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Right Ventricular Performance in Essential Hypertension JACK FERLINZ, M.D. SUMMARY Effects of systemic hypertension on right ventricular (RV) performance have not been previously investigated. In this study, 10 normal patients were compared to 20 patients with uncomplicated, asymptomatic essential hypertension (defined as cuff diastolic blood pressure 2 100 mm Hg) after a complete hemodynamic and RV cineangiographic evaluation. The mean intra-arterial pressure in the normal group was 93 ± 11 vs 120 ± 13 mm Hg in the essential hypertension group (p < 0.01). All right-sided pressures were sub- stantially higher in the hypertensive than in the normal patients (mean right atrial pressure: 2 ± 1 mm Hg for normals, 5 ± 3 mm Hg for hypertensives,p < 0.01; RV end-diastolic pressure: 3 ± 2 mm Hg for normals, 5 ± 2 mm Hg for hypertensives, p < 0.05; mean pulmonary artery pressure: 12 ± 3 mm Hg for normals, 17 ± 5 mm Hg for hypertensives, p < 0.01; mean pulmonary capillary wedge pressure: 6 ± 1 mm Hg for normals, 9 ± 3 mm Hg for hypertensives, p < 0.01. Cardiac index in normal and hypertensive patients was nearly iden- tical (2.93 ± 0.80 1/min/m2 in normals, 3.11 ± 0.67 1/min/m2 in hypertensives, NS). In contrast, a markedly lower cineangiographic RV ejection fraction was present in the hypertensive compared with the normal patients (68 ± 6% vs 59 ± 7%, p < 0.01). The lower RV ejection fraction was due to the proportionately greater increase in the RV end-systolic volume index (22 ± 5 mI/M2 for normals, 34 ± 8 mI/m2 for hyperten- sives, p < 0.01) than in the end-diastolic volume index (69 ± 13 ml/m2 for normals, 82 ± 16 mI/M2 for hypertensives, p < 0.04) in the hypertensive patients. It is concluded that 1) hypertensive patients have higher right-sided pressures than normals, and 2) RV performance in essential hypertension may be characterized by a lower RV ejection fraction than in normal subjects. RIGHT VENTRICULAR (RV) performance in adult heart disease has received only scant attention compared with the efforts designed to study the left ventricular function. The most extensively in- vestigated area of potential RV dysfunction is cor- onary artery disease, where RV ejection fraction has been measured in patients with and without the right coronary artery occlusion." 2 Furthermore, patterns of RV asynergy have been evaluated in acute3 and chronic4 ischemic coronary disease. Attempts have been also made to determine the extent of RV dysfunction in chronic obstructive pulmonary disease5 and adult congenital heart disease with RV pressure and volume overload,6 and to compare these findings with the results in normal adult population.7 Very lit- tle is known, however, about the nature of RV perfor- mance when the left ventricle is exposed to a chronic pressure overload that takes place in essential hypertension. Because the distortions of the normal geometry of the two ventricles influence each other's performance,8"16 this study was designed to investigate the impact of chronic left ventricular pressure over- load in patients with essential hypertension on RV function and to compare these performance characteristics with the RV function seen in the con- comitantly studied normal subjects. From the Cardiology Section, Medical Service, Veterans Ad- ministration Medical Center, Long Beach, California, and the University of California School of Medicine, Irvine, California. Address for correspondence: Jack Ferlinz, M.D., Chief, Cardiac Catheterization Laboratory, Veterans Administration Medical Center, 5901 East Seventh Street, Long Beach, California 90822. Received February 1, 1979; revision accepted June 28, 1979. Circulation 61, No. 1, 1980. Materials and Methods Thirty patients were selected for this study. All gave informed consent and were divided into two groups. Ten patients had the chest pain syndrome and were evaluated with a complete hemodynamic assess- ment, selective left ventriculography and coronary arteriography. When cardiac catheterization failed to reveal any organic cardiac pathology, these patients were allocated to the normal group (NI), and served as control subjects. The other 20 patients had documented essential hypertension for at least 3 months. Their sphygmomanometer-determined diastolic blood pressure was consistently . 100 mm Hg, and they were allocated to the essential hyperten- sion group (EH). None of the EH patients had a history of cerebrovascular disease, pulmonary dis- orders, congestive heart failure or significant valvular or congenital lesions. While coronary anatomy was not studied in the hypertensive subjects, and latent coronary artery disease could therefore have been present in some of them, none had a history or symp- toms indicative of coronary disease or electrocar- diographic evidence of a prior myocardial infarction. All subjects were in normal sinus rhythm and had no conduction abnormalities. Funduscopic examination was normal in all patients, and none of the subjects had elevated serum creatinine. A clinical profile for the entire patient population is presented in table 1. Some of the EH patients were receiving an- tihypertensive medications; these were stopped at least 2 weeks before the study. These patients were closely monitored after the antihypertensive medications were discontinued in order to detect immediately a poten- tially dangerous acceleration of hypertension. This did not occur in any of the subjects, and they did not develop new symptoms or complications. 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Right Ventricular Performancein Essential Hypertension

JACK FERLINZ, M.D.

SUMMARY Effects of systemic hypertension on right ventricular (RV) performance have not beenpreviously investigated. In this study, 10 normal patients were compared to 20 patients with uncomplicated,asymptomatic essential hypertension (defined as cuff diastolic blood pressure 2 100 mm Hg) after a completehemodynamic and RV cineangiographic evaluation. The mean intra-arterial pressure in the normal group was93 ± 11 vs 120 ± 13 mm Hg in the essential hypertension group (p < 0.01). All right-sided pressures were sub-stantially higher in the hypertensive than in the normal patients (mean right atrial pressure: 2 ± 1 mm Hg fornormals, 5 ± 3 mm Hg for hypertensives,p < 0.01; RV end-diastolic pressure: 3 ± 2 mm Hg for normals, 5 ±

2 mm Hg for hypertensives, p < 0.05; mean pulmonary artery pressure: 12 ± 3 mm Hg for normals, 17 ± 5mm Hg for hypertensives, p < 0.01; mean pulmonary capillary wedge pressure: 6 ± 1 mm Hg for normals, 9± 3 mm Hg for hypertensives, p < 0.01. Cardiac index in normal and hypertensive patients was nearly iden-tical (2.93 ± 0.80 1/min/m2 in normals, 3.11 ± 0.67 1/min/m2 in hypertensives, NS). In contrast, a markedlylower cineangiographic RV ejection fraction was present in the hypertensive compared with the normalpatients (68 ± 6% vs 59 ± 7%, p < 0.01). The lower RV ejection fraction was due to the proportionatelygreater increase in the RV end-systolic volume index (22 ± 5 mI/M2 for normals, 34 ± 8 mI/m2 for hyperten-sives, p < 0.01) than in the end-diastolic volume index (69 ± 13 ml/m2 for normals, 82 ± 16 mI/M2 forhypertensives, p < 0.04) in the hypertensive patients. It is concluded that 1) hypertensive patients have higherright-sided pressures than normals, and 2) RV performance in essential hypertension may be characterized bya lower RV ejection fraction than in normal subjects.

RIGHT VENTRICULAR (RV) performance inadult heart disease has received only scant attentioncompared with the efforts designed to study the leftventricular function. The most extensively in-vestigated area of potential RV dysfunction is cor-onary artery disease, where RV ejection fraction hasbeen measured in patients with and without the rightcoronary artery occlusion." 2 Furthermore, patternsof RV asynergy have been evaluated in acute3 andchronic4 ischemic coronary disease. Attempts havebeen also made to determine the extent of RVdysfunction in chronic obstructive pulmonary disease5and adult congenital heart disease with RV pressureand volume overload,6 and to compare these findingswith the results in normal adult population.7 Very lit-tle is known, however, about the nature of RV perfor-mance when the left ventricle is exposed to a chronicpressure overload that takes place in essentialhypertension. Because the distortions of the normalgeometry of the two ventricles influence each other'sperformance,8"16 this study was designed to investigatethe impact of chronic left ventricular pressure over-load in patients with essential hypertension on RVfunction and to compare these performancecharacteristics with the RV function seen in the con-comitantly studied normal subjects.

From the Cardiology Section, Medical Service, Veterans Ad-ministration Medical Center, Long Beach, California, and theUniversity of California School of Medicine, Irvine, California.Address for correspondence: Jack Ferlinz, M.D., Chief, Cardiac

Catheterization Laboratory, Veterans Administration MedicalCenter, 5901 East Seventh Street, Long Beach, California 90822.

Received February 1, 1979; revision accepted June 28, 1979.Circulation 61, No. 1, 1980.

Materials and MethodsThirty patients were selected for this study. All gave

informed consent and were divided into two groups.Ten patients had the chest pain syndrome and wereevaluated with a complete hemodynamic assess-ment, selective left ventriculography and coronaryarteriography. When cardiac catheterization failed toreveal any organic cardiac pathology, these patientswere allocated to the normal group (NI), and served ascontrol subjects. The other 20 patients haddocumented essential hypertension for at least 3months. Their sphygmomanometer-determineddiastolic blood pressure was consistently . 100 mmHg, and they were allocated to the essential hyperten-sion group (EH). None of the EH patients had ahistory of cerebrovascular disease, pulmonary dis-orders, congestive heart failure or significant valvularor congenital lesions. While coronary anatomy wasnot studied in the hypertensive subjects, and latentcoronary artery disease could therefore have beenpresent in some of them, none had a history or symp-toms indicative of coronary disease or electrocar-diographic evidence of a prior myocardial infarction.All subjects were in normal sinus rhythm and had noconduction abnormalities. Funduscopic examinationwas normal in all patients, and none of the subjectshad elevated serum creatinine. A clinical profile forthe entire patient population is presented in table 1.Some of the EH patients were receiving an-

tihypertensive medications; these were stopped at least2 weeks before the study. These patients were closelymonitored after the antihypertensive medications werediscontinued in order to detect immediately a poten-tially dangerous acceleration of hypertension. This didnot occur in any of the subjects, and they did notdevelop new symptoms or complications. Therefore,

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RV PERFORMANCE IN ESSENTIAL HYPERTENSION/Ferlinz

TABLE 1. Clinical Profile of Patient PopulationAverage of six hypertensive

Age BP readings (d= sD) during Cardiomegaly(years) 2 weeks before study (CT ratio >

No. (mean ± Sryst Diast Electrocardiogram 0.50) on chestGroup pts SD) (mm HIg) (mm Hg) WNTL LVIH x-ray

Normal 10 46 9 None None All None None

Hypertensive 20 51 8 169 ± 15 110 8 13 (6.55%) 7 (35%) None

Abbreviations: BP blood pressure; CT cardiothoracic; LVH - left ventricular hypertrophy; WNL-within normal limits.

none of the patients had to be excluded because thewithdrawal of medication was poorly tolerated.

All patients in both groups were studied with a com-bined hemodynamic-angiographic approach. Cir-culatory measurements and angiograms were per-formed in the fasting state, in the supine position, andwithout premedication. Cardiac output (CO) andpressure data were collected before the right ven-triculogram. CO was determined with the Lyons in-docyanine green indicator-dilution computer byaveraging four sequential measurements. All pres-sures - aortic (AP) and pulmonary artery (PAP)systolic, diastolic, and mean; RV systolic and end-diastolic; mean right atrial (RAP); and meanpulmonary capillary wedge pressure (PCWP) - weremeasured in each case with Statham model P23Dbstrain gauges and recorded with an Electronics forMedicine DR-12 Simultrace recorder over three fullrespiratory cycles. Heart rate (HR) was monitoredthroughout the study. In addition, systemic vascularresistance (SVR = [mean AP -mean RAP] / CO)and pulmonary vascular resistance (PVR = [meanPAP - mean PCWP] / CO) were calculated for eachpatient.

Single-plane, cine right ventriculograms in the 30Oright anterior oblique (RAO) projection were per-formed in all 30 patients. Fifty-five to 65 ml of 76%megluminie sodium diatrizoate (Renografin 76) wereinjected over a 3-second interval into the RV chamberthrough a #8 Eppendorf or NIH catheter in each case,and right ventriculograms recorded at 64 frames/sec

on 35-mm Ilford Cinegram F film with Philips 9-inchimage intensifier. Only the first six beats after com-plete opacification were analyzed by two independentobservers. Whenever different values for the RV ejec-tion fraction were obtained, the two values wereaveraged. In general, there was only a negligiblevariance in the calculated values; the largest dis-crepancy was only 4%, and the correlation coefficientfor the two observers was 0.96. If a premature ven-tricular contraction occurred, at least two successivenormal sinus beats (after the premature beat) had tooccur before a frame was selected for volumetricanalysis. A typical high-resolution frame (EH patient16) is presented in figure 1.

RV volumes were determined with the methodfor single-plane RV volume measurements previouslydeveloped in our laboratory.'7 This method is quite ac-curate (r = 0.93) compared with the very precisebiplane RV volumetric analysis.' End-diastolicvolume index (EDVI), end-systolic volume index(ESVI), stroke volume index (SVI) and ejection frac-tion (EF = SVI/EDVI) were calculated for eachpatient.

All data were analyzed with the t test for nonpairedvariables.18

Results

The complete mean hemodynamic and volumetricdata for both groups are given in table 2, and a sum-mary of key cardiovascular findings for each Nl andEH patient in tables 3 and 4.

FIGURE 1. A representative right ventricular cineangiogram in end-systole (left) and end-diastole (right).

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VOL 61, No 1, JANUARY 1980

Volumetric Data for Normal

Normal Hypertensivepatients patients

(mean 5= SD) (mean + SD) SignificanceParameter n = 10 n = 20 (p)

Syst AP(mm Hg) 132 19 163 23 <0.01

Diast AP(mm Hg) 71 11 92 11 <0.01

Mean AP(mm Hg) 93 11 120 =t 13 <0.01

Mean RAP(mm Hg) 2 s= 1 5 83 <0.01

RV syst press(mmHg) 22 - 6 27 5 <0.02

RVEDP(mm Hg) 3 2 5 2 <0.05

Syst PAP(mm Hg) 20 i= 6 26 6 <0.02

Diast PAP(mmHg) 8 2 11 5 <0.03

Mean PAP(mm Hg) 12 3 17 5 <0.01

Mean PCWP(mm Hg) 6 - 1 9 *3 <0.01

SVR (dyn-sec-cm-5) 1502 - 469 1609 527 NS

PVR (dyn-sec-cm-5) 104 i= 53 108 57 NS

HR (beats/min) 75 12 77=-9 NS

CI (l/min/m2) 2.93 - 0.80 3.11 - 0.67 NS

RV EDVI(m1/m2) 69 - 13 82 - 16 <0.04

RV ESVI(m1/m2) 22 - 5 34 - 8 <0.01

RV SVI(mi/M2) 47 11 48 12 NS

RVEF(%) 68 - 6 59 - 7 <0.01

Abbreviations: AP = arterial pressure; CI = cardiacindex; EF - ejection fraction; EDVI = end-diastolic volumeindex; ESVI = end-systolic volume index; HR = heartrate; n = number of patients; PAP = pulmonary arterypressure; PCWP = pulmonary capillary wedge pressure;PVR = pulmonary vascular resistance; RAP = right atrialpressure; RV = right ventricular; RVEDP right ven-tricular end-diastolic pressure; SD = standard deviation;SVI = stroke volume index; SVR = systemic vascularresistance.

The EH patients are characterized by a substan-tially higher (p < 0.01) systolic, diastolic, and meansystemic intra-arterial pressures than their normalcounterparts. The diastolic pressure for the EH groupwas > 90 mm Hg - a reading that has beenassociated with a greater incidence of cardiovascularcomplications than in control subjects.'9-21 SVR wasalso higher in the EH patients, but this difference didnot reach statistical significance, possibly because the

SVR in the hypertensive group was partially loweredby the higher CO and RAP than was present in thecontrol group.

All right-heart pressures, including the right and leftventricular filling pressures (mean RAP and PCWP,respectively) were significantly higher in the EHpatients. The relationship between the systemic andthe right-sided pressures is depicted in figure 2. PVR,however, was only slightly greater in hypertensivethan in the normal subjects, probably again reflectinghigher CO and PCWP in the EH group.

There was no appreciable difference in HR betweenthe two groups. Cardiac index was higher in the EHpatients, but this increase was not statistically signifi-cant. In contrast, RV volumetric analysis revealedthat the RV EDVI and ESVI are substantially greaterin the EH patients (p < 0.04 and < 0.01, respectively),while the RV SVI is almost the same in both groups.Because the increase in the RV ESVI is proportionallymuch larger than the increase in the RV EDVI (ESVIincreased from 22 to 34 ml/m2, representing a rise of55%; EDVI rose from 69 to 82 ml/m2, representing anincrease of only 19%), RV EF is significantly lower (p< 0.01) in the EH patients than in the controls. Therange of RV EF for normal subjects was 56-78% (onlyone patient had a RV EF less than 60%), while in theEH subjects the RV EF varied from 51-71% (with 10,or 50%, of all patients having an RV EF that was lessthan 60%). The relationship between the RV EDVI vs

RVEDP, and the RV ESVI, SVI and EF vs RV fill-ing pressure (that is, mean RAP), is presented infigure 3.

In a recent report,22 Olivari et al. suggested that theRV function in systemic hypertension can be predictedon the basis of a standard ECG. If the ECG of the EHpatients shows evidence of left ventricular hyper-trophy without strain, the RV function is likely to besupernormal. If left ventricular hypertrophy withstrain is seen, however, RV performance purportedlydeteriorates below the normal levels. This differentia-tion between the normal and abnormal RV functionbased on ECG could not be confirmed in the presentstudy. The patient (EH patient 6) with the mostseverely abnormal ECG (SV, + RV, = 46 mm withstrain) had one of the highest RV EFs in the EH group(70%). However, a better correlation between the RVperformance and ECG might emerge if more of ourEH patients had abnormal ECG tracings.

DiscussionThis study demonstrates that right-sided circulation

is not immune to the effects of systemic hypertension.The increase in the right-heart pressures among theEH patients is significantly different from the values inthe normotensive controls in this study and in theclassic study of normal subjects by Fowler et al.23Earlier reports have suggested that pulmonarypressures remain normal in essential hypertension.24-27More recently, relative elevation of right-sided pres-sures in hypertensive patients has been reported.22 28

Some investigators have postulated that when

TABLE 2. Hemodynamic andand Hypertensive Patients

CIRCULATION158

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RV PERFORMANCE IN ESSENTIAL HYPERTENSION/Ferlinz 159

TABLE 3. Summary of Key Cardiovascular Findings for Each Normal Patient

Pt Mean AP Mean RAP RVEDP Mean PAP Mean PCWP CI RV EDVI RV ESVI RV EFno. (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (I/min/M2) (mi/M2) (ml/m2) (%)

1 80 2 4 13 6 3.24 76 21 722 106 1 1 10 4 2.10 77 24 693 95 1 1 10 6 3.06 73 16 784 105 3 4 12 6 3.60 64 22 665 80 1 2 12 5 3.20 67 23 666 85 3 6 14 8 2.87 59 26 567 110 4 4 18 6 2.23 90 27 708 93 2 5 12 7 4.58 63 23 639 92 2 2 10 7 2.22 44 12 73

10 82 2 3 10 4 2.20 80 27 66

MeaniSD 93d11 2 1 3 -2 12 3 6 1 2.93 - 0.80 69 -13 22 5 68 6

Abbreviations: See table 2.

pulmonary pressures rise in patients with essential major mechanism responsible for the elevated right-hypertension, this increase reflects the increasing sided pressures of the EH patients. However, becausediastolic pressures in the failing left ventricle.25 29, 30 an impaired cardiac pump function can be detectedNone of the EH patients in this study had clinical, during exercise even in patients with early, un-chest x-ray or hemodynamic findings suggestive of complicated essential hypertension,3" a latent left ven-even borderline left ventricular decompensation. Left tricular failure in the hypertensive group cannot beventricular failure, therefore, cannot be considered the completely excluded, and this incipient cardiac in-

TABLE 4. Summary of Key Cardiovascular Findings for Each Hypertensive Patient

Pt Mean AP Mean RAP RVEDP Mean PAP Mean PCWP CI RV EDVI RV ESVI RV EFno. (mm Hg) (mm Hg) (mm Hg) (mm Hg) (mm Hg) (I/min/M2) (mi/M2) (mi/M2) (%)

1 125 1 1 16 15 3.47 81 34 582 110 4 5 14 10 2.93 58 25 563 110 4 6 18 7 3.60 92 45 514 110 3 4 11 7 2.90 59 23 615 115 1 1 10 6 2.21 75 34 556 120 6 6 18 12 3.56 74 22 707 130 10 10 32 12 5.02 80 36 55

8 107 3 3 13 8 3.56 76 33 579 128 8 8 19 14 3.37 72 32 56

10 108 2 3 14 10 3.39 99 44 5611 160 3 5 14 5 2.02 102 30 7112 115 6 6 19 12 3.13 106 37 6513 130 3 3 14 7 3.18 89 42 5314 112 4 5 17 6 2.79 81 37 5415 113 2 4 10 5 2.48 55 26 5316' 130 4 6 15 9 3.42 77 31 6017 112 9 9 18 11 3.10 93 46 5118 120 6 8 21 11 2.54 96 29 7019 110 5 9 20 10 3.07 66 21 6820 130 6 6 20 12 2.37 100 44 56

MeanSD 120 13 5 43 5 2 17 - 5 9 3 3.11 -0.67 82 i 16 34 -8 59- 7

Abbreviations: See table 2.

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CIRCULATION VOL 61, No 1, JANUARY 1980

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right ventricular end-diastolic pressure;PAP = pulmonary artery pressure; PCWP= pulmonary capillary wedge pressure.

sufficiency may contribute to the rise in right-sidedpressures.

However, if it is accepted that left ventricular func-tion is virtually intact in the EH patients, and it there-fore plays only a minor (or no) role in increasingpulmonary pressures, the cause for elevated right-sided pressures in hypertensive subjects becomesobscure. Decades ago it was postulated that systemichypertension may cause hypertrophy of the left ven-tricular septum, which encroaches on the right ven-tricular chamber to such an extent that there is a func-tional obstruction within the RV cavity (theBernheim's syndrome).32" 33 As a result, peripheralvenous and right atrial pressures increase, resulting ineventual right-heart failure. The very existence of this

syndrome, however, is still in doubt.34 Furthermore,even if it is real, it is probabl' not a factor in the EHpatients in this study because in the Bernheim's syn-drome pulmonary circulation should remain un-affected and RV volumes should decrease; yet our EHsubjects have higher pulmonary arterial pressures andRV volumes than the normal controls. Potentiallymuch more important than the Bernheim's syndromeis the effect of various humoral mechanisms on right-sided circulation. Patients with essential hypertensionhave enhanced sympathetic activity35 36 and haveresting plasma catecholamine concentrations that aresubstantially increased.36 37 Furthermore, the rate ofangiotensin generation is clearly elevated in most ofthese subjects.38 Because pulmonary circulation

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FIGURE 3. Relationship between rightventricular (R V) volumes and ejection frac-tion (EF) vs R V pressures for normotensiveand hypertensive groups. The R V end-diastolic volume index (ED VI) and end-systolic volume index (ESVI) are sig-nificantly higher, and R V EF is significantlylower in hypertensive patients. RV strokevolume index (SVI) is virtually identicalin both groups.

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RV PERFORMANCE IN ESSENTIAL HYPERTENSION/Ferlinz

responds readily to norepinephrine and angiotensinwith pulmonary vasoconstriction and elevatedpulmonary pressures,39-44 increased right-heartpressures in essential hypertension may reflectenhanced activity of catecholamines, angiotensin, orsome other humoral substance that is capable ofproducing pulmonary vasoconstriction.45 Whetherthese humoral agents are also responsible for the re-

cent observation that the decreased vascular com-pliance in essential hypertension is not limited to thearterial system, but is also present in the venous cir-culation,46 is still unresolved.CO has been reported to be elevated in uncompli-

cated essential hypertension,35 41, 41 as has the restingHR.35 48 49-51Most investigators believe that the highresting CO is a direct result of the increase in HR.3'Only one study reports a normal HR and a marked in-crease in cardiac index.47 No significant difference inCO and HR between the NI and EH subjects was

noted in this study. Therefore, it must be concludedthat CO and HR frequently remain normal in patientswith essential hypertension a finding consistentwith reports from many other investigators.46 52 54

Ventricular EF is one of the most sensitive indicesof cardiac function.55 5 The volumetric analysis of RVperformance in Nl and EH patients is, therefore, thecornerstone of this study. Compared with the normalsubjects, the RV EF is significantly lower in thehypertensive patients, indicating that RV emptyingmay become impaired in essential hypertension.

Several mechanisms may account for this finding. Ithas been demonstrated that the end-systolic dimen-sions increase, and ventricular contractility decreaseswith increases in afterload.58 Because of the increasedpulmonary pressures in the EH patients (fig. 2), theRV afterload becomes augmented, and the RVresponds with larger ESVI and lower EF (fig. 3). Thisstudy, therefore, does not confirm prior findings in ex-

perimental animals that systemic hypertensiongenerates a stimulus in response to the increased func-tional requirements of myocardium, which, until theleft ventricle fails, causes the RV to function in an

augmented state;59' 60 or that RV performance can beincreased by the right-sided Anrep effect.61

Other mechanisms that may depress the RV perfor-mance in systemic hypertension may occur because ofthe interdependence of the two ventricles.8 16 62 Thus,

a stressed left ventricle may adversely affect RV per-formance and bring about changes in the RV volume-pressure characteristics. This influence may be exertednot only by the interventricular septum, which is com-prised of a thin right and a relatively thick left musclemass,63"65 but also by the circular and spiral bundles ofmuscle fibers that encircle both ventricles.66' 67

In conclusion, the concept that the right ventricle isimmune from the effects of uncomplicated systemichypertension is no longer tenable. RV pressures,volumes, and EF change significantly even with earlyabnormal increases in the arterial pressure. Systemichypertension therefore exerts its influence on thewhole heart, strengthening the concept that the right

and left ventricles physiologically represent a singlefunctional unit. The causes for right-heart changesseen in essential hypertension are complex. Toevaluate these mechanisms further, simultaneous rightand left ventricular volume-pressure relationshipsmust still be investigated.

AcknowledgmentThe expert secretarial assistance of Wilma Mottin is greatly ap-

preciated.

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