Objective: The control of myocardial temperature is very important in myocardial protection methods. We investigated the validity of myocardial protection methods at our institution using noninvasive thermography as a means of determining the effectiveness of myocardial protection, with the aim of confirming that myocardial protection solution is correctly infused. Methods: Of 52 extracorporeal circulation cases with cardiac arrest from May 2020 to June 2022, 10 cases with cardiac arrest by progressive myocardial protection with Microplegia, a blood myocardial protection, were included. Infusion was performed at an infusion temperature of 20℃, with an intracircuit pressure of less than 300 mmHg and a flow rate of 250-350 ml/min maintained in a progressive manner. Myocardial temperature in the anterior region of the heart was measured using a thermographic camera at a distance of 80 cm from the heart. Results: The cardiac surface temperature before the start of myocardial protection was 32.5±1.0℃. After the start of infusion, the cardiac surface temperature at the time cardiac arrest was obtained was 27.4±1.3℃. In all cases, the cardiac surface temperature at the time of cardiac arrest was visually heterogeneous. Further infusion was continued, and the average time to reach the lowest visually uniform surface temperature was 342±23 s. The mean cardiac surface temperature at the end of myocardial protection was 22.4±1.3℃. At the start of myocardial protection solution infusion, the myocardial surface cooled faster in muscle than in visible fat, in the order aorta>myocardium from the apex>cardiac base. The postoperative course was generally good in all cases with respect to EF, CKMB, catecholamine use, extubation time, postoperartive hospital stay, and outcomes. Conclusion: It was found that a time of about 360 s is needed to uniformly cool the myocardial temperature during infusion of myocardial protection solution. Furthermore, by confirming the cooling of the base of the heart, it is suggested that it is inferred that the whole is cooled. To avoid problems caused by inadequate myocardial protection, it is suggested that measuring myocardial temperature using a non-invasive, simple thermal imaging camera can assist in determining the effectiveness of myocardial protection, and is expected to establish the safety of further myocardial protection.

BACKGROUND/AIMS: The influences of Helicobacter pylori eradication therapy on the disease course of inflammatory bowel disease (IBD) are still unclear. We therefore conducted a multicenter, retrospective cohort study to evaluate the safety of H. pylori eradication therapy for IBD patients. METHODS: IBD patients with H. pylori eradication from 2005 to 2015 (eradication group) and control patients (non-eradication group; 2 paired IBD patients without H. pylori eradication matched with each eradicated patient) were included. IBD exacerbation (increased/additional IBD drug or IBD-associated hospitalization/surgery) and disease improvement based on the physicians’ global assessment were investigated at baseline, and at 2 and 6 months after eradication or observation. RESULTS: A total of 429 IBD (378 ulcerative colitis, 51 Crohn’s disease) patients, comprising 144 patients in the eradication group and 285 patients in the non-eradication group, were enrolled at 25 institutions. IBD exacerbation was comparable between groups (eradication group: 8.3% at 2 months [odds ratio, 1.76; 95% confidence interval, 0.78–3.92; P=0.170], 11.8% at 6 months [odds ratio, 1.60; 95% confidence interval, 0.81–3.11; P=0.172]). Based on the physicians’ global assessment at 2 months, none of the patients in the eradication group improved, whereas 3.2% of the patients in the non-eradication group improved (P=0.019). Multivariate analysis revealed that active disease at baseline, but not H. pylori eradication, was an independent factor for IBD exacerbation during 2 months’ observation period. The overall eradication rate was 84.0%–comparable to previous reports in non-IBD patients. CONCLUSIONS: H. pylori eradication therapy does not alter the short-term disease activity of IBD.
Clarithromycin ; Cohort Studies ; Colitis, Ulcerative ; Helicobacter pylori* ; Helicobacter* ; Humans ; Inflammatory Bowel Diseases* ; Metronidazole ; Multivariate Analysis ; Retrospective Studies