Tomoko Hayano

Efficacy of N-acetylcysteine and aminophylline in preventing contrast-induced nephropathy

BACKGROUND Contrast-induced nephropathy (CIN) is one of the important complications of coronary angiography (CAG) and percutaneous coronary intervention (PCI), especially in patients with chronic kidney disease (CKD). Prophylactic administration of N-acetylcysteine (NAC) and aminophylline has been reported to be effective in some trials, but the results still remain controversial. We investigated the efficacy of NAC or aminophylline in preventing CIN. METHODS AND RESULTS Forty-five consecutive patients undergoing CAG and/or PCI were randomly assigned to receive hydration and NAC (704 mg orally twice daily; NAC group, n=15), hydration and aminophylline (250 mg intraveneously 30 min before CAG and/or PCI; aminophylline group, n=15), or hydration alone (control group, n=15). We compared serum creatinine (SCr), creatinine clearance (Ccr), blood beta-2 microglobulin, and urinary beta-2 microglobulin levels at baseline and 48h after CAG and/or PCI. In the NAC group, SCr decreased from 1.00 + or - 0.36 to 0.67 + or - 0.16 mg/dl (p<0.01), and Ccr significantly increased from 62.4 + or - 15.6 to 80.4 + or - 8.39 ml/min (p<0.01). In the aminophylline group, SCr and Ccr were unchanged. In the control group, SCr significantly increased from 0.94 + or - 0.21 to 1.28 + or - 0.21 mg/dl (p<0.01), and Ccr significantly decreased from 63.7 + or - 16.1 to 46.1 + or - 10.6 ml/min (p<0.01) after CAG and/or PCI. In the NAC group, mean blood beta-2 microglobulin significantly decreased from 2.38 + or - 0.58 to 1.71 + or - 0.38 mg/dl (p<0.01), and in the aminophylline group, mean urinary beta-2 microglobulin concentration significantly decreased from 337 + or - 31.0 to 239 + or - 34 microg/ml (p<0.01). CONCLUSIONS These results suggest that both prophylactic NAC and aminophylline administration are effective in preventing CIN, but not with hydration alone. It appears that the two compounds work in different ways against CIN.

Assessment of right atrial mapping and P wave—triggered signal-average in patients with paroxysmal atrial fibrillation

Abstract To assess right atrial mapping and P wave—triggered signal-averaged electrocardiogram (ECG) in patients with paroxysmal atrial fibrillation (PAF), this study examined right atrial electrograms using atrial mapping and parameters by P wave—triggered signal-averaged ECG in 39 patients without sick sinus syndrome. Subjects were divided into those with PAF (n = 13; 60 ± 13 years old) and a control group (n = 26; 49 ± 19 years old). The total number of abnormal right atrial electrograms per patient was significantly greater in the PAF group (3.2 ± 1.9) than in the control group (1.1 ± 0.9; P P = .06). The filtered P wave duration was significantly longer in the PAF group than in the control group (144 ± 21 vs 125 ± 14 ms [ P P P 1.5 μV (2.2 ± 1.8 vs 1.3 ± 1.3 [ P

Paradoxical effects of pirenzepine on parasympathetic activity in chronic heart failure and control

We studied the effect of intravenous pirenzepine (3 mg) in normal subjects (n=15, 43+/-16 years old) and in patients with chronic heart failure (n=15, 61+/-12 years old) to assess the effect of low-dose pirenzepine on vagal activity. R-R intervals and the standard deviations, low-frequency power (LF: ln ms2, 0.04-0.15 Hz), high-frequency power (HF: ln ms2, 0.15-0.40 Hz) and the ratio of low- to high-frequency power (LF/HF ratio) were measured 10 min before and after pirenzepine using a Holter analysis system. Pirenzepine was found to cause a significant increase in the R-R interval from 903+/-112 to 956+/-129 ms in the control group (P<0.0001) and from 927+/-141 to 958+/-168 ms in patients with chronic heart failure (P<0.01). Pirenzepine also increased HF significantly from 4.29+/-0.32 to 5.16+/-0.38 ln ms2 in the control group (P<0.0001) and from 4.04+/-0.16 to 4.48+/-0.24 ln ms2 in the chronic heart failure group (P<0.05). Pirenzepine did not significantly alter the LF/HF ratio in either group. We emphasize that pirenzepine appears to have a vagoinimetic effect in patients with chronic heart failure and that it may be useful for augmenting vagal control of the heart in some patients with chronic heart failure.

An autopsy case of tako-tsubo cardiomyopathy presenting ventricular tachycardia after pacemaker implantation

We herein report a rare autopsy case of tako-tsubo cardiomyopathy (TTC) presenting ventricular tachycardia after pacemaker implantation. A 69-year-old male received a dual-chamber pacemaker implantation for complete atrioventricular block. He had no chest symptoms after the operation. Three days later, he developed severe chest pain, followed by syncope. Electrocardiogram showed sustained monomorphic ventricular tachycardia. Despite the use of amiodarone and frequent electrical defibrillation, ventricular tachycardia and ventricular fibrillation were repeated incessantly. He died 24 h after the syncope. The autopsy revealed no hemopericardial effusion, or perforation of leads. There were also no obstructive lesions in the coronary arteries. Myocardial necrosis was observed in the entire circumference and the all layers of the left ventricle. Microscopically, myocardial necrosis was plurifocal and contraction band necrosis. We speculate that catecholamine cardiotoxicity caused ventricular tachycardia in this case. Further studies are needed to clarify the heterogeneity of this disease. <Learning objective: Tako-tsubo cardiomyopathy should be considered a potential complication of pacemaker implantation. Physicians should recognize that this disorder can occur unexpectedly during medical examination or treatment.>.

Double Ventricular Response by a Single Ventricular Extrastimulus to the Inner Loop of Reentry in a Patient Without Apparent Heart Disease

SHIMIZU, A., et al.: Double Ventricular Response by a Single Ventricular Extrastimulus to the Inner Loop of Reentry in a Patient Without Apparent Heart Disease. In a patient without apparent heart disease, a ventricular extrastimulus delivered from the left ventricular apex where the electrogram was recorded 30 ms after the onset of the QRS complex during VT advanced the second QRS complex, but not the first QRS complex. The morphology of the second QRS complex was the same as that of VT. The postpacing interval was the same as the cycle length of the VT. These findings indicated that the site of stimulation was at the inner loop of the reentry circuit of the VT. A ventricular extrastimulus with a shorter coupling interval advanced the first and second QRS complexes, indicating that the ventricle was activated by antidromic and orthodromic activation from the extrastimulus. Radiofrequency ablation at that site of stimulation terminated the VT and no further VT could be induced.