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(Chest. 2001;120:825-833.)
© 2001 American College of Chest Physicians

Angiographic and Prognostic Correlates of Cardiac Output by Cardiopulmonary Exercise Testing in Patients With Anterior Myocardial Infarction*

Riccardo Bigi, MD; Alessandro Desideri, MD; Riccardo Rambaldi, MD, PhD; Lauro Cortigiani, MD; Carlo Sponzilli, MD and Cesare Fiorentini, MD

* From the Cardiovascular Research Foundation (Drs. Bigi, Desideri, and Cortigiani), "S. Giacomo" Hospital, Castelfranco Veneto, Italy; and Division of Cardiology (Drs. Rambaldi and Sponzilli), "S. Paolo" Hospital; The Institute of Biomedical Sciences (Dr. Fiorentini), University of Milan, Milan, Italy.

Correspondence to: Riccardo Bigi, MD, via Visoli, 1, 23037 Tirano (SO), Italy; e-mail: rbigi{at}tiscalinet.it


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objective: To assess the diagnostic and prognostic value of cardiac output assessed by cardiopulmonary exercise testing in patients with anterior acute myocardial infarction (AMI) and left ventricular dysfunction.

Patients and setting: Forty-six patients with AMI (7 female patients; mean ± SD age, 55 ± 8 years; ejection fraction, 39 ± 7%) underwent cardiopulmonary exercise testing and coronary angiography following hospital discharge.

Measurement and results: Cardiac output was estimated from oxygen uptake (O2) during exercise according to a method based on the linear regression between arteriovenous oxygen content difference and percent maximum O2. Angiograms were scored using Gensini and Duke "jeopardy" scores. Cardiac output at anaerobic threshold (COAT) <= 7.3 L/min was the best cutoff value for identifying multivessel coronary artery disease (relative risk, 3.1). Angiographic scores were significantly higher in patients with COAT < 7.3 L/min as compared to those with COAT > 7.3 L/min (82 ± 8 vs 53 ± 7 and 6 ± 2 vs 4 ± 3, respectively; p < 0.05) and were inversely and significantly correlated to COAT. Conversely, no correlation was found with ECG changes. COAT, O2 at anaerobic threshold, and peak O2 were univariate prognostic indicators. However, using Cox’s model, COAT was the only multivariate predictor of outcome (odds ratio, 0.28; 95% confidence interval [CI], 0.09 to 0.9). Moreover, COAT < 7.3 L/min was associated to an increased risk of further cardiac events (odds ratio, 5; 95% CI, 1.4 to 17) and provided a significant discrimination of survival for the combined end point of cardiac death, reinfarction, and clinically driven revascularization.

Conclusions: COAT is a safe and feasible tool providing additional diagnostic and prognostic information in patients with AMI.

Key Words: acute myocardial infarction • cardiac output • cardiopulmonary stress testing


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Noninvasive selection of patients eligible for invasive procedures represents the recommended approach for risk stratification of patients recovering from acute myocardial infarction (AMI).1 Although exercise ECG remains the pivot of this strategy, due to its safety, feasibility, and general availability, preexisting as well as infarct-induced abnormalities can make ECG interpretation problematic during exercise. In particular, large anterior infarctions represent a major limiting factor for diagnostic exercise ECG, so that nuclear or echocardiographic imaging is generally suggested in these patients.

Clinical utilization of exercise-induced transient systolic dysfunction as marker of myocardial ischemia is well established and carries with it prognostic information.2 Even though noninvasive measurement of ejection fraction by radionuclide ventriculography has been the most widely employed technique to prognostically assess ventricular function during exercise in post-AMI patients,3 4 5 6 7 8 9 directly measured cardiac output at rest or during exercise also showed a prognostic value in prior studies.10 11 12 However, both techniques are not generally available and are burdened by high costs.

Cardiopulmonary exercise testing monitors several noninvasive parameters during exercise. Many are independent of pulmonary function and are mainly related to the systolic function of the heart (eg, oxygen pulse, lactic acidosis, and maximal oxygen uptake [O2]). The prognostic value of O2 has been demonstrated by several studies13 14 15 in different clinical settings. It has been suggested16 17 that cardiac output and stroke volume can be easily measured from O2 and heart rate (HR) during exercise on the basis of the predictability and reduced variability of arteriovenous oxygen content difference (C[a-v]O2). The aims of the present study were (1) to evaluate the feasibility of this method in the clinical setting of AMI; and (2) to correlate cardiac output assessed by cardiopulmonary exercise testing with ECG, angiographic, and prognostic data of patients with anterior AMI.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Study Population
The study population consisted of 46 consecutive patients (mean ± SD age, 56 ± 9 years; 7 female patients) with AMI diagnosed according to present European Society of Cardiology/American College of Cardiology recommendations.18 All but three of the patients underwent thrombolytic therapy within 6 h of the onset of symptoms. The anterior site of the infarction was confirmed by the presence of echocardiographically detected wall motion abnormalities in the vascular territory of the left anterior descending coronary artery.19 Ventriculographic mean ejection fraction was 39 ± 8%. Patients underwent cardiopulmonary exercise testing 20 ± 5 days following hospital discharge, after withdrawing ß-blockers, calcium antagonists, and nitrates for five half-lives. Coronary angiography was obtained within 1 month of the index exercise test. A 24-month follow-up was carried out for the combined end point of cardiac death, nonfatal reinfarction, heart failure, and clinically driven revascularization procedures. Exclusion criteria were as follows: (1) age > 75 years, (2) underlying lung disease, (3) anemia, (4) arterial hypoxemia, (5) dysthyroidism, (6) significant valvular heart disease,(7) inability to exercise, and (8) conditions precluding ECG interpretability during exercise (such as ventricular hypertrophy, digitalis therapy, bundle branch blocks, etc). The study was approved by the institutional review committee, and the subjects gave informed consent.

Exercise Test Protocol
Patients performed a symptom-limited, incremental exercise test on an electromagnetically braked cycle ergometer in sitting position. The work rate increased in 10-W steps every minute, and the pedaling frequency was maintained from 60 to 70 revolution per minute. The 12-lead ECG was continuously monitored throughout the test for rhythm, rate, and ST-T wave changes using a computer-assisted system (Marquette Case 15 System; Marquette Electronics; Milwaukee, WI). The occurrence of significant anginal pain, ventricular tachycardia, major conduction abnormalities, ST-segment depression > 3 mm, limiting symptoms (such as dyspnea, dizziness, leg fatigue, etc), or excessive elevation (> 230 mm Hg), as well as significant drop (>= 30 mm Hg) in systolic BP, were regarded as interruption criteria. Significant ECG changes were defined as horizontal or downsloping ST-segment depression > 1 mm measured 80 ms after the J point in one or more leads, excluding aVR and V1, and ST-segment elevation > 1 mm measured 40 ms after the J point.

Gas Exchange Analysis
Expired volume was measured with a pneumotachograph calibrated with known volumes of room air. Expired air was sampled continuously at the mouthpiece for measurement of PO2 (polarographic analyzer) and PCO2 (infrared analyzer). Precision analyzed mixtures were used for calibration. Electrical signals from these devices underwent analog-to-digital conversion and were processed (max; SensorMedics; Yorba Linda, CA) for breath-to-breath determination of pulmonary gas exchange variables. Peak O2 was defined as O2 averaged over the last 30 s of exercise. Ventilatory anaerobic threshold (AT) was assessed using the multisegmental linear regression analysis of a plot of carbon dioxide delivery vs O2 (V-slope method).20

Cardiac Output Estimation
Cardiac output was noninvasively estimated using the Stringer method16 based on the linear relation between C(a-v)O2 and percent peak O2 during exercise. Accordingly, the O2 at any given exercise level was expressed as percent of the maximal achieved O2; C(a-v)O2 was then derived by the following regression equation: C(a-v)O2 = 5.72 + 0.10 x peak O2. Thus, the standard equation of the Fick principle for oxygen,21 cardiac output = O2/C(a-v)O2, was applied for cardiac output determination at rest and cardiac output determination at AT (COAT) and peak exercise. The method is summarized in Figure 1 , where cardiac output is plotted as a function of mean C(a-v)O2 with O2 isopleths.21



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  		Figure 1.. Cardiac output as a function of C(a-v)O2 with superimposed O2 isopleths. C(a-v)O2 values are expressed as mean ± SE.

 
Coronary Angiography
Selective coronary angiography was performed using Judkins’s or Sones’s technique. Multiple views of each coronary artery were obtained, including craniocaudal views. All coronary and left ventricular angiograms were interpreted by two experienced observers blinded to cardiopulmonary exercise test result. Differences in interpretation were resolved by consensus. Clinically significant coronary stenosis was defined as > 70% reduction of luminal diameter in any of the three coronary arteries or their main branches or > 50% lumen narrowing of the left main coronary artery. Angiograms were scored using the method of Gensini,22 reflecting the severity of coronary artery disease, and the Duke "jeopardy" score,23 reflecting the extension of area at risk. Ejection fraction was calculated using left ventriculography.

Follow-up
Outcome was determined from patient interviews, from hospitals chart reviews and/or telephone interviews with a close relative, or the referring physician. Target events were cardiac death, nonfatal infarction, New York Heart Association class III-IV heart failure, and clinically driven revascularization procedures. Death was defined as cardiac if strictly related to proven cardiac causes (fatal reinfarction, acute heart failure, or malignant arrhythmias). Myocardial infarction was diagnosed on the basis of present European Society of Cardiology/American College of Cardiology recommendations. Only the worst event was taken into account for statistical analysis in order to avoid overlap. Nonclinically driven revascularization, performed just on the basis of coronary angiography result, was not considered a target end point. Consequently, patients were censored at the time of the procedure in this case.

Statistical Analysis
Data are expressed as mean ± SD or SE. The 95% confidence interval (CI) is reported when appropriate. Continuous variables were compared using Student’s t test. Normality was assessed by Kolmogorov-Smirnov test. Kruskal-Wallis analysis of variance on ranks was used for multiple comparison in case of nongaussian distribution. Correlation between two variables was tested by linear regression analysis using Pearson’s r coefficient in case of normal distribution and Spearman’s r coefficient in case of nonnormal distribution. Categorical variables were compared by {chi}2 statistics. Sensitivity, specificity, positive, and negative predictive value relied on the standard definitions.

The capability of exercise testing variables to predict outcome was assessed by the Cox proportional-hazard model using univariate and stepwise multivariate procedures.24 The following variables were entered into the model: oxygen pulse, O2 at AT, peak O2, maximal HR, HR reserve (ie, difference between peak and rest HR), maximal double product, COAT, and peak cardiac output. The log-rank test was used to compare Kaplan-Meier event-free survival curves. The cutoff value of COAT providing the best discrimination of risk was selected by means of receiver operating characteristic curves method.25 Statistical significance was set at a p < 0.05, and statistical software (SPSS release 7.5.1 for Windows; SPSS; Chicago, IL) was used for analysis.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
No complication was observed during cardiopulmonary exercise testing. The most frequent complaint was "dry mouth" sensation in six subjects (13%). Eighteen patients (39%) were unable to attain their age-predicted maximal HR. Reasons for stopping the test were muscular fatigue (20 subjects), exhaustion (11 subjects), dyspnea (10 subjects), and chest pain (5 subjects). Functional capacity was 70 ± 28 W. Clinical, exercise testing, and angiographic data in the individual patient are reported in Table 1 .


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  		Table 1.. Clinical, Exercise Testing, and Angiographic Data in the Individual Patients*

 
ECG Changes
Exercise-induced ECG changes were observed in 28 patients (61%): ST-segment elevation in Q-wave leads in 23 patients and ST-segment depression in non–Q-wave leads in 5 patients. Mean time to ECG changes was 295 ± 80 s. No significant ECG modification was found in the remaining 18 patients.

Hemodynamic Changes
Modifications of hemodynamic parameters during exercise are illustrated in Figure 2 . Stroke volume was maximal at AT (67 ± 20 mL/beat) and decreased at peak exercise (63 ± 19 mL/beat). Conversely, cardiac output and cardiac index increased from AT (7.5 ± 2.4 L/min and 4.0 ± 1.2 L/min/m2, respectively) to peak exercise (8.7 ± 2.9 L/min and 4.6 ± 1.4 L/min/m2) due to significant increase in HR (from 113 ± 20 to 140 ± 23 beats/min; p < 0.0001). Thus, we considered the pure inotropic response to be maximal at AT, which was reached at 69 ± 9% of peak O2.



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  		Figure 2.. Modification of hemodynamic parameters during cardiopulmonary exercise testing. The box extends from the 25th percentile to the 75th percentile, with a horizontal line at the median (50th percentile). Whiskers extend down to the smallest value and up to the largest. SV = stroke volume; CO = cardiac output; CI = cardiac index.

 
No significant correlation was found between resting ejection fraction and COAT. The COAT of patients with exercise-induced ECG changes was significantly lower than that of patients without ECG changes (6.8 ± 0.4 L/min vs 8.6 ± 0.6 L/min; p < 0.05).

Angiographic Correlates
Twenty-five patients had multivessel disease, and 17 patients had single-vessel coronary artery disease. Five patients had nonocclusive coronary artery disease, with one patient having no disease at all. The left ventricular descending coronary artery was occluded in 17 patients, while it presented significant stenosis in 18 patients and nonocclusive stenosis in 10 patients. A detailed description of coronary anatomy in the individual patients is reported in Table 1 . Median Gensini score was 70 (range 4 to 155; first and third quartiles, 39 and 100, respectively), while median jeopardy score was 6 (range, 0 to 12; first and third quartiles, 4 and 7, respectively).

Significant ECG changes were observed in 16 patients with and 12 patients without multivessel disease, while 9 of 18 patients without ECG changes also had multivessel disease. No significant difference was found between Gensini and jeopardy score of patients with and without exercise-induced ECG changes (72 ± 36 vs 73 ± 44 and 5.6 ± 2.6 vs 5.1 ± 3.4, respectively).

Receiver operating characteristic curve analysis selected 7.3 L/min COAT as the best cutoff value for predicting multivessel disease. Table 2 shows sensitivity, specificity, positive, and negative predictive value of this criterion as compared to ECG modifications. Gensini and jeopardy scores were significantly and inversely correlated with COAT (Fig 3 ), while no correlation was found between rest-peak and rest-COAT variations. Moreover, both scores were significantly higher among patients with COAT < 7.3 L/min as compared to those with COAT > 7.3 L/min (82 ± 8 vs 53 ± 7 and 6 ± 2 vs 4 ± 3, respectively; p < 0.05).


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  		Table 2.. Sensitivity, Specificity, Positive and Negative Predictive Value of ECG Changes and COAT for Predicting Multivessel Coronary Artery Disease*

 


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  		Figure 3.. Correlation between COAT and Gensini and jeopardy scores.

 
Of patients with no significant ECG changes, multivessel coronary artery disease was found in 3 of 11 patients with COAT > 7.3 L/min and in 6 of 7 patients with COAT < 7.3 L/min (relative risk, 3.1; 95% CI, 1.1 to 8.6). However, multivessel disease was found in 4 of 9 patients with COAT > 7.3 L/min and 12 of 19 patients with COAT < 7.3 L/min (relative risk, 1.4; 95% CI, 0.6 to 3.1) among those with significant ECG changes.

Prognostic Correlates
Twenty-two target events occurred during follow-up: cardiac death (n = 6), myocardial infarction (n = 4), New York Heart Association class IV heart failure requiring hospitalization (n = 2), and revascularization procedures (n = 10; including coronary angioplasty [n = 1] and bypass surgery [n = 9]) that were clinically driven by unstable angina or recurrent anginal symptoms refractory to full medical therapy. The median time to revascularization in these patients was 225 days (range, 195 to 360 days; first quartile, 220 days; third quartile, 270 days). Eleven patients underwent direct, nonclinically driven revascularization: bypass surgery (n = 6) and percutaneous transluminal coronary angioplasty (n = 5).

Significant exercise-induced ECG changes were observed in 14 of 22 patients (64%) with and 14 of 26 patients (54%) without events (odds ratio, 1.5; 95% CI, 0.4 to 4.8). However, COAT < 7.3 L/min was found in 16 of 22 patients (73%) with events and in 9 of 26 patients (35%) without events (odds ratio, 5; 95% CI, 1.4 to 17; p < 0.01). COAT of patients with spontaneous events was significantly (p < 0.05) lower as compared to that of patients without events at follow-up (Fig 4 ).



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  		Figure 4.. COAT according to the outcome. revasc = revascularization.

 
Three exercise testing covariates (COAT, O2 at AT, and peak O2) were univariate predictors of further cardiac events. However, multivariate analysis indicated COAT as the only variable independently and inversely associated to the outcome (odds ratio, 0.28; 95% CI, 0.09 to 0.9). Finally, the event-free survival of patients with COAT < 7.3 L/min was significantly lower than that of patients with COAT > 7.3 L/min (Fig 5 ), while no significant difference was found between patients with and without exercise-induced ECG changes.



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  		Figure 5.. Kaplan-Meier event-free survival curves according to COAT.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
The main goals of exercise testing following AMI are to evaluate the extent and severity of the underlying coronary artery disease and to assess prognosis. In patients with anterior infarctions, impaired functional capacity and uninterpretable ECG represent major obstacles to these aims. Many studies on exercise testing in post-AMI patients have shown that hemodynamic parameters (such as maximal workload, BP, ejection fraction, etc) outperform exercise-induced ECG changes, especially in the anterior infarction group. The results of the present study add COAT as another parameter providing important diagnostic and prognostic information that can be obtained at submaximal level of exercise and, therefore, are available even in patients unable to exercise maximally.

We found that COAT represents an effective measure of the inotropic reserve during exercise, any further increase in cardiac output being mainly sustained by the chronotropic reserve. Koike et al26 demonstrated that the AT strongly correlates with the O2, above which left ventricular function decreases during exercise in patients with chronic heart failure. Our results fit this finding and support previously observed27 relations between AT and severity of exercise impairment in cardiac patients. Indeed, cardiac output depends much more on peak O2 than on C(a-v)O216 in patients with left ventricular dysfunction and, consequently, can be estimated from the O2 at AT, since it is unlikely to rise much further with increasing exercise intensity. Interestingly, cardiac output change from resting value to AT was a worse predictor of coronary artery disease as compared to the absolute value of COAT in our study. This is in keeping with previous reports28 showing that the absolute level of exercise ejection fraction, which reflects both the degree of permanent muscle loss and the extent of myocardium in jeopardy, is the best indicator of coronary artery disease severity.

AT occurred at approximately 70% of peak O2 in our patients, which is at odds with the common finding of values closer to 50% in untrained or heart disease subjects. A possible explanation is that, due to the substantially impaired functional capacity, true maximal O2 was not achieved by our patients.

Infarct-related abnormalities make ECG interpretation doubtful during exercise in patients with anterior infarctions, as they may confound the determination of ischemia.29 30 ST-segment depression can be detected only in anteroseptal infarctions and generally reflects ischemia in the lateral or inferoposterior region. However, ST-segment elevation in Q-wave leads has been associated to left ventricular dysfunction,31 to the presence of viable myocardium at jeopardy,32 33 to wider necrosis in the anteroseptal and apical regions, and to wider extent of ischemia in the lateral region.34 ECG changes were associated to significantly lower COAT in this study, but COAT showed a superior ability to assess the total burden of the underlying coronary artery disease (Fig 3) . However, it should be noted that, even though a significant inverse correlation was found between COAT and both Gensini and jeopardy scores, the considerable scatter of data makes this correlation of little clinical value and should be confirmed over larger populations.

The threshold of ischemic ECG changes during exercise has a well-known prognostic significance.35 However, since the exercise tolerance was uniformly reduced in our study group, a substantially overlap occurred that obscured the prognostic value of this parameter.

Resting ejection fraction showed no correlation with COAT or its AT-rest variation. Indeed, many other factors (such as age, sex, level of exercise, presence of collateral vessels, site of stenosis, number of diseased vessels, exercise protocol, and training) can modulate the response of left ventricular function to exercise besides its resting value in patients with coronary artery disease.

In addition to diagnostic information, COAT was able to convey a significant discrimination of risk as clearly demonstrated by the Kaplan-Meier event-free survival curves in Figure 5 . This was not obtained with other stress-testing parameters and emphasizes the additional value of cardiopulmonary stress testing over exercise ECG in this clinical setting.

Comparison With Nuclear Studies
Our results are in keeping with the large amount of data from previous nuclear studies on the diagnostic and prognostic value of ventricular function during exercise. Although the ability to gear stroke volume to metabolic demand during exercise may not be inevitably reduced in coronary patients,36 end-diastolic as well as end-systolic left ventricular volumes increase in presence of severe multivessel coronary artery disease37 with secondary reduction in cardiac output. Determination of peak systolic function and its peak-rest change during exercise by nuclear techniques have been used to identify extensive coronary artery disease38 39 and to assess prognosis after AMI.3 4 5 6 7 8 9 More recently, ejection fraction at peak exercise has been found to provide additional prognostic information over its resting value among patients enrolled in the Thrombolysis in Myocardial Infarction II study.40

Clinical Implications
The results of this study suggest that noninvasive assessment of cardiac output by O2 during exercise is a safe and feasible tool for risk stratification of patients with AMI. According to the international guidelines,1 exercise ECG is the first clinical test performed for patients recovering from AMI and serves as a "gate keeper" for more complex and expensive diagnostic procedures; however, this approach may be the limited by the diagnostic accuracy of the exercise ECG in patients with AMI. The noninvasive assessment of cardiac output by cardiopulmonary exercise testing can provide useful diagnostic and prognostic information when compared to exercise ECG and radionuclide ventriculography.


   Footnotes
 
Abbreviations: AMI = acute myocardial infarction; AT = anaerobic threshold; C(a-v)O2 = arteriovenous oxygen content difference; CI = confidence interval; COAT = cardiac output determination at AT; HR = heart rate; O2 = oxygen uptake

Received for publication August 21, 2000. Accepted for publication March 21, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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