Yusuke Kawai

Remote ischemic preconditioning reduces contrast-induced acute kidney injury in patients with ST-elevation myocardial infarction: A randomized controlled trial

BACKGROUND Contrast medium-induced acute kidney injury (CI-AKI) is a cardiovascular complication after myocardial infarction treated with emergency percutaneous coronary intervention. The aim of this randomized, sham-controlled trial was to evaluate the impact of remote ischemic preconditioning (RIPC) on CI-AKI in patients with ST-elevation myocardial infarction who received emergency primary percutaneous coronary intervention. METHODS AND RESULTS Patients with a suspected ST-elevation myocardial infarction were randomly assigned at a 1:1 ratio to receive percutaneous coronary intervention either with (n=63) or without (n=62) RIPC (intermittent arm ischemia through three cycles of 5min of inflation and 5min of deflation of a blood pressure cuff). A total of 47 RIPC patients and 47 control patients met all study criteria. The primary endpoint was the incidence of CI-AKI, which was defined as an increase in serum creatinine >0.5mg/dL or >25% over the baseline value 48-72h after administration of contrast medium. The incidence of CI-AKI was 10% (n=5) in the RIPC group and 36% (n=17) in the control group (p=0.003). The odds ratio of CI-AKI in patients who received RIPC was 0.18 (95% confidence interval: 0.05-0.64; p=0.008). CONCLUSIONS In patients with ST-elevation myocardial infarction, RIPC before percutaneous coronary intervention reduced the incidence of CI-AKI.

Clinical characteristics of responders to treatment with tolvaptan in patients with acute decompensated heart failure: Importance of preserved kidney size

BACKGROUND Recent clinical trials have demonstrated the efficacy of short-term treatment with tolvaptan, an oral vasopressin V2 receptor antagonist, in patients with heart failure. However, the response to tolvaptan varies among patients. The aim of this study was to determine factors associated with response to tolvaptan in patients with acute decompensated heart failure (ADHF). METHODS The Tolvaptan Registry, a prospective, observational, multicenter cohort study performed in Japan, aims to determine factors affecting the responsiveness of tolvaptan in patients with ADHF. We enrolled ADHF patients treated with tolvaptan and they were divided into two groups: responders and non-responders. Responders were defined as subjects who met all of the following three conditions: (1) increasing urine volume during a 24-hour period after the start of tolvaptan treatment; (2) improvement in New York Heart Association functional class; and (3) decrease in cardiothoracic ratio assessed by chest X-ray on day 3 of tolvaptan administration. RESULTS Among the 114 patients, treatment with tolvaptan improved three conditions of heart failure in more than half of all the cohorts (71 patients, 62%). As for baseline characteristics, estimated glomerular filtration rate, urine osmolality, and kidney size were significantly greater in responders than in non-responders. Multivariate logistic analysis revealed that kidney size was independently associated with responders (odds ratio: 1.083, p=0.001, 95% confidence interval 1.031-1.137). CONCLUSIONS The main clinical characteristic of responders to treatment with tolvaptan is that kidney size is preserved.

Effect of remote ischemia or nicorandil on myocardial injury following percutaneous coronary intervention in patients with stable coronary artery disease: A randomized controlled trial

BACKGROUND The effect of remote ischemic preconditioning (RIPC) and nicorandil on periprocedural myocardial injury (pMI) in patients with planned percutaneous coronary intervention (PCI) remains controversial. The aim of this randomized trial was to evaluate the effect of RIPC or nicorandil on pMI following PCI in patients with stable coronary artery disease (CAD) compared with a control group. METHODS Patients with stable CAD who planned to undergo PCI were assigned to a 1:1:1 ratio to control, RIPC, or intravenous nicorandil (6mg/h). Automated RIPC was performed by a device, which performs intermittent arm ischemia through three cycles of 5min of inflation and 5min of deflation of a pressure cuff. The primary outcome was the incidence of pMI, determined by an elevation in high-sensitive troponin T or creatine kinase myocardial band at 12 or 24h after PCI. The secondary outcomes were ischemic events during PCI and adverse clinical events at 8months after PCI. RESULTS A total of 391 patients were enrolled. The incidence of pMI following PCI was not significantly different between the control group (48.9%) and RIPC group (39.5%; p=0.14), or between the control group and nicorandil group (40.3%; p=0.17). There were no significant differences in ischemic events during PCI or adverse clinical events within 8months after PCI among the three groups. CONCLUSIONS This study demonstrated moderate reductions in biomarker release and pMI by RIPC or intravenous nicorandil prior to the PCI consistently, but may have failed to achieve statistical significance because the study was underpowered.

USEFULNESS OF POSITIONAL ANGIOGRAPHY AND CATHETERIZATION STUDY: A CASE OF PLATYPNEA-ORTHODEOXIA SYNDROME SUCCESSFULLY TREATED WITH TRANSCUTANEOUS FORAMEN OVALE CLOSURE

Platypnea-orthodeoxia syndrome(POS) is a rare condition detected by through history taking. Further investigation and management are often required. A 75 year old female with long history of osteoporosis and rheumatoid arthritis, who had compression lumbar fracture 3 months before presentation was

Association between changes in platelet reactivity during elective percutaneous coronary intervention and periprocedural myocardial infarction: A pilot study

BACKGROUND High platelet reactivity before percutaneous coronary intervention (PCI) reportedly increases the risk of PCI-related myocardial infarction (PMI) following elective PCI. We conducted a pilot study to evaluate changes in platelet reactivity during PCI and their association with the incidence of PMI. METHODS In total, 133 consecutive patients undergoing elective PCI after pretreatment with dual antiplatelet therapy for at least 7 days were prospectively enrolled. Platelet reactivity was measured by the VerifyNow® assay (International Technidyne Corporation, Edison, NJ, USA) immediately before and after PCI. RESULTS Platelet reactivity significantly increased from 177.3 ± 53.4 P2Y12 reaction units (PRU) before PCI to 203.4 ± 52.8 PRU immediately after PCI (p < 0.001). Absolute changes in platelet reactivity were significantly greater in patients with than without PMI (32.4 ± 29.0 vs. 21.2 ± 24.8 PRU, respectively; p = 0.021). In the multivariable logistic regression analysis, the absolute change in PRU was an independent predictor of the incidence of PMI. Receiver operating characteristic curve analysis of the change in PRU during PCI for discriminating PMI showed a sensitivity, specificity, and the cut-off value of 46%, 76%, and 37 PRU, respectively (area under the curve = 0.607, p = 0.0235). When the patients were divided into two groups, namely a greater (change in PRU ≥ 37) and smaller (change in PRU < 37) increase group, the incidence rate of PMI was significantly higher in the greater than smaller increase group (59.1% vs. 34.8%, respectively; p = 0.008). Additional exploratory analyses by intracoronary imaging demonstrated that the proximal reference lumen area in the greater increase group was significantly smaller than that in the smaller increase group (6.5 ± 2.4 vs. 7.7 ± 3.1 mm2, respectively; p = 0.032). CONCLUSION An increase in platelet reactivity after elective PCI is possibly associated with PMI. This finding should be validated by a larger-scale study.

Effect of Intensive and Standard Pitavastatin Treatment With or Without Eicosapentaenoic Acid on Progression of Coronary Artery Calcification Over 12 Months ― Prospective Multicenter Study ―

BACKGROUND The effect of lipid-lowering agents on progression of coronary artery calcification (CAC) remains unclear. We evaluated the effects of pitavastatin 2 mg/day (PIT2), pitavastatin 4 mg/day (PIT4), and PIT2 combined with eicosapentaenoic acid (PIT2+EPA) on CAC progression.Methods and Results:This prospective multicenter study in Japan included patients with an Agatston score of 1-999, hypercholesterolemia, and no evidence of cardiovascular disease. Patients were allocated into PIT2, PIT4, or PIT2+EPA groups. The primary outcome was the annual percent change in Agatston score in all patients. In total, 156 patients who had multi-detector row computed tomography without any artifacts were included in the primary analysis. Pitavastatin did not significantly reduce the annual progression rate of the Agatston score (40%; 95% CI: 19-61%). The annual progression rate of Agatston score in the PIT2 group was not significantly different from that in the PIT4 group (34% vs. 42%, respectively; P=0.88) or the PIT2+EPA group (34% vs. 44%, respectively; P=0.80). On post-hoc analysis the baseline ratio of low- to high-density lipoprotein cholesterol was a significant predictor of non-progression of Agatston score by pitavastatin (OR, 2.17; 95% CI: 1.10-44.12; P=0.02). CONCLUSIONS Pitavastatin does not attenuate progression of CAC. Intensive pitavastatin treatment and standard treatment with EPA does not reduce progression of CAC compared with standard treatment.