Takeshi Senoo

Contrast-Induced Nephropathy in Patients Undergoing Emergency Percutaneous Coronary Intervention for Acute Coronary Syndrome

Contrast-induced nephropathy (CIN) is associated with significantly increased morbidity and mortality after coronary angiography and percutaneous coronary intervention (PCI). The aim of the present study was to assess the clinical features and in-hospital outcomes of CIN after emergency PCI. The serum creatinine (SCr) concentration was measured from days 0 to 30 in 338 consecutive patients with acute coronary syndrome undergoing emergency PCI. CIN was defined as an increase in SCr of >25% or >0.5 mg/dl within 2 days after PCI. Overall, 94 patients (28%) developed CIN. The mean SCr on admission was not significantly different between patients with CIN and those without CIN. The CIN group had significantly greater SCr at days 1, 2, and 30 than did the no CIN group. Multivariate analysis showed female gender (odds ratio [OR] 2.38, 95% confidence interval [CI] 1.12 to 5.07, p = 0.025), a culprit lesion in the left anterior descending artery (OR 2.37, 95% CI 1.31 to 4.27, p = 0.0042), contrast agent volume >200 ml (OR 3.60, 95% CI 1.96 to 6.62, p <0.001) and end-diastolic pulmonary arterial pressure >15 mm Hg (OR 2.03, 95% CI 1.02 to 4.04, p <0.01) to all correlate independently with CIN. The in-hospital mortality rate was greater in the CIN group than in the no CIN group (9.6% vs 3.3%, respectively; p = 0.025). In conclusion, CIN is a frequent complication of emergency PCI for acute coronary syndrome and is associated with a greater mortality rate and persistent renal dysfunction.

Urinary liver-type fatty acid-binding protein level as a predictive biomarker of contrast-induced acute kidney injury.

Eur J Clin Invest 2012; 42 (5): 557–563

Prevention of contrast-induced nephropathy by chronic pravastatin treatment in patients with cardiovascular disease and renal insufficiency

BACKGROUND Contrast-induced nephropathy (CIN) is known to increase morbidity and mortality of cardiovascular disease. Recent studies have shown statins prevented CIN after contrast media exposure, but optimal statin type and dosage are still unknown. PURPOSE The aims of the present study were to evaluate whether chronic pravastatin treatment before scheduled coronary angiography or percutaneous coronary intervention could reduce the incidence of CIN and to elucidate the factors related to CIN in patients with renal insufficiency. METHODS We studied 431 consecutive patients with renal insufficiency. One hundred ninety-four patients were receiving pravastatin treatment as standard chronic treatment of hypercholesterolemia. Serum creatinine levels were measured at baseline (pre-procedure) and within 48 h after contrast media exposure (peak post-procedure). CIN was defined as an increase in the serum creatinine values of > or = 25% or > or = 0.5 mg/dl after contrast media exposure. Logistic regression analysis was performed to evaluate the important factors related to CIN using four variables: age, pravastatin, pre-procedure serum creatinine, and contrast volume. RESULTS CIN was observed in 36 patients (8.4%). Patients without pravastatin (p<0.01), high level pre-procedure serum creatinine (p<0.01), and high contrast volume (p=0.034) had a significantly higher incidence of CIN. Logistic regression analysis revealed that pravastatin treatment (chi(2)=6.549, p=0.011, odds ratio=0.34), pre-procedure serum creatinine (chi(2)=6.294, p=0.009, odds ratio=2.78), and contrast volume (chi(2)=4.484, p=0.034, odds ratio=1.01) were independently related to the decreased risk of CIN. CONCLUSIONS Chronic pravastatin treatment before contrast media exposure was important for preventing CIN in patients with renal insufficiency. Also, reducing the dose of contrast media was important for preventing CIN in patients with high-baseline serum creatinine levels.

Real Time Three‐Dimensional Transesophageal Echocardiographic Images of Platypnea‐Orthodeoxia Due to Patent Foramen Ovale

A 74-year-old man with a patent foramen ovale was admitted with dyspnea and cyanosis that had become progressively worse along with dehydration. Transthoracic echocardiography (iE33, Philips Medical Systems, Andover, MA, USA) revealed a normal ventricular size and function and no evidence of intracardiac shunting by Doppler color interrogation. Neither chest x-ray nor chest computed tomography (Aquilion 64, Toshiba Medical Systems, Otawara, Japan) revealed any apparent pulmonary disease that could cause his dyspnea. A right and left heart catheterization demonstrated normal coronaries with a mean right atrial pressure of 3 mmHg and a normal mean pulmonary artery pressure of 13 mmHg. Careful history taking revealed that he developed dyspnea in a sitting position, whereas the symptoms were relieved in a supine position. The transesophageal echocardiographic images taken in the supine position showed the foramen ovale was closed (Fig. 1 right), and no apparent right-to-left shunt by Doppler color flow (Fig. 1 left). The images taken in the sitting position showed the foramen ovale was wide open (Fig. 2 right, Fig. 3), with a massive rightto-left shunt across the patent foramen ovale by Doppler color flow (Fig. 2 left), caused hypoxemia and dyspnea. The patient was given the diagnosis of platypnea-orthodeoxia syndrome. Platypnea-orthodeoxia, a syndrome character-

Efficacy of Oxycodone for Dyspnea in End-stage Heart Failure with Renal Insufficiency

A 67-year-old man with dilated cardiomyopathy and renal insufficiency was admitted to our hospital with dyspnea secondary to end-stage heart failure. We introduced oxycodone for medically refractory dyspnea instead of morphine because of the patients renal insufficiency. After the administration of oxycodone, his dyspnea was alleviated without any adverse opioid effects, such as respiratory depression. After treating his heart failure, he was able to leave the intensive care unit. Oxycodone may therefore be a reliable agent for the treatment of dyspnea in patients with end-stage heart failure and renal insufficiency.