Noriko Mori

Impaired fibrinolysis early after percutaneous transluminal coronary angioplasty is associated with restenosis

This study examined the role of fibrinolytic components in the process of restenosis after percutaneous transluminal coronary angioplasty (PTCA). Seventy-two patients with single-vessel disease who underwent successful PTCA were prospectively selected. Tissue plasminogen activator (TPA), free plasminogen activator inhibitor-1 (free PAI-1), TPA/PAI-1 complex, and total PAI-1 antigen levels were measured before, at 1 week after, and at 3 months after PTCA. Six months after PTCA, the study patients were divided into two groups: 41 patients without restenosis and 31 patients with restenosis. There were no significant differences with regard to sex, age, coronary risk factors, or morphologic changes in the target lesions between the two groups. There were no significant differences in plasma TPA, TPA/PAI-1 complex, or total PAI-1 levels at each sampling period, or in the time courses between the two groups, except for total PAI-1 levels at 1 week after PTCA. Although no significant differences in free PAI-1 levels before PTCA were observed, free PAI-1 levels after PTCA in the patients with restenosis were significantly higher than those in the patients without restenosis. In addition, each group had a significant change in the time course of free PAI-1 levels. The results suggest that impaired fibrinolysis early after PTCA might affect the repair process of vascular injury, which leads to restenosis, and also that serial determination of free PAI-1 levels could help predict restenosis.

Circadian fluctuations of tissue plasminogen activator antigen and plasminogen activator inhibitor-1 antigens in vasospastic angina

To elucidate the circadian variation of fibrinolytic components in vasospastic angina, plasma levels of tissue plasminogen activator antigen (t-PA), free plasminogen activator inhibitor antigen (free PAI-1), t-PA/PAI-1 complex, and total PAI-1 were measured in venous plasma samples. Samples were taken every 6 hours (6:00 AM, noon, 6:00 PM, and midnight) for 24 hours in 14 patients with vasospastic angina, in 9 patients with exertional angina, and in 19 normal subjects. Twenty-four-hour Holter monitoring (Holter monitor, Del Mar Avionics, Irvine, Calif.) was also carried out in all subjects. All of the fibrinolytic components showed circadian variation, with a peak level at 6:00 AM in every study group except for the t-PA/PAI-1 complex in the group of patients with exertional angina. The values for all or the fibrinolytic components at each sampling time were higher in patients with coronary artery disease than in normal subjects. In particular, the mean value of free PAI-1 at 6:00 AM in patients with vasospastic angina was significantly higher than that in normal subjects and that in patients with exertional angina. This value of free PAI-1 in patients with vasospastic angina was closely associated with the duration of ischemic attacks. These results suggested that the circadian fluctuation of fibrinolytic components may be an important factor that leads to coronary thrombosis at the time of coronary spasm, especially in the early morning.

Significance of intimal tears in the mechanism of luminal enlargement in percutaneous transluminal coronary angioplasty: correlation of histologic and angiographic findings in postmortem human hearts.

Transluminal coronary angioplasty was performed in 17 coronary arteries with stenotic lesions of 15 postmortem human hearts. Morphologic changes of dilated vessels were examined angiographically and histologically. Angiographic evidence of coronary dissection was present in 8 (47%) of the 17 vessels. Histologic examination showed that intimal, medial, and adventitial tears were present in 17 (100%), 11 (65%), and one (6%) of the 17 vessels, respectively. In vessels with angiographic evidence of coronary dissection, the tear extended to more than one fourth of the circumference of the vessel. The tear was histologically demonstrated also in vessels which had no angiographic evidence of coronary dissection. Circumferential extension of the tear was greater in women than in men. There were no significant relationships between severity of the tear and histologic or angiographic characteristics of the target lesions. These results suggest that intimal or medial tears may frequently occur also in clinical cases treated with percutaneous transluminal coronary angioplasty and may be necessary for the success of the procedure.

Physiologic capacity of well-developed collaterals in patients with isolated left anterior descending artery disease.

To assess the physiologic significance of well-developed collaterals, 34 patients, with isolated left anterior descending artery disease (LAD) and without overt prior myocardial infarction, underwent cardiac catheterization and exercise thallium-201 emission computed tomography. The patients were divided into 3 groups; 11 patients with 90% stenosis of the proximal LAD and without collaterals (group 1), 11 with 99% stenosis of the proximal LAD, and without collaterals (group 2) and 12 with a total occlusion of the proximal LAD which was completely filled by well-developed collaterals (group 3). On left ventriculography, shortening fractions of the anterior wall were significantly reduced in group 2 as compared to group 1 and 3 (group 1 vs group 2: p< 0.01, group 2 vs group 3: p< 0.05), which reflected the lower ejection fraction of group 2 (p< 0.01 and p< 0.05, respectively). The perfusion defects of the anterior wall on both the initial and the delayed images were severer in groups 2 and 3 than in group 1 (group 1 vs group 2 and group 1 vs group 3 on the initial image: p< 0.01, for both, group 1 vs group 2 and group 1 vs group 3 on the delayed image: p< 0.05, for both). However, recovery of the perfusion defects from the initial image to the delayed image was better in group 3 than in groups 1 and 2 (group 1 vs group 2 and group 1 vs group 3: p< 0.05, for both). Therefore, coronary blood flow through well-developed collaterals was considered to be comparable to the flow through a diseased vessel with 90% stenosis at rest. During maximal exercise, blood flow through well-developed collaterals was considered to be comparable to the flow through a diseased vessel with 99% stenosis, although the blood flow through well-developed collaterals was considered to be better than that through 99% stenosis during the recovery period. These findings suggest that patients with well-developed collaterals must be treated like those with severe stenosis.

Value of thallium-201 early reinjection for assessment of myocardial viability.

To assess the efficacy of early reinjection forpredicting post intervention improvement in thallium-201 (Tl) uptake and regional wall motion, we reinjected a small dose of Tl following post-stress imaging and obtained reinjection early images (10 min after early reinjection) and reinjection delayed images (3 hr afterwards) in 40 patients who were referred to us for revascularization (group I). Twenty-nine patients in group I also underwent conventional stress-redistribution Tl scintigraphy (group II). Conventional stress-redistribution Tl scintigraphy was repeated after intervention. Contrast left ventriculography was performed before and after intervention and changes in regional wall motion were assessed in 22 of 40 patients. In group I, the predictive value for improvement and no improvement (the accuracy) of reinjection early images in perfusion was 83%, while that of reinjection delayed images was 91%. Furthermore, the accuracy of reinjection early images in regional wall motion was 80%, while it was 91% for reinjection delayed images. In group II, the accuracy in perfusion was 78% and the value in regional wall motion was 70%. Both accuracy in perfusion and in regional wall motion obtained from reinjection delayed images were significantly higher than the values in group II (p < 0.05). These data suggest that early reinjection is useful for predicting postintervention thallium uptake and regional wall motion.

Circulating myosin light chain I levels after coronary reperfusion: A comparison with myocardial necrosis evaluated from single photon emission computed tomography with pyrophosphate

This study was performed to assess the influence of coronary reperfusion on the serial serum myosin light chain (LC)I levels and to evaluate the relationship between the peak LCI level and the infarct size calculated from single photon emission computed tomography (SPECT) with technetium-99m pyrophosphate (Tc-99m PYP) in 11 patients who underwent coronary reperfusion. Blood was drawn before reperfusion, immediately after reperfusion, and once a day for 14 days, to estimate the time course of serum LCI release. The infarct size estimated by Tc-99m PYP ranged from 7.3 to 62.4 ml. The LCI levels obtained before reperfusion were less than 2.5 ng/ml but those obtained immediately after reperfusion were much higher. The value ranged from 2.7 to 9.7 ng/ml and that expressed as a percentage of peak LCI (% peak LCI) ranged from 19 to 83%. Collateral circulation, reperfusion arrhythmia and the degree of residual stenosis had no influence upon the % peak LCI. The correlation between peak LCI levels and SPECT-determined infarct size was good, with a correlation of 0.76 (p< 0.01, regression line by least squares method y= −3.31+1.53x). Early serum LCI might be influenced by coronary reperfusion but the peak LCI value reflected acute myocardial necrosis in patients who underwent coronary reperfusion.

Clinical effects of intravenous diltiazem hydrochloride on renal hemodynamics.

Summary: We administered diltiazem HCl i.v. (0.05 mg/kg in bolus followed by 0.01 mg/kg/min for 45 min), and determined the changes in blood pressure (BP), glomerular filtration rate (GFR), renal blood flow (RBF), total renal resistance, urinary volume (UV), urinary sodium (UNa) and potassium excretion, urea and osmolar clearance, and tubular reabsorption ratio of sodium (TRNa%). The serum concentration of diltiazem achieved was similar to the maximum level after a single oral dose of 120 mg. GFR and RBF were measured by i.v. infusion of sodium thiosulfate and sodium p-aminohippurate, respectively, as indicators. The subjects included 12 cases of essential hypertension (EH), 10 of chronic glomerular nephritis (CGN) with hypertension, 12 of CGN without hypertension, 12 of ischemic heart disease (IHD), and 10 of normotensive controls. BP decreased in hypertensives but not in normotensives. In patients with EH, GFR and RBF increased markedly (by 25.3 ± 33.8% and 30.7 ± 39.5%, respectively). In patients with IHD, GFR increased slightly by 9.8 ± 17.6%, whereas in patients with CGN with hypertension, GFR decreased by −4.3 ± 14.3%. No significant change of these indices was observed in normal subjects and in patients with CGN without hypertension. UV and UNa increased and TRNa% decreased in all groups. Urea and osmolar clearance increased in almost every group.

Living related renal transplantation for end-stage renal disease after liver transplantation from a brain-dead donor.

Abstract  We report a case in which a living related renal transplantation was successfully performed for end‐stage renal disease that had progressed after a liver transplantation from a brain‐dead donor for liver cirrhosis associated with type C hepatitis. Because the transplanted liver function had been excellent with the use of tacrolimus and mycophenolate mofetil, the same immunosuppressive agents with prednisolone were employed for the renal transplantation. Both grafts are functioning well without recurrence of hepatitis at 10 months after the renal transplantation. From our experience, renal transplantation should not be contraindicated even if the patient has undergone liver transplantation or has hepatitis C viral infection.