Potential Predictors for Mental Stress-Induced Myocardial Ischemia in Patients with Coronary Artery Disease
Coronary artery disease (CAD) remains a leading cause of death worldwide, with a significant portion of patients experiencing myocardial ischemia induced by mental stress. Mental stress-induced myocardial ischemia (MSIMI) is associated with adverse cardiac events, making it crucial to identify potential predictors for this condition. This study aimed to explore whether biomarkers and blood pressure could serve as predictors for MSIMI in patients with CAD.
The study enrolled 82 patients with documented CAD between June 1, 2017, and November 9, 2017. Patients were divided into MSIMI-positive and MSIMI-negative groups based on diagnostic criteria. Blood samples were collected at rest and after a 5-minute mental arithmetic task, which served as the mental stressor. The study measured various biomarkers, including high-sensitivity cardiac troponin I (hs-cTnI), N-terminal pro-brain natriuretic peptide (NT-proBNP), creatine kinase-muscle/brain (CK-MB), myoglobin, C-reactive protein (CRP), and D-dimer. Blood pressure and heart rate were also recorded at rest, during, and after the stressor.
The results revealed that patients with MSIMI had significantly higher median resting NT-proBNP levels (141.02 pg/mL vs. 57.95 pg/mL) and mean systolic blood pressure (SBP) (145.56 mmHg vs. 134.92 mmHg) compared to those without MSIMI. After the mental stress task, patients who developed MSIMI exhibited higher elevations in post-stressor hs-cTnI (0.020 ng/mL vs. 0.009 ng/mL) and post-stressor NT-proBNP (138.96 pg/mL vs. 61.55 pg/mL). Receiver operating characteristic (ROC) curves and logistic regression analyses identified optimal cut-off values for these biomarkers and blood pressure, which were associated with increased risks of developing MSIMI.
The study found that patients with post-stressor hs-cTnI levels ≥0.015 ng/mL had a seven-fold increased risk of developing MSIMI. Similarly, patients with resting NT-proBNP levels ≥80.51 pg/mL had an eight-fold increased risk, and those with post-stressor NT-proBNP levels ≥98.80 pg/mL had a 35-fold increased risk. Additionally, patients with resting SBP ≥129.50 mmHg had an 11-fold increased risk of MSIMI. These findings suggest that hs-cTnI, NT-proBNP, and SBP could serve as potential predictors for MSIMI in patients with CAD.
The study also explored the relationship between mental stress and myocardial ischemia. Mental stress is hypothesized to trigger myocardial ischemia through mechanisms such as inflammatory responses, hyperactivation of the sympathetic nervous system, increased catecholamines, and psychological factors like anger, depression, and anxiety. Previous research has shown that MSIMI is associated with a two-fold increased risk of adverse cardiac events in patients with CAD. This study aimed to build on these findings by identifying biomarkers and blood pressure as potential predictors for MSIMI.
The diagnostic criteria for MSIMI included the development or worsening of wall motion abnormalities or a reduction in left ventricular ejection fraction (LVEF) by ≥5% during mental stress compared to rest. Echocardiography was used to assess wall motion and LVEF, with images analyzed by an experienced sonographer. The study also utilized the Gensini scoring system to evaluate the severity of coronary artery stenosis, although no significant differences were found between the MSIMI-positive and MSIMI-negative groups.
The study’s statistical analysis involved linear regression, ROC curves, and logistic regression. Linear regression was used to assess the relationship between resting and post-stressor biomarker levels. ROC curves were plotted to determine optimal cut-off values for hs-cTnI and NT-proBNP, with the area under the curve (AUC) used to estimate diagnostic accuracy. Logistic regression was then used to test the predictive value of these cut-off values and other selected parameters.
The results showed that patients with MSIMI had slightly higher baseline resting hs-cTnI levels and significantly greater resting NT-proBNP levels compared to those without MSIMI. After the mental stress task, patients who developed MSIMI exhibited higher elevations in post-stressor hs-cTnI and NT-proBNP levels. These findings were consistent with previous research indicating that hs-cTnI and NT-proBNP are sensitive markers of myocardial stress and ischemia.
The study also found that patients with MSIMI had significantly higher resting SBP and peri-stressor SBP compared to those without MSIMI. However, no significant differences were observed in diastolic blood pressure (DBP) or heart rate between the two groups. The ROC curve for resting SBP yielded a cut-off value of 129.50 mmHg, with a sensitivity of 93.8% and a specificity of 40.9%. Patients with resting SBP ≥129.50 mmHg had an 11-fold increased risk of developing MSIMI.
The study’s findings have important clinical implications. Identifying patients at higher risk of MSIMI could help clinicians implement targeted interventions to reduce the risk of adverse cardiac events. For example, patients with elevated hs-cTnI, NT-proBNP, or SBP levels could be monitored more closely and provided with stress management interventions or pharmacological treatments to mitigate the effects of mental stress on myocardial ischemia.
The study also highlights the need for further research to explore the mechanisms underlying MSIMI and to identify additional predictors. Future studies could investigate the role of other biomarkers, such as inflammatory markers or genetic factors, in predicting MSIMI. Additionally, larger multicenter studies with longer follow-up periods could provide more robust evidence on the association between MSIMI and adverse cardiac events.
In conclusion, this study demonstrates that patients with CAD who have higher hs-cTnI levels, greater NT-proBNP levels, or elevated SBP are at increased risk of developing MSIMI. These findings suggest that hs-cTnI, NT-proBNP, and SBP could serve as potential predictors for MSIMI, providing valuable insights for clinicians in managing patients with CAD. Further research is needed to validate these findings and to explore additional predictors and interventions for MSIMI.
doi.org/10.1097/CM9.0000000000000260
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