Akira Tamura

Background: Contrast-induced nephropathy is the leading cause of in-hospital acute renal failure. This side effect of contrast agents leads to increased morbidity, mortality, and health costs. Ensuring adequate hydration prior to contrast exposure is highly effective at preventing this complication, although the optimal hydration strategy to prevent contrast-induced nephropathy still remains an unresolved issue. Former meta-analyses and several recent studies have shown conflicting results regarding the protective effect of sodium bicarbonate. The objective of this study was to assess the effectiveness of normal saline versus sodium bicarbonate for prevention of contrast-induced nephropathy. Methods: The study searched MEDLINE, EMBASE, Cochrane databases, International Pharmaceutical Abstracts database, ISI Web of Science (until 15 December 2008), and conference proceedings for randomized controlled trials that compared normal saline with sodium bicarbonate-based hydration regimen regarding contrast-induced nephropathy. Random-effects models were used to calculate summary odds ratios. Results: A total of 17 trials including 2,633 subjects were pooled. Pre-procedural hydration with sodium bicarbonate was associated with a significant decrease in the rate of contrast-induced nephropathy (odds ratios 0.52; 95% confidence interval 0.34–0.80, P = 0.003). Number needed to treat to prevent one case of contrast-induced nephropathy was 16 (95% confidence interval 10–34). No significant differences in the rates of post-procedure hemodialysis (P = 0.20) or death (P = 0.53) was observed. Conclusion: Sodium bicarbonate-based hydration was found to be superior to normal saline in prevention of contrast-induced nephropathy in this updated meta-analysis.

Background Carvedilol may reduce the severity of central sleep apnea (CSA) in patients with chronic heart failure (CHF). Methods and Results This study prospectively examined the effect of carvedilol on the severity of CSA in patients with CHF. Polysomnographic findings, left ventricular (LV) function, and plasma brain natriuretic peptide (BNP) level were evaluated before and 6 months after induction of carvedilol in 16 patients with CHF (New York Heart Association functional class II or III and LV ejection fraction 5 with dominant central apneic events). All patients tolerated carvedilol. The 6-month treatment with carvedilol increased the LV ejection fraction (32±7.4% to 45±9.8%, P<0.001) and decreased the BNP level (159 [69-458] pg/ml to 38 [16-193] pg/ml, P=0.017). The polysomnographic findings showed that the treatment decreased the apnea-hypopnea index (34±13 to 14±13, P=0.003) and CAI (13±11 to 1.9±4.3, P<0.001), whereas it increased the obstructive apnea index (1.1±1.5 to 3.1±3.4, P=0.04). Conclusion This preliminary study shows that treatment with carvedilol reduces the severity of CSA in patients with CHF, but that episodes of obstructive sleep apnea sometimes increase after the treatment. (Circ J 2009; 73: 295 - 298)

A 46-year-old woman with mitral stenosis was admitted to our hospital because of exertional dyspnea. She had undergone open mitral commissurotomy 15 years ago. Doppler echocardiography showed that the mitral valve area was 0.8 cm² without mitral regurgitation. She underwent diagnostic cardiac catheterization including transseptal puncture. After several attempts of the transseptal puncture, a Brockenbrough's needle was successfully advanced into the left atrium. The pressure gradient in the diastolic phase between the left atrium and the left ventricle was 10 mmHg, and the mitral valve area calculated by the Gorlin formula was 0.8 cm². Coronary angiography performed after the transseptal puncture revealed a fistula from the atrial branch in the left circumflex coronary artery into the right atrium (RA) (Panels A and B, white arrows). A significant step-up in the O₂ saturation was not observed in the RA, and echocardiography did not showed echo free space. After 1 week, she successfully underwent percutaneous mitral valvuloplasty using an Inoue balloon without any complications. Because the fistula did not produce any adverse effects, including a coronary steel phenomenon, we decided to perform conservative management for it. To the best of our knowledge, this is the first report of a coronary-RA fistula caused by the transseptal puncture.

We examined the frequency of side-branch occlusion of the sinus node (SN) artery and of the subsequent sinus arrest in 80 consecutive patients who underwent percutaneous coronary intervention (PCI) for proximal right coronary artery (RCA) lesions. Side-branch occlusion of the SN artery occurred during PCI in 14 (17.5%) patients. Sinus arrest with junctional escape rhythm developed in 4 (28.6%) of these 14 patients. Temporary ventricular pacing was performed for one patient. The junctional escape rhythm disappeared in all of the patients within 3 days of the SN artery occlusion. The frequency of a single blood supply to the SN by the SN artery originating from the RCA did not differ significantly between the patients with and without sinus arrest (4/4 [100%]) vs 9/10 [90%]). In conclusion, although side-branch occlusion of the SN artery often occurs during PCI for proximal RCA lesions, where the SN artery originated, it does not always produce sinus arrest even in cases of a single blood supply to the SN by the SN artery originating from the RCA. Even though sinus arrest is caused by the occlusion of the SN artery, this bradyarrhythmia seems to disappear in the short term.