Incidence and significance of decreases in systolic blood pressure during graded treadmill exercise testing

Incidence and Significance of Decreases in Systolic Blood Pressure During Graded Treadmill Exercise Testing

STEPHEN N. MORRIS, MD, FACC JOHN F. PHILLIPS, MD, FACC JOHN W. JORDAN, MD PAUL L. McHENRY, MD, FACC Indianapolis,

Indiana

From the Krannert Institute of Cardiology, the Department of Medicine, Indiana University School of Medicine, and the Veterans Administration Hospital, Indianapolis, Indiana. This study was supported in part by the Herman C. Krannert Fund, Indianapolis, Indiana; by Grants HL-06308, HL05363 and HL-07192 from the National Heart, Lung, and Blood Institute of the National Institutes of Health, U.S. Public Health Service, Bethesda, Maryland; and by a want-in-aid from the Amer%Xn Heart Association, Dallas, Texas and the American Heart Association, Indiana Affiliate, Indianapolis, Indiana. Manuscript received May 20, 1977: revised manuscript received July 20, 1977, accepted July 21, 1977. Address for reprtnts: Stephen N. Morris, MD, Department of Medicine, 1100 West Michigan Street, Indianapolis, Indiana 46202.

The incidence of decreases in peak systolic blood pressure during treadmill exercise was investigated in 460 patients with definite or,suspected coronary heart disease. All patients were studied with coronary cineangiography. Exercise was continued to one of the following end points: chest pain, 85 to 90 percent of the patient’s age-predicted maximal heart rate, ventricular tachycardla or a sustained decrease of 10 mm Hg or more below the peak level of systolic blood pressure. Twenty-two patients with 75 percent or greater stenosis of one or more major coronary arteries manifested a decrease in systolic pressure 10 mm Hg or more during exercise. These included 15 (i7 percent) of 88 pattents with three vessel, 7 (7 percent) of 101 with two vessel and 0 of 90 with single vessel disease. The decrease in pressure was reproducible in the seven patients who underwent a second exercise test before alteration of therapy; this decrease was abolished in the six patients who exercised again after coronary bypass graft surgery. A decrease in systolic pressure of 10 mm Hg or more also occurred during exercise testing in 3 of 23 patients with noncoronary organic heart dlsease; all 3 had an obstructive cardiomyopathy that had not been suspected clinically. Only I of 158 subjects with chest pain and no demonstrable heart disease had a decrease in systolic blood pressure with exercise. Declines in blood pressure were not observed during 650 maxlmal exercise tests performed on 590 clinically normal men. In conclusion, if one excludes subjects with cardiomyopathy or significant heart valve disease, a sustained exercise-Induced decrease in peak systotic blood pressure of 10 mm Hg or more is a highly specific sign of multiple vessel coronary artery dtsease. This phenomenon Is best explained by acute left ventricular pump failure secondary to extensive myocardial ischemia.

In normal subjects exercise produces an increase in systolic blood pressure, and this increase is usually accompanied by a decrease in the diastolic blood pressure with a widening of the pulse pressure.Q A decrease in systolic blood pressure below resting levels has been observed during treadmill exercise testing in some patients with severe valve, hypertensive or coronary heart disease3; a decrease in systolic pressure below resting levels at the onset of treadmill exercise-induced angina has been reported as a reliable sign of severe multiple vessel coronary artery disease.4 However, Baker et al.5 reported that a decreasing systolic blood pressure may be observed during graded exercise in the absence of significant coronary artery disease, especially in women. Other study results6v7 have suggested that a reduction in systolic pressure may be a normal physiologic response during prolonged strenuous exercise. Thus, there are conflicting reports regarding the significance of decreasing systolic blood pressure during graded exercise testing. Furthermore, it is not known how great a decrease in systolic blood pressure is necessary

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to be of potential

diagnostic aid when evaluating patients with suspected coronary artery disease. This report deals with the findings of a prospectively designed study of the blood pressure responses during treadmill exercise testing of 460 patients with known or suspected coronary heart disease. During the time of this study we also evaluated the blood pressure responses of 560 normal male members of the Indiana State Police Force who underwent a total of 650 maximal treadmill exercise tests. Material and Methods cases: A total of 1,020 persons from two patient populations were evaluated by treadmill exercise testing. Group I consisted of 560 clinically healthy male members of the Indiana State Police Force who underwent periodic maximal exercise testing during the study period as part of a continuing cardiovascular evaluation program being conducted at the Indiana University Medical Center.8 Group II consisted of 460 consecutive patients who underwent both treadmill exercise testing and coronary cineangiographic studies at our institution between July 1,1973 and September 30,1976 because of known or suspected coronary artery disease. Our modified Balke multistage exercise protocol and our electrocardiographic recording techniques have previously been described.8,g Blood pressure recordings: All exercise blood pressure levels were measured by the same observer during each individual exercise test. However, three of us participated in the supervision of the exercise tests reported in this study, and serial testing of the same patient was occasionally performed by a different physician. The blood pressure recordings were made with a Tycos cuff adapted to a Baumanometer sphygmomanometer and a standard stethoscope with the diaphragm placed over the right brachial artery. Blood pressures were recorded in the subjects in Group I during sitting and standing rest and during the last minute of each 3 minute stage of exercise. Blood pressures in the patients in Group II were recorded at least once per minute during each 3 minute stage of exercise. During exercise all blood pressure recordings were made with the subject’s hand resting on a side rail and his arm flexed slightly at the elbow. This technique reduces the amount of mechanical or arm movement artifacts and assures accurate and reproducible blood pressure measure-

ments. Whenever a decrease was observed in the systolic pressure, the blood pressure recordings were repeated one or more times at approximately 15 second intervals to confirm the accuracy of the reading and to demonstrate that the decrease was sustained. By study protocol design, a decrease in systolic blood pressure of 10 mm Hg or more that was sustained during two or more consecutive determinations was considered an end point for the exercise test. Coronary cineangiographic studies: In the patients in Group II these studies were performed utilizing the Judkins transfemoral approach.lO Each coronary artery was filmed in multiple projections using 35 mm cineangiography. All coronary cineangiograms were reviewed and interpreted by three of us, and arteries unanimously graded as having a 75 percent or greater luminal narrowing were considered significantly narrowed. The presence and extent of left ventricular wall motion abnormalities were estimated using a left ventriculogram filmed in the right anterior oblique position. Left ventricular end-diastolic pressure was measured in the resting state before the left ventricular and coronary cineangiographic injections. Exercise protocol: The subjects in Group I underwent a thorough history, physical and laboratory examination before exercise testing.8 All men with definite or suspected heart disease were excluded from this study. Also excluded were subjects with persistent systolic blood pressure at rest exceeding 160 mm Hg or diastolic pressure exceeding 96 mm Hg. The end point of exercise for these highly motivated subjects was a self-determined maximal effort; all subjects attained an exercise heart rate exceeding 90 percent of their age-predicted maximal rate.” The exercise end points for the patients in Group II were one of the following: (1) chest pain, (2) an exercise heart rate

of 85 to 90 percent of the patient’s age-predicted maximal rate, (3) ventricular tachycardia, or (4) a decrease in systolic blood pressure of 10 mm Hg or more sustained during repeat blood pressure determinations. In patients who experienced chest pain during exercise, the test was terminated shortly after the onset of pain if a diagnosis of coronary heart disease was already established or if the S-T segment response was interpreted as abnormal by the monitoring physician (1.0 mm or more of horizontal or downsloping S-T depression). If the S-T segment response remained normal or equivocal at the time of exercise-induced chest pain and a diagnosis of coronary heart disease was not established, the test was sometimes continued in an effort to elicit an abnormal S-T segment re-

TABLE I Prevalence of Exercise-Induced Decreases in Systolic Blood Pressure (EDBP) in the Study Populations

Subiects Group

I

Group IIA Group IIB Group IIC

Clinically normal state police Chest pain-no significant coronary ariery disease’ _ Significant coronary arterv diseaset Noncorbnary heart disease*

Mean Age((rryge)

With EDBP no. 00

Exercised (no.)

Sex (no.)

560

M-560 F-O M-89 F-70

38(28-61)

0

0

47(26-68) 50(17-68)

1+ 0

0.6

M-242 F-37 M-17 F-5

51(18-69) 54(35-69) 43(30-6 1j 47(43-50)

159 279 22

22 0

7.9 13.6

03

No coronary stenosis greater than 50 percent. There were no obstructive lesions in 145 (91 percent) of the 159 subjects. + The only patient in the study who was receiving methyldopa and propranolol at the time of exercise testing. t One or more major coronary arteries with 75 percent or greater stenosis. 5 Includes 19 patlents with cardiomyopathy. The three patients with exercise-induced decreases in systolic blood pressure were the only ones in this study group with obstructive cardiomyopathy. l

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sponse. However, the patient’s chest pain was never allowed to exceed the intensity of that he experienced during his usual daily activities. All exercise electrocardiograms were recorded on magnetic tape. Upon completion of the exercise test the S-T segment changes were quantitated using previously described computer techniques9 In patients with a normal baseline ST-T segment, the computed S-T response was considered abnormal if the S-T depression was 1.0 mm or greater and the algebraic sum of the S-T depression in millimeters and the S-T slope in millivolts/second was less than zero.9 These computed values were used to compare the incidence of abnormal S-T segment responses in patients with and without exerciseinduced declines in systolic blood pressure. Results

Group I (normal subjects): The 560 clinically normal subjects in Group I underwent a total of 650 maximal exercise tests during the study period. None of these subjects demonstrated a decrease in systolic blood pressure during exercise (Table I). Group II (known or suspected coronary artery disease): The patients in this group were divided into three subgroups according to their final clinical diagnosis (Table I). Group IIA consisted of 159 patients who were evaluated for symptoms of chest pain but found to have no coronary artery stenosis exceeding a 50 percent luminal narrowing by coronary cineangiography; the majority (91 percent) demonstrated no coronary artery disease or only minor luminal irregularities. In one patient, a 41 year old man with essential hypertension, systolic pressure decreased 24 mm Hg during exercise. He had no chest pain and at the time of the exercise test he was taking propranolol (40 mg four times a day), methyldopa (250 mg three times a day) and long-acting nitrates (Nitrobid@, 6.5 mg three times a day). Group IIB consisted of 279 patients who demonstrated a 75 percent or greater stenosis of one or more of the three major coronary arteries on coronary cineangiography. In this subgroup there were 22 patients (7.9 percent) who demonstrated a decrease in systolic blood pressure of 10 mm Hg or more during exercise. Group IIC consisted of 22 patients with noncoronary organic heart disease; 16 had nonobstructive cardiomyopathy, three had obstructive cardiomyopathy, two

ET AL.

had aortic insufficiency and one had a partial absence of the pericardium. Three of these patients demonstrated a decrease in systolic blood pressure during exercise and all three had an obstructive cardiomyopathy.

Patients with exercise-induced decline in systolic blood pressure: A total of 39 exercise tests were per-

formed in these 26 patients. All of the repeat exercise tests were performed in the 22 patients with coronary artery disease in Group IIB. The Group IIB patients demonstrated a mean decline in systolic blood pressure of 23 mm Hg during their initial exercise test (Table II). The systolic blood pressure level during exercise dropped below that recorded during standing rest in only 9 of the 22 patients. Sixteen of these 22 patients had angina before the decrease in blood pressure; the limiting symptoms in the remaining 6 were dyspnea in 3, leg fatigue in 2 and giddiness in 1. A second exercise test was obtained in 7 of the 22 patients with coronary disease who demonstrated a decrease in systolic blood pressure during their initial test (Group IIB, Table II). The repeat tests were performed without intervening alterations in therapy and after time intervals ranging from 2 weeks to 17 months (the interval was 2 to 5 weeks in all but one patient). The decrease in systolic blood pressure during exercise was reproducible in ail seven patients. The most dramatic and abrupt decreases in systolic pressure were observed in the three patients with obstructive cardiomyopathy (Group IIC, Table II). These patients were being evaluated because of chest pain of uncertain origin and they did not have heart murmurs at rest or pathologic Q waves in the resting electrocardiogram. Prominent systolic murmurs were observed immediately after exercise, and a diagnosis of obstructive cardiomyopathy was subsequently confirmed with echocardiography and left heart catheterization. Effect of surgery: Saphenous vein coronary bypass graft surgery was subsequently performed in 12 of the 22 patients with coronary artery disease (Group IIB). To date we have repeated the exercise test in 6 of the 12 patients postoperatively including 4 patients who demonstrated a decrease in systolic blood pressure during repeat exercise testing before surgery (Table II).

TABLE II Magnitude and Reproducibility of Exercise-Induced Decrease in Systolic Blood Pressure (EDBP) in 26 Patients During 39 Exercise Tests Patients (no.) Group IIA Group IIB First TMET Repeat TMET Repeat TMET after CABG Group IIC

With TMET (no.)

With EDBP (no.)

1

1

22

22

:*

I:

3

3

Mean and Range of EDBP (mm f-fg)

With EDBP Below Standing BP at Rest (no.)

24

1

23 (10-46) 20 (10-34)

9 2

39 (20-56)

2

2:

.

.

3

Four of these patients were in the subgroup of seven patients who had a second or repeat treadmill test. All four had a reproducible exerciseinduced decrease in systolic blood pressure before surgery. BP = blood pressure; CABG = coronary bypass graft surgery; TMET = treadmill exercise test. l

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All six of the patients demonstrated an increase in the peak systolic blood pressure attained during repeat exercise testing after surgery (Fig. 1). The mean increment in systolic pressure was 29 mm Hg (range 4 to 68). Two of the six patients still experienced angina during the postoperative exercise test, but every patient was able to exercise for a longer period than before surgery (mean duration 308 seconds preoperatively versus 638 seconds postoperatively). Clinical characteristics of patients with a decrease in systolic blood pressure during exercise (Table III): The 22 patients with coronary artery disease and exercise-induced decreases in systolic blood pressure were, as a group, 4.4 years older than the 257 patients who did not have a decrease in systolic blood pressure during exercise. This age difference between the two subgroups was not statistically significant. All 22 patients were men (22 of 242). There were 37 women in the study group with significant coronary artery disease. The absence of a decrease in systolic blood pressure in women compared with men (0 of 37 versus 22 of 242) was not quite significant at the 0.05 level. This apparent sex difference was most likely due to a predominance of single vessel disease in the women and to a much greater prevalence of triple vessel disease in the men. No significant differences were observed between the two subgroups (those with and without a decrease in systolic blood pressure) in the frequency of com-

puter-quantitated S-T segment abnormalities with exercise, the presence of ventricular premature complexes, the prevalence of previous myocardial infarction, evidence of akinesia or dyskinesia in the left ventriculogram or the level of mean left ventricular end-diastolic pressure (Table III). The coronary arteriographic findings in the 22 patients with coronary artery disease and exercise-induced decreases in systolic blood pressure are summarized in Table IV. Three patients had significant stenosis of the left main coronary artery, and an additional 14 patients had a 75 percent or greater stenosis of the luminal diameter of both the left anterior descending and left circumflex coronary arteries. Therefore, 17 of the 22 patients had lesions that have been regarded by some investigators4 as equivalent to a left main stem coronary artery stenosis. Fifteen (68 percent) of the patients had significant three vessel coronary disease. The remaining seven patients had at least two major coronary arteries with a 75 percent or greater stenosis and four of these patients also had a 50 percent stenosis of the third major coronary artery. The prevalence rate of exercise-induced decreases in systolic blood pressure in the 279 patients with coronary

TABLE III

Characterlstlcs of 279 Patients With Significant Coronary Artery Disease 22 With EDBP

I

70 _ 60 _ 50 _ 40 d G u J zK :

30_ 20 _-

P Value

F:;;n”o”,” (yr)

55.2

50.8

Male’ Female S-T depression with exercise testing* VPC Previous documented myocardial infarction Akinesia or dyskinesia on left ventriculography Mean LVEDP (mm Hg)

22

220

880% (15/17)

7:&

(142/183)

NS NS

55% (12122) 48% (10/22j

49% (1281257) 49% (125/357j

NS NS

32% (7/22)

39% (98/254)t

NS

11.7

11.2

NS

NS

Includes only patients with a normal baseline ST-T segment. t A left ventriculogram was not obtained in three patients. EDBP = exercise-induced decrease in systolic blood pressure; LVEDP = left ventricular end-diastolic blood pressure: NS = not significant; P = probability; VPC = ventricular premature complexes at rest or with treadmill exercise. l

; 10 _ 6 tz :: O_ nw ,’ 3 -10 __ z 3

257 Without EDBP

-20 _

TABLE IV Coronary Arterlographlc Findlngs in 22 Patients (Group IIB)

-30 _

Patients

(no.) -40 I

1 PRE OP

POST

175 % stenosis of: Left main coronary artery Left anterior descending artery (LAD) Left circumflex artery (LC) Right coronary artery (RCA) LAD and LC LAD and RCA 2 maior vessels 3 major vessels

OP

FIGURE 1. Effect of coronary bypass surgery in six patients. Preoperatively (PRE OP) these six patients had a mean decrease of 23 mm Hg from peak exercise systolic blood pressure level (E.P.). Postoperatively (POST OP) each patient attained a higher peak systolic blood pressure level than on the preoperative exercise test, with a mean increment of 29 mm Hg.

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artery disease was 7.9 percent, but this varied considerably within our study population depending on the number of coronary vessels involved (Table V). None of the 90 patients with single vessel disease manifested a decrease in systolic blood pressure during exercise whereas 7 percent (7 of 101) of the patients with two vessel disease and 17 percent (15 of 88) of those with three vessel disease demonstrated an abnormal systolic blood pressure response during exercise. Thus, a decrease in systolic blood pressure during exercise was observed in 11.6 percent (22 of 189) of patients with cineangiographic evidence of multiple vessel coronary artery disease. The prevalence rate of abnormal blood pressure responses in patients with left main coronary artery disease was 17 percent (3 of 181, which was the same as that observed in patients with significant three vessel disease. All three patients with significant left main coronary artery stenosis and an abnormal blood pressure response during exercise also had a 75 percent or greater stenosis of the right coronary artery. Discussion

Incidence and clinical significance of exerciseinduced drop in systolic blood pressure: Our results reaffirm the clinical value of accurate blood pressure recordings during graded exercise testing. Previous reports3!4 dealing with the exercise blood pressure responses of patients with heart disease have considered flat systolic blood pressure responses or a reduction in systolic blood pressure below resting levels to be abnormal. Our results show that a sustained and reproducible decrease in peak systolic blood pressure during exercise as small as 10 mm Hg is clinically significant. This observation holds true even when the initial expected increment in systolic blood pressure occurs during exercise. In patients with coronary artery disease a decrease of this magnitude in systolic blood pressure is highly suggestive of significant multiple vessel involvement. In our study population, 11.6 percent (22 of 189) of the patients with coronary cinenagiographic findings of advanced two or three vessel coronary artery disease demonstrated an abnormal decrease in blood pressure during exercise. Of the 88 patients who had triple vessel disease, 15 (17 percent) had an abnormal blood pressure response. Abnormal decreases in systolic blood pressure were not observed in healthy subjects or in patients with single vessel coronary artery disease. The 22 study patients with exercise-induced decreases in systolic blood pressure were all identified on exercise tests performed before coronary cineangiography, and therefore there was no retrospective influence on their selection. None of the patients had orthostatic hypotension, hypovolemia, obstructive heart valve disease or evidence of congestive heart failure, and none had cardiac arrhythmia at the time of the exercise blood pressure determinations. Although one can question the accuracy of brachial arterial cuff pressure measurements taken during exercise, the reproducibility of an exercise-induced decrease in systolic blood pressure in all seven subjects undergoing a second exercise test and the absence of this finding in 560 normal

TABLE V Correlation of Severity of Coronary Artery Disease and Frequency of Exercise-Induced Decrease in Systolic Blood Pressure (EDBP) in 279 Patients Patients (no.1 Single vessel with 275% stenosis Two vessels with 275% stenosis Three vessels with 275 % stenosis

90 101 88

With EDBP IlO.

%

0

0

1:

1:

men during maximal treadmill testing confirms that the blood pressure can be recorded during exercise with a high degree of reliability. Causes of exercise-induced fall in systolic blood pressure: The decrease in the peak systolic blood pressure during exercise in patients with multiple vessel coronary artery disease is best explained by acute left ventricular pump failure secondary to extensive myocardial ischemia. This hypothesis is supported by an absence of abnormal blood pressure responses in our 90 patients with single vessel coronary disease, in whom less myocardium is at risk of ischemic compromise, and by the restoration of a normal blood pressure response to exercise in patients with multiple vessel disease after coronary artery bypass graft surgery. Because a decline in systolic blood pressure during exercise is primarily dependent upon the area of myocardium rendered ischemic, it is possible that some subjects with single vessel coronary artery disease will eventually be shown to manifest this abnormality. This could especially be: the case when a maximal exercise protocol is used because the area of exercise-induced ischemia may be more extensive under these circumstances. The abnormal blood pressure responses observed in the three patients with obstructive cardiomyopathy can best be attributed to an accentuation of the left ventricular outflow tract obstruction during treadmill testing. This is most likely due to a combination of an upright posture and the increase in circulating catecholamines that accompanies exercise.12 The explanation for the single patient with a “false positive” decrease in blood pressure among the 159 patients with chest discomfort and normal coronary arteriograms is less obvious. This patient was the only person in the study who was tested while receiving a combination of propranolol, methyldopa and longacting nitrates. This drug combination has the potential for reducing maximal cardiac output while simultaneously augmenting the peripheral vasodilatation that accompanies exercise. lt1-i5 Therefore, certain pharmacologic agents may obliterate the adaptive mechanisms normally operative during exercise to maintain the systolic blood pressure. Role of thermoregulatory mechanisms: Prolonged exhaustive exercise has been shown to cause a decrease in systolic blood pressure even in normal subjects.s7 This response is thought to be mediated through sympathetic vasodilatation of skin vasculature in order to

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dissipate the heat load generated by the prolonged muscular work. As a larger percentage of the cardiac output is shifted to the skin for cooling purposes, the total peripheral vascular resistance decreases. If cardiac output is already near maximal, both the systolic and mean arterial blood pressures may decrease. This thermoregulatory or so-called “cardiovascular drift” phase of exercise7 occurs only with vigorous exertion maintained over a prolonged period. This phenomenon was not observed by Saltin and Sternbergs using an exercise protocol including 15 minutes of warm-up followed by a maximal work load that would exhaust the subjects in another 6 minutes. With our modified Balke treadmill exercise protocol8 none of the patients with an exercise-induced decline in systolic blood pressure walked more than 12 minutes (mean 4.9 minutes, range 2 to 12 minutes). Thus it is highly unlikely that the decrease in systolic pressure observed in the 22 Ijatients was initiated by thermoregulatory mechanisms. Our patient population was predominantly male but we did not observe an abnormal blood pressure response in any of the 37 women with coronary artery disease or in any of the 70 women who had chest pain but who were free of significant coronary artery disease on coronary cineangiography. Thus our results failed to confirm the finding of Baker et al., 5 who reported that exerciseinduced hypotension occurs more frequently in women and is often not associated with coronary artery disease.

Clinical implications: Our results show that a decrease in systolic blood pressure of 10 mm Hg or more below peak values during treadmill exercise is a reliable indicator of multiple vessel coronary artery disease provided the following conditions are met: (1) the decrease in pressure is sustained during one or more repeat determinations obtained at 15 to 20 second intervals after the initial recording; (2) there is no coexistent cardiomyopathy, heart valve disease, hypovolemia, orthostatic hypotension or evidence of congestive heart failure at rest; (3) there are no cardiac arrhythmias at the time of blood pressure recording; (4) the patient is not receiving a combination of pharmacologic agents that would significantly reduce cardiac output or augment the vasodilatation accompanying exercise, or both; and (5) exercise is at least 1 minute in duration. This latter condition is designed to exclude “false positive” decreases in systolic pressure in very anxious subjects whose pressure may decrease early in the first stage of exercise as they begin to relax. It is not necessary for the final systolic blood pressure to drop below that recorded at standing rest. Also, some subjects had normal exercise S-T segments (two patients) or did not experience angina (six patients). Therefore, when the criteria listed are fulfilled, we believe that an exercise-induced decrease of 10 mm Hg or more below peak systolic blood pressure is a useful, highly specific and easily elicited sign of severe compromise of the coronary circulation.

References 1. Fraser RS, Chapman CB: Studies on the effect of exercise on cardiovascular function. II. The blood pressure and pulse rate. Circulation 9:193-198, 1954 2. Bruce RA, Gey GO Jr, Cooper MN, et al: Seattle Heart Watch: initial clinical, circulatory and electrocardiographic responses to maximal exercise. Am J Cardiol33:459-469, 1974 3. Bruce RA, Cobb LA, Kalsura S, et al: Exertional hypotension in cardiac patients. Circulation 19543-551. 1959 4. Thomson PD, Kelernan MH: Hypotension accompanying the onset of exertional angina. Circulation 52:28-32, 1975 5. Baker T, Levites R, Anderson GJ: The significance of hypotension during treadmill exercise testing (abstr). Circulation 54:Suppl ll:ll-11, 1976 6. Saltln B, Sternberg J: Circulatory response to prolonged severe exercise. J Appl Physiol 19:833-838, 1964 7. Smith EE, Guyton AC, Manning RD, et al: Integrated mechanisms of cardiovascular response and control during exercise in the normal human. Prog Cardiovasc Dis 18:421-443, 1976 8. Farls JV, k&Henry PL, Jordan JW, et al: Prevalence and reproducibility of exercise induced ventricular arrhythmias during maximal exercise testing in normal men. Am J Cardiol37:617-622, 1976 9. k&Henry PL, Phillips JF, Knoebel SB: Correlation of computer-

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10. 11.

12.

13.

14. 15.

quantitated treadmill exercise electrocardiogram with arteriographic location of coronary artery disease. Am J Cardiol 30: 747-752, 1972 Judkihs NIP: Percutaneous transfemoral selective coronary arteriography. Radio1 Clin North Am 6:467-492, 1968 McHenry PL, Morris SN: Exercise electrocardiography-current state of the art, chap 14. In, Advances in Electrocardiography, Vol II (Schlant RC, Hurst JW, ed). New York, Grune & Stratton, 1976, p 275 Braunwald E: Idiopathic hypertrophic subaortic stenosis (obstructive cardiomyopathy), chap 74. In. The Heart, third edition (Hurst JW, Logue RB, ed). New York, McGraw-Hill, 1974, p 1346 Maxwell RA: Adrenergic blocking drugs, adrenergic neuron blocking drugs and drugs altering biochemical mechanisms in adrenergic neurons, chap 34. In. Drill’s Pharmacology in Medicine, fourth edition (DiPalma JR, ed). New York, McGraw-Hill, 1971, p 685 Brlggs AH, Holland WC: Antihypertensive drugs, chap 41. In Ref 13, p 860 Angelakos ET: Coronary vasodilators, chap 39. In Ref 13, p 814-815

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