Effect of exercise and cavity size on right ventricular function in morbid obesity

Effect of Exercise and Cavity Size on Right Ventricular Function in Morbid Obesity Martin A. Alpert, MD, Amolak Singh, MD, Boyd E. Terry, MD, Diana L. Kelly, RDMS, M.S. Sharaf El-Deane, MD, Vaskar Mukerji, MD, Daniel Villarreal, MD, and Andre K. Artis, MD

To assess the effect of exercise and to determine the Muence of the right ventricular (RV) internal dimension on RV systolii function in morbid obesity, M-mode and P-dimensional echocardiography and radiii ventriculography were performedon22patientswhosebodyweightwasat least twice the ideal body weight and who had no clinical or laboratory evidence of underlying organic heart disease or pulmonary disease. RV ejection fraction was measured at rest and during peak suupine hicycle exercise. RV exercise response was deftned as the change in RV ejection fraction during peak exercise. There was a significant negative correlation between percent over ideal body weight and RV exercise response (r = 0.86, p
From the Departments of Medicine, University of Missouri Health SciencesCenter and Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri. Manuscript receivedApril 27, 1989;revisedmanuscript receivedand acceptedAugust 7, 1989. Address for reprints: Martin A. Alpert, MD, Division of Cardiology, Room lE-65, University of Missouri Health SciencesCenter, One Hospital Drive, Columbia, Missouri 65212.

I

t is well established that complications of morbid obesitysuchashypoxia may producepulmonary arterial hypertension and clinical manifestations compatible with right ventricular (RV) dysfunction.1-4 In recent years it has become increasingly clear that extreme obesity may produce alterations in left ventricular (LV) structure even in the absenceof systemic hypertension and underlying organic heart disease.5-12 These structural abnormalities include LV dilatation that evolves from the increase in circulating blood volume and cardiac output associatedwith excessiveadiposetissue accumulation and secondary or “eccentric” hypertrophy that occurs in accordancewith the law of LaPlace.’l-l3 Prior studies have demonstratedthat resting LV systolic dysfunction commonly occurs in nonhypertensive morbidly obese individuals without underlying organic heart disease.9J0Whether these hemodynamic stressesaffect the RV in a similar fashion in the absenceof LV failure, mitral valve diseaseor pulmonary arterial hypertension is uncertain. Moreover, little is known about the effect of exercise on RV function in extreme obesity. The objectives of this study were to assessresting RV systolic function in morbidly obese patients and to determine the effect of exerciseon RV systolic function in such individuals with special reference to the RV internal dimension. METHODS Patient relection: Study patients were selectedfrom

those referred for surgical therapy of morbid obesity (gastroplication).14Patients entering the study were required to weigh at least twice their ideal body weight for 15 years.Patients with systemichypertension,those with clinical or laboratory evidenceof organic heart disease not directly related to obesity (including patients with clinical or radiographic evidence of LV failure) and those receiving drugs that might alter LV or RV function were excluded from the study. Also excluded were patients with hypoxemia, hypercarbia, evidenceof moderateto severeobstructive or restrictive lung disease or those with impaired diffusion capacity on pulmonary function tests.15J6 Protocol evaluation: A medical history, physical examination, resting electrocardiogram,chest x-ray, echocardiogram (M-mode and 2-dimensional) and radionuelide ventriculogram (obtained at rest and during incremental supine bicycle ergometry) were performed on each patient before surgery.

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RIGHT VENTRICULAR FUNCTION IN MORBID OBESITY

TABLE I Individual and Mean Clinical, Hemodynamic

% Overweight

Pt

RV internal dimension <2.0 cm 122 1 124 2 100 3 104 4 100 5 104 6 104 7 108 8 133 9 106 10 120 11 122 12 112f 11 Mean f 1 SD RV internal dimension >2 cm 142 1 122 2 119 3 124 4 239 5 113 6 125 7 195 8 158 9 160 10 150*4O Mean f 1 SD Mean& 1 SD 129f34 for all patients BP = blood pressure;

EX = exercise;

and Echocardiographic

Rv Internal Dimension (cm)

RV Ejection Fraction (%) Rest

Ex

1.7 1.8 1.7 1.9 1.8 1.7 1.9 1.6 1.8 1.8 1.5 1.7 1.7fO.l

31 42 32 36 45 58 44 34 58 34 57 53 43flO

50 47 59 48 75 54 62 47 80 49 68 60 58fll

2.4 2.1 2.3 2.5 2.1 2.0 2.1 2.1 2.1 2.3 2.2 f 0.2 2.0 f 0.3

24 38 57 53 55 29 39 33 61 40 43f13 43f 11

24 39 38 50 32 42 40 32 61 42 4OflO 5Of14

LV = left ventricular;

RV = right ventricular;

A

THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 64

Heart Rate (beats/min)

Mean BP (mm Hg)

Rest

Ex

Rest

Ex

Rest

Ex

19 5 27 12 30 -4 18 13 22 15 11 7 15f9

41 70 40 57 62 68 62 47 51 48 58 51 54flO

73 76 65 67 84 63 75 47 58 51 65 61 65fll

69 76 76 70 82 843 70 80 81 80 72 82 76f5

107 116 122 126 124 126 115 135 135 130 120 118 122f8

98 96 102 95 90 102 93 98 93 90 93 92 95f4

128 112 138 125 130 121 124 121 123 125 123 126 124*6

0 1 -19 -2 -23 13 1 -1 0 2 -3flO 7f13

39 62 61 57 72 39 45 49 48 32 50f12 53fll

28 73 59 52 66 39 55 54 43 33 5Of14 58f14

67 76 79 76 80 70 70 74 76 62 73f6 75-+5

107 125 120 124 119 115 126 118 124 131 121 f 7 122f8

97 100 97 103 96 93 102 102 103 101 99f3 97zt4

117 123 125 129 126 124 138 123 129 127 126f5 125f6

SD = standard

Echocardiograms were performed using a HewlettPackard model 77020A ultrasonograph with a 2.25MHz scanning head in the semirecumbentand left lateral positions in accordance with the American Society of Echocardiography recommendations.l 7 Normal ranges for echocardiographic measurementswere set in accordance with American Society of Echocardiography standards.17The key echocardiographic measurement, the RV internal dimension, was obtained in the semirecumbentposition (normal range 0.7 to 2.3 cm).17 RV systolic function was measuredusing multigated equilibrium cardiac blood pool scintigraphy using a pre viously described technique.*8-21A single observer analyzed the data and the intraobserver variability was 13% (ejection fraction units). Normal radionuclide RV ejection fraction is 235% and normal RV exercise responseis an increase in RV ejection fraction by 15%. Both resting and exercisegated blood pool imageswere acquired at the time of each examination in all patients. Supine exercise studies were acquired in the same projection as the resting studies.Using a bicycle ergometer, patients were exercisedat 40-watt workload increments. After an initial warm-up period of 2 minutes, data were acquired for 2 minutes while the patients exercisedat a constant speed.Subsequently,a l-minute warm-up and a 2-minute data collection interval were used for each level of exerciseuntil the symptom-limited endpoint was reached. LV ejection fraction was obtained in a similar 1362

Data in 22 Morbidly Obese Patients

LV Ejection Fraction (%)

deviation.

manner using__standard techniques for data acquisition _. and analysis.2uJ1RV and LV exercise responseswere defined as the changesin RV and LV ejection fractions, respectively; during peak exercise. Blood pressure was measured using a mercury sphygmomanometerand arm cuff. Mean blood pressure was calculated by adding onethird of the pulse pressure to the diastolic blood pressure. StatWeal -sir: Student paired and non-paired t tests were used to compare mean data. Correlations were performed using the least square linear regression analysis to calculate Pearson correlation coefficients and determine p values. A p value <0.05 was considered statistically significant. RESULTS Patient characteristics: The study population consistedof 22 patients; 17 women and 5 men with a mean age of 36 f 8 years. The mean body weight was 142 f 32 kg. The mean amount over ideal bcdy weight was 129 f 26%. Study groups anaiymk In analyzing the data we choseto scrutinize the study population as a whole, the subgroup with a high-normal or enlarged RV internal dimension (22.0 cm) and the subgroup whose RV internal dimension was <2.0 cm. Although comparisonof subgroups with normal and enlarged RV internal dimensionsand normal and depressedresting RV ejection

fractions would have been desirable, there were too few patients with a frankly enlarged RV internal dimension or depressedresting RV ejection fraction for meaningful statistical analysis.

exercise response.There was a significant increase in mean RV ejection fraction for the group as a whole from 43 f 11% at rest to 50 f 14% during peak exercise (p <0.05). Exercise produced a significant increase Effect of exercise on right ventricular systolic funcin mean heart (p
l l l

\re

l

RGUREl.-ofright(RV) intemd dimedon and RV exercise rospomo.ThorowasasigMhntnogative comlathbetw~RVintemaldimedon and RV exercise nespmse.

‘e

l

‘x l l

,,,,,,

r = 0.60

p < 0.005

-30

-20

-10

RV Exercise

0

10

Response

20

30

(%I

Fl6uRE2.cbveuonofpercentovlEr idealbodyweightdrightvebiadar (RV) exercise respome. Therowasa . * Ilerrlicantnagativebehvoempercontovor~bedyweight and RV exercise respome.

I

-30

I

-20

1

-10

RV Exercise

I

I

I

I

0

10

20

30

Response

(%I

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RIGHT VENTRICULAR FUNCTION IN MORRID OBESITY

22.0 cm, 3 had a depressedresting RV ejection fraction and 9 had abnormal RV exercise response.Three patients had a frankly enlarged RV internal dimension. In the subgroup of patients whose RV internal dimension was <2.0 cm, mean RV ejection fraction increasedsignificantly from 44 f 11% at rest to 58 f 11% at peak exercise (p <0.03), whereasin the subgroup whose RV internal dimension was 22.0 cm, mean RV ejection fraction did not significantly change (43 f 13% at rest and 40 f 11% during peak exercise). Moreover, the magnitude of change in mean RV ejection fraction with exerciseshown for those with an RV internal dimension <2.0 cm (15 f 9) and those with an RV internal dimension 12.0 (-3 f 10) was significantly different (p <0.005, Table I). The differences in the magnitude of increase in mean heart rate and mean blood pressure induced by exercise were not significant. Mean workloads were 63 f 21 watts in the subgroup whose RV internal dimension was 22.0 cm and 67 f 20 watts in the subgroup whose RV internal dimension was <2.0 cm. Key eon=elatIons: There was significant negative correlation between RV internal dimension and RV exercise response(Figure 1, r = 0.60, p
THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 64

dance with the law of LaPlace.11J2,26 Such hypertrophy may reduce diastolic compliance leading to elevation of LV filling pressure.11,12If hypertrophy keeps pace with dilatation, resting systolic LV function is preserved9J1~12*25 If hypertrophy fails to keep pace with dilatation, wall stresscontinues to be high and resting LV systolic dysfunction may ensue. Obeseindividuals with preservedresting LV systolic function may not be entirely normal. We recently reported that morbidly obese patients with increasedLV masscommonly have an abnormal LV exerciseresponseeven when resting LV systolic function is normal.25Whether the RV of nonhypertensivemorbidly obesepatients free from underlying cardiopulmonary diseaseis similarly affected by these hemodynamic stresses is uncertain. Accordingly, we sought to assessresting RV systolic function and determine the effect of exercise on RV systolic function in such individuals. Resting RV systolic dysfunction occurred in 23% of patients in this study. Prior studies using similar patient populations have reported resting LV systolic dysfunction in 32 to 56% of ca~es.~J~*~~ There was however, a significant positive correlation between resting RV and LV systolic function. Thii suggeststhat the hemodynamic stressesthat affect resting LV systolic function in nonhypertensivemorbidly obeseindividuals without underlying heart diseasemay affect RV systolic function in a similar fashion, but to a lesserextent. Our results indicate that measurementof RV ejection fraction during exerciseis superior to measurement of resting RV ejection fraction as a means of assessing RV function and reserve.Whereas only 23% of our patients had resting RV systolic dysfunction, 50% had an abnormal RV exercise response.Moreover, 8 of the 11 patients with an abnormal RV exerciseresponsehad a normal RV ejection fraction at rest. There was a significant positive correlation between RV and LV exercise response.This may suggest that hemodynamic factors affecting RV systolic function during exerciseare similar to those affecting LV systolic function during exercise; however, without data derived from direct measurement of ventricular filling pressure,pulmonary and systemicarterial pressuresand cardiac output, this conclusion remains speculative. The lack of correlation between resting RV ejection fraction and RV exerciseresponseindicates that resting RV ejection fraction is a poor predictor of RV systolic functional reserve. This was underscored by the presence of normal RV exercise responsein 2 of the 5 patients with resting RV systolic dysfunction and an abnormal RV exercise responsein 8 of the 17 patients with normal resting RV systolic function. Clearly, factors other than the state of RV systolic function at rest influence the RV responseto exercisein morbidly obese patients. Messerli et a111J2have demonstratedthat systemic hypertension in obese patients produces impairment of LV function over and above that of obesity alone. Pulmonary hypertension may impose a similar additive impairment of RV function.1-4 However, our study population was selectedto minimize the likelihood

of pulmonary hypertension being present; thus, it is unlikely that our observationsare attributable to an elevation in pulmonary vascular resistance. The results of our study indicate the presenceof a relation betweenthe RV internal dimension and RV exercise response.Patients with a high-normal or frankly enlarged RV internal dimension (22.0 cm) experienced no significant change in RV ejection fraction with exercise, whereaspatients whoseRV internal dimension was <2.0 cm experienceda significant increase in RV ejection fraction during exercise. Of the 10 patients whose RV internal dimension was 12.0 cm, 3 had resting RV systolic dysfunction and 9 had an abnormal RV exercise response.This suggeststhat RV dilatation (even within the normal range) may precede overt RV systolic dysfunction. Thus, in nonhypertensive morbidly obesepatients without underlying cardiopulmonary disease,exercise may elicit abnormalities of RV systolic function that may not be apparent at rest and the presenceof a high-normal or frankly enlarged RV internal dimension identifies patients who are likely to have an abnormal RV exercise response. Acknowledgment: We thank Peggy Smith for assistance in preparing this manuscript.

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