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(Chest. 2000;118:329-335.)
© 2000 American College of Chest Physicians

Percutaneous Transluminal Coronary Angioplasty Improves Oxygen Uptake Kinetics During the Onset of Exercise in Patients With Coronary Artery Disease*

Hiromasa Adachi, MD; Akira Koike, MD; Akihiro Niwa, MD; Akira Sato, MD; Toshihiko Takamoto, MD; Fumiaki Marumo, MD and Michiaki Hiroe, MD

* From the Second Department of Internal Medicine (Drs. Adachi, Sato, Marumo, and Hiroe), Tokyo Medical and Dental University, Tokyo, Japan; The Cardiovascular Institute (Dr. Koike), Tokyo, Japan; Musashino Red Cross Hospital (Dr. Niwa), Tokyo, Japan; and Hokushin General Hospital (Dr. Takamoto), Nagano, Japan.

Correspondence to: Akira Koike, MD, The Cardiovascular Institute, 3-10, Roppongi 7-chome, Minato-ku, Tokyo 106-0032, Japan; e-mail: koike{at}cepp.ne.jp


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: Although percutaneous transluminal coronary angioplasty (PTCA) is known to have beneficial effects on exercise capacity, its effects on the cardiovascular response during the onset of exercise have not been clarified. The present study was undertaken to determine the effects of PTCA on the kinetics of oxygen uptake (O2) during constant-work-rate exercise in patients with coronary artery disease, as well as on their indexes of maximal work capacity.

Methods: Seventeen patients with coronary artery disease who received successful PTCAs performed a 50-W constant-work-rate exercise test for 6 min and a symptom-limited incremental exercise test both before and 4 months after the PTCA procedure. O2 was calculated from breath-by-breath analysis of respired gases. The time constant of O2 kinetics during the onset of 50-W exercise was determined by fitting a single exponential function to the O2 response.

Results: In 14 patients without coronary restenosis, the time constant of O2 kinetics was significantly shortened from (mean ± SD) 57.4 ± 12.6 before PTCA to 48.2 ± 9.5 s after PTCA (p = 0.0035), indicating improved kinetics of the O2 response. In these subjects, the peak O2 obtained during maximal exercise testing also increased from 23.1 ± 3.5 to 26.5 ± 3.2 mL/min/kg, respectively (p = 0.0005). However, there was no improvement in these indexes in the patients who had restenosis after undergoing PTCA (n = 3).

Conclusion: Indexes of cardiopulmonary exercise testing, which reflect an efficiency of oxygen flow to the exercising muscle, can be used as an objective, noninvasive, and cost-effective guide for understanding which patients will not have coronary restenosis following PTCA.

Key Words: coronary artery disease • oxygen uptake • percutaneous transluminal coronary angioplasty • restenosis


   Introduction
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 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
A symptom -limited incremental exercise test with the measurement of expired gas is widely performed for evaluating exercise capacity in cardiac patients and for stratifying patients with heart fail-ure.1 2 3 Among indexes of cardiopulmonary exercise testing, the peak oxygen uptake (O2) measured at maximal exercise has been considered a "gold standard" because it reflects maximal cardiac output.3 4 5 However, the measurement of peak O2 requires physical exhaustion by a subject and is not necessarily reproducible.6 Thus, there is considerable interest among cardiologists in obtaining objective information based on submaximal, rather than maximal, exercise.2 7 8 9 10 11

In a 1995 study, it was found that the kinetics of O2 during the onset of submaximal exercise correlate well with peak O2 and other indexes of maximal exercise capacity.11 It was found also that the administration of a coronary vasodilator speeds the kinetics of O2 increase in patients with coronary artery disease.12 13 The O2 kinetics are assumed to reflect the rise in cardiac output during the onset of exercise in patients with cardiovascular disease.14

Percutaneous transluminal coronary angioplasty (PTCA) is one of the most advanced techniques that has been in use for treating coronary artery disease over the past 10 years. Although PTCA can be relied on to improve maximal exercise capacity by reducing myocardial ischemia and raising the threshold of the onset of anginal pain, PTCA also may speed the kinetics of the cardiac output increase during exercise. An improved rise in cardiac output can be expected to speed the O2 kinetics during exercise.

In the present study, we investigated the effects of PTCA on the kinetics of O2 during constant-work-rate exercise as well as on the maximal exercise capacity of patients with coronary artery disease. We hypothesized that PTCA might not only improve exercise capacity, but might also speed up the kinetics of the increase in O2 in patients with coronary artery disease.


   Materials and Methods
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 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
We initially enrolled 18 consecutive patients with coronary artery disease who received elective PTCA at Musashino Red Cross Hospital. The patients had been screened to exclude any patient > 70 years or any patient who could not perform the exercise testing due to a physical disturbance. The data on 1 of the 18 enrolled patients were excluded from analysis because of an unsuccessful PTCA. Thus, the data on the remaining 17 patients who received successful PTCAs were used for the following analysis (Table 1 ). Six patients had had a previous myocardial infarction. One of the 17 patients (patient 1 in Table 1 ) was in atrial fibrillation, and the others were in sinus rhythm. At the start of the study, every patient was clinically stable. All patients were treated with aspirin along with nitrates and/or calcium antagonists. The same medications were maintained through the study period. The patients were all sedentary and were not involved in any special exercise training programs before or during the 4 months after PTCA. The nature and purpose of the study, as well as the risks involved, were explained to each patient, and informed consent was obtained prior to enrollment. The study was approved by the institutional committee on human research.


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  		Table 1.. Physical Characteristics, Cardiac Diagnoses, and Angiographic Findings Before and After PTCA in Each Patient*

 
Exercise Tests, Coronary Angiography, and PTCA
Both exercise testing and coronary angiography were performed within a week before the patients underwent PTCA, and at 4 months after undergoing PTCA, according to the protocol of follow-up coronary angiography after PTCA for our hospital. An upright, electromagnetically braked cycle ergometer (model 930; Siemens-Elema AB; Solna, Sweden) was used for the exercise testing.11 Each subject performed a 50-W constant-work-rate test for 6 min starting from rest and then an incremental exercise test. The incremental exercise test began with a 3-min warm-up at 20 W and 60 rotations/min, and then the load was increased incrementally by 1 W every 6 s to the symptom-limited maximal load. The interval between the two tests was approximately 40 min. A 12-lead ECG (model ML-8000; Fukuda Denshi; Tokyo, Japan) was monitored continuously throughout the tests. Measurements of cuff BP were made every minute with an automatic indirect manometer (model STBP-680F; Collin Denshi; Aichi, Japan).15

Angiographic findings were evaluated by the caliper method by an experienced cardiologist who had no knowledge of the results of the cardiopulmonary exercise testing. PTCA was performed using the standard procedures of our institution. A successful PTCA was defined as a reduction of the initial measured stenosis of >= 75% of the diameter to a residual stenosis of < 50% of the diameter without a major complication. Restenosis after PTCA was defined as a luminal narrowing of > 75% at the site of the PTCA.

Measurements of O2 During Exercise Testing
O2 was measured (model AE-280 Respiromonitor; Minato Medical Science; Osaka, Japan) on a breath-by-breath basis throughout the exercise periods, as previously described.11 14 The monitor consists of a hot-wire flowmeter, oxygen and carbon dioxide gas analyzers (zirconium element-based oxygen analyzer and infrared carbon dioxide analyzer), and a microcomputer. The 90% response time was approximately 150 ms for both the oxygen and carbon dioxide analyzers. Gas was sampled through a filter by a suction pump through the gas analyzers at a rate of 220 mL/min. The system was calibrated before each study.

Data Analysis
Resting O2 was determined as the average uptake measured during the 2 min prior to starting exercise while sitting on the ergometer. The O2 after 6 min of exercise was determined as the average O2 level measured between the time periods of 330 and 360 s during 50-W exercise. Peak O2 was defined as the highest O2 attained over a 10-s period during incremental exercise. The gas exchange (anaerobic) threshold was determined by the V-slope method.16

A five-point moving average of the breath-by-breath data was used to evaluate O2 kinetics during the 50-W constant-work-rate exercise. The time constant of O2 kinetics was determined by fitting a single exponential function to the O2 response starting at the onset of exercise (Fig 1 ).11 14 17 The general form of this equation can be written as follows:

where O2(t) is O2 at time t, O2(b) is the baseline O2 at rest, A is the amplitude of the O2 response (the increment above baseline), and {tau} is the time constant. A and {tau} were derived by nonlinear regression using least squares and iterative techniques with a computer (SigmaPlot Scientific Graph System; Jandel Scientific Corporation; San Rafael, CA). The methodology for determining the time constant of O2 kinetics already has been described in our previous reports11 12 13 14 ; reproducibility of the kinetics of O2 on separate test days in cardiac patients has been shown by Sietsema et al.10



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  		Figure 1.. The effects of PTCA on the O2 response during 6 min of 50-W constant-work-rate exercise in a representative patient (patient 8 in Table 1 ). The values to the left at 0 minutes are measured at rest. Exercise was terminated immediately at 6 minutes. The curved lines are the computer-derived representation of the best fit of the single exponential model of the O2 response. The time constant ({tau}) after PTCA was shorter (the kinetics were faster) than that before PTCA.

 
Statistical Analysis
Data are reported as mean ± SD. After dividing the subjects into two groups (patients with restenosis and those without restenosis), differences in the variables between the test before PTCA and that after PTCA were analyzed by paired t tests. Comparisons of the variables among subgroups were made by unpaired t tests. A p value < 0.05 was considered to indicate statistical significance.


   Results
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 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
The end point of the maximal incremental exercise before PTCA was chest pain in 7 patients and dyspnea or leg fatigue in the remaining 10 patients (Table 1) . Four months after undergoing PTCA, only three patients felt chest pain during maximal exercise. Significant ST-segment depression or elevation was observed during maximal exercise in 11 patients before undergoing PTCA and in 9 patients after undergoing PTCA.

The intensity of 50 W corresponded to 51.9 ± 7.5% of the maximal work rate, and O2 at 6 min during 50-W exercise corresponded to 67.8 ± 11.0% of the peak O2 from the exercise test results before PTCA. From the results after PTCA, the intensity of 50 W corresponded to 46.4 ± 7.1% of the maximal work rate, and the O2 at 6 min during 50-W exercise corresponded to 62.2 ± 11.5% of the peak O2. All the subjects could easily sustain 6 min of 50-W exercise both before and after undergoing PTCA.

For the exercise tests performed before the patients underwent PTCA, there were no significant differences in the indexes of exercise capacity, including the time constant between patients with previous myocardial infarction (n = 6) and those without it (n = 11). Also, there was no difference in these indexes between patients with single-vessel disease (n = 11) and those with two- or three-vessel disease (n = 6).

Coronary angiography performed 4 months after PTCA revealed that 3 of the 17 patients had restenosis in the target segment of a coronary vessel. Thus, for the following analysis, we divided the subjects into two groups: 14 patients who underwent successful PTCA without significant restenosis; and 3 patients who had restenosis in the coronary arteries 4 months after successful PTCA (Table 1) . There were no significant differences in age, height, or body weight between the groups.

Effects of PTCA on Hemodynamic Variables and ECG Changes
Table 2 demonstrates heart rate, BP, and O2 at rest and at 6 min of 50-W constant-work-rate exercise in patients with and without restenosis. These variables did not differ between pre-PTCA and post-PTCA for both groups. In the patients without restenosis, the maximum ST depression measured at 6 min of 50-W exercise was 0.96 ± 1.18 mm before they underwent PTCA, which was significantly reduced to 0.15 ± 0.32 mm after patients underwent PTCA (p = 0.020). However, PTCA did not influence the maximum ST depression in the patients with restenosis.


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  		Table 2.. Heart Rate, BP, and O2 Before and After PTCA*

 
Effects of PTCA on Indexes of Exercise Testing
Figure 2 shows the indexes of exercise testing before and after PTCA in patients with and without restenosis in the coronary arteries. Resting O2 and the O2 attained at the end of the 50-W constant-work-rate exercise were not influenced by PTCA (Table 2) . However, in the patients without restenosis, the time constant of O2 during 6 min of 50-W exercise was significantly shortened from 57.4 ± 12.6 s before undergoing PTCA to 48.2 ± 9.5 s 4 months after undergoing PTCA (p = 0.0035), indicating the improved response of O2 kinetics. In these patients, the peak O2 obtained during the incremental exercise testing was 23.1 ± 3.5 mL/min/kg before undergoing PTCA, which significantly increased to 26.5 ± 3.2 mL/min/kg after undergoing PTCA (p = 0.0005). Similarly, the gas-exchange threshold and maximal work rate were significantly increased by PTCA (Fig 2) . The gas-exchange ratio at peak exercise during incremental exercise also was increased by PTCA from 1.02 ± 0.06 before PTCA to 1.05 ± 0.07 after PTCA (p < 0.05) in the patients without restenosis.



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  		Figure 2.. The effects of PTCA on the time constant of O2, the gas-exchange threshold (GET), peak O2, and the maximal work rate in 14 patients without restenosis (•) and in 3 patients with restenosis ({circ}). Large circles represent mean values.

 
In the patients who had restenosis in the coronary arteries, indexes of exercise capacity, including the time constant, were not changed and, in some cases, even worsened after PTCA (Fig 2) . The gas-exchange ratio at peak exercise was not influenced by PTCA in these patients.

The percentage of increase in peak O2 after PTCA was 16.2 ± 13.7% in the patients without restenosis and was significantly greater than that in the patients with restenosis (-11.8 ± 9.4%; p = 0.005). The percentage of increase in maximal work rate was also significantly greater in the patients without restenosis (p = 0.007). However, differences in the changes of the other indexes between the two groups were not statistically significant, partly due to the small number of subjects.


   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The incidence of restenosis following PTCA has been reported to be as high as 30 to approximately 50%.18 19 20 Although symptom-limited maximal exercise testing is a useful method for screening patients with ischemic heart disease, the diagnostic value of ECG changes during exercise testing of PTCA patients is low.21 22 Therefore, exercise-induced ST-segment changes are not necessarily reliable markers of coronary restenosis after PTCA.21 22 While exercise testing performed with myocardial perfusion imaging improves the sensitivity and specificity for the detection of restenosis, this technique is prohibitively expensive. Accordingly, a supplemental and cost-effective technique to improve the diagnostic accuracy of exercise testing is needed.

The increase in oxygen transport to muscle cells during the onset of exercise depends on circulatory function and is reflected in muscular O2 kinetics. Thus, noninvasive analysis of the kinetics of pulmonary O2, a parameter which closely reflects muscular O2 kinetics, provides useful information on circulatory function in patients with cardiovascular disease. The kinetics of O2 can be objectively determined in terms of the time constant by fitting an exponential model to the increase of O2 during a short period of low-intensity constant-work-rate exercise.

In the present study, we discovered that a successful PTCA not only increases the peak O2, maximal work rate, and gas-exchange threshold, but also significantly speeds up the kinetics of the increase in O2 during the onset of submaximal constant-work-rate exercise. However, in the patients who had restenosis in the coronary arteries after PTCA, there was no improvement in these indexes. Measuring the time constant of O2 kinetics has an advantage over that of measuring peak O2 in that it does not require a subject’s maximal effort.

The time constant of O2 was shortened by an average of 9.2 s 4 months after successful PTCA. We have reported that the administration of coronary vasodilators such as isosorbide dinitrate13 or nicorandil (2-nicotinamidoethyl nitrate)12 significantly shortens the time constant of O2 during exercise by as much as about 5 s. It has been shown that the time constants of O2 in cardiac patients with relatively higher left ventricular ejection fractions (40 ± 5%) are an average of 12 s shorter than those of the patients with lower ejection fractions (30 ± 3%).14 Moreover, the difference in the time constant of O2 between healthy subjects and cardiac patients was reported to be 12 to approximately 13 s in our previous report.11 Thus, we believe that shortening of the time constant of O2 after PTCA by 9 s reflects a sufficient improvement in O2 response in a patient with coronary artery disease.

Given that O2 is the product of cardiac output and the difference in the oxygen content of arterial and venous blood, the significant shortening of the time constant of O2 noted in the present study could be attributed either to a faster increase in cardiac output or to a more rapidly increasing arteriovenous oxygen difference at the onset of exercise. In the former case, the faster increase in cardiac output during exercise in patients after they had undergone PTCA would be likely to be primarily attributable to a faster increase in stroke volume due to an improvement in myocardial contractility attained via a reduction in myocardial ischemia. In the latter case, raising the threshold of anginal pain by successful PTCA must have extended the daily activity during the 4 months after PTCA. This might have resulted in a more effective redistribution of the cardiac output to the exercising muscle, thereby allowing a more rapid increase in the arteriovenous oxygen difference, which reflects the efficiency of the rate-limiting steps of the oxidative metabolism. However, it is difficult to differentiate whether the shortening of the time constant reflects an improved function of the myocardium after a prolonged period of relative ischemia or whether it reflects an improvement of the rate-limiting steps of the oxidative metabolism in the skeletal muscle.

In the present study, the activity levels of the patients during the study period were not evaluated. However, improvements in ST changes during exercise and maximal exercise capacity suggest that the activity levels of the patients without restenosis were substantially increased by PTCA.

We determined a time constant of O2 in a single exercise session using a 5-breaths moving average of the breath-by-breath data. By using a moving average, visual evaluation of the kinetics becomes easier (Fig 1) . On the other hand, a moving-average technique may obscure the actual response of O2, especially for the immediate increase at the start of exercise lasting approximately 20 s (ie, the phase I period).23 In our experience, however, a moving average <= 5 breaths does not significantly influence the time constant of O2 during 6-min of moderate-intensity exercise. While several repetitions of exercise testing and superimposition of these data without a moving average might be necessary to distinguish the phase I response from the subsequent increase in O2, it is not easy to submit a cardiac patient to multiple repetitions in order to obtain the parameters of exercise capacity.

The present study used an ergometer (model 930; Siemens-Elema) that requires approximately 10 s after the start of exercise to reach the established work rate. Therefore, the actual work rate was probably < 50 W in the first 10 s. The characteristics of the ergometer at the start of pedaling might have partly affected the calculated time constant.

We used 6 min of moderate-intensity exercise at 50 W to determine the time constant of O2. A further study will be needed to evaluate whether the time constant of O2 could be obtained accurately by exercise testing at lower intensity or within a shorter testing period. A special exercise training program would help to speed up the kinetics of O2 during exercise in patients with coronary artery disease. However, a controlled study recruiting many more subjects will be necessary to establish the clinical significance of the improved O2 kinetics and to clarify whether a shortening of the O2 time constant is related to improvements in the quality of life in these patients.

We conclude that indexes of cardiopulmonary exercise testing, which reflect an efficiency of oxygen flow to the exercising muscle, can be used as an objective, noninvasive, and cost-effective guide for identifying patients without coronary restenosis following PTCA.


   Acknowledgements
 
We appreciate the invaluable assistance of Tohru Obayashi, MD, Kazuo Kobayashi, MD, and Noritaka Shimizu, MD, of the Tokyo Medical and Dental University.


   Footnotes
 
Abbreviations: PTCA = percutaneous transluminal coronary angioplasty; O2 = oxygen uptake

Supported in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science, and Culture of Japan.

Received for publication June 18, 1999. Accepted for publication February 1, 2000.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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