Prophylactic use of carvedilol in patients receiving ANT may protect both systolic and diastolic functions of the left ventricle.
The chronic systemic inflammation and oxidative stress are important features in chronic obstructive pulmonary disease (COPD). Atherosclerosis is accepted as an inflammatory disease. Both local and systemic inflammation and oxidative stress negatively affect the atherosclerotic process. Metabolic alterations, systemic inflammation, and neurohormonal activation frequently occur in patients with COPD. However, the impact of COPD on intensity and severity of atherosclerosis and morphology of stenotic lesions in patients with established coronary artery disease by coronary angiography is unknown. Eighty-eight patients who were diagnosed with COPD disease were enrolled in the study. Eighty-two patients without any pulmonary disease were included in the control group. Coronary angiography and blood gases analysis were performed in all patients. Gensini score and Extent score were used to evaluate the intensity and severity of atherosclerosis. Lesion morphologies were defined in all patients. The mean number of affected coronary arteries was 2.5 +/- 0.6 in the COPD group and 2.1 +/- 0.7 in the control group (P = 0.004). The mean Extent score was 37 +/- 16 in the COPD group and 23 +/- 11 in the control group (P = 0.001). The Gensini score in the COPD group was significantly higher than that in the control group (respectively 10.9 +/- 6.3 vs 6.6 +/- 4.1, P = 0.01). The number of critical lesions, and type B and C lesions were higher in the COPD group. Multivariate analysis demonstrated that COPD was independently predictive for Gensini score (odds ratio 1.371; 95% confidence interval 1.682-9.228; P = 0.002) and Extent score (odds ratio 1.648; 95% confidence interval 2.023-13.339; P = 0.001). Severity and intensity of atherosclerosis increases in COPD and atherosclerotic lesions have worse morphological properties in COPD.
IMA levels after the exercise test increased in patients with CAD. Our study results indicate that postexercise IMA levels can be helpful markers in the diagnosis of stable CAD in clinical practice.
Ischemia-Modified Albumin and Myocardial IschemiaSbarouni et al. (1) reported on "Ischemia-Modified Albumin [IMA] in Relation to Exercise Stress Testing [EST]" in a previous issue of the Journal. Although the investigators found significant differences in the IMA values at baseline, peak exercise, and after EST, there was no relation between the IMA changes and the result of the EST. The researchers stated that changes in IMA levels do not reflect myocardial ischemia and that IMA does not seem to improve the accuracy of EST. Although these are highly interesting results, some important points must be considered in this study.Previous studies have shown that IMA is a marker of myocardial ischemia, and it was accepted that IMA is an early marker to help in ruling out patients with acute coronary syndrome (2,3). Interestingly, Sbarouni et al.(1) concluded that IMA levels do not indicate myocardial ischemia different from these other studies. False negative and false positive results of exercise testing are important clinical problems in diagnosis of coronary artery disease (CAD). The sensitivity and specificity of EST range between 60% and 70% (4,5). Approximately 30% to 40% more false negative results may be obtained in clinical practice. Therefore, each positive EST is not accepted as a sign of myocardial ischemia. However, in the study by Sbarouni et al. (1), a positive stress test is accepted as indicative of myocardial ischemia. It is not mentioned how many patients with positive EST have myocardial ischemia. In our opinion, lack of this important information may change the study results.Other conflicts and controversial subjects are related to results from postexercise IMA levels. Because plasma IMA levels increase within minutes after myocardial ischemia, peak exercise IMA levels may not indicate myocardial ischemia. However, postexercise IMA levels may be helpful to determine myocardial ischemia during exercise. Previously, it was demonstrated that IMA levels decrease after physical exercise, and it was hypothesized that this immediate decrease may have been attributable to interference in the IMA measurement by lactate produced during skeletal muscle ischemia (6,7) However, release of lactate after EST in patients with peripheral vascular disease has been reported (8) Although Sbarouni et al. (1) concluded that a decrease in IMA levels is associated with hemoconcentration, it was unknown whether peripheral vascular disease was present in the study population. Therefore, possible peripheral vascular disease in patients may affect IMA levels via increased lactate concentration.
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