Left Ventricular Mechanical Efficiencyin Man with Heart Disease

WILLIAM A. BAXLEY, M.D., HAROLD T. DODGE, M.D., CHARLES E. RACKLEY, M.D.HAROLD SANDLER, M.D., AND DAVID PUGH, M.D.

SUMMARY Thirty-eight adults with valvular and/or myocardialdisease had heart catheterization with coronary blood flow and myo-cardial 02 consumption (MVO2) per 100 g measured by the nitrousoxide washout technique. Quantitative biplane angiocardiographywas performed to assess left ventricular volume, mass, ejection frac-tion and work. Left ventricular efficiency was calculated from work,MVO2/100 g and mass. Efficiency ranged from 4 to 40% and wasnormal in some patients with severe ventricular pressure-volume work

MECHANICAL EFFICIENCY is a performance param-eter of energy-transfer systems, most commonly used in anengineering context. Expressed as a percent, it is the dimen-sionless ratio of mechanical work performed to energyutilized over a given time period. In terms of human left ven-tricular dynamics, energy utilized has been shown to resultrelatively exclusively from aerobic metabolism in theabsence of ischemic coronary disease.1 2 Thus left ven-tricular efficiency can be calculated from its rate of perform-ing work and the rate of energy consumption (oxygen con-sumption or MVO2) over the same time interval.' In thisway ventricular efficiency has been calculated in animals.4 Inman, methods utilized for coronary blood flow determina-tion have included the nitrous oxide washout,3' 68 heliumwashout9 and other techniques.'0 MVO2 is then computed asthe product of coronary blood flow and coronary arterial-venous oxygen difference. The values of MVO2 obtained bythese methods are expressed in MVO2/min/100 g of myo-cardium. Thus, knowledge of the left ventricular weight ormass is also necessary to calculate total left ventricularMVO2 and hence left ventricular efficiency. Left ventricularmass in normal humans has been estimated for this purpose,and ventricular efficiency calculated.3 However, the vari-able degrees of ventricular hypertrophy associated withchronic left ventricular hemodynamic abnormalities makeventricular mass measurements necessary for determinationof efficiency in patients with long-standing disease. Previousreports of left ventricular efficiency calculated with ven-tricular mass measurements in resting patients with chronicvalvular or myocardial disease have not been reported. Inthe present investigation, 38 adults with such diseases werestudied by quantitative angiocardiographic techniques withcoronary blood flow/100 g measured by the nitrous-oxidewashout technique. Calculation of left ventricular mass andchamber volumes in combination with left ventricular pres-sure measurements and MVO2 values permitted determina-

From the Departments of Medicine, University of Washington, Seattle,Washington and University of Alabama Medical Center, Birmingham,Alabama.

Supported in part by the Cardiovascular Research and Training Center,HL 13517, University of Washington; Program Project Grant HE 11310(NIH), and Vocational Rehabilitation Grant RD-22 19, University ofAlabama.

Address for reprints: William A. Baxley, M.D., Associate Professor ofMedicine, 1919 7th Avenue South, Birmingham, Alabama 35294.

Received April 23, 1976; revision accepted November 11, 1976.

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overloads. Total left ventricular MVO2 ranged up to 461 ml/min.Neither total MVO2 nor MVO2/100 g was significantly related toventricular work, ejection fraction, or tension-time index. These datasuggest 1) a relationship between left ventricular efficiency and myo-cardial function in chronic valvular or myocardial disease, 2) thatefficiency may be normal in hypertrophied ventricles, and 3) thatchronic increases in resting ventricular metabolic requirements aremet by hypertrophy rather than by increased MVO2/100 g.

tion of total left ventricular MVO2, coronary blood flow,work, and efficiency values together with ejection fraction asa measure of myocardial function. These data providefurther information on the functional characteristics of theleft ventricle in man with chronic valvular and myocardialdisease.

Materials and Methods

The subjects of this investigation were 38 adult male pa-tients, age range 25-65 years, studied by right and left heartcatheterization and biplane angiocardiography at theUniversity of Alabama Hospital, the University ofWashington Hospital or the Seattle Veterans Administra-tion Hospital. The patients all had valvular or myocardialdisease with symptoms of heart failure, at least NYHA classIII. None had evidence of coronary artery disease by historyor electrocardiogram. All were studied as part of adiagnostic evaluation. Initially coronary sinus and systemicarterial catheterization were performed. Coronary bloodflow per 100 g of left ventricular myocardium was measuredby the N20 desaturation curves following a 15 minute periodof 15% N20 inhalation.7 The desaturation curves were con-structed from N20 analysis data from multiple arterial andcoronary sinus blood samples drawn simultaneously over a10 minute period immediately following cessation of theN20 inhalation. The 02 content of the coronary sinus andsystemic arterial blood was determined by the Van Sykemethod, and coronary arteriovenous 02 difference calcu-lated. MVO2/100 g myocardium was then computed as theproduct of coronary flow/100 g and coronary arteriovenous02 difference. Following completion of the coronary sinusportion of the study, pulmonary artery catheterization wasperformed, and left heart catheterization was done by theretrograde arterial or transseptal approach. The cathetersutilized were #8 French fluid-filled, and pressures were mea-sured with Statham P23d transducers recorded on an Elec-tronics for Medicine recorder. Cardiac output was measuredby the Fick technique. Finally biplane left heart angiocar-diography was performed during quiet respiration at filmingrates of 6 or 12 per second with power injection of 50-75 mlof contrast material. Coronary angiography was not per-formed in these patients, since there was no clinical evidenceof coronary disease. Left ventricular volumes, mass, forwardand regurgitant flows, and ejection fraction were calculated

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TABLE 1. Hemodynamic Data in 38 PatiintsRanges of values

Mean standard Pressure VolumeLeft ventricular variable deviation All patients PMD* group overload group overload group Mixed group**

End-diastolic volume (ml) 235 i 101 83490 226407 110-270 213490 83-371Stroke volume (ml) 118 54 38-323 40-92 72-167 101-323 38-150Ejection fraction 0.53 0.18 0.10-0.86 0.10-0.25 0.43-0.86 0.30-0.75 0.36-0.77Total output/minute (L/min) 8.21 3.35 3.40-20.00 3.40-5.34 6.01-9.47 8.88-20.00 3.65-10.24Forward cardiac output (L/min) 4.38 1.15 2.58-7.28 2.58-3.50 3.21-5.70 3.41-7.28 3.07-6.94Regurgitant flow (L/min) 3.76 2.96 0.00-15.10 0.82-2.16 1.84-4.50 4.98-15.10 0.00-4.44Mass (g) 321 126 106-609 283-343 185-483 198-609 106-504End-diastolic pressure (mm Hg) 14 9 3-40 12-26 8-25 740 3-32Peak systolic pressure (mm Hg) 121 29 68-196 90-104 150-196 68-142 91-146Tension-time index (mm Hg/sec/min) 2840 818 1724-5537 1921-3017 2772-4378 19514800 1724-5537Stroke work (g-m) 198 104 49-510 54-118 147-445 134-510 49-288Work/minute (kg-m/min) 13.3 5.90 4.03-31.10 4.23-7.83 12.60-21.30 9.65-31.10 4.03-17.83Coronary blood flow/100 g (ml/min-100 g) 78.5 25.2 46.1-157.4 48.2-96.9 54.0-96.0 46.1-122.3 47.4-157.4Total coronary blood flow (ml/min) 219 105 36-461 136-275 99430 50401 3646102 consumption/100 g (ml/min-100 g) 10.7 3.3 5.9-19.4 6.2-14.5 7.8-14.0 6.4-19.4 5.9-17.3Total 02 conLsumption (ml/min) 33.3 13.4 7.9-60.6 17.6-49.7 16.9-57.1 24.3-54.7 7.9-60.6Efficiency (%) 21 9 440 4-19 12-36 13-36 940*PMD - primary myocardial disease.**Mixed group contains one patient with isolated mitral stenosis.

by quantitative biplane angiographic techniques describedpreviously.'"'2 It would have been of interest to calculate leftventricular wall stress in these patients. However, filmingrates of 6/second were not considered adequate for con-

struction of accurate stress curves. Left ventricular strokework and work per minute were calculated utilizing theproduct of angiographic stroke volume (end-diastolic vol-ume minus end-systolic volume) and mean ventricular sys-

tolic ejection pressure. Mean pressure was obtained byplanimetry of the area under the left ventricular pressurecurve from the time of mitral valve opening to aortic valveclosure. Total left ventricular MVO2 was computed as ven-tricular mass/100 g X MVO2/100 g. Left ventricular effi-ciency was calculated by relating left ventricular work tototal left ventricular MVO2 as described by Bing.3 Theassumed energy equivalent for oxygen was 2.059 kg-m ofenergy liberated per ml of 02 metabolized;3 left ventricularefficiency in percent was determined as:

Left ventricular work in kg-m/minTotal MVO2 in ml/min X 2.059

These calculations involve the following assumptions: 1)Coronary blood flow as measured by the N20 method, withcoronary sinus sampling, provides a measure of left ven-

tricular blood flow.657 Although the N20 washout methodmay give falsely elevated values of coronary blood flow inpatients with coronary disease,1'-15 none of the patients inthis series had evidence of coronary disease. 2) Venous bloodsampled from the coronary sinus reflects the 02 content ofthe left ventricular myocardial venous drainage. 3) Thevalue of the energy equivalent of 02 assumes a respiratoryquotient of 0.823. 4) The physiologic condition of the pa-tient remains relatively unchanged between the time of cor-

onary blood flow determination and the time of quantitativeangiography. 5) Anaerobic myocardial metabolism is negli-gible in the absence of evidence of coronary artery disease.1'26) The mass value computed by the angiographic methodrepresents perfused tissue for which N20 determined bloodflow measurements is applicable. 7) Left ventricular work as

determined from total stroke volume and mean systolic ejec-

tion pressure prcvides a reasonable measure of the externalwork of the ventricle.The data acquired by these studies were tabulated accord-

ing to major disease categories and analyzed statistically.

Results

Of the 38 patients, four were found to have primary myo-cardial disease; they had ejection fractions < 0.25 withoutevidence of significant valvular abnormality. Six had pre-

dominant left ventricular pressure overload due to aorticvalve stenosis, and 12 patients had predominant aorticand/or mitral regurgitation causing left ventricular volumeoverload. The 16 remaining patients had either pure mitralstenosis (one patient) or mixed lesions with combinations ofmitral and aortic involvement. Table 1 shows the hemo-dynamic data for the 38 patients both collectively and sub-divided into the four diagnostic categories. A wide spectrumof values is seen, with end-diastolic volumes ranging up to490 ml, ejection fractions as low as 0.10, mass values as highas 609 g, and ventricular work up to 31.1 kg-m/min. Totalleft ventricular coronary blood flow was as high as 461ml/min, and MVO2 to 60.6 ml/min. Left ventricular effi-ciency extended from 4 to 40% within the patient group.

Figure I shows graphically the coronary blood flow andMVO2 values per 100 g of myocardium, grouped accordingto major cardiac diagnosis. No significant differences amongthe various disease categories were present. It is noteworthythat a three to four-fold range of these values contrasts witha ten-fold range of values for stroke work, total left ven-

tricular coronary flow, and efficiency; and a seven-fold rangeof values for total MVO2.

Left ventricular mass did not correlate significantly witheither coronary blood flow or with MVO, where these valueswere expressed per 100 g myocardium. Significant correla-tions between mass and total coronary flow or MVO, wouldbe expected since the mass itself is utilized in the calculationof these total values.* It is noteworthy that the amount of

*r = 0.82 and 0.70, respectively.

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20 A

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FIGURE 1. Left ventricular oxygen consumption per 100 g myo-cardium (left vertical axis) and coronary bloodflow per 100 g myo-cardium (right vertical axis) grouped according to major diagnosticcategory. L V = left ventricle. The horizontal lines designate meanand standard deviation.

hypertrophy compared to the left ventricular work isgenerally similar for the different types of workloads in thevalve patients. Thus, mass/work ratio was 22.68 ± 8.81 g-min/kg-m for the pressure-load patients, 23.03 ± 9.00 forthe volume-load group, and 25.76 + 9.76 for the mixed-valve group. There was no significant difference betweenthese groups.

Figure 2 shows the relationship of left ventricular workand total MVO2 for the 38 patients, with symbols depictingthe different diagnoses. The mathematically computed iso-grams reveal the relationship between these two variablesexpressed as efficiency. A graphic expression of this typehelps clarify the relationship between the three variables ofventricular work, MVO2 and mechanical efficiency. No sig-nificant grouping according to disease type is noted, otherthan the self-evident relatively low ventricular work valuesfor the primary myocardial disease patients. Likewise, thetension time index was not significantly correlated with

*= Primary Myocardial Disease30 A=LV Pressure OverloadIj=LV Volume Overload o ,Z Mixed L /

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either total MVO2 (r = 0.03) or MVO2 per 100 g (r = 0.08).Figure 3 shows ejection fraction, as a measure of myo-

cardial function, plotted against left ventricular efficiency.The relationship between these two parameters was not close(r = 0.58). No particular grouping of patient diagnoses isevident other than the low values exhibited by the myo-cardial disease patients. Ejection fraction did not correlatesignificantly with coronary blood flow nor with MVO2, ex-pressed either in total terms or per 100 g of myocardium.Also, there was no correlation whatsoever in comparing cor-onary arterial venous 02 difference with efficiency or withejection fraction.A comparison of left ventricular ejection fraction with

ventricular work per 100 g of myocardium is shown in figure4. The patients with primary myocardial disease, in additionto having low ejection fraction, have the lowest work per-formed per 100 g of myocardium, indicating excessive ven-tricular hypertrophy relative to mechanical workload. Noneof the 38 patients had low ejection fraction with average orhigh work values per 100 g.

Discussion

This report describes quantitatively the mechanical effi-ciency of the left ventricle, in terms of external work per-formed compared to energy utilized, in a series of restingadult patients with valvular and/or myocardial disease. Therange of efficiency values was 4 to 40%, with the lowestvalues found in those patients with primary myocardial dis-ease. A weak association (r = 0.58) existed between efficien-cy and ejection fraction. It is of interest that left ventricularefficiency may be normal in the setting of severe chronic ven-tricular work overload if myocardial function is good.Indeed, as shown in figure 2, the six patients with the highestventricular workloads all had efficiency values greater than24%. These findings reflect the relationships among efficien-cy, hypertrophy, and myocardial function in the resting,chronically diseased human heart. These relationships arecomplex and, as noted by others,1" the factors influencingefficiency are difficult to analyze and discuss. Starling andVisscher commented in 1926 that as the "heart tires,"mechanical efficiency decreases.17 In 1949, Bing et al.calculated efficiency values utilizing estimates of ventricularweights derived from separate autopsy data rather thanfrom in vivo ventricular mass measurements of the subjects

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566 CIRCULATION

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studied.3 Similar to the present findings, they describedvalues from 19.2-24.5% in normal humans; those with heartfailure had efficiencies down to 12.9%. In 1973, Malik et al.induced chronic left ventricular pressure overloads in dogsand later studied multiple parameters of ventricular func-tion, including efficiency, in the intact heart.4 Compared tocontrols, the hypertrophied ventricles exhibited normal orabove normal values of efficiency and ventricular function.Also, Cooper et al. induced chronic right ventricular volumeoverload in cats by surgical creation of atrial septal defects.'8Myocardial function, including MVO2 per unit tensiondevelopment at maximum muscle length, was found to benormal, in spite of the ventricular hypertrophy present.The two variables which determine efficiency are ven-

tricular work and MVO2. It is noteworthy that the ranges ofboth the MVO2 and coronary blood flow values per 100 g ofmyocardium were generally unrelated to the type of left ven-tricular hemodynamic abnormality (fig. 1.). Also, as shownin table 1, these values per 100 g did not extend over as widea range in this series as did other parameters of total leftventricular dynamics, such as stroke work, total MVO2 andcoronary flow, and efficiency. Indeed, as shown in the table,total MVO2 extended up to 60.6 ml/min and coronary flowto 461 ml/min, in patients with severely hypertrophied leftventricles. These figures indicate that left ventricular VO2and coronary flow may represent a significant portion oftotal body VO2 and cardiac output in these disease states.Furthermore, these data support in quantitative terms theprinciple suggested by Bing- that chronically increased rest-ing left ventricular workloads and hence chronically in-creased ventricular metabolic requirements are fulfilled byhypertrophy more than by increased coronary flow andMVO2 per unit of myocardium. He reported a range ofvalues for MVO2/100 g myocardium of 3.5 to 18.8 ml indifferent diseases;3 the values for patients in heart failurewere only slightly higher than the normal controls. Also,Badeer noted that MVO2 per unit myocardium is relativelyconstant in different size dog hearts.19 Thus, the extent ofhypertrophy, rather than the left ventricular workload, is amajor determinant of total resting MVO2 in chronic diseasestates. It is of interest that the amount of hypertrophy com-pared to the workload appears generally the same invalvular heart disease whether the workload is from pres-

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sure or volume or mixed. Thus there was no significantdifference between the three work-overload groups whenmass/work ratio values were compared.

Previously published findings concerning MVO2 changesin response to acute intervention in animals are difficult tointerrelate with data obtained in the chronically diseased,resting state in humans. Thus, numerous animal studies,primarily of in vitro muscle preparations or intact isolatedhearts, have described the factors influencing MVO2. Inthese studies, acute hemodynamic or pharmocologic in-terventions have been instituted and the resultant alterationsin MVO2 measured. Classically the findings have been thatMVO2 is primarily related to myocardial tension or stress,contractile state, and heart rate with less importantrelationships to myocardial work or contractile elementwork, basal metabolism, and the energy of activation forcontraction and relaxation.20-31 The tension-time indexcalculated as the area under the systolic portion of the aorticpressure curve82' 33 and the product of blood pressure timesheart rate," have been regarded as major determinants ofMVO2. Multiple reports have shown that acute pressureloads on the. left ventricle increase MVO2 more than dovolume loads.24 In one such study, Urschel et al. producedacute mitral incompetence in dogs, and noted that MVO2 in-creased only slightly although work was significantly in-creased.85 Ventricular efficiency has also been measuredafter acute intervention. Rodbard and co-workers mea-sured MVO2 and efficiency in dogs with different acute ven-tricular hemodynamic alterations and found efficiencyvalues from 3.9 to 32.7%."" These values varied propor-tionally but nonlinearly with stroke volume. Studies ofhumans by Gorlin revealed that the left ventricular efficiencyindex, calculated without use of ventricular weight, in-creased with exercise in normals." Levine et al. reportedthat this efficiency index was low in a series of patients withheart failure and failed to rise normally with exercise.98Rowe et al. reported that MVO2/100 g and coronaryflow/100 g rose with exercise both in normal patients andthose with aortic valve disease.6 The reason that efficiencymay increase with exercise in normals is unclear, since theaugmented contractility with exercise should increase the °2cost per unit work. Decreasing ventricular size with exercisein normals, but not in disease states, has been implicated,since this should reduce wall tension.38

In contrast to left ventricular responses to acute hemo-dynamic changes, the left ventricle cavity size and masschange significantly in response to chronic alteration inworkload and myocardial function.3' In comparison to thefindings in acute hemodynamic alterations in individualhearts, the data of this study were obtained from a series ofresting patients with chronic disease. Thus, as expected,there is no significant relationship between the tension-timeindex and either total MVO2 or MVO2/ 100 g. In long-stand-ing volume overload conditions such as mitral or aorticvalvular incompetence, the left ventricular end-diastolicvolume usually increases to allow a greater stroke volumewithout increase in ejection fraction.Y In chronic left ven-tricular pressure overloads such as aortic valve stenosis thechamber volumes may remain normal." In conditions withdiffusely decreased myocardial function, with or without co-existent valvular disease, the end-diastolic volume usuallyincreases out of proportion to the stroke volume, with resul-

0 2 4 6 8 10

L.V. WORK/MASS (KG - M/100 GM - MIN)FIGURE 4. Left ventricular ejection fraction compared to left ven-tricular work/mass, or work per gram of myocardium.

0.0

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568 CIRCULATION

tant decrease in ejection fraction.'2 `-4a The MVO, shoulddecrease with decreased ventricular function.28 In thisregard, Henry and co-workers reported a significant correla-tion between circumferential fiber shortening velocity andMVO2/l00 g measured by helium washout techniques in 14patients.9 Left ventricular transmural wall tension, on theother hand, is related to both intracavitary pressure andchamber dimensions by the La Place relationship.42 Thus,either elevated ventricular end-diastolic volume or highsystolic pressure loads will increase wall tension. In thesesituations, the left ventricular mass tends to increase to theextent that wall stress per cm' cross-sectional area regressestoward normal." With this increase in left ventricular masscomes increased total MVO. Consideration of all these fac-tors leads to the theoretical possibility that decreased ven-tricular function could, by virtue of decreased MVO2, in-crease efficiency. However, as indicated by the data of thisstudy and others,3 4 19. 38 apparently the hypertrophy andventricular shape changes assume primary significance, suchthat efficiency is usually decreased with chronic myocardialfailure. Although this study reveals the range of theseefficiency values in this group of patients, the basic etiologyof low efficiency remains unknown. It is suspected that lowefficiency results from a primary abnormality in conversionof energy to contractile work. Other possibilities, however,such as internal cellular alignment abnormalities with in-effective coordination of contraction must also be con-sidered.

In this group of 38 patients with various combinations ofpressure overload, volume overload and decreased ven-tricular function, there is evident reason for the observedwide spectrum of values for ventricular mass, workload, andefficiency.

References

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VOL 55, No 4, APRIL 1977

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W A Baxley, H T Dodge, C E Rackley, H Sandler and D PughLeft ventricular mechanical efficiency in man with heart disease.

Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 1977 American Heart Association, Inc. All rights reserved.

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