional chest pain and excessivefatigue. ECG abnormalities included evidence of right ventricular hypertrophy in all but two of the patients; one patient had complete right bundle branch block. Seven of the patients underwent open-lung biopsy after hemodynamic monitoring wascompleted to establishthe histopathologic diagnosis of pulmonary hypertension (Table I).

septal seen

defect; BP = systolic arterial on biopsy; PH = pulmonary

blood pressure; hypertension;

Echocardiograms. Two-dimensional and two-dimensional-directed M-mode echocardiogramswere obtained within 24 hours of hemodynamic monitoring in all patients. A Diasonic ultrasonoscopewith a 1.25 cm diameter, 2.25 MHz transducer with a repetition frequency of 1000 cycleslsec was used, and data were collected on a strip-chart recorder at paper speedsof 50 or 100 mm/set. Echoeswere recorded with patients recumbent in the left semilateral position. Tracings were recorded of the right and left sidesof the septum and of the endocardium and epicardium of the posterior left ventricular wall at the level of the chordae tendineae at end expiration. Measurements were made only when the echoeswere clear and continuous throughout the cardiac cycle. M-mode echocardiogramswere interpreted by a single observer who was unaware of the diagnosisor the hemodynamic data collected on individual patients. For each patient, overall septal motion was characterized as either normal (group I) or abnormal (group II). Septal motion was read as normal when the septum moved posteriorly simultaneous to the onset of the QRS and when peak posterior excursion of the septum wasobservedbefore the peak anterior motion of the posterior wall and peak posterior wall thickening occurred. If septal motion was not normal in theserespects,it wasclassifiedasabnormal, so that borderline or slightly abnormal caseswere read as abnormal (group II). More objective specifics of septal position and motion were analyzed by delineating seven points (i.e., T,,-T, in Fig. 1) along both the right and left sides of the septum during a single cardiac cycle of the M-mode echocardiogram. The midpoint of the cycle, T3,

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max

0

200

400

000

so0

1000

moec

1. Relative septal motion was determined by delineating seven points along the right and left sidesof the septumasdepicted from the computer-assisteddrawing of a single cardiac cycle. T3 = time of maximum posterior wall thickening (PWs max) (seetext for details).

Fig.

was taken at the point of maximum posterior wall thickness and was considered to represent end systole. End diastole, T,, wasdefined asbeing coincident with the peak of the R wave of the QRS complex. The remainder of systole, T, and T,, and diastole, T, and Tg, was divided into equal thirds. A minimum of three cardiac cycles were analyzed for eachpatient. So that a description of relative septal position could be made and group averaging performed, measurementswere normalized by subtracting the distance at T, (centimeters) from the distancesat T, through T,. Thus, septal position could be compared irrespective of individual left ventricular cavity size or length of cardiac cycle. Echocardiograms were digitized as previously described,‘6and plots were madeof continuous left ventricular cavity dimension (LVD) and septal and posterior wall thicknesses.From these data, cavity, septal, and posterior wall dynamics were computed. The following parameters were derived from these measureddimensions.(1) Percentageof shortening of left ventricular cavity minor-axis dimension: %ALV = LVDd-LVDs/LVDd x 100, where LVDd = end-diastolic dimension and LVDs = end-systolic dimension. (2) Peak rate of increaseof left ventricular dimension during diastole, referred to hereafter as peak left ventricular filling rate: +dLVD/dt, where t = time in seconds.(3) Peak rate of velocity of circumferential fiber shortening. (4) Rapid filling period: defined as the time from minimum left ventricular dimension (T3) to the time when the left ventricular filling rate decreasedto 20% of its maximum value. Minimum left ventricular dimension was defined as the point at which left ventricular filling rate changedfrom negative to positive. (5) Percentage of systolic septal thickening: %AVS = VSs-VSd/VSs X 100, where VSs = maximum systolic thickness and VSd = minimum diastolic thickness. (6) Percentage of systolic posterior wall thickening: %APW = PWs-PWd/ PWs X 100, where PWs = maximum systolic thickness and PWd = minimum diastolic thickness. (7) Peak rate of

Heart

Journel

systolic septal thickening: +dVS/dt. (8) Peak rate of systolic posterior wall thickening: +dPW/dt. Analysis of regional and global left ventricular function and septal motion and position in the patients with pulmonary hypertension were comparedwith echocardiographic data obtained from 10 normal volunteer subjects with a mean ageof 38 f 7 years. The normal subjectshad no historic or clinical evidenceof heart diseaseat the time of study. Hemodynamic monitoring. Right heart catheterization was performed via an antecubital vein with the use of a flow-directed, balloon-tipped, thermodilution catheter. Systemic arterial pressurewas measuredwith standard sphygmomanometry. Serial supine hemodynamic measurements were taken during a 4%hour period during pharmacologictesting; the results reported represent values recorded in the first 3 hours of monitoring, prior to drug intervention, and represent the averageof triplicate readingsthat varied I 10% . Statistical analysis. All data are presented as mean f one standard deviation unlessotherwise indicated. Group comparisonswere analyzed by meansof one-way, repeated-measuresanalysis of variance. A probability (p) value of <0.05 was consideredsignificant. RESULTS Hemodynamics. As detailed in Table I, the patients with pulmonary hypertension ranged in age from 16 to 71 years; there were seven women and six men studied. Six patients had a clinical history and/or lung biopsy results consistent with idiopathic pulmonary hypertension, whereas the remaining patients were classified into more specific etiologic categories. Patients Nos. 1, 3, and 10 had clinical signs of tricuspid regurgitation which included systolic murmur with positive Carvallo’s sign, prominent jugular venous “c-v” and hepatic pulsations, and right-sided S,. None of the patients had pulmonary venous hypertension, as evidenced by a pulmonary capillary wedge pressure less than 12 mm Hg (mean 7 k 1 mm Hg). Mean values for right ventricular systolic and mean pulmonary artery pressures were 71 + 26 mm Hg and 46 k 16 mm Hg, respectively. A transseptal systolic pressure gradient, AP, was calculated for each patient by subtracting right ventricular systolic pressure from systolic arterial pressure. Septat motion. Septal motion was interpreted from the M-mode echocardiograms as normal in seven of the patients with pulmonary hypertension (group I), whereas six patients displayed a distinctly abnormal septal motion on the M-mode echocardiogram (group II). Closer inspection of relative septal motion in the patients revealed two separate patterns of abnormal septal movement as compared to that of normal subjects. Fig. 2 depicts the relative

Volume Number

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1.0,

a5 4 t 3 $

0,

x B L 1

-a5 I # i

3

I I I

i E s

-10,

r

1

I

I

1

I

I

4 t I 8 oxz ?i -LO-

Fig. 2. Relative septal motion (dashed lines, solid symbols) of seven patients in group I who were interpreted as

having normal septal motion on M-mode echocardiogram. line, open symbols representsnormal septal motion from 10 normal subjects. Note significant differences in septal motion during diastole. Data shown are mean f 2 SD.

Solid

the patients in group I which were interpreted as “normaI” and compares it to the septal motion of the control population for both the right ventricular and left ventricular sides of the septum. As can be seen, a normal posterior excursion of the interventricular septum occurred throughout systole in group I,

Fig. 3. Relative septal motion (dashed lines, solid symbols) of six patients in group II who were interpreted as

having abnormal septal motion on M-mode echocardiogram. Significant anterior movement of septum toward the right ventricle throughout systole is seenin this group of patients when compared to normal septal motion (solid line, open symbols). Data shown are mean + 2 SD.

buthe wuA&dhutCdeadmiHthsr4hbf anterior motion of the septum contrast, Fig. 3 illustrates the six patients in group II who having abnormal septal motion There was a markedly abnormal of the septum throughout all

during diastole. In septal pattern of the were interpreted as on echocardiograms. anterior movement of systole and early

May 1987

1118

Jessup et al.

American

,

MO.02

,

0 Fig. 4. Systolic pressure gradient across the septum, or

AP, for patients in group I (pulmonary hypertension with “normal” septal motion on M-mode echocardiogram) and in group II (pulmonary hypertension with abnormal septal motion on M-mode echocardiogram).

Heart Journal

with grossly abnormal septal motion (p < 0.05), in contrast to group I patients and normal subjects. Regional and global indices of left ventricular function, as derived from computer-assisted analysis of the echocardiograms, are presented in Table II. There was no evidence of depressed left ventricular performance at rest in those patients with chronic right ventricular pressure overload. The percentage of shortening of cavity minor axis was significantly higher than normal as was the peak rate of circumferential fiber shortening, but probably reflects the smaller internal dimension of the left ventricle in the patients with pulmonary hypertension. Peak left ventricular filling rate and the duration of the rapid filling period were similar for normal subjects and the patient population. Despite the abnormal septal motion, there was no difference in the percentage of systolic thickening of the septum or the posterior wall in either group I or group II compared to normal; neither was there a difference in the peak rate of systolic posterior wall thickening. However, there was a statistically significant increase in the peak rate of systolic septal thickening in patients with chronic pulmonary hypertension (p < 0.05). Thus, although the septal to free wall dimension of the left ventricle was reduced in all patients with pulmonary hypertension, regional and global dynamics of left ventricular performance were normal. DISCUSSION

diastole, but the remainder of diastolic motion was no different from the normal pattern. The only hemodynamic parameter which distinguished these two patterns was AP, or the transseptal pressure gradient (Fig. 4). In the seven patients from group I, the systolic pressure gradient across the septum was 65 f 16 mm Hg, significantly higher than the gradient of 21 t- 24 mm Hg calculated for the patients in group II with abnormal systolic septal motion 07 < 0.02). Neither mean pulmonary artery pressure, peak pulmonary systolic pressure, nor right ventricular systolic pressure correlated well with the two septal motion patterns described. Left ventricular size and function. The left ventricu-

When an excessive pressure or volume overload is imposed on a ventricle, myocardial hypertrophy develops as a primary compensatory mechanism that allows the ventricle to sustain this load. This fundamental concept has long been recognized as the reason for the development of right ventricular hypertrophy in response to pulmonary arterial hypertension of diverse etiologies. However, early reports by several different laboratories noted the regular and unexplained occurrence of concomitant hypertrophy of the left ventricle in patients with car pulmonale.3-5 Thus, considerable speculation arose

lar septal-free wall dimension throughout the cardiac cycle was significantly smaller in patients with pulmonary hypertension as compared to normal subjects, illustrated in Fig. 5. The result of chronic pulmonary hypertension on myocardial wall thickness is shown in Fig. 6. The septum tended to be thicker in all patients but was within normal limits statistically. However, the left ventricular posterior wall was significantly thicker in group II patients

causes of left ventricular abnormalities in patients with right ventricular pressure overload. These investigations have been confounded in the past by the use of more traditional descriptors of left ventricular function. For example, alterations of the left ventricular pressure-volume relationship have been well described in animals and patients with elevated pulmonary and right ventricular pressures,17-22suggesting that left ventricular compliance

about the incidence] functional si nificancel and 6

Volume Number

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8.0 1

Pulmonary

END-DIASTOLE

6.0

and LV function

hypertension

ENPDIASTOLE

ENDSYSTOLE

P
1.2

2

1.2

: :: z

0.72

z 0 I c

0.46

i *s

0.46

0.24

% p E

0.24

3

0.0

0.0

ML 6rnUP vmxp I II

P
0.96

2

li

Fig.

T-

P=NS 2

z VI 0.72

f

5. Left ventricular (LV) internal dimensions as measured by M-mode echocardiography for normal control subjects (NL) and patients with pulmonary hypertension in groups I and II.

I

ENPDIASTOLE

P=NS

0.96

1119

WI. vmup I

P

6. Septal and posterior wall myocardial thickness as measuredby M-mode echocardiography. Abbreviations as in Fig. 5. Fig.

was abnormal in this population. However, several investigations in dogs, with the use of acute or chronic models of pulmonary hypertension, have indicated that these abnormalities are the result of the consequences of right ventricular distension and septal displacement, rather than true changes in left ventricular myocardial stiffness.7”*23,24 Other resting hemodynamic indices, such as left ventricular stroke volume or stroke work index, may be likewise depressed because of a reduction in right ventricular stroke output.21 Frequently, the study populations have included a majority of men with chronic obstructive lung disease, many of whom may have had asymptomatic coronary artery disease or significant arterial hypoxemia. For these reasons, several investigators have concluded that left ventricular performance was impaired in the presence of right ventricular pressure overload.17-18~20 The present study examined the effect of right ventricular pressure overload secondary to chronic pulmonary arterial hypertension on left ventricular size and function in 13 patients in whom coronary artery disease, hypertension, and hypoxemia were excluded. Regional and global left ventricular function was assessed by a computer-assisted analysis of two-dimensional-directed M-mode echocardiograms obtained within 24 hours of a hemodynamic study. The use of the two-dimensional view enhanced the selection of the most representative short-axis view of the left ventricle, Left ventricular cavity dimensions and wall thickness were measured by means of standard echocardiographic methods and were compared to those of 10 normal control subjects. The validity of echocardiographic measurements of left ventricular minor axis and its rate of change has been established by comparison with angiographic data in normal patients and in those

with abnormal septal motion.25-27 Moreover, an analysis of septal and posterior wall dynamics in terms of percentage and peak rates of systolic thickening has been particularly useful in those situations where septal motion is abnormal, such as atrial septal defect and asymmetric hypertrophic cardiomyopathy. X,28-29 From our results, we would submit that resting left ventricular function is well preserved in patients with even severe degrees of pulmonary hypertension. These results are in agreement with those of Krayenbuehl et aL30 who studied 10 women with chronic pulmonary hypertension by left ventricular micromanometry and cineangiography. They concluded that left ventricular performance was normal at rest as evidenced by the following contractile indices: dP/dk, (maximal rate of rise of left ventricular pressure), V, (peak measured velocity of contractile element shortening), and V,, (extrapolated maximal velocity of contractile element shortening). Likewise, Frank et al.lg reported normal left ventricular myocardial blood flow, oxygen extraction, and contractility in 11 patients with chronic car pulmonale. Analogous conclusions, summarized by Bove and Santamore, have been drawn by several other groups of investigators who have evaluated left ventricular function in patients with chronic obstructive pulmonary disease. Although we and others have demonstrated that left ventricular function is normal at rest, cardiac performance may be reduced in these patients during exercise or other forms of stress. Krayenbuehl et a1.,30 in the study referred to earlier, found that handgrip exercise data significantly distinguished a

1120

Table

Jessup et al.

may 1987 Heart Journal

Amarlcan

II. Echocardiographic indices of left ventricular function Normal % A LV Peak LV filling rate Peak Vcf Rapid filling period % AVS %APW peak +dVSfdt peak +dPWfdt

33.3 15.2 2.2 160 49.2 87.0 3.3 4.3

subjects

k 4.2% -t 2.2 cmhec + 0.2 se& f 50 cm/set + 12.5% ‘- 15.6% + 0.6 cm/set k 1.2 cm/set

Pulmonary

hypertension

45.7 2 9.3% 15.3 * 4.0 cm/set 3.4 * 9 see-’ 139.4 t- 18 cmhec 51.3 t 18.4% 77.2 f 21.3% 4.3 5~ 1.2 cmhec 3.9

f

0.9

cm/set

p Value
NS
Abbreviations: 7; A Lv = percentage of shortening of left ventricular cavity minor-axis dimension; ‘0 A VS = percentage of systolic septal thickening; PW = percentage of systolic posterior wall thickening; + dVS/dt = peak rate of systolic septal thickening; + dPW/dt = peak rate of systolic posterior thickening; NS = no significant difference between normal subjects and patients with pulmonary hypertension; Vcf = velocity of circumferential shortening.

normal population from a group of patients with pulmonary hypertension. The contractile indices V, and V, increased during handgrip exercise in control subjects but were essentially unchanged in the patients with pulmonary hypertension. These findings have been confirmed by Badkes in dogs with chronic pulmonary artery banding. He reported normal left ventricular function at rest in this model of chronic right ventricular pressure overload, but induced regional abnormalities of left ventricular contraction when the dogs were exercised on a treadmill. He suggested that this systolic dysfunction was mediated by a reduced contribution of the ventricular septum to left ventricular ejection during exercise. While it may be true that the abnormal septum displays less than normal contractility during exercise, we found no evidence of decreased septal function at rest. Despite abnormal septal motion and position, the duration of rapid filing, peak velocity of circumferential fiber shortening, and peak left ventricular filling rate were normal and can best be explained by the compensatory increase in the peak rate of septal systolic thickening in the patient population. Latent abnormalities of left ventricular performance in patients with severe right ventricular pressure overload may be partially accounted for by other causes.3-5 These include increased bronchopulmonary shunting causing an

5% A wall fiber

had normal systolic motion of the interventricular septum with associated decreased anterior motion during diastole. The remaining six patients in group II had marked systolic distortion of the septum but relatively normal diastolic movement. Abnormal septal motion has been described previously in some patients with pulmonary hypertension, but was often attributed to the association of concomitant tricuspid regurgitation.32 Diamond et al.‘* had argued earlier that septal motion was normal in patients with pure right ventricular systolic pressure overload. However, recent work by Yock and Poppa has suggested that 90% of patients with suspected right ventricular pressure overload have Dopplerdetected tricuspid regurgitation. Moreover, the absence of any significant hemodynamic differences between groups I and II makes it unlikely that tricuspid regurgitation was less common in one group compared to the other, and the clinical examination of our patients was not helpful in this regard. Goldman34 has reviewed a number of mechanisms by which septal motion can be seen to vary in echocardiographic studies. For example, Meyer et alI4 have proposed that abnormal septal motion in cases of right ventricular overload is the result of the marked dilatation of the right ventricle and a resultant exaggerated anterior movement of the entire

increased cardiac output and exercised-induced heart during systole,providing a net systolic anterihypoxemia. However, we saw no evidence of abnormally elevated cardiac output in our patients, and only one patient showed significant arterial oxygen desaturation during exercise. Thus, it would seem that an assessment of septal motion and position is crucial to any evaluation of cardiac function in patients with chronic pulmonary hypertension. Our analysis of relative septal motion revealed two distinct patterns as compared to that of normal subjects. The seven patients in group I

or motion of the septum. Pearlman et all6 concluded that the direction and magnitude of septal motion during systole is determined by the intracardiac position of the septum at end diastoIe. Weyman et al.36 suggested that paradoxical septal motion in patients with right ventricular overload is a result of a change in the diastolic shape of the left ventricle. In addition, the intrinsic contractility of the septum it&f influences interventricular septal motion. Most important, the gradient in force (i.e., pres-

Volume Number

113 5

sure times surface area) across the interventricular septum influences septal position and configuration.” Normally, the transseptal systolic gradient creates a dominant axiaI force on the left ventricular septal surface, thereby bowing the septum into the right ventricle. A change in the transseptal gradient between the ventricles will result in septal displacement and will be accompanied by changes in the configuration and size of each ventricle. Tanaka et al.36 recorded simultaneous pressure tracings of the right and left ventricles and the instantaneous interventricular pressure gradient in patients with pulmonary hypertension and abnormal septal motion, all of which were correlated with the septal configuration seen on M-mode echocardiogram. They demonstrated that the abnormal diastolic motion of the septum seen in their patients was a result of the negative interventricular pressure gradient between the left and right ventricles during diastole. Kingma et al.37 have likewise reported that in dogs with chronic pulmonary artery banding, abnormal septal motion always occurred in response to a major reduction in, or reversal of, the transseptal enddiastolic pressure gradient. The results of the present study confirm these previous observations. Of interest is the lack of agreement as to when septal deformity is more profound, in systole or diastole. Ryan et a1.3s reported on patients with either right ventricular pressure or volume overload, and suggested that in the former group, left ventricular deformity persisted throughout the cardiac cycle, but the degree of deformity was greater at end systole. Other authors have noted a predominance of diastolic abnormalities.35 We have observed abnormal septal motion in both diastole (group I) and systole (group II), which was also reported by Krayenbuehl et a130 We would suggest that many of these discrepancies are accounted for by the marked individual variations in the instantaneous pressure gradient across the septum, which is not easily measured. Finally, our observations about septal and posterior wall thicknesses in patients with pulmonary hypertension tend to support earlier work. Badke8 noted the development of septal hypertrophy in dogs with chronic pulmonary artery banding. He suggested that the hypertrophy of the septum might be a compensatory factor that occurred to restore left ventricular ejection to normal levels. Krayenbuehl et aL30 also reported septal hypertrophy in their patients with car pulmonale, as did Goodman et a1.32 Many of our patients had increased septal thickness, although the group as a whole showed no statistical difference in septal size compared to a

Pulmonary

hypertension

and LV function

1121

normal population. The potential mechanisms that promote the development of left ventricular hypertrophy in the absence of systemic hypertension remain unclear. We are indebted to David Ward, Tom Nuskickei, and Virginia Andrews for providing their assistance during the course of the study, and to Nicole Glimp for manuscript preparation.

REFERENCES

1. Bernheim PI. De l’asystolie veineuse dans l’hypertrophie du coeur gauche par stenose concomitante du ventricule droit. Rev Med 1910;39:785. 2. Dexter L. Atria1 septal defect. Br Heart J 1956;18:269. 3. Fluck DC. Chandrasekar RG. Gardner FV. Left ventricular hypertrophy in chronic bronchitis. Br Heart J 1966;28:92. Michaelson N. Bilateral ventricular hypertrophy due to chronic pulmonary disease. Dis Chest 196838435. Kountz WB, Alexander HL, Prinzmetal M. The heart in emphysema. AM HEART J 1936;11:163. Weber KT, Janicki JS, Shroff SG, Likoff MJ, St. John Sutton MG. The right ventricle: physiologic and pathophysiologic considerations. Crit Care Med 1983:11:323. 7. Weber KT, Janicki JS, Shroff S, Fishman AP. Contractile mechanics and interaction of the right and left ventricles. Am J Cardiol 1981;47:686. 8. Badke FR. Left ventricular dimensions and function during right ventricular pressure overload. Am J Physiol 1982; 242zH611. 9. Badke FR. Left ventricular dimensions and function during exercise in dogs with chronic right ventricular pressure overload. Am J Cardiol 1984:53:1187. 10. Stool EW, Mullins CB, Le&n SJ, Mitchell JH. Dimensional changes of the left ventricle during acute pulmonary arterial hypertension in dogs. Am J Cardiol 1974;33:868. 11. Popp RL, Wolfe SB, Hirata T, Feigenbaum H. Estimation of right and left ventricular size by ultrasound. Am J Cardiol 1969;24:523. 12. Diamond MA, Dillon JC, Haine CL, Chang S, Feigenbaum H. Echocardiographic features of atria1 septal defect. Circulation 1971;43:129. 13. Assad-Morel1 JL, Tajik AJ, Giuliani ER. Echocardiographic analysis of the ventricular septum. Prog Cardiovasc Dis 1974;17:219. 14. Meyer RA, Schwartz DC, Benzing G, Kaplan S. Ventricular septum in right ventricular volume overload. Am J Cardiol 1972;30:349. 15. Pearlman AS, Clark CE, Henry WL, Morganroth J, Itscoitz SB, Epstein SE. Determinants of ventricular septal motion. Influence of relative right and left ventricular size. Circulation 1976;54:83. 16. St. John Sutton MG, Tajik AJ, Mercier L, Seward JB, Giuliani ER, Ritman EL. Assessment of left ventricular function in secundum atrial septal defect by computer analysis of the M-mode echocardiogram. Circulation 1979; 66~1082. 17. Rao S, Cohn KE, Eldridge FL, Hancock EW. Left ventricular failure secondary to chronic pulmonary disease. Am J Med 1968;45:229. 18. Baum GL, Schwartz A, Llamas R, Castillo C. Left ventricular function in chronic obstructive lung disease. N Engl J Med 1971;285:361. 19. Frank MJ, Weisse AB, Moschos CB, Levinson GE. Left ventricular function, metabolism, and blood flow in chronic car pulmonale. Circulation 1973;27:798. 20. Khaia F. Parker JO. Right and left ventricular nerformance in chronic obstructive-lung disease. AM Hx&r J 1971; 82:319. 21. Moulopoulos SO, Sorcas A, Stamatelopoulos S, Arealis E.

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Left ventricular performance during by-pass or distention of the right ventricle. Circ Res 1965;17:484. 22. Kelly DT, Spotnitz HM, Beiser GD, Pierce JE, Epstein SE. Effects of chronic right ventricular volume and pressure loading on left ventricular performance. Circulation 1971;44:403. 23. Taylor RR, Cove11 JW, Sonnenblick EH, Ross J Jr. Dependence of ventricular distensibility on filling of the opposite ventricle. Am J Physiol 1967;213:711. 24. Bemis CE, Serur JR, Borkenhagen D, Sonnenblick EH, Urschel CW. Influence of right ventricular filling pressure on left ventricular pressure and dimension. Circ Res 1974; 34:498. 25. Feigenbaum H, Popp RL, Wolfe SB, Troy BL, Pombo JF, Haine CL, Dodge HT. Ultrasound measurements of the left ventricle: a correlative study with angiocardiography. Arch Intern Med 1972;129:461. 26. Gibson DG, Brown D. Measurement of instantaneous left ventricular dimension and filling rate in man, using echocardiography. Br Heart J 1973;35:1141. 27. Gibson DG, Brown DJ. Measurement of peak rates of left ventricular wall movement in man: comparison of echocardiography with angiography. Br Heart J 1975;37:677. 28. St. John Sutton MG, Trail1 TA, Ghafour AS, Brown DJ, Gibson DG. Echocardiographic assessment of left ventricular filling after mitral valve surgery. Br Heart J 1977;39:1283. 29. St. John Sutton MG, Tajik AJ, Gibson DF, Brown DJ, Seward JB, Giuliani ER. Echocardiographic assessment of left ventricular filling and septal and posterior wall dynamics in idiopathic hypertrophic subaortic stenosis. Circulation 1978;57:512.

American

May 1987 Heart Journal

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