Changes in myocardial electrical impedance induced by coronary artery occlusion in pigs with and without preconditioning: correlation with local ST-segment potential and ventricular arrhythmias

BACKGROUND: Myocardial ischemia increases tissue electrical resistivity leading to cell-to-cell uncoupling, and this effect is delayed by ischemic preconditioning in isolated myocardium. Alterations in myocardial resistivity elicited by ischemia in vivo may influence arrhythmogenesis and local ST-segment changes, but this is not well known. METHODS AND RESULTS: Myocardial impedance (resistivity [omega x cm] and phase angle [degrees]), epicardial ST segment, and ventricular arrhythmias were analyzed during 4 hours of coronary artery occlusion in 11 anesthetized open-chest pigs; these were compared with 13 other pigs submitted to a similar coronary occlusion preceded by ischemic preconditioning. Myocardial resistivity rose slowly during the first 34+/-7 minutes of occlusion (237+/-41 to 359+/-59 omega x cm), increased rapidly to 488+/-100 omega x cm at 60 minutes, and reached a plateau value (718+/-266 omega x cm, ANOVA; P<.01) at 150+/-69 minutes. By contrast, phase-angle changes began after 17 minutes of ischemia (-3.0+/-1.6 degrees to -4.2+/-1.2 degrees at 29+/-8 minutes) and evolved faster thereafter (-12.5+/-5.3 degrees at 144+/-56 minutes). Marked changes in myocardial impedance were observed during the reversion of ST-segment elevation that occurred 1 to 4 hours after occlusion, but impedance changes were less apparent during the early ST-segment recovery seen at 15 to 35 minutes of ischemia. The second arrhythmia peak (30+/-5 minutes) coincided with the fast change in tissue impedance, and both were delayed (P<.05) by ischemic preconditioning. CONCLUSIONS: A rapid impairment of myocardial impedance occurs after 30 minutes of coronary occlusion, and its onset is better defined by shift in phase angle than by rise in tissue resistivity. Phase 1b arrhythmias are associated with marked impedance changes, and both are delayed by preconditioning. Reversion of ST-segment elevation is partially associated with impairment of myocardial impedance, but other factors play a role as well.     

Effect of coronary artery reperfusion on transmural myocardial remodeling in dogs

BACKGROUND: The effects of reperfusion after coronary occlusion on transmural remodeling of the ischemic region early and late after nontransmural infarction must importantly affect the recovery of regional function. Accordingly, analysis of local volume and three-dimensional strain was performed using a finite element method to determine regional remodeling. Systolic and remodeling strains were measured using radiographic imaging of three columns (approximately 1 cm apart) of four to six gold beads implanted across the left ventricular posterior wall in 6 dogs. METHODS AND RESULTS: After a control study, infarction was produced by 2 to 4 hours of proximal left circumflex coronary artery occlusion followed by reperfusion. Follow-up studies were performed at 2 days, 3 weeks, and 12 weeks with the dogs under anesthesia and in closed-chest conditions. Biplane cineradiography was performed to obtain the three-dimensional coordinates of the beads. At 2 days, end-systolic strains were akinetic with loss of normal transmural gradients of shortening and thickening. Remodeling strains (RS) were determined by use of a nonhomogeneous finite element method by referring the end-diastolic configuration during follow-up studies to its control state at matched end-diastolic pressures and heart rates. Tissue volume at 2 days increased substantially, more at the endocardium (30 +/- 7%) than at the epicardium (5 +/- 12%, P < .01); the increase was associated with an average RS in the wall-thickening direction of 0.18 +/- 0.15 (P < .01) with all other RS near zero. At 12 weeks systolic function partially recovered, with normal wall thickening in the epicardium (radial strain, 0.081 +/- 0.056 [control] versus 0.113 +/- 0.088 [12 weeks]) but with dysfunction in the endocardium (0.245 +/- 0.108 [control] versus 0.111 +/- 0.074 [P < .01] [12 weeks]). This inability of the inner wall to recover function may be related to increased transmural torsional shear and negative longitudinal-radial transverse shear in the inner wall. Volume loss occurred at 12 weeks in the endocardium (-36 +/- 16%) corresponding to transmural gradients in longitudinal RS and both transverse shear RS. Negative longitudinal RS was greater at the endocardium (-0.20 +/- 0.10) than at the epicardium (-0.06 +/- 0.05, P < .01). CONCLUSIONS: These results indicate the presence of marked subendocardial edema 2 days after reperfusion following 2 to 4 hours of coronary occlusion. At 3 months after reperfusion, however, there was volume loss in the inner wall due to shrinkage along the myofiber direction with reduced transmural function and loss of longitudinal shortening, while both tissue volume and function recovered completely in the outer wall.     

Effects of N-nitro-L-arginine on coronary artery tone and reactive hyperemia after brief coronary occlusion in conscious dogs

AIM: To determine the role of an endothelium-derived relaxing factor (nitric oxide) in controlling basal coronary tone and coronary vasomotion after brief coronary occlusion (reactive hyperemia). METHODS: In 10 chronically instrumented conscious dogs, we studied the diameter changes of the large epicardial coronary artery and coronary blood flow in response to intracoronary administration of acetylcholine (0.1 and 1 microgram) and brief coronary occlusion for 5 and 20 s before and after intracoronary infusion of N-nitro-L-arginine (LNNA). RESULTS: Intracoronary infusion of LNNA (1, 3, and 10 mg) decreased the diameter of the large epicardial coronary artery and coronary blood flow in a dose-dependent manner without altering arterial pressure and heart rate. LNNA (10 mg) significantly attenuated the increase in artery diameter and coronary blood flow by acetylcholine. The ratio of artery dilation to the blood flow response after acetylcholine was not affected by LNNA. LNNA (10 mg) significantly decreased the ratio of repayment to debt flow volume of reactive hyperemia, but did not affect the ratio of peak to resting flow; it also significantly attenuated the reactive dilation of the large epicardial coronary artery after reactive hyperemia. The ratio of artery dilation to repayment flow volume (micron/ml) during reactive hyperemia was attenuated significantly by LNNA. CONCLUSION: These findings suggest that endothelium-derived nitric oxide may contribute to basal coronary tone and that reactive dilation of the large epicardial coronary artery during reactive hyperemia was caused by flow-mediated nitric oxide release, whereas coronary artery dilation after acetylcholine was caused largely by the direct receptor-mediated release of nitric oxide.     

Effects of unilateral stellate ganglion blockade on the arrhythmias associated with coronary occlusion

In anesthetized dogs the circumflex and/or the anterior descending coronary artery were briefly occluded (10 to 90 seconds) and ectopic beats occurring during the occlusion or for 60 seconds following release were counted. Control occlusions were alternated with occlusions performed during complete, reversible, unilateral blockade of either the right or the left stellate ganglion. This was achieved with thermodes through which coolant was circulated. In this way the shortcomings associated with stellectomy, which is irreversible, are avoided. Blockade of the right stellate ganglion increased the number of ectopic beats associated with coronary occlusion. The occurrence of episodes of ventricular tachycardia and fibrillation was also greater. By contrast, blockade of the left stellate ganglion reduced or abolished occlusion-induced arrhythmias. These effects are independent of changes in heart rate or vegal activity; they depend solely upon unilateral alteration in sympathetic tone, and are not demonstrable when such tone is low. We suggest that the right and left cardiac sympathetic nerves have a different influence upon cardiac excitability.     

Postoperative arrhythmias and myocardial electrolytes in patients undergoing coronary artery bypass grafting

Electrolyte changes in right atrial and skeletal muscle pre- intra- and postoperatively, and their relationship to the development of postoperative atrial fibrillation or flutter were evaluated in 31 patients with coronary artery bypass grafting (CABG). Such postoperative arrhythmias occurred in 14 patients (45%). Before CABG the skeletal muscle potassium concentration was lower in these patients than in the others: median 261.4 (range 148.2-329.5) vs 298.6 (167.1-416.4) mumol/g dry weight, p = 0.017. The right atrial potassium concentration was normal, but sodium levels were higher in the patients with, than in those without postoperative arrhythmias: median 340.3 (263.7-454.9) vs 296.3 (203.9-355.0) mumol/g dry weight, p = 0.008, indicating disturbed transmembrane electrolyte transfer. During CABG the potassium levels fell and sodium increased in both right atrium and skeletal muscle, and on postoperative day 2 the potassium content in skeletal muscle was not yet restored. Magnesium levels showed no changes in right atrium or skeletal muscle, but serum magnesium declined postoperatively. As the observed electrolyte derangements may be important in the development of postoperative arrhythmias, concomitant potassium and magnesium supplement postoperatively may be beneficial in restoring cellular potassium concentration.     

Effects of prostacyclin on myocardial hemodynamics and metabolism after coronary artery bypass grafting

OBJECTIVE: To evaluate the impact on clinical behavior of a 3-day workshop designed to increase trainees' rates of smoking cessation counseling and reminders about Pap smears in routine consultations. DESIGN: Randomized control trial. SETTING: Accredited teaching practices of the Royal Australian College of General Practitioners' Training Program. SUBJECTS: Thirty-four trainees and 1,500 consecutive adult patients ages 16-65 years. METHOD: Trainees randomly allocated to the experimental group participated in a 3-day interactive workshop on disease prevention during their 13-week family medicine term. Audiotapes of consultations with adults conducted by trainees at the beginning and end of the rotation were analyzed blind to compare assessment of patients' smoking status and, for women, date of last Pap smear. A questionnaire mailed to each patient after the consultation also allowed identification of smokers and women overdue for a smear. Consultations with these patients at risk were analyzed for preventive counseling. Inter- and intrarater reliability was calculated for audiotape analysis. RESULTS: Preworkshop rates of questions about smoking were low, occurring in 22% of consultations. While trainees allocated to the experimental workshop were more likely to ask a routine question about smoking at the end of the term than those in the control group (P = 0.01), two-thirds of smokers remained undetected irrespective of trainee group and fewer than one in five were advised to stop smoking. Reminders about Pap smears did not change as a result of training and remained low in fewer than 20% of consultations. kappa values demonstrated high reliability of audiotape analysis. CONCLUSION: This direct measurement of clinical behavior revealed that low levels of preventive care provided by trainees are resistant to skills training without reinforcement in clinical practice. In view of the importance of prevention in routine consultations, we recommend continued evaluation of more intensive educational programs. Those withstanding rigorous evaluation could be considered for implementation in similar training contexts seeking to improve the frequency and quality of disease prevention in primary medical care.     

Relation of absence of ST reelevation immediately after reperfusion and success of reperfusion with myocardial salvage

To examine whether resolution in ST elevation without ST reelevation immediately after reperfusion indicates successful reperfusion with myocardial salvage, we studied 40 patients who had an extensive acute myocardial infarction with early reperfusion: 24 patients had ST reelevation and 16 patients had no ST reelevation. Results indicate that (1) in the group with ST reelevation, rapid progression of myocardial damage occurs by reperfusion itself (i.e., reperfusion injury) and (2) in the group without ST reelevation, myocardial damage had already been extensive and irreversible at the time of reperfusion; thus, the absence of ST reelevation is not always a sign of reperfusion with myocardial salvage.     

Relationship between epicardial ST-segment elevation and myocardial ischemic damage after experimental coronary artery occlusion in dogs

The relationship between early and late epicardial electrocardiographic changes as well as those in regional myocardial blood flow (MBF) and the severity of myocardial damage was determined in 12 anesthetized dogs with left anterior descending coronary artery ligation. Radioactive microspheres (15 mum) were used to measure regional MBF at 15 min (early) and 24 h (late) after coronary occlusion. Severity of myocardial damage was assessed by the extent of myocardial creatine phosphokinase depletion 24 h after coronary ligation. There was a close linear correlation between myocardial creatine phosphokinase activity and regional MBF both early (r=0.93, 2P less than 0.001) and late (r=0.88, 2P less than 0.001). An inverse but less precise relationship existed between acute epicardial ST-segment elevation and early (r=-0.41, 2P less than 0.001), or late (r=0.35, 2P less than 0.05) regional MBF. Similarly, a weak correlation was found between myocardial creatine phosphokinase (IU/mg protein) at 24 h and early epicardial ST (millivolt) elevation (r=-0.36, 2P less than 0.02). In the center zones of the infarct with MBF 1/10 of normal, about 35% of the areas with normal QRS width had no epicardial ST-segment elevation 15 min after coronary occlusion. About 44% of the areas which developed pathological Q-waves in the electrocardiogram at 24 h had no ST elevation 15 min after coronary ligation. Late evolution of abnormal Q-waves occurred almost invariably in areas in which the early MBF was reduced to less than 50% of normal and in areas which subsequently had myocardial creatine phosphokinase levels reduced to less than 60% of normal. After coronary occlusion, the severity of the ultimate myocardial damage, which was directly proportional to the degree of reduction in MBF, was therefore not reliably predicted by the early epicardial ST-segment elevation. The data obtained in these studies suggest the need for caution in the use of acute ST-segment elevation as a predictive index of the extent or severity of myocardial ischemic damage.     

The distinction between coronary and myocardial reperfusion after thrombolytic therapy by clinical markers of reperfusion

BACKGROUND: On the basis of a previous experience in a chronic sheep model in which partial mitral allografts remained viable and properly functioning 12 months after operation, we assessed the results obtained by replacing the tricuspid valve with fresh antibiotic-preserved mitral allografts. METHODS: Twenty 3-month-old sheep with a mean weight of 23.7 +/- 2.3 kg underwent cardiopulmonary bypass and had a fresh antibiotic-preserved mitral allograft implanted in the tricuspid position with the heart beating under normothermic conditions. The tricuspid valve apparatus was not excised. After a mean follow-up of 13.2 months, the allograft was evaluated by gross inspection and light and electron microscopy. RESULTS: Nine sheep died of technical causes within the first week after operation and 2 at 4 and 6 months of infective endocarditis of the allograft. The hemodynamic study before heart explantation revealed residual tricuspid incompetence in 3 of the 9 survivors. Macroscopic examination showed flexible valves with no signs of structural deterioration, calcification, or thrombosis. Under light and scanning electron microscopic examination, allografts were almost completely denuded of endothelial cells and showed loosely arranged connective tissue with scarce signs of inflammatory reaction. Despite these findings, allografts were free from major structural damage. CONCLUSIONS: The mitral homograft could be an alternative to replacement of the tricuspid valve with a bioprosthesis or a mechanical prosthesis.     

Effect of dorsal root section on the arrhythmias associated with coronary occlusion

In anesthetized vagotomized dogs and cats the circumflex and/or the anterior descending coronary artery were briefly occluded (5-90 s), and ectopic beats occurring during the occlusion and for 60 s following release were counted. When arrhythmias were regularly produced for a given occlusion, the dorsal roots from C8 to T5 were transected and the occlusions were repeated. Dorsal root section produced minor changes in heart rate and blood pressure. Dogs and cats did not differ in their responses. Dorsal root section was performed in eight animals and decreased the absolute number of ectopic beats by 63 +/- 19% compared to control values (P less than 0.05). In four animals the effect on ectopic beats produced by repeated occlusions without dorsal root section was investigated and found to be increased by 35 +/- 24% compared to contrl values. Most of the somatic afferents contained in the dorsal roots were damaged by the surgical preparation. Therefore, repeated occlusions and interruption of somatic afferents do not appear to have influenced our results. The arrhythmogenic interaction between the local effects of myocardial ischemia and the sympathetic activity, whose outlow contained in the ventral roots remained intact, was still possible after dorsal root section and this explains why ectopic beats were reduced but not almost suppressed as is usually the case after bilateral stellectomy. We conclude that dorsal root section reduces the number of ectopic beats associated with short-lasting coronary artery occlusions and that the most likely mechanism is the interruption of the cardiocardiac sympathetic reflex which depends upon afferent fibers running through the dorsal roots.     

Effects of transient coronary occlusion on the capillary network in the left ventricle of rat

The objective was to examine the changes in the capillary network in the left ventricle of rats subjected to transient occlusion of the left coronary artery followed by reperfusion (I-R). Eighteen Wistar rats were divided into three groups and all rats were anaesthetized with ethyl ether and artificially ventilated. The I-R 1 rats were subjected to a 3 min occlusion followed by reperfusion; the I-R 3 rats had three 3 min occlusions separated by 3 min of reperfusion; the Sham-operated rats underwent surgery but the coronary artery was not occluded. The thorax was closed at the end of the procedures and the rats were sacrificed for isolation of the hearts 30 d after treatment. Frozen sections of the left ventricles were cut and differential staining was used to classify the capillary portions. Five additional rats treated as the I-R 1 group were sacrificed at 120 min after reperfusion. Their left ventricles were used for immunohistochemical investigation of the early expression of bFGF and VEGF. By comparison with the Sham-operated rats, both I-R groups showed increases in the capillary density of total and venular capillary portions, an increased capillary : myocyte (C : M) ratio and a decrease in the capillary domain area in the three capillary portions. The changes in the I-R 1 group were significantly greater than those in the I-R 3 group, suggesting that the frequent experience of ischemic attack reduces the capacity of angiogenesis. In the rats sacrificed 120 min after the start of reperfusion, bFGF and VEGF were expressed on capillaries and in some myocytes. Punctate bFGF or VEGF staining was observed even 30 d after the transient ischemia. One 3 min occlusion of the left coronary artery followed by reperfusion produced changes in capillarity that would increase the oxygen supply to ventricular tissues. These effects may be attributed to the bFGF and VEGF expressed around capillaries. Repeated occlusions interspersed with a short period of reperfusion reduced the advantageous effects on capillarity.     

Incomplete infarct and delayed neuronal death after transient middle cerebral artery occlusion in rats

BACKGROUND AND PURPOSE: The clinical syndrome of transient ischemic attacks is accompanied in a significant percentage of patients by brain lesions or neuroimaging abnormalities whose structural counterparts have not been defined. The objective of this study was to analyze, in an experimental model of short-term (< 25 minutes) focal ischemia and long-term (< or = 28 days) reperfusion, the extent and nature of the structural abnormalities affecting neurons and glia located within the territory of the transiently occluded artery. METHODS: Adult Wistar rats (n = 121) had the origin of one middle cerebral artery (MCA) occluded with a nylon monofilament for periods of 10 to 25 minutes. Experiments of transient MCA occlusion were terminated at variable periods ranging from 1 day to 4 weeks. Control experiments consisted of (1) MCA occlusion without reperfusion (n = 7) lasting 7 to 14 days and (2) sham operations (n = 2) followed by 1- to 4-day survival. After in situ fixation, brain specimens were serially sectioned and subjected to detailed morphometric evaluations utilizing light and electron microscopes. The statistical method used to evaluate the results was based on ANOVA followed by Bonferroni's corrected t test and Student's t test comparisons. RESULTS: Brain lesions were not detectable in the sham-operated controls. All brains with permanent MCA occlusion (7 to 14 days) had large infarctions with abundant macrophage infiltration and early cavitation. Forty-five (37%) of the experiments involving transient MCA occlusion had no detectable brain lesions after 4 weeks. Selective neuronal necrosis was found in 76 of 121 rats (63%) with transient MCA occlusion. Neuronal necrosis always involved the striatum, and in 29% of the brains with ischemic injury, necrosis also included a short segment of the cortex. In the striatum, the length of the arterial occlusion was the main determinant of the number of necrotic neurons (20 minutes [22.6 +/- 19] is worse than 10 minutes [4.9 +/- 7]) (P < .0001). In the cortex, the length of reperfusion determined the number of necrotic neurons appearing in layer 3. Experiments with reperfusion of 4 to 7 days' duration yielded more necrotic neurons per microscopic field (2.02 +/- 3) than those lasting fewer days (0.04 +/- 0.1) (P < .05). The histological features of these lesions underwent continuous change until the end of the fourth week, at which time necrotic neurons were still visible both in the striatum and in the cortex. CONCLUSIONS: Arterial occlusions of short duration (< 25 minutes) produced, in 76 of 121 experiments (63%), brain lesions characterized by selective neuronal necrosis and various glial responses (or incomplete infarction). This lesion is entirely different from the pannecrosis/cavitation typical of an infarction that appears 3 to 4 days after a prolonged arterial occlusion. Delayed neuronal necrosis, secondary to a transient arterial occlusion or increasing numbers of necrotic neurons in experiments with variable periods of reperfusion, was a response observed only at a predictable segment of the frontoparietal cortex.     

Spatial stability of extracellular potassium ion and blood flow distribution in rat cerebral cortex after permanent middle cerebral artery occlusion

Extracellular potassium ion activity ([K+]o) increases precipitously during brain ischemia when blood flow falls below threshold values less than approximately 15 mL/100 g/min. This flow threshold for increase of [K+]o occurs also in focal ischemia producing gradient from ischemic core to adjacent normally perfused brain. In this study we investigated the spatial and temporal stability of extracellular potassium ion and blood flow gradients after permanent middle cerebral artery occlusion (MCAO) in rats. [K+]o and regional CBF were measured, respectively, with K+-sensitive and polarographic hydrogen-sensitive microelectrodes at different cortical locations in the middle cerebral artery distribution region. Spatial assessment of [K+]o and regional CBF was conducted at 30, 90, and 180 minutes after MCAO. [K+]o in the more lateral cortex (core) increased from near 3 mmol/L before MCAO to greater than 50 mmol/L and was associated with flow values less than 25% of pre-ischemic levels. Measurements medial to the core (penumbra) indicated progressively decreasing levels of [K+]o and improvement of CBF. There was a tendency for [K+]o in penumbral zones to decrease toward normal levels with time, but there was little dissipation of [K+]o in core regions. In contrast, the spatial CBF profile remained remarkably constant for the entire recording period. Thus, unlike infarction which has been reported to expand with time after focal ischemia, the spatial [K+]o disturbance tends to contract primarily due to decreasing [K+]o with time in the penumbra. Thus, steady state levels of [K+]o after focal ischemia may not be a valuable predictor of cell viability.     

Release of endothelin from the porcine heart after short term coronary artery occlusion

OBJECTIVE: Endothelin is increased in plasma following myocardial infarction. Whether brief periods of myocardial ischaemia not leading to myocardial infarction increase plasma endothelin is not known. Thus, the present study was designed to examine cardiac endothelin balance in association with a 10 min coronary artery occlusion followed by reperfusion. METHODS: Venous blood was selectively sampled from the transiently ischaemic myocardium using a shunt between the anterior interventricular vein and the right atrium in eight pentobarbitone anaesthetised pigs. Flow in the shunt was measured with a Doppler flow probe. Arterial blood was drawn from the aortic arch. Plasma endothelin was measured using an Endothelin 1-21 specific [125I] assay system. This assay system has no cross reactivity with big endothlin. RESULTS: A net cardiac endothelin uptake of 0.7(0.3-1.4) fmol.min-1 x g-1 (median, 95% confidence interval) in the control period shifted to a net release during the first 10 min of reperfusion. The release reached a maximum of 2.8(0.4-6.0) fmol.min-1 x g-1 after 1.5 min of reperfusion. Cardiac venous endothelin concentration increased from 3.4(2.5-4.8) to 4.4(3.6-6.9) and 4.4(3.6-6.6) fmol.ml-1 at 1.5 and 5 min of reperfusion, respectively (p < 0.001 for both). Arterial endothelin concentration decreased from 4.8(3.9-6.1) to 2.7(2.4-4.3) fmol.ml-1 at 10 min of reperfusion (p < 0.001). CONCLUSION: Endothelin is released from the heart for several minutes during reperfusion following a brief coronary artery occlusion.     

Assessment of sensorimotor neglect after occlusion of the middle cerebral artery in the rat

Evaluating the efficacy of neuroprotective drugs in rat models of focal cerebral ischemia has involved histological and behavioral batteries to examine treatment outcome. However, the behavioral tests used to date provide little insight into the nature of the neurological impairments. To provide an analysis of a possible "neglect" syndrome after occlusion of the middle cerebral artery, M. I. Posner's (1980) visual attentional paradigm was adapted for use in the rat. A paw-reaching task and a test of somatosensory "neglect" also were used to assess forelimb sensorimotor function. The lesion group displayed unilateral deficits; however, there was no evidence of attentional dysfunction. Results are consistent with the conclusion that the behavioral deficits identified arise from a somatosensory deficit rather than hemineglect due to dysfunctional spatial attention.     

New electrocardiographic criteria for predicting the site of coronary artery occlusion in inferior wall acute myocardial infarction

In patients with inferior wall acute myocardial infarction (AMI), the site of the culprit lesion is an important determinant of outcome. Patients with right ventricular infarction have a poor prognosis, whereas those with occlusion of the left circumflex coronary artery (LCx) have a good prognosis. Therefore, we assessed whether standard 12-lead electrocardiograms obtained on admission could identify the site of coronary artery occlusion, (i.e., a site proximal to the origin of the right ventricular branch of the right coronary artery [RCA], a site distal to the origin of the right ventricular branch of the RCA, or a site in the LCx). The ratio of ST depression in lead V3 to ST elevation in lead III (V3/III ratio) was evaluated immediately before coronary angiography in 152 patients with a first inferior wall AMI confirmed by coronary angiography within 12 hours after the onset of symptoms. For occlusion of the proximal RCA, distal RCA, and LCx, V3/III ratio was 0.2+/-0.3, 0.8+/-0.5, and 2.5+/-2.5 (p = 0.0001), respectively. The V3/III ratio <0.5 identified proximal RCA occlusion, 0.5 相似文献   

Effectiveness of digitalis with or without acebutolol in preventing atrial arrhythmias after coronary artery surgery

In this study, a beta-adrenergic blocker in combination with digoxin provided marginal protection against atrial fibrillation/flutter after coronary artery surgery. The economic comparison of patients who did and did not develop atrial fibrillation/flutter indicates that prevention of these arrhythmias can have a significant impact on length of hospital stay and cost of this common surgical procedure.     

Amelioration by quinapril of myocardial infarction induced by coronary occlusion/reperfusion in a rabbit model of atherosclerosis: possible mechanisms

BACKGROUND: The increased severity of the myocardial injury produced by coronary occlusion-reperfusion in models of atherosclerosis is associated with an increase in leukocyte accumulation in the ischemic myocardium. Expression of P-selectin, an adhesion molecule involved in the interaction between leukocytes and endothelium, is increased in atherosclerotic vessels. Long-term angiotensin-converting enzyme (ACE) inhibition has been shown to reduce atherosclerotic vascular change in experimental models. METHODS AND RESULTS: We examined changes in the size of the infarct resulting from coronary occlusion/reperfusion in normally fed and cholesterol-fed rabbits that were chronically treated with quinapril. Infarct size was significantly larger in the cholesterol-fed versus normally fed rabbits. ACE activity in the ischemic and nonischemic myocardium was significantly reduced by quinapril. Chronic quinapril administration significantly ameliorated the increased myocardial injury in cholesterol-fed rabbits. Quinapril administration markedly increased the myocardial cGMP content and reduced the myeloperoxidase activity in the border region of the ischemic myocardium in cholesterol-fed rabbits. The enhanced expression of P-selectin in myocardial tissue of cholesterol-fed rabbits was also effectively reduced by quinapril treatment. The above effects of quinapril were eliminated by blockade of bradykinin B2 receptors or inhibition of nitric oxide synthesis. CONCLUSIONS: Chronic quinapril treatment ameliorated the severity of myocardial injury produced by coronary occlusion/reperfusion in cholesterol-fed rabbits, possibly because of reversal of the enhanced interaction between leukocytes and endothelium in the ischemic myocardium via a bradykinin-related pathway.     

Effect of suture closure of coronary artery fistula on aneurysmal coronary artery and myocardial ischemia

This study indicates the importance of coronary angiography and myocardial scintigraphy on long-term follow-up of patients after surgery for coronary arterial fistula in view of the progression to coronary artery obstruction and myocardial ischemia.     

Emergency coronary artery surgery after failed PTCA: myocardial protection with continuous coronary perfusion of beta-blocker-enriched blood

MK-801 (dizocilpine), a noncompetitive N-methyl-D-aspartate antagonist, induces dystonia in monkeys at doses of 0.08 mg/kg. This syndrome was tested with the dopamine D1 receptor antagonist NNC 756, the DA D2 receptor antagonist raclopride, the atypical antipsychotic clozapine, the dopamine D1 receptor agonist SKF 81297, the dopamine D2/D3 receptor agonist quinpirole, the anticholinergic biperiden, amphetamine, and the benzodiazepine midazolam in 7 Cebus apella monkeys previously treated with dopaminergic agents. NNC 756 (0.004 and 0.01 mg/kg), raclopride (0.004 and 0.01 mg/kg), SKF 81297 (0.3 and 0.6 mg/kg), quinpirole (0.1 and 0.2 mg/kg), amphetamine (0.25 and 0.5 mg/kg), and biperiden (0.125 and up to 1.0 mg/kg), had no significant effect on MK-801-induced dystonia. In contrast, both clozapine (2.0 mg/kg) and midazolam (0.4 and 1.0 mg/kg) reduced the dystonia caused by MK-801. Dystonia induced by dopamine D1 and D2 antagonists is easily antagonized by biperiden and dopamine agonists, whereas these drugs had no significant effect on MK-801-induced dystonia. It has been proposed that dystonia may be caused by a sudden drop in the output from the basal ganglia that is primarily GABAergic. Midazolam's enhancing effect on the GABAergic tone is consistent with this hypothesis. The effect of clozapine is more difficult to explain, but this drug has a rich pharmacology and suggests an agonistic glutamatergic effect.