Geometric and compositional appearance of atheroma in an angiographically normal carotid artery in patients with atherosclerosis.

BACKGROUND AND PURPOSE: Arterial remodeling may enable atherosclerotic disease without luminal stenosis. We sought to assess the prevalence and characteristics of atherosclerosis in angiographically normal carotid arteries. MATERIALS AND METHODS: Forty-six arteries with 0% stenosis by MRA were evaluated with multicontrast carotid MR imaging at 3T. For each artery, the percentage wall volume (wall volume/[lumen volume + wall volume] x 100%) and the presence versus absence of an LRNC, calcification, IPH, and fibrous cap rupture were recorded. In addition, the relative size of each plaque component (eg, percentage LRNC = LRNC volume/wall volume x 100%), when present, was calculated. RESULTS: The mean of percentage wall volume in arteries with 0% stenosis was 43.0 +/- 6.9% with a range from 31.6% to 60.1%. An LRNC was present in 67.4% (31/46) of arteries, calcification was present in 65.2% (30/46), IPH was present in 8.7% (4/46), and fibrous cap rupture was present in 4.3% (2/46). In arteries with an LRNC (n = 31), the average percentage LRNC volume was 8.8 +/- 7.3% with a range from 1.0% to 31.5%. For calcification (n = 30), the mean percentage calcification volume was 3.8 +/- 4.2% with a range of 0.1%-17.4%. The mean percentage IPH volume (n = 4) was 2.7 +/- 1.7% with a range of 0.5%-4.1%. CONCLUSIONS: These findings indicate that stenosis by MRA may underestimate the presence of carotid atherosclerosis, and they demonstrate the need for improved methods for accurately identifying carotid atherosclerotic plaque severity.

[Ischemic preconditional protection of ischemia reperfusion injury on isolated hearts of ground squirrel and rat].

The protective effects of ischemic preconditioning on ischemia-reperfusion injury was investigated using isolated Langendorff perfusing hearts from ground squirrel and rat. In Preconditioning I group hearts were first perfused with Krebs-Henseleit solution for 10 min to establish a steady state, then stopped for 15 min to establish global ischemia, and finally followed by 10 min ischemia and 10 min reperfusion. In Preconditioning II group there were three cycles of 5 min ischemia + 5 min reperfusion after 10 min equilibration and then the final 10 min ischemia and 10 min reperfusion were followed. It was found that in group I during the final 10 min ischemia period there was remarkable augmentation of CK release from both animal's hearts. But in group II CK release decreased markedly during the same ischemic period. CK release during final 10 min reperfusion period also decreased significantly in group II in comparison with group I. The incidence of arrhythmias occurred in both animal's hearts was markedly reduced in group II rather than group I. In conclusion, short episode ischemic preconditioning protect subsequent ischemia-reperfusion injury on isolated hearts from ground squirrel and rat.

[Electrophysiological effects of antiarrhythmic drug UK-68798 on different AV nodal cells in rabbit heart].

By means of microelectrode techniques the electrophysiological effects of a new class III antiarrhythmic agent, UK-68798 (Dofetilide), were investigated on atrionodal (AN), nodal (N), nodal-His (NH) and His (H) cells in the AVN area of rabbit heart. UK-68798 (5 x 10(-9) to 5 x 10(-6) mol/L) had no effect on APA and RP of the 4 kinds of cells but caused a dose-dependent decrease in AVN spontaneous rhythm without changing the A-H conduction time. APD50 and APD90 were prolonged markedly by the drug in a dose-dependent manner. Among the 4 kinds of cells, N cell had the highest percentage increment in APD, indicating a prominent sensitivity to the drug. For example, at 5 x 10(-6) mol/L, the prolongation percentages of APD90 are: 95 +/- 26% (N), 75 +/- 22% (AN), 63 +/- 26% (H), 46 +/- 26% (NH). The effective refractory periods (ERP) of the 4 kinds of cells were lengthened also in a dose-dependent manner, while the ERP increment percentages (delta ERP%) of the 4 kinds of cells did not show significant difference. However, ERP corresponding repolarization membrane potentials (ERP-RMP) of the 4 kinds of cells were not affected by the drug. The above results suggested that though ERP increased in parallel with APD prolongation, the homogeneous delta ERP% and unchanged ERP-RMP values of the 4 kinds of cells would prevent the AVN area from becoming a source of reentry arrhythmias under the action of UK-68798.

[The biphasic creatine kinase release from isolated rat heart induced by global ischemia and early period of reperfusion].

The present study provided a model with which the kinetics of CK release in the early phase of reperfusion was investigated. By using Langendroff method the isolated rat heart was first perfused for 10 min for establishing equilibrium, then stopped for 10 min to establish global ischemia, and finally followed by reperfusion for sample collection in every 15 s for the measurement of CK activity (U/L) as an index of cellular damage. A characteristic biphasic release of CK was shown under condition of 3 min reperfusion with Krebs-Henseleit (K-H) solution without glucose. The 1st peak of CK release appeared abruptly in the first 15 s of reperfusion and the 2nd one, during 120-180 s of reperfusion. The appearance of the 2nd peak was shifted to 30-75 s by adding glucose (11.1 mmol/L) into the perfusate. The 1st peak mainly reflects ischemic injury while the 2nd represents reperfusion injury. Anoxia (95% N2 + 5% CO2) or glucose addition may delay or decrease both peaks, but low Ca2+ (0.05 mmol/L) only delays the appearance of the 2nd peak to 3 min. The results suggest that the oxygen paradox rather than calcium paradox is involved in both phases of CK release. As for low Ca2+ decreasing the 2nd peak may be attributed to its effect of reducing Ca2+ inflow and overload injury secondary to oxygen paradox.

[Effects of lipoic acid on reperfusion induced arrhythmias and myocardiac action potential alterations induced by free radical generating system].

By means of Langendorff method the isolated rat heart was perfused with Krebs Henseleit solution. Following ligation of the left descending coronary artery for 10 min the heart was reperfused for 3 min. The incidence of ventricular fibrillation in the reperfusion period was 100%, and the normal sinus rhythm time was shortened to 29 s within 3 min of reperfusion. Administration of lipoic acid (6.8 X 10(-6)-1.7 X 10(-4) mol/L) to the perfusate significantly reduced the incidence of ventricular fibrillation to 33-50% and prolonged the normal sinus rhythm time to 97-107 s. APA, RP, and Vmax recorded from the guinea pig papillary muscle were depressed due to the deleterious effect of xanthine oxidase and hypoxanthine free radical generating system. Under the treatment of lipoic acid (3.5 X 10(-5) mol/L), the depression of APA, RP, and Vmax were significantly relieved. This confirms that lipoic acid treatment, owing to its free radical scavenger effect, is able to protect myocardium from free radical induced electrophysiological abnormalities, and consequently decrease the incidence of malignant arrhythmias.

[Effects of ciwujia (Acanthopanax senticosus Harms) on reperfusion-induced arrhythmia and action potential alterations in the isolated rat heart].

By means of Langendorff method and standard microelectrode techniques the effects of Ciwujia on reperfusion induced arrhythmias and action potential alterations were studied in isolated rat heart with transient coronary occlusion. Inclusion of Ciwujia extract (equivalent to 1.2 and 2.4 mg crude drug/ml) was found helpful in reducing reperfusion induced ventricular fibrillation and ventricular tachycardia. Associated with this reduction in rhythm disturbances was an increase in the total duration of normal sinus rhythm during the 3 min reperfusion period. With the administration of Ciwujia the number of cells with abnormal action potential configurations was significantly reduced. This confirms that Ciwujia can protect myocardium from electrophysiological abnormalities, and therefore reduces the incidence of malignant arrhythmias.

Arrhythmogenic effects of toxic concentrations of the antiarrhythmic drug lorcainide on the isolated canine ventricle.

The effect of the new antiarrhythmic drug lorcainide was studied on the specialized conducting system of isolated canine ventricle. Transmembrane action potentials were recorded simultaneously from three subendocardial sites within the ventricular basis, free wall and apex. At concentrations of 3 x 10(-6) and 2.4 x 10(-5) M, lorcainide caused a dose-dependent decrease in maximum rates of rise and in amplitude of the action potential; 0.6 x 10(-6) M had no significant effect, resting potential and action potential duration remained unchanged with 0.6 x 10(-6) M and 3 x 10(-6) M. The most prominent effect of 2.4 x 10(-6) M lorcainide was the appearance of an increasing notch resulting in clear separation of the action potential in an initial short spike depolarization (50-120 msec) with or without a subsequent plateau depolarization 280-370 msec). Both components demonstrated an independent and inhomogeneous conduction through functionally different pathways. Changes in stimulation rate or premature stimuli resulted in nonstimulated reexcitations resembling bigemini, ventricular tachycardia or regional ventricular fibrillation. The results indicate that dissociation of the action potential in two components is due to toxic alterations of ionic channels of the fiber membrane and that nonstimulated reexcitations are due to reentry via functionally fast and slow pathways.