Comparison of myocardial perfusion by distal protection before and after primary stenting for acute myocardial infarction: angiographic and clinical results of a randomized controlled trial.

OBJECTIVES: To assess the myocardium-reperfusing effect of a distal protection device, GuardWire Plus (GuardWire Plus), in patients with acute myocardial infarction (AMI). BACKGROUND: Distal embolization may result in reduced myocardial perfusion, increasing the risk of non-Q-wave myocardial infarction and death. Distal protection devices may protect the microcirculation from embolic debris, improving short- and long-term clinical outcomes. METHODS: From February 2002 to July 2003, a total of 341 AMI patients at 22 institutions in Japan were enrolled in the present, multicenter, prospective, randomized trial. Patients experiencing AMI within 12 hr of symptom onset, who were considered treatable by stenting and who met the inclusion criteria, were eligible for randomization. Stenting with and without GuardWire Plus was conducted to examine whether the device provides faster and more complete ST-segment resolution, smaller infarct size, and improved myocardial blush score. RESULTS: The rates of slow flow and no-reflow immediately after PCI were 5.3 and 11.4% in the GuardWire Plus and control groups, respectively (P = 0.05). Blush score 3 acquisition rates immediately after PCI were 25.2 and 20.3% in the GuardWire Plus and control groups, respectively (P = 0.26), and the rates at 30 days after PCI were 42.9 and 30.4%, respectively (P = 0.035). CONCLUSIONS: A significant difference was found between the GuardWire Plus and control groups with respect to the total incidence of distal embolization, indicating that GuardWire Plus angiographically improved myocardial perfusion without demonstrating the preventive effect of myocardial damage.     

Predictor of respiratory disturbances during gastric endoscopic submucosal dissection under deep sedation

BACKGROUND Sedation is commonly performed for the endoscopic submucosal dissection(ESD) of early gastric cancer. Severe hypoxemia occasionally occurs due to the respiratory depression during sedation.AIM To establish predictive models for respiratory depression during sedation for ESD.METHODS Thirty-five adult patients undergoing sedation using propofol and pentazocine for gastric ESDs participated in this prospective observational study. Preoperatively, a portable sleep monitor and STOP questionnaires, which are the established screening tools for sleep apnea syndrome, were utilized. Respiration during sedation was assessed by a standard polysomnography technique including the pulse oximeter, nasal pressure sensor, nasal thermistor sensor, and chest and abdominal respiratory motion sensors. The apnea-hypopnea index(AHI) was obtained using a preoperative portable sleep monitor and polysomnography during ESD. A predictive model for the AHI during sedationwas developed using either the preoperative AHI or STOP questionnaire score.RESULTS All ESDs were completed successfully and without complications. Seventeen patients(49%) had a preoperative AHI greater than 5/h. The intraoperative AHI was significantly greater than the preoperative AHI(12.8 ± 7.6 events/h vs 9.35 ± 11.0 events/h, P = 0.049). Among the potential predictive variables, age, body mass index, STOP questionnaire score, and preoperative AHI were significantly correlated with AHI during sedation. Multiple linear regression analysis determined either STOP questionnaire score or preoperative AHI as independent predictors for intraoperative AHI ≥ 30/h(area under the curve [AUC]: 0.707 and 0.833, respectively) and AHI between 15 and 30/h(AUC: 0.761 and 0.778, respectively).CONCLUSION The cost-effective STOP questionnaire shows performance for predicting abnormal breathing during sedation for ESD that was equivalent to that of preoperative portable sleep monitoring.     

Associations between serum lipoprotein(a) levels and the severity of coronary and aortic atherosclerosis

To elucidate the associations between Lp(a) levels and coronary and aortic atherosclerosis, we performed aortic MRI in 143 patients undergoing coronary angiography. Severity of aortic atherosclerosis was represented as plaque scores. Of the 143 patients, 104 had coronary artery disease (CAD). Thoracic and abdominal aortic plaques were found in 89 and 131 patients. Lp(a) levels increased stepwise with the number of stenotic coronary vessels: 15.7 (CAD(-)), 21.2 (1-vessel), 21.4 (2-vessel), and 22.9 mg/dl (3-vessel) (P<0.05). For aortic atherosclerosis, 143 patients were divided into quartiles by plaque scores. Lp(a) did not differ among quartiles of thoracic plaques: 17.1, 19.0, 23.5, and 21.2 mg/dl (P=NS), whereas Lp(a) increased stepwise with quartiles of abdominal plaques: 17.1, 19.2, 19.1, and 24.0 mg/dl (P<0.05). Lp(a) was an independent factor for CAD and abdominal aortic plaques, but not thoracic plaques. Thus, Lp(a) levels were associated with aortic atherosclerosis, especially in abdominal aorta, as well as coronary atherosclerosis.