Background: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule...Background: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. Method: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels(group I, 11 male, 6 female, mean age=48± 9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow(group II, 11 male, 9 female, mean age=50± 8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count(TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects(group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. Results: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow(ICAM-1: 545± 198 ng/ml vs. 242± 113 ng/ml respectively, p< 0.001, VCAM-1: 2040± 634 ng/ml vs. 918± 336 ng/ml respectively, p< 0.001, E-selectin: 67± 9 ng/ml vs. 52± 8 ng/ml respectively, p< 0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1(r=0.550, p< 0.001), VCAM-1(r=0.569, p< 0.001) and E-selectin(r=0.443, p=0.006). Conclusion: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.展开更多
Context: Carbon monoxide(CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of moderate to severe CO poisoning. While the in- hospital mortality for t...Context: Carbon monoxide(CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of moderate to severe CO poisoning. While the in- hospital mortality for these patients is low, the long- term outcome of myocardial injury in this setting is unknown. Objective: To determine the association between myocardial injury and long- term mortality in patients following moderate to severe CO poisoning. Design, Setting, and Participants: Prospective cohort study of 230 consecutive adult patients treated for moderate to severe CO poisoning with hyperbaric oxygen and admitted to the Hennepin County Medical Center, a regional center for treatment of CO poisoning, between January 1, 1994, and January 1, 2002. Follow- up was through November 11, 2005. Main Outcome Measure: All- cause mortality. Results: Myocardial injury(cardiac troponin I level ≥ 0.7 ng/mL or creatine kinase- MB level ≥ 5.0 ng/mL and/or diagnostic electrocardiogram changes) occurred in 85(37% ) of 230 patients. At a median follow- up of 7.6 years(range: in- hospital only to 11.8 years), there were 54 deaths(24% ). Twelve of those deaths(5% ) occurred in the hospital as a result of a combination of burn injury and anoxic brain injury(n=8) or cardiac arrest and anoxic brain injury(n=4). Among the 85 patients who sustained myocardial injury from CO poisoning, 32(38% ) eventually died compared with 22(15% ) of 145 patients who did not sustain myocardial injury(adjusted hazard ratio, 2.1; 95% confidence interval, 1.2- 3.7; P=.009). Conclusion: Myocardial injury occurs frequently in patients hospitalized for moderate to severe CO poisoning and is a significant predictor of mortality.展开更多
Background: We undertook a prospective electrocardiogram(ECG) substudy in the ESSENCE trial and hypothesized that patient subgroups with ST-segment deviation would experience greater benefit from enoxaparin, as compar...Background: We undertook a prospective electrocardiogram(ECG) substudy in the ESSENCE trial and hypothesized that patient subgroups with ST-segment deviation would experience greater benefit from enoxaparin, as compared with unfractionated heparin(UFH). Methods: Of the 3171 patients in the trial, 3087 had a qualifying ECG available for analysis by the core laboratory. Patients were divided into 4 mutually exclusive groups based upon the qualifying ECG:(1) ST-segment elevation,(2) ST-segment depression,(3) T-wave inversions, or(4) others. Results: The 30-day and 1-year primary outcomes(death, myocardial infarction, or recurrent angina) were significantly lower among patients with ST elevation or ST depression who received enoxaparin, as compared with UFH(20.8%vs 28.0%, P=.0019 and 32%vs 40.4%, P=.0011, respectively). The greatest absolute benefit of enoxaparin over UFH was seen in patients with ST depression(primary end point at 30 days, 24.6%vs 32.4%, P=.018; at 1 year, 35.5%vs 44.5%, P=.012). Conclusion: Specific recognition of patients with ST-segment depression appears to identify those not only at high risk for adverse outcome, but also patients most likely to derive the greatest benefit from enoxaparin, as compared with UFH therapy.展开更多
文摘Background: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1(ICAM-1), vascular cell adhesion molecule-1(VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. Method: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels(group I, 11 male, 6 female, mean age=48± 9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow(group II, 11 male, 9 female, mean age=50± 8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count(TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects(group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. Results: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow(ICAM-1: 545± 198 ng/ml vs. 242± 113 ng/ml respectively, p< 0.001, VCAM-1: 2040± 634 ng/ml vs. 918± 336 ng/ml respectively, p< 0.001, E-selectin: 67± 9 ng/ml vs. 52± 8 ng/ml respectively, p< 0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1(r=0.550, p< 0.001), VCAM-1(r=0.569, p< 0.001) and E-selectin(r=0.443, p=0.006). Conclusion: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.
文摘Context: Carbon monoxide(CO) poisoning is a common cause of toxicological morbidity and mortality. Myocardial injury is a frequent consequence of moderate to severe CO poisoning. While the in- hospital mortality for these patients is low, the long- term outcome of myocardial injury in this setting is unknown. Objective: To determine the association between myocardial injury and long- term mortality in patients following moderate to severe CO poisoning. Design, Setting, and Participants: Prospective cohort study of 230 consecutive adult patients treated for moderate to severe CO poisoning with hyperbaric oxygen and admitted to the Hennepin County Medical Center, a regional center for treatment of CO poisoning, between January 1, 1994, and January 1, 2002. Follow- up was through November 11, 2005. Main Outcome Measure: All- cause mortality. Results: Myocardial injury(cardiac troponin I level ≥ 0.7 ng/mL or creatine kinase- MB level ≥ 5.0 ng/mL and/or diagnostic electrocardiogram changes) occurred in 85(37% ) of 230 patients. At a median follow- up of 7.6 years(range: in- hospital only to 11.8 years), there were 54 deaths(24% ). Twelve of those deaths(5% ) occurred in the hospital as a result of a combination of burn injury and anoxic brain injury(n=8) or cardiac arrest and anoxic brain injury(n=4). Among the 85 patients who sustained myocardial injury from CO poisoning, 32(38% ) eventually died compared with 22(15% ) of 145 patients who did not sustain myocardial injury(adjusted hazard ratio, 2.1; 95% confidence interval, 1.2- 3.7; P=.009). Conclusion: Myocardial injury occurs frequently in patients hospitalized for moderate to severe CO poisoning and is a significant predictor of mortality.
文摘Background: We undertook a prospective electrocardiogram(ECG) substudy in the ESSENCE trial and hypothesized that patient subgroups with ST-segment deviation would experience greater benefit from enoxaparin, as compared with unfractionated heparin(UFH). Methods: Of the 3171 patients in the trial, 3087 had a qualifying ECG available for analysis by the core laboratory. Patients were divided into 4 mutually exclusive groups based upon the qualifying ECG:(1) ST-segment elevation,(2) ST-segment depression,(3) T-wave inversions, or(4) others. Results: The 30-day and 1-year primary outcomes(death, myocardial infarction, or recurrent angina) were significantly lower among patients with ST elevation or ST depression who received enoxaparin, as compared with UFH(20.8%vs 28.0%, P=.0019 and 32%vs 40.4%, P=.0011, respectively). The greatest absolute benefit of enoxaparin over UFH was seen in patients with ST depression(primary end point at 30 days, 24.6%vs 32.4%, P=.018; at 1 year, 35.5%vs 44.5%, P=.012). Conclusion: Specific recognition of patients with ST-segment depression appears to identify those not only at high risk for adverse outcome, but also patients most likely to derive the greatest benefit from enoxaparin, as compared with UFH therapy.
