In all 21 patients, the bicycle exercise was terminated by exercising muscle fatigue without chest pain or ischemic electrocardiographic response. Exercise duration was 9±3 min in patients with anterior MI and 9 ± 2 min in those with inferior MI; the difference was not significant.
Size of Infarction
There were no significant differences in creatine kinase, lactate dehydrogenase, left ventricular ejection fraction and left ventricular end-diastolic volume index between anterior (2,516 ±1,355 IU/L, 1,752 ± 958 IU/L, 49 ±7 percent, and 86 ±15 ml/m2) and inferior MI (2,445±1,179 IU/L, 1,679 ± 657 IU/L, 53 ±5 percent, and 78 ±8 ml/m2). Data appear in Tables 1 and 2. The right coronary artery was responsible for inferior MI in eight patients and the left circumflex artery was responsible in two patients. The left anterior descending coronary artery was responsible for anterior MI in all 11 patients. None of the patients had regional wall motion abnormalities remote from the infarct site. There was no significant difference between the two groups in the number of segments with wall motion abnormality (2.7 ±0.9 and 2.5 ±1.0, anterior MI and inferior MI, respectively). During myocardial perfusion scintigraphy, a small transient defect was observed in the infarct area in two patients (one patient with anterior and one patient with inferior infarction), but none of the patients had positive S-T segment change or anginal pain.
Hemodynamic Response During Exercise
Hemodynamic response to exercise in individual patients in relation to patency of infarct-related coronary artery, myocardial perfusion study, and segmental wall motion are shown in Tables 2 and 3. There were no significant differences between the two groups in HR, blood pressure, cardiac index, and stroke volume index at rest and at peak exercise. Although there was no significant difference in pulmonary artery wedge pressure at rest, patients with anterior MI had significantly higher pulmonary artery pressure than those with inferior MI at peak exercise. None of the patients had a large V wave on the pulmonary artery wedge pressure tracing at rest and during exercise.
DT-HR and QS2-HR Relationships During Exercise
To obtain the DT-HR and QS2-HR relationships, DT and QS2 were plotted against the corresponding HR at rest and at peak exercise. The DT and HR had a nonlinear inverse relationship, the equations of which were as follows: DT=e*7 67-0 021 xHR) for anterior MI (r= -0.98, p<0.01) and DT=e<-°024xHR> for inferior MI (r= —0.99, p<0.01) at rest, whereas DT = 0(6.63—0.012xhr) for anterior MI (r= -0.92, p<0.01) and DT=e<e M-° 012xHR> for inferior MI (r= -0.94, p<0.01) at peak exercise. The QS2 and HR had a linear inverse relationship, the equations for which were as follows: QS2 = 554 —2.4 x HR for anterior MI (r= —0.80, p<0.01) and QS2=522—1.8 x HR for inferior MI (r= —0.82, p<0.01) at rest, whereas QS2=463 — 1.3 x HR for anterior MI (r= —0.89, p<0.01) and QS2 = 405-1.0 x HR for inferior MI (r= -0.84, p<0.01) at peak exercise. When DT-HR and QS2-HR relationships in patients with anterior and inferior MI were compared, despite no significant difference in DT and QS2 at rest, significant prolongation of QS2 (p<0.01) with consequent shortening of DT (p<0.01) was observed in patients with anterior MI at peak exercise (Fig 1 and 2).
Plasma norepinephrine level increased significantly at peak exercise, but there was no significant difference between the two groups at rest and at peak exercise (Table 3). To obtain the QS2-norepinephrine relationship during exercise, QS2 was plotted against the corresponding norepinephrine at peak exercise. The QS2 and norepinephrine had a linear inverse relationship (QS2 = — 0.01 X norepinephrine + 285 [r=0.63, p<0.05]) at peak exercise in inferior MI, but QS2 was not related to norepinephrine in anterior MI.
Table 1—Clinical Characteristics
|Anterior MI(n = H)||Inferior MI (n = 10)||p Value*|
|Age, yr||57 ±9||57 ±6||NS|
|Peak creatine kinase, IU/L||2,516±1,355 2,445± 1,179||NS|
|Peak lactate dehydrogenase, IU/L||1,752 ±958||1,679 ±657||NS|
|Ejection fraction, %||49 ±7||53±5||NS|
|Left ventricular end-diastolic volume index, ml/m2||86± 15||78 ±8||NS|
Table 2—Hemodynamic Response to Exercise in Relation to Coronary Artery Potency and Segmental Wall Motion
|Patients||ReperfusionTherapy||InfarctArtery||AsynergicSegment!||TransientDefect||Cardiac Index, L/min/m*||PAW, mm Hg|
|3||Totally occluded||2, 3,6||–||1.91||6.65||10||35|
|8||PTCA||Patent||1, 2, 3, 6||–||2.26||6.61||5||18|
|10||Totally occluded||2, 3,6||–||1.41||4.97||13||37|
|4||Totally occluded||4, 5,7||–||2.57||4.61||8||20|
|8||Totally occluded||4, 5,7||–||1.56||4.22||12||25|
ТаЫе 3—Hemodynamic Response to Exercise