Masayuki Motohiro

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.

Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction.

Motohiro M, Yuasa F, Hattori T, Sumimoto T, Takeuchi M, Kaida M, Jikuhara T, Hikosaka M, Sugiura T, Iwasaka T: Cardiovascular adaptations to exercise training after uncomplicated acute myocardial infarction. Am J Phys Med Rehabil 2005;84:684–691. Objective: This study examined the cardiovascular adaptations of an exercise training program and evaluated the role of peripheral vasodilator capacity in contributing to these adaptations after myocardial infarction. Design: A total of 44 consecutive patients with uncomplicated myocardial infarction underwent 3 wks of exercise training. Controls (n = 12) with comparable myocardial infarction were selected from our database and were restricted to a program with minimal activity. All patients performed cardiopulmonary exercise testing with hemodynamic measurements. Forearm and calf reactive hyperemic flow were measured by venous occlusive plethysmography as indices of peripheral vasodilator capacity. Results: Despite no change in arteriovenous oxygen difference at peak exercise after training, training resulted in significant increases in oxygen consumption, cardiac output, and stroke volume and a significant decrease in systemic vascular resistance at peak exercise (overall, P < 0.05). Calf reactive hyperemic flow increased significantly after training (P < 0.001), but forearm reactive hyperemic flow did not. Furthermore, increase in calf reactive hyperemic flow after training had a positive correlation with increases in peak cardiac output, stroke volume, and oxygen consumption after training and an inverse correlation with peak systemic vascular resistance. Conclusions: Exercise training improved exercise tolerance by improving hemodynamic responses to exercise after myocardial infarction. This improved exercise performance was linked to a training-induced increase in calf vasodilator capacity.

A new protocol using sodium bicarbonate for the prevention of contrast-induced nephropathy in patients undergoing coronary angiography.

Contrast-induced nephropathy (CIN) is associated with increased morbidity and mortality rates. Although a previous study reported that pretreatment with sodium bicarbonate is more effective than sodium chloride for prophylaxis of CIN, this has not been a universal finding. We performed a prospective randomized trial to investigate whether CIN can be avoided using sodium bicarbonate. In total 155 patients with a glomerular filtration rate (GFR) <60 ml/min/1.73 m(2) who were undergoing coronary angiography were enrolled. We assigned patients to sodium chloride plus sodium bicarbonate (bicarbonate group, n = 78) or sodium chloride alone (chloride group, n = 77). Infusion of sodium bicarbonate at 1 ml/kg/hour continued from 3 hours before to 6 hours after coronary angiography. CIN was defined as a 25% increase in serum creatinine from baseline value or an absolute increase of ≥0.5 mg/dl, which appeared within 2 days of contrast. Baseline GFR was not significantly different between the 2 groups. Patients in the bicarbonate group had a higher GFR than those in the chloride group on day 2 (45.8 ± 13.4 vs 40.9 ± 14.6 ml/min/1.73 m(2), p = 0.031) and at 1 month (49.5 ± 14.7 vs 43.7 ± 15.5 ml/min/1.73 m(2), p = 0.019). CIN occurred in 10 patients (13%) in the chloride group but in only 2 patients (2.6%) in the bicarbonate group (p = 0.012). Sodium chloride plus sodium bicarbonate is more effective than sodium chloride alone for prophylaxis of CIN and can lead to retention of better long-term renal function.

Candesartan and arterial baroreflex sensitivity and sympathetic nerve activity in patients with mild heart failure

The purpose of this study was to investigate the effects of candesartan on arterial baroreflex sensitivity (BRS) and sympathetic activity in patients with mild heart failure (HF). Arterial pressure, heart rate, plasma renin activity, plasma angiotensin II and noradrenaline, and muscle sympathetic nerve activity (MSNA) were measured before therapy and after 4 weeks in 20 patients with mild HF. Patients were assigned to a candesartan group (n = 10) or a placebo group (n = 10). Baroreflex sensitivity was assessed by using phenylephrine. Candesartan induced an increase in plasma renin activity and plasma angiotensin II associated with a reduction in arterial pressure without affecting heart rate. Although plasma noradrenaline was unchanged (320 ± 322 pg/ml to 339 ± 104 pg/ml), MSNA decreased significantly (52 ± 11 bursts/min to 42 ± 9 bursts/min; p < 0.01)) and BRS increased significantly (6.9 ± 3.6 msec/mm Hg to 10.2 ± 3.3 msec/mm Hg; p < 0.01) after candesartan. However, there were no significant changes in the measured variables in the placebo group. These data indicate that candesartan treatment enhanced BRS and reduced sympathetic activity in patients with mild HF. Thus, the inhibitory effect of candesartan on sympathetic activity may, at least in part, contribute to the beneficial effect of angiotensin II receptor blockade in patients with mild HF.

Skeletal muscle hypoperfusion during recovery from maximal supine bicycle exercise in patients with heart failure

Leg blood flow (LBF) and its relation to central hemodynamics were examined during recovery following maximal supine bicycle exercise in 11 patients with heart failure and 20 patients with normal exercise capacity after myocardial infarction. The results indicate that LBF was markedly reduced in patients with heart failure, and that decreased cardiac output response and enhanced peripheral vasoconstriction, which functioned to prevent hypoperfusion in the nonexercising vital regions and to maintain arterial blood pressure, were responsible for the reduced LBF during recovery in heart failure.

Iodine 123-metaiodobenzylguanidine imaging reflect generalized sympathetic activation in patients with left ventricular dysfunction

Background:  Iodine 123‐metaiodobenzylguanidine (MIBG) imaging has been used to assess cardiac sympathetic nerve abnormalities. To determine the role of MIBG imaging as a measure of generalized sympathetic nerve activity, MIBG imaging was evaluated with muscle sympathetic nerve activity (MSNA) and plasma norepinephrine (noradrenaline) level in patients with old myocardial infarction.

Effect of angiotensin-converting enzyme inhibitor on cardiopulmonary baroreflex sensitivity in patients with acute myocardial infarction ☆

We evaluated the effect of angiotensin-converting enzyme inhibition (quinapril) on cardiopulmonary baroreflex sensitivity in 30 patients with uncomplicated myocardial infarction (quinapril group, 15 patients; placebo group, 15 patients) at 5 and 10 days after the onset of myocardial infarction. This study indicates that quinapril improved cardiopulmonary baroreflex and thus reduced sympathetic outflow in patients with acute myocardial infarction.

Correlation of Heart Rate Turbulence with Sympathovagal Balance in Patients with Acute Myocardial Infarction

To examine the relationship among heart rate turbulence parameters, arterial baroreflex sensitivity, and cardiac sympathetic nerve activity, 15 patients with acute myocardial infarction, presenting with sinus rhythm and ≧3 ventricular premature beats/24hr were studied at least 2 weeks after acute myocardial infarction. Turbulence onset (TO) and turbulence slope (TS) were averaged from 3 respective ventricular premature beats. Early heart-to-mediastinum ratio (H/M), delayed H/M, and washout rate were calculated from iodine-123-metaiodobenzylguanidine (123I MIBG) scintigraphy. Arterial baroreflex sensitivity was calculated by phenyrephrine method. Arterial baroreflex sensitivity correlated significantly with TO (r = − 0.75, p < .01) and TS (r = 0.53, p < .05). TO had no correlations with early H/M, delayed H/M, and washout rate. There were no significant correlations between TS and early H/M. However, TS had significant correlation with delayed H/M(r = 0.74, p < .01) and washout rate (r = − 0.71, p < .01). Thus, heart rate turbulence of TO and TS parameters depend on sympathovagal balance.