JACC Vol. 22, No . 3September 1993 : 65 9-64

Systolic Blood Pressaire As - . : .- : : During Exercise AcoveryWith Angin- _D-c~wis

MASAKI HASHIMOTO MD, MITSUNORI OKAMOTO, MD, TOGO YAMAGATA, MD,*

TETSUYA YANMANE, MD,* MITSUMASA WATANABE, MD,* YUKIKO TSUCHIOKA, MHIDEO MATSUURA, MD,* GORO KAJIYAMA, MD*

Hiroshima City, Japan

Abilo .fib

Objectives. This study was conducted to clarify the eases laanisaatsof the abnormal systolic blood pressure response after exercise inpatients with angina pectoris.

Background. An abnormal systolic blood pressure response inpatients with angina pectoris has been observed not only duringexercise beat also during the recovery period after exercise .However, the mechanisms of this abnormal response duringrecovery have not been elucidated .

Methods . Thirty-five patients with angina pectoris and 17control subjects underwent bicycle ergometric studies after inser-tion of a Swan-Ganz catheter .

Results . In control subjects, all hemodynandc variables de-creased rapidly after exercise . In 7 of the 35 patients, systolicblood pressure increased after exercise . The patients with anginawere classified into two groups. In group 1 (17 patients), changesin systolic blood pressure during recovery were smaller than those

It is well established that a decrease or an inadequateincrease; in systolic blood pressure during exercise stresstesting is frequently observed in patients with angina pecto-ris and severe coronary artery disease (1-11) . A change insystolic blood pressure during exercise in patients withangina is suggestive of myocardial ischemia or severe coro-nary artery disease . Moreover, we (12-14) previously re-ported that an abnormal systolic blood pressure response inpatients with angina was observed not only during exercisebut also during the recovery phase ; that is, some patientswith angina showed an inadequate increment in systolicblood pressure during exercise and a lesser decrease insystolic blood pressure during the recovery phase . How-ever, the mechanisms of these abnormal systolic bloodpressure responses during exercise and recovery have notbeen elucidated . The present study was performed to clarifythe mechanisms of the abnormal systolic blood pressure

From the Department of Cardiology, Hiroshima Prefectural HiroshimaHospital and the *First Department of Internal Medicine, Hiroshima Univer-sity, School of Medicine, Minami-ku, Hiroshima City, Japan .

Manuscript received August 3, 1992 ; revised manuscript received Febru-ary 9, 1993, accepted March 2, 1993 .

Address for correspondence : Masaki Hashimoto, MD, Department ofCardiology, Hiroshima Prefectural Hiroshima Hospital, 1-5-54 Ujinakanda,Minami-ku, Hiroshima City, Japan 734 .

©1993 by the American College of Cardiology

659

in control subjects . In group 11 (IS patients) recovery of systolicblood pressure was normal . Changes in stroke index front rest topeak exercise were smaller in group I than in group 11 . Strokeindex in both patient groups increased paradoxically duringrecovery. The increase in systemic vascular resistance indexduring recovery and the ratio of plasma norepineplarine concen-tration to cumulative work load were greater in group 1 than ingroup 11 .

Conclusions . An abnormal systolic blood pressure resafter physical exercise in patients with angina pectoris is indicativeof severe myocardial ischenain during ekmoise and may be causedby an increase in stroke volume due to recovery from myocardialischenfla and increased systemic vascular resistance secondary toexaggerated sympathetic nervous activity .

(J Am Coll Cardiol 1993,22 :659-64)

response during recovery after exercise in patients withangina pectoris .

MethodsStudy patients (Table 1) . The study group comprised 17

control subjects (12 men and 5 women) and 35 patients (26men and 9 women) with stable effort angina pectoris who hadtransient attacks of chest pain with evidence of myocardialischemia and significant ST-T wave changes . The age of the35 patients ranged from 28 to 73 years (mean 60) and 22 hada history of myocardial infarction . The age of the controlsubjects ranged from 22 to 70 years (mean 50) . All patientsunderwent coronary angiography within 6 months of thestudy. Fifteen patients had single-vessel, nine had double-vessel and I I had triple-vessel disease . Patients with recentmyocardial infarction (within 3 months) or prior coronaryrevascularization were excluded . All patients were with-drawn from all antianginal drugs (beta-adrenergic blockers,calcium blockers and nitrates) for 2t2 days . Control subjectswere patients with a chest pain syndrome who had normalresults on chest X-ray study, electrocardiogram, echocardio-gram and thallium-201 exercise stress myocardial imaging .All patients and control subjects gave written informed

0755-1097/931$6 .00

660

HASHIMOTO ET AL .BLOOD PRESSURE RECOVERY IN ANGINA

TAle 1 . Clinical Characteristics of the Study Groups

Control

Patients withSubjects

Angina Pectoris

wed as number of subjects or patients or mean value ± SECAD - coronary artery disease : F - female : M - male ; MI - myocardiAmurcOn .

consent, and the study protocol was approved by the HumanStudies Committee of Hiroshima University .

E%evdse protocol. A Swan-Ganz catheter was insertedthrough the subelavian vein and positioned in the pulmonaryartery . Baseline values for blood pressure, heart rate, pul-monary artery pressure, cardiac output and left ventricularejection fraction (by radionuclide ventriculography) weremeasured . Blood sampling for measurement of plasmanorepinephrine concentration was also performed at rest .The exercise test was performed in the supine positionusing a bicycle ergometer . Exercise was started at 25 W,and the work load was increased by 25 W every 4 min .The exercise rate was constant at 6C rpm . Exercise wascontinued until the patient develops A chest pain or at-tained the target heart rate . Blood pressure, heart rate,pulmonary artery pressure, cardiac output and weft ventric-ular ejection fraction were measured, and blood samplingfor plasma norepinephrine was also performed at peakexercise. Exercise capacity was defined as the product ofexercise duration (in min) multiplied by t,.ie work load (in W)of each exercise level (integration of work loads) . Afterexercise, blood pressure, heart rate, pulmonary artery pres-sure and cardiac output were measured 1, 3 and 6 min afterthe end of exercise . Left ventricular ejection fraction wasmeasured -2 to 4 and e5 to 7 min after the end of exercise(Fig . 1).

Hemodynamic measurements. Blood pressure was meausured by a standard cuff technique and cardiac outputby a thermodilufion method. Stroke index and systemicvascular resistance index were calculated from standardformulas.

Radionuclide ventricuk4raphy . To obtain the left ventric-ular ejection fraction, multigated radionuclide vcntriculogra-PhY was recorded by labeling red blood cells in vivo with20 mCi of technetium-99m. Radionuclide ventriculographywas Performed using a scintillation camera with a multipur-pose collimator and hardware zoom and R wave-triggeredgate interfaced with an ADAC system l computer. Thecamera head was positioned in the left anterior obliqueprojection to maximize the separation of the right and leftventricles (usually 45°). Data were processed using conven-

HRBPCtPADPLVEFPNE

Peak Ex .

t

t

JACC Val . 22, No. 3September 1993 :659-64

t

t

t

t

11t

Figure 1 . Exercise (Ex .) protocol and measurements of hemody-namic variables. BP blood pressure : Cl = cardiac index ; HR =heart rate : LVEF left ventricular ejection fraction: PADP =pulmonary artery diastolic pressure ; PNE -T plasma norepinephrincconcentration. Arrows indicate when measurements were made .

tional software prcgrams, which included automated calcu-lation of the left ventricular ejection fraction .

Norepinephrine levels. Mixed venous blood samples weredrawn through a Swan-Ganz catheter and centrifuged .Plasma was stored at -60'C for subsequent determination ofplasma norepinephrine levels using a modification of themethod described by Sato et al . 15 .

Statistical analysis . Data are presented as mean value tSD. The data were analyzed with multiple comparisonScheR test with SAS statistical software SAS Institute .The significance level was taken at < 0.05 of the alphavalue. Differences in categoric variables were analyzed bychi-square analysis; a value of p < 0.05 was consideredstatistically significant .

Results

Systolie blood pressure response during recovery. Themean change in systolic blood pressure from peak exerciseto recovery in control subjects was -37, -58 and--65 mm Hg at 1, 3 and 6 min, respectively, after terminationof exercise . Seven of the 35 patients with angina pectorisshowed an increase in systolic blood pressure after exercise .Then, according to the criteria of Acanfora et al . 16 andAmon et al . 17 of an abnormal systolic blood pressureresponse during recovery, we defined the upper limits as2 SD of the control value for the change in systolic bloodpressure from peak exercise to each recovery point . We thenclassified the patients into two groups . Group I included I -,patients 12 men and 5 women, mean age 65 years with anabnormal systolic blood pressure response increase or poordecay in recovery compared with peak exercise duringrecovery. Group II consisted of 18 patients 14 men and 4women, mean age 57 years with normal systolic bloodpressure decay during recovery Fig. 2 .

Characteristics of patients with an abnormal systolic bloodpressure response during exercise and recovery . The fre-quency of an abnormal systolic blood pressure response

Total group 17 35MIF 12/5 26/9Ale (yr) 50 ± 14 60 ± 11Prior MI 0 22CAD (with prior MI)

I-vessel 0 15(9)2-vessel 0 9(8)3-vessel 0 11(5)

JACC Vol . .22, No . 3September 1 , 93 ae59- A

mm Hq

~ alphd,D 05 n Coqt~oj 0 Group I

Oup II

Cow,

1

Yes

#"W"5 now,

No

min

Figure 2. Changes delta in systolic blood pressure from peak exerciseto recovery. Patients were classified into two groups . Group I includedpatients with an abnormal systolic blood pressure response duringrecovery . Group 11 consisted of those with a normal systolic bloodpressure response during recovery . Control u. control subjects .

during recovery did not differ significantly in patients with orwithout prior myocardial infarction, but it was significantlygreater in patients with multivessel than in those withsingle-vessel disease 65 vs. 27 , respectively Table 2 .According to the criteria for an abnormal systolic bloodpressure response during exercise described by Morris et al .7 and Weiner et al . 10 , 7 of the 35 patients with anginashowed an abnormal systolic blood pressure response duringexercise. The sensitivity, specificity and accuracy of diag-nosing multivessel disease were, respectively, 30 , 93 and57 for an abnormal systolic blood pressure response duringexercise and 65 , 73 and 69 for an abnormal systolicblood pressure response during recovery Table 3 , whereaccuracy = True positive + True negative /All patientsx 100.

Exercise work load, hetnodynatnic variables and plasmanorepinephrine concentration at rest and at peak exerciseTable 4 . Exercise work load in group I was significantlyless than that in control subjects or group 11 . Heart rate andsystolic blood pressure at peak exercise did not differsignificantly among the three groups . Stroke indexes at restand at peak exercise were significantly lower in group I thanin group 11 control subjects. Systemic vascular resistance

Table 2. Characteristics of Patients With Group I or WithoutGroup 11 an Abnormal Blood Pressure Response During Recovery

No . of SignificantPrior MI

Stenoses

Single

Multiple

Group I 11 6 4 13Group 11

11

7

11

7p value group I vs, group [W

NS

< 0.05

By chi-square analysis . Group I = abnormal blood pressure responseduring recovery ; Group II = normal blood pressure response during recovery .Group I included more patients with multivessel disease than did group If .MI = myocardial infarction .

FASUMOTO ET AL .BLODO PRESSURE RECOVERY IN ANGINA

'able 3 . Sensitivity, Specificity and Accuracy of DiagnosingMultivessel Disease by Abnormal Blood Pressure ResponseDuring Exercise Versus During Recovery

661

An abnormal blood pressure response during recovery was more sensi-tive than that during exercise for diagnosing multivessel coronary arterydisease. Data are expressed as number of patients .

index at peak exercise was significantly higher in group Ithan in group It and in control subjects . Left ventricularejection fraction at rest and at peak exercise did not differsignificantly among all study subjects . Plasma norepineph-rine concentration at peak exercise was higher in group Ithan in control subjects, bat this difference did not reachstatistical significance .

Changes in hemodynamic variables from rest to peakexercise . Changes in heart rate in group 1 48 ± 20 beats/mlwere smaller than those in group 11 60 ± 19 beats/min or incontrol subjects 68 ± 29 beats/min . Changes in systolicblood pressure in group 1 33 ± 21 min Hg were significantlysmaller than those in group 11 51 ± 17 mm Hg or in controlsubjects 62 ± 21 mm Hg . Changes in stroke index in groupI 1 ± 6 mi/m 2 were smaller than those in group 11 5 ±8 ml/m2 or in control subjects 9 ± 8 MI/M2 Fig. 3 . Leftventricular ejection fraction decreased from rest to peakexercise in group I -3 ± 7 but increased in the other twogroups 2 ± 9 in group 11, 17 ± 11 in control subjects .The change in pulmonary diastolic blood pressure in group Iwas greater than that in control subjects .

Changes in ltemodynamic variables from peak exercise toeach recovery period. The decrease in heart rate was almostthe same in each group Fig. 4 . Stroke index ml/n121decreased during the recovery phase in control subjectsI min -7 ± 6 ; 3 min -8 7; 6 min -6 ± 6 but increased

in both patient groups 4 8, 3 ± 6, 2 ± 6, respectively, ingroup I and 3 ± 5, 3 ± 8, 2 ± 6, respectively, in group IIFig. 5 . Left ventricular ejection fraction units de-

creased in control subjects 2 to -4 min -5 ± 8 ; 5 to -7 min-10 ± 9 but increased in both patient groups 8 6,9 ± 9, respectively, in group I and I I ± 5, 7 9,respectively, in group 11 . The increases in stroke volumeand left ventricular ejection fraction in each patient groupwere nearly equal . Increases in systemic vascular resistanceindex dynes-s-cm - 5 . M2 in group 1 1 min 291 ± 339 ; 3 min526 ± 237; 6 min : 479 t 275 were greater than those in theother two groups 70 ± 217, 182 ± 305, 161 ± 274, respec-tively, in group II and 252 ± 237, 348 ± 220, 405 ± 244,respectively, ira control subjects Fig. 6 .

Abnormal Blood Pressure ResponseExercise Recovery

Sensitivity 6120 30 INN 65Specificity 14/15 93 11115 73Accuracy 20135 57 24/35 69

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HASHIMOTO ET AL .BLOOD PRESSURE RECOVERY IN ANGINA

Table 4. Exercise Work Loads, Hemodynamic Variables and Plasma Norepinephrine Concentrations at Rest and During Peak Exercise

Group 1108 ± 74 W/min f

Exercise work load . talpha < 0 .05 versus control subjects . Wpha < 0 .05 versus group 11 . Values are expressed as mean value ± SD . C1 = cardiac index -,Ex - exercise ; Group I - patients with an abnormal systolic blood pressure SHP response during recovery ; Group 11 = those with a normal systolic bloodpressure response during recovery ; HR - heart rate ; LVEF - left ventricular ejection fraction : PADP = pulmonary artery diastolic pressure ; PNE = plasmanorepinephrine; SI - stroke index ; SVR - systemic vascular resistance .

Ratio of plasma norepinephrine concentration to cumula-tive work load at peak exercise . The ratio of plasma norepi-nephrine concentration to cumulative work load in group Iwas greater than that in the other two groups Fig. 7 .

DiscussionPrevious studies 1-11 have reported that patients with

angina and an abnormal systolic blood pressure responseduring exercise generally include those with severe coronaryartery lesions . In the present study, the patients with anabnormal systolic blood pressure response during exerciseincluded more patients with severe coronary artery lesions .Recently, abnormal systolic blood pressure response wasexamined not only during exercise but also during therecovery phase 1414 . Mantra et al . 16 and Anion et al .

Figure 3. Changes delta in systolic blood pressure left panel andstroke index right pond from rest to peak exercise in each group .Changes in systolic blood pressure were significantly lower in groupI than in grout 11 or control subjects . The increase in stroke index ingroup I was significantly less than that in control subjects . Defini-tions as in Figure 2 .

m Um2fh

-10L~Gam:

0 00hu 0 05 WS Group Ll

4WW005V8CWW

Gmup comw

Group II

Control Subjects277 ± 196 W/min rf

589 ± 480 W/min

7 reported that an abnormal ratio of recovery to peakexercise systolic blood pressure was more sensitive thanexercise-induced angina or ST segment depression for diag-nosing the severity of coronary artery lesions . In the presentstudy, 13 65 of 20 patients with multivessel disease butonly 4 27 of 15 patients with single-vessel disease showedan abnormal systolic blood pressure response during recov-ery. These findings suggest that there is a close correlationbetween this response and the severity of coronary arterylesions . Kawakubo et al . 18 compared abnormal systolicblood pressure responses during graded treadmill exercisetesting and during recovery for diagnosing the severity ofcoronary artery lesions and found no difference in specificitybut a higher sensitivity for an abnormal systolic bloodpressure response during recovery than for an abnormalexercise response . The results of the present study usingsupine bicycle ergometry were similar .

Thus, an abnormal systolic blood pressure response isimportant not only during exercise but also during recovery,although the mechanisms of the abnormal response duringrecovery have not been elucidated . Systolic blood pressureis determined by the product of stroke volume and systemic

Figure 4 . Serial changes delta in heart rate from peak exercise torecovery in each group . Heart rate decreased similarly in each groupduring the recovery phase . Definitions as in Figure 2 .

beaw!in

0

-20

-1001 3

JACC Vol. 22, No . 3September 1993 :659-64

6

I

min

Rest Peak Ex Rest Peak Ex Rest Peak Ex

HR beats/min 70 ± 11 117 ± 22 68 ± 12 128 ± 18 66 ± 8 Q34 ± 26

SHP mm Hg 139 ± 22 172 ± 31 140 ± 20 192 ± i 1 132 ± 16 03 ± 23

CI liters/min per m 2 2.75 ± 0.47t 4.79 ± 0 .94tt 3 .11 ± 0.35 6.62 ± 1 .12 3.09±0 .51 1.38±1 .75

SI MI/ral 40 ± 84 41 ± 7# 47±7 52±7 47±7 56± I I

PADP mm Hg 11±4 26±9 12±3 26± 11±3 22±7

SVR dynes- S . Cro -5 .m2 2,893 542 1,918 ± 327tt 2,532 ± 443 1,533 ± 285 2,489 ± 426 1,375 ± 337

LVEF 47 14 45±15 50 ± 11 51 ± 14 62°9 79±I1

PNE pgol 171 72 1,083 ± 646 163 ± 91 937 ± 678 134 ± 60 599 ± 318

JACC Vot. 22, No. 3Soixe -fiber 399.3 :659-64

r4 I m P

I

Figure 5, Serial charges delta in stroke index from pealk exerciseto recovery in each group . Stroke index increased in groups I and 11but decreased in control subjects . The increase in stroke index wasnearly equal in both patient groups . Definitions as in Figure 2 .

vascular resistance . In the present study, the stroke volumeincreased paradoxically from peic,~ exercise to recovery illthe patient groups, whereas it decreased in control subjecis .previously, we 12,13 found that all increase in cai-diacindex from peak exercise to early recovery in patients withangina pectoris correlated negatively with a decrease in leftventricular ejection fraction from rest to peak exercise . Wethen suggested that the decrease in myocardial contractilityof the left ventricle due to myocardial ischemia during peakexercise improved after termination of exercise and that therecovery of reduced myocardial contractility results in anincrease in cardiac index early after cessation of exercise . Inthe present study, because the change in heart rate frompeak exercise to recovery was the same in the two patientgroups, we considered the increase in stroke volume in thesepatients to be based on the recovery from myocardialischemia during peak exercise. In both patient groups, theincrease in pulmonary diastolic pressure from rest to peakexercise was greater than that in normal subjects, and the

Figure 6. Serial -iianges delta in systemic vascular resistanceindex from pr.K exercise to recovery in each group . Systemicvascular resistance index increased in each group and was greetin group I and smallest in group 11 . Definitions as in Figure 2 .

dyn -sec - cm' 5 . m2

1

3

3

6

6

min

min

HASHIMOTO ET AL .BLOOD PRESSURE RECOVERY IN ANGINA

Gfoup s

Group 11

Control

Figure 7. Plasma norepinephrine PNE concentration at peak, ex-ercise Ex I divided by the sum of the work loads in each group . Theconcentration was greatest in group I and smallest in conlrc4subjects . Definitions as in Figure 2 .

decrease in pulmonary diastolic pressure during recoverywas the same in the three groups. Thus, in the patientgroups, a high preload continued during recovery, whichmay be related to the increase in stroke index duringrecovery by means of the Frank-Starling mechanism . More-over, stroke volume increased during recovery because of afaster decrease in heart rate than the decrease in cardiacoutput resulting from metabolic demands 19- .26 . In con-trast, there have been no reports on the changer in systemicvascular resistance during recovery . In this study, the in-crease in systemic vascular resistance index during recoveryin group I was greater than that in group 11 or in controlsubjects, and this greater increase in systemic vascularresistance coupled with a greater increase in stroke volumemay be the cause of the higher systolic blood pressure inpatients with severe coronary artery disease . In group 1, thechange in stroke index and left ventricular ejection fractionfrom rest to peak exercise was smaller than that in group 11 .Thus, myocardial ischemia was greater in group I than ingroup 11 . In group 1, the ratio of plasma norepinephrineconcentration to cumulative work load was higher than thatin group II . Thus, an abnormal systolic blood pressureresponse after physical exercise in patients with anginapectoris may indicate the presence of severe myocardialischemia during physical exercise . i t may be caused by anincrease in stroke volume due to recovery of myocardialischemia and an increase in systemic vascular resistancesecondary to exaggerated sympathetic nervous activity .

Limitations of the study . In this study, the number ofpatients was small. Further investigation is necessary toestablish a multiple regression function for evaluating isch-

663

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HASHIMOTO ET AL .BLOOD PRESSURE RECOVERY IN ANGINA

emic ST-T wave changes and systolic blood pressure re-sponse in patients with angina pectoris .

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;53:1532-7 .24 . Hagberg JM, Hickson RC, Mclane JA, Ehsani AA, Winder WW . Disap-

pearance of norepinephrine from the circulation following strenuousexercise . J Appl Physiol 1.79;47:1311-4 .

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