A risk prediction model is a statistical model based on a series of characteristics used to estimate the probability of individual risks or clinical outcomes. In clinical practice, a risk prediction model is primarily used to stratify disease severity and predict disease risk or prognosis. Compared to traditional imaging examinations and noninvasive stress imaging, CPET has great advantages in terms of economy and objective accuracy[13]. More importantly, CPET can be used to obtain a series of parameters closely related to cardiopulmonary function and prognosis[14]. Anuradha Lala et al.[3] reported that many CPET parameters have a clear predictive value for death in patients with heart disease and rehospitalization in patients with HF.
In this study, we found that the CPET parameters of peakVO2, PETCO2, and VE/VCO2slop were important factors in predicting the prognosis of patients with AMI after PCI. SHAP was used to analyze the importance of the modeling factors, which confirmed that the peakVO2, PETCO2, and VE/VCO2slop had clear predictive values for the recurrence of AMI, HF, hospitalization, and death of patients after PCI. Moreover, peakVO2 ≥ 20 ml/min/kg and VE/VCO2slop < 33 significantly reduced the risk of adverse prognosis. The ROC curves of the three logistic models were drawn using the verification set, and the results showed that they had good differentiation, a high fit, and a good working effect. The results of internal and external verification showed that the model has good stability and clinical practicability and can be used to predict the prognosis of patients with AMI after PCI.
In 2016, the American medical community officially listed cardiorespiratory fitness (CRF) as a “clinical vital sign.” PeakVO2, as an important indicator for evaluating CRF, has become an important parameter for clinical evaluation of patient status, rehabilitation treatment effect, and prediction of life and health. Matsumura et al.[15] found that the New York Heart Association (NYHA) classification has a good correlation with peakVO2 and AT, indicating that HF symptoms are closely related to the body’s ability to transport oxygen. Based on the peakVO2 and AT values, Weber and Janicki[16] more objectively divided the cardiac function of patients with HF into four levels. Most scholars believe that peakVO2 and AT are more reliable and independent predictors of survival in HF than the NYHA classification or left ventricular ejection fraction[17–19]. Our results also showed that peakVO2 was an independent factor affecting the prognosis of AMI after PCI, and a peakVO2 ≥ 20 ml/min/kg significantly reduced the incidence of adverse events and improved the prognosis of patients. Therefore, patients with AMI after PCI should initiate aerobic exercises as soon as possible to improve their functional abilities. Functional capacity can be used as a risk factor for predicting death. For every 1 MET increase in functional capacity (3.5 ml/kg/minVO2), the risk of death can be reduced by 13–35%[20]. However, improvements in functional ability are mainly achieved by increasing the peakVO2 value through aerobic exercise.
The VE/VCO2slop is an indicator of the gas exchange efficiency. Ferreira et al.[21] found that VE/VCO2slop ≥ 43 is an ideal cut-off value for judging the presence of HF; indeed, compared to the classical peakVO2-based criteria, it can accurately reclassify 18.3% of HF. Patients with HF with VE/VCO2slop ≥ 45 and peakVO2 < 10.0 ml/min/kg have a very poor prognosis in the next 4 years[22]. Studies have shown that aerobic exercise capacity and ventilation efficiency are important reference indicators in evaluating the prognosis of patients with mild obstructive hypertrophic cardiomyopathy[23]. This evidence suggests that the VE/VCO2slop can predict the prognosis of patients with cardiovascular diseases. This study also found that the VE/VCO2 slope was an independent factor affecting the prognosis of patients with AMI after PCI, where the higher the value, the higher the risk of adverse events. Several studies have confirmed that the ventilation efficiency of patients with coronary heart disease improves after exercise training[24–30]. Additionally, the VE/VCO2slop was reduced by 6–23% in patients with chronic HF after the exercise training program. In this regard, Gademan et al.[27] showed improvements in the ventilation efficiency of patients with HF after exercise (VE/VCO2slop, before training = 35.8 ± 3.9 vs. after training = 31.0 ± 6.1, decreased by 14%). In summary, patients with AMI after PCI should start cardiac rehabilitation exercises as soon as possible after achieving a stable condition to increase peakVO2 and improve ventilation efficiency.
PETCO2 is the end-tidal carbon dioxide partial pressure that reflects pulmonary ventilation and pulmonary blood flow. Arena et al. showed that ventilation efficiency (especially VE/VCO2slop) and PETCO2 peak during exercise are related to pulmonary hypertension caused by late diastolic dysfunction of left ventricular hypertrophy and that PETCO2 is an important predictor of cardiac-related events in patients with HF[31]. A previous study suggested that PETCO2AT is superior to peakVO2 in the prognosis of adverse events in patients undergoing CRT[6]. Moreover, Matsumoto et al.[32] found that in a group of patients with HF, PETCO2 at the ventilation threshold was significantly correlated with cardiac output during peak exercise. The sensitivity and specificity of PETCO2 (< 38.5 mmHg) in predicting low cardiac output during exercise (cardiac index < 5.11 L/min/m2 at peak exercise) were 76.5% and 75.0%, respectively. Tanabe et al.[33] also reported a significant correlation between PETCO2 and cardiac index during peak exercise in patients with HF. The results showed that PETCO2 can better reflect the cardiac output response during exercise and has a diagnostic value. Thus, this study found that PETCO2 is an independent predictor of HF during follow-up in patients with AMI after PCI and reported that the risk of HF is 1.21 times higher for every unit increase in PETCO2. In summary, PETCO2 is not only a prognostic predictor of patients with HF but also a predictor of HF after AMI.
This study has some limitations that warrant discussion. First, this is a retrospective cohort study, and some patients were not included in the analysis because of data loss. Second, during the CPET, some patients did not reach the maximum exercise level owing to the symptom-restricted exercise strategy adopted by individual patients; thus, the HRmax could not be obtained. Lastly, the study participants included patients who underwent CPET in tertiary hospitals, which may not represent the entire AMI population, limiting the generalizability of our results at the grassroots level.
Our results revealed that CPET can well predict the prognosis of adverse events after PCI in patients with AMI and that the risk of adverse events was significantly reduced when peakVO2 ≥ 20 ml/min/kg and VE/VCO2slop < 33. Therefore, patients with AMI should start aerobic rehabilitation training as soon as possible to promote cardiac function recovery, improve oxygen uptake and ventilation efficiency, reduce the incidence of re-AMI and HF, and improve prognosis.
Table 1
Comparison of clinical data (x ± s)
Item | No-event group (n = 269) | Event group (n = 41) |
---|
Age (years) | 56.53 ± 10.94 | 59.27 ± 12.79 |
Sexuality | M 230 (85%) F 40 (15%) | M 36 (88%) F 5 (12%) |
BMI (kg/m2) | 25.47 ± 3.57 | 25.95 ± 3.35 |
LVEF (%) | 60.1 ± 4.94 | 58.56 ± 5.02 |
Clinical diagnosis | | |
STEMI | 135 (50%) | 28 (68%) |
NSTEMI | 134 (50%) | 13 (32%) |
Laboratory examination | | |
Hemoglobin (g/L) | 137.75 ± 17.36 | 137.68 ± 15.35 |
BNP (pg/ml) | 100.87 ± 135.14 | 134.06 ± 146.25 |
Total cholesterol (mmol/L) | 4.12 ± 1.10 | 3.78 ± 1.20 |
Triglyceride (mmol/L) | 1.85 ± 2.20 | 1.74 ± 0.94 |
Low-density lipoprotein (mmol/L) | 2.40 ± 1.50 | 2.16 ± 0.90 |
High-density lipoprotein (mmol/L) | 1.03 ± 0.33 | 1.04 ± 0.24 |
Serum creatinine (µmol/L) | 66.79 ± 27.26 | 65.71 ± 23.06 |
Troponin (µg/L) | 2.66 ± 6.90 | 1.09 ± 2.06 |
Creatine kinase-MB (U/L) | 1.43 ± 2.88 | 1.25 ± 1.12 |
Smoking history | | |
Never or have quit smoking | 159 (59.1%) | 21 (51.2%) |
Smoking | 110 (40.9%) | 20 (48.8%) |
Drinking history | | |
Never or have quit drinking | 188 (70%) | 25 (61%) |
Drinking | 81 (30%) | 16 (39%) |
Case history | | |
Diabetes | 60 (22%) | 10 (24%) |
Hypertension | 128 (47.6%) | 25 (61%) |
Medication | | |
Antiplatelet aggregation drugs | 269 (100%) | 41 (100%) |
Calcium channel blockers | 128 (47.6%) | 27 (65.9%) |
Atorvastatin | 255 (94.8%) | 41 (100%) |
β-blockers | 229 (85.1%) | 36 (87.8%) |
Coronary artery disease | | |
Triple vessel disease ≥ 50% | 66 (24.5%) | 12 (29.3%) |
LAD ≥ 50% | 189 (70.3%) | 35 (85.4%) |
LCX ≥ 50% | 128 (47.6%) | 15 (36.6%) |
RCA ≥ 50% | 134 (49.8%) | 20 (48.8%) |
LMCA ≥ 50% | 8 (3.0%) | 3 (7.3%) |
Number of brackets | 1.27 ± 0.56 | 1.24 ± 0.74 |
Count data in the table represent [number of cases (%)]. Compared to the no-event group. *P < 0.05, **P < 0.01. BMI: body mass index, LVEF: left ventricular ejection fraction, STEMI: acute ST-segment elevation myocardial infarction, NSTEMI: non-acute ST-segment elevation myocardial infarction, BNP: brain natriuretic peptide, LAD: left anterior descending branch, LCX: left circumflex branch, RCA: right coronary artery, LMCA: left main coronary artery.
Table 2
Comparison of CPET parameters (x ± s)
Item | No-event group (n = 269) | Event group (n = 41) | re-AMI group (n = 20) | HF group (n = 25) |
---|
HRmax (time/min) | 109.51 ± 18.00 | 102.51 ± 15.29* | 102.35 ± 11.96 | 101.76 ± 16.48* |
Peak workload (W) | 97.39 ± 30.38 | 89.12 ± 30.28 | 93.6 ± 20.80 | 88.20 ± 30.79 |
METmax | 5.04 ± 1.05 | 4.22 ± 0.86** | 4.42 ± 0.73* | 4.13 ± 0.85** |
PeakVO2 (ml/kg/min) | 17.64 ± 3.67 | 14.73 ± 2.99** | 15.37 ± 2.48** | 14.44 ± 2.98** |
AT (ml/kg/min) | 14.73 ± 3.29 | 12.84 ± 2.54** | 13.29 ± 2.49 | 12.67 ± 2.64** |
VE (L/min) | 44.28 ± 13.29 | 41.87 ± 11.95 | 44.85 ± 10.48 | 41.64 ± 13.08 |
Peak oxygen pulse (ml/beat) | 11.40 ± 2.86 | 10.94 ± 2.80 | 11.90 ± 2.27 | 10.60 ± 2.86 |
VE/VCO2slop | 30.43 ± 4.99 | 36.10 ± 8.94** | 35.78 ± 8.23** | 37.83 ± 9.34** |
PETCO2 (mmHg) | 35.77 ± 4.62 | 33.78 ± 5.39* | 34.10 ± 4.23 | 33.48 ± 5.55** |
BR (%) | 62.51 ± 9.34 | 64.07 ± 9.20 | 64.93 ± 7.48 | 62.58 ± 10.80 |
OUES (ml/min/L/min) | 1858.71 ± 449.32 | 1765.73 ± 512.70 | 1875.50 ± 409.60 | 1709.32 ± 513.46 |
Borg | 14.86 ± 0.99 | 15.12 ± 0.93 | 15.00 ± 1.03 | 15.04 ± 0.98 |
HRR (time/min) | 38.68 ± 14.76 | 32.85 ± 13.52* | 32.60 ± 10.95 | 33.36 ± 13.28 |
%pred | 61.71 ± 13.27 | 55.95 ± 15.53* | 53.00 ± 12.81** | 58.20 ± 17.84 |
Compared to the no-event group: *P < 0.05, **P < 0.01.
HRmax: peak heart rate, HRrest: rest heart rate, peakVO2: peak oxygen uptake, METmax: peak metabolic equivalent, AT: anaerobic threshold oxygen uptake, PETCO2: peak end-tidal carbon dioxide partial pressure, VE/VCO2slop: carbon dioxide ventilation equivalent slope, %pred: percentage of peak oxygen uptake to predicted value, VE: peak ventilation, BR: peak respiratory reserve, OUES: oxygen uptake efficiency slope, HRR: HRmax-HRrest.
Table 3
Logistic multivariate regression of the three groups
Group | Item | OR | 95% CI: | P |
Lower limit | Upper limit |
No-event group and event group | PeakVO2 | 0.724 | 0.568 | 0.924 | 0.009 |
VE/CO2slop | 1.169 | 1.064 | 1.284 | 0.001 |
Constant | 0.000 | | | 0.054 |
No-event group and re-AMI group | VE/CO2slop | 1.140 | 1.047 | 1.242 | 0.030 |
Constant | 0.013 | | | 0.073 |
No-event group and HF group | PeakVO2 | 0.705 | 0.527 | 0.944 | 0.019 |
VE/CO2slop | 1.232 | 1.091 | 1.391 | 0.001 |
PETCO2 | 1.210 | 1.028 | 1.424 | 0.022 |
Constant | 0.000 | | | 0.016 |
peakVO2: peak oxygen uptake, PETCO2: peak end-tidal carbon dioxide partial pressure, VE/VCO2slop: carbon dioxide ventilation equivalent slope.