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PubMed1985

Different effects of thiopental in severe hypoxia, total ischemia, and low-flow ischemia in rat heart muscle.

The effect of thiopental (100 mg X 1(-1] during total ischemia, low-flow ischemia, and severe hypoxia with maintained flow was investigated in the isolated perfused rat heart. During total ischemia the rate of decline of tissue creatine phosphate and adenosine triphosphate was no different in thiopental-treated and untreated hearts. The development of ultrastructural damage during total ischemia, the release of creatine kinase on reperfusion, and the exacerbation of ultrastructural damage after reperfusion were unaffected by thiopental. When thiopental was added to the perfusate during hypoxia and during low-flow ischemia at a normal pH(7.4), creatine kinase release during reoxygenation and during reperfusion was significantly less (P less than 0.005 and P less than 0.05, respectively) than in the untreated groups. After low-flow ischemia at a low pH (6.5), creatine kinase release was no different in thiopental-treated and untreated hearts. Thus, thiopental afforded protection of the myocardium in hypoxia and low-flow ischemia at pH 7.4 but not in total ischemia and low-flow ischemia at pH 6.5. The data are consistent with the hypothesis that during total ischemia and low-flow ischemia at pH 6.5, acidosis favors the entry of thiopental into the cell, causing inhibition of mitochondrial function and reduction of ATP production. During hypoxic perfusion and low-flow ischemia at pH 7.4, when the decrease in pH is less, the cardiodepressant effect of thiopental may offset any deleterious effect of the drug on intracellular organelles such as mitochondria.

Adenosine Triphosphate↗
PubMed1996

Comparison of skeletal muscle microcirculation between clamp ischemia and microsurgical ischemia.

We compared ischemia reperfusion injury-associated vasospasm and perfused capillary density (PCD) at the microcirculatory level between clamp ischemia and microsurgical ischemia in rat skeletal muscle. Rat cremaster muscle was prepared as an island flap, attached only with pudic-epigastric vessels branching from external iliac vessels. Two types of ischemia, with clamping only or with microvascular anastomosis, were applied at the external iliac vessels for 2 hours followed by 1-hour reperfusion before in vivo microscopic examination for hemodynamic changes. At the end of observation, small segments of the vessels at the clamping site and microsurgical anastomoses site were also harvested for histological examination. It was found that the first- and second-order arterioles had about 12-15% diameter reductions in both groups, whereas diameter reductions of the third-order arterioles were up to 37.8% in the microsurgical ischemia group, much greater than that in the clamp ischemia group (2.3%). There was also no significant difference in PCD reduction between the two groups, although the red blood cell velocity was much slower in the microsurgical ischemia group. Histological examination of the anastomosis site showed massive accumulation of polymorphonuclear neutrophils on the venous endothelium. These results suggested a different degree of endothelial damage and local leukocyte activation between microsurgical ischemia and clamp ischemia. Therefore, we conclude that clamp ischemia cannot replace microsurgical ischemia for studying microcirculatory changes in free tissue transfer.

Anastomosis, Surgical↗
PubMed2005

Prolonged cold ischemia in rat cardiac allografts promotes ischemia-reperfusion injury and the development of graft coronary artery disease in a linear fashion.

BACKGROUND: Prolonged cold ischemia is thought to exacerbate ischemia-reperfusion injury and graft coronary artery disease (GCAD). We investigated the effect of varying lengths of cold ischemia on inflammation and apoptosis during ischemia-reperfusion injury and correlated this with the degree of GCAD in rat cardiac allografts. METHODS: PVG rat (RT1c) hearts subjected to 30, 60, 90, 120, or 150 minutes of cold ischemia were heterotopically transplanted into ACI rats (RT1a). Grafts were procured after 4 hours of reperfusion and analyzed for superoxide generation, myeloperoxidase activity, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta), and monocyte chemoattractant protein-1/chemokine (C-C motif) ligand 2 (MCP-1/CCL2) production, cardiomyocyte apoptosis, and caspase-2, -3, -8, -9 activities. Additional transplanted animals received cyclosporine A (7.5 mg/kg/day) for 10 days as chronic rejection models. Indices of GCAD were determined at 90 days. RESULTS: A direct linear correlation was found between cold ischemic time, ischemia-reperfusion injury, and GCAD. Superoxide generation, myeloperoxidase activity, TNF-alpha, IL-1beta, MCP-1/CCL2 production, cardiomyocyte apoptosis, and caspase-2, -3, -8, and -9 activities increased with ischemic time, peaking at 120 minutes and plateauing at 150 minutes. GCAD, assessed by the percentage of luminal narrowing, the intima/media ratio, and the percentage of diseased vessels, worsened with increased ischemic time, peaking at 120 minutes and plateauing at 150 minutes. All tested variables in both the acute and chronic phases were significantly increased with 120-minute ischemia compared with 30-minute ischemia. CONCLUSIONS: These data indicate that the degree of cardiomyocyte apoptosis and inflammatory response in cardiac allografts during ischemia-reperfusion injury depends on the duration of cold ischemia. More important, that prolonged cold ischemia correlates with increased GCAD.

Animals↗
PubMed1986

[Experimental study on reversibility of cerebral ischemia--residual blood flow and duration of ischemia].

This experimental study was designed to estimate the flow thresholds and the time thresholds for reversibility of cerebral ischemia. We used a "canine model of completely ischemic brain regulated with a perfusion method", in which the cerebral blood flow (CBF) could be controlled. The residual blood flow was reduced to 10%, 20%, 30% or 40% of normal CBF, and the recirculation was started after 1, 2, 3 or 4 hours of ischemia. CBF was measured by a laser doppler flow meter. EEG and somatosensory evoked potential (SEP) was monitored and used as a parameter expressing the brain function. In the 10% and 20% ischemia group, functional recovery could not be obtained even if reperfusion was started at 1 hour after the onset of ischemia. On the other hand, in the 30% ischemia group, nearly complete recovery of EEG and SEP could be seen when reperfusion was done at 1 hour from the onset of ischemia. But recirculation after 2 hours of ischemia did not lead to significant functional recovery. In the 40% ischemia group, reperfusion within 3 hours of ischemia allowed full recovery of ischemic brain. On the contrary, reperfusion after 4 hours of ischemia showed a gradual deterioration of EEG and SEP. Accordingly, it was clearly demonstrated that the reversibility of ischemic brain was critically correlated to severity and duration of cerebral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Effect of ischemia duration and nitric oxide on coronary vasoconstriction after ischemia-reperfusion.

The effects of the duration of ischemia on coronary vasoconstriction after ischemia-reperfusion were analysed in rat hearts. After 15, 30 or 45 min of global zero-flow ischemia and 15 min reperfusion, the coronary response to endothelin-1 (10(-10)-10(-7) M) and the thromboxane A2 analogue 9,11-dideoxy-1a,9a-epoxymethanoprostaglandin F2alpha (U46691, 10(-8)-10(-6) M) was recorded. Vasoconstriction induced by endothelin-1 only increased after short 15 min periods of ischemia. In contrast, the vasoconstriction induced by U46619 remained unmodified by short ischemias but was reduced after longer periods of ischemia (30 and 45 min). Inhibition of nitric oxide synthesis with the Nw-nitro-L-arginine methyl ester (L-NAME, 10(-4) M) augmented the vasoconstriction induced by endothelin-1 in non-ischemic hearts, but not following ischemia. Similarly, L-NAME increased the vasoconstriction induced by U46619 to a greater extent in non-ischemic hearts than following ischemia. These results suggest that ischemia-reperfusion inhibits nitric oxide production, causing an increased coronary response to endothelin-1 after brief ischemias. Longer ischemias may non-specifically inhibit coronary vasoconstriction and reduce nitric oxide production.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

Influence of groin incision, duration of ischemia, and prostaglandin E1 on ischemia-reperfusion injury of the lower limb.

OBJECTIVE: The influences of groin incision, duration of ischemia, and the effects of prostaglandin E1 (PGE1) on ischemia-reperfusion (I/R) injury of the hind limb in rabbits were evaluated. DESIGN: A prospective study. SETTING: Laboratory. PARTICIPANTS: In 64 rabbits, bilateral hind limb ischemia was induced by occlusion of the abdominal aorta. Volume changes, neuromuscular function of the hind limb, and creatine kinase (CK) release were measured as variables of tissue injury. INTERVENTIONS: Eight rabbits served as untreated controls (CON). In 2 groups (each n = 14), 3 hours of ischemia were followed by 3 hours of reperfusion (I/R). In 2 different groups (each n = 14), 45 minutes of ischemia were followed by 2 hours of reperfusion. To determine effects of PGE1, 1 I/R group of each ischemia duration was treated intravenously with 80 ng/kg/min of PGE1 starting 30 minutes after the onset of ischemia (I/R-PGE1). To determine effects of groin incision on edema formation, volume changes were determined in the "operated" right (CON-R, 3h-R, 3h-PGE1-R and 45 min-R, 45 min-PGE1-R) or in the "nonoperated" left hind limb (CON-L, 3h-L, 3h-PGE1-L and 45 min-L, 45 min-PGE1-L), representing a subgroup analysis. MEASUREMENTS AND MAIN RESULTS: Volume changes after I/R occurred only in operated legs after ischemia (3h-R: 2.3 +/- 0.3 mL, p < 0.0001 v CON-R and 3h-L; 45 min-R: 0.8 +/- 0.2 mL, p < 0.01 v 45 min-L). PGE1 reduced edema formation in the operated legs (3h-PGE1-R: 1.0 +/- 0.4 mL, p < 0.0001 v 3h-R; 45 min-PGE1-R: 0.5 +/- 0.3 mL, p = 1.0 v 45 min-R). Groin incision without I/R had no effect on edema formation (CON-R: -0.13 +/- 0.17 mL of baseline). The increase of CK release from 616 +/- 584 U/L in controls to 5,921 +/- 2,156 U/L after 3 hours of ischemia (p < 0.001) was attenuated by treatment with PGE1 (3,732 +/- 2,653, p < 0.05 v I/R). Forty-five minutes of ischemia did not lead to cellular damage as measured by CK release (I/R: 606 +/- 364 U/L). Recovery of neuromuscular function was not affected by PGE1. CONCLUSION: Development of edema during I/R depends on groin incision of the hind limb and on the duration of ischemia. The I/R injury is attenuated by PGE1 treatment, in terms of reduced edema formation and CK release, but not in terms of neuromuscular function.

Alprostadil↗
PubMed2001

Differences in prolonged ischemia length using ischemic preconditioning in the rabbit heart. Tolerable limitation time for surgically induced myocardial ischemia during normothermic cardiac operation.

BACKGROUND: To determine the effect of the tolerable limitation time of prolonged ischemia after ischemic preconditioning on postischemic functional recovery and infarct size reduction in the rabbit heart. METHODS: White rabbits (n=30) were used for Langendorff perfusion. Control hearts were perfused at 37 degrees C for 180 min; 30 min global ischemia hearts (30GI) received 30 min global ischemia and 120 min reperfusion; IPC+30GI hearts received 5 min zero flow global ischemia and 5 min reperfusion prior to 30 min global ischemia; 20 min global ischemia hearts (20GI) received 20 min global ischemia and 120 min reperfusion; IPC+20GI hearts received 5 min zero flow global ischemia and 5 min reperfusion prior to 20 min global ischemia. RESULTS: Infarct size in the 30GI hearts was 33.5+/-4.0% and 1.7+/-0.5% in the control hearts. The 20GI hearts and IPC+30GI hearts decreased infarct size, as compared with the 30GI hearts (13.0+/-1.8% and 16.6+/-1.7%, respectively; p<0.001, 20GI vs 30GI; p<0.01, IPC+30GI vs 30GI; p>0.05, 20GI vs IPC+30GI) but did not enhance postischemic functional recovery. The IPC+20GI hearts (3.5+/-0.6%) significantly decreased infarct size as compared with the 20GI hearts (p<0.05, IPC+20GI vs 20GI), and there was no significant difference between the IPC+20GI and the control hearts (p>0.05), but the IPC+20GI hearts did not enhance postischemic functional recovery. CONCLUSIONS: A 20 min ischemia may be the tolerable limitation time of prolonged ischemia after ischemic preconditioning in an isolated rabbit heart model.

Animals↗
PubMed1998

Glibenclamide does not prevent action potential shortening induced by ischemia in anesthetized rabbits but reduces ischemia-induced arrhythmias.

The possible ischemia-selective Class III anti-arrhythmic action (selective action potential widening in ischemia) of the IKATP blocker glibenclamide was assessed in anesthetized rabbits during ischemia induced by complete occlusion of a coronary artery. Coronary artery occlusion caused an initial prolongation in monophasic action potential (MAP) duration at 90% repolarization from 145 +/- 2.8 ms (mean +/- S.E.M., n = 14) to 162 +/- 4.5 ms (P < 0.05) 1 min after ischemia. This was followed by a rapid and sustained shortening to 104 +/- 4.9 ms 5 min after the onset of ischemia (P < 0.05 from both values). Glibenclamide (3, 6, 12 or 24 mg/kg, i.v.) caused a statistically significant, dose-related reduction in the rate of MAP shortening induced by ischemia, whereas 0.3 mg/kg was without effect. The effective dose for a 50% maximal effect (ED50) was 13 +/- 0.8 mg/kg (n = 28). Despite this, there was no effect on the final magnitude of MAP shortening. Five min after induction of ischemia, there were no longer any detectable effects of glibenclamide on MAP duration. Glibenclamide significantly reduced the incidence of ventricular fibrillation, although the effect was not dose related. No differences were found in the latency to ventricular fibrillation between groups. Ventricular fibrillation occurred 10.6 +/- 1.1 min (n = 19) after the start of ischemia. In a similar experiment, 0.3 mg/kg glibenclamide i.v. did not affect the rate of MAP shortening, the final magnitude of MAP shortening or the occurrence of arrhythmias caused by ischemia. Since the action potential widening effects of glibenclamide in ischemic tissue were not observed at the time when arrhythmias occurred, it is unlikely that an ischemia-selective Class III anti-arrhythmic action contributes to the limited antiarrhythmic actions of glibenclamide.

Action Potentials↗
PubMed1993

Discordance between effects of anti-ischemic therapy on ambulatory ischemia, exercise performance and anginal symptoms in patients with stable angina pectoris. The Angina and Silent Ischemia Study Group (ASIS).

OBJECTIVES: We sought to define the extent to which the therapeutic efficacy of three single-drug regimens on ambulatory ischemia paralleled efficacy on other clinical manifestations of ischemia, specifically exercise test performance and anginal symptoms. BACKGROUND: Some studies have shown that the presence and severity of ambulatory ischemia are predictive of anginal symptoms and exercise test performance, whereas other studies have not. Less is known about effects of antianginal treatment and whether response to therapy for one clinical manifestation reflects therapeutic responses for other clinical manifestations. METHODS: We studied 50 patients in the Angina and Silent Ischemia Study who had documented coronary disease, an exercise test positive for ischemia, the presence of ambulatory and asymptomatic ischemia on ambulatory electrocardiographic (ECG) Holter monitoring and stable anginal symptoms. Patients received maximally tolerated doses of sustained release propranolol (mean 293 mg/day), sustained release diltiazem (mean 350 mg/day), nifedipine (mean 79 mg/day) and placebo, each for 2-week periods in a double-blind, crossover fashion. Patients' responses to treatment were assessed by 48-h ambulatory ECG monitoring, exercise test (standard Bruce protocol) and diaries of angina. Levels of efficacy for each agent and for each clinical measure were compared using Spearman correlation analysis. RESULTS: With placebo there was no correlation among the frequency of ischemic episodes by ambulatory ECG monitoring, exercise time to 1.0-mm ST segment depression or frequency of anginal episodes. Furthermore, for a given patient the efficacy of each active medication in reducing ambulatory ischemia was not correlated with response in anginal symptoms or exercise test performance (r = -0.21 to 0.24, p = NS). Within each of these clinical measures, efficacy of one drug was more strongly correlated with efficacy of another drug (r = 0.64 to 0.81 for ambulatory ischemia, 0.48 to 0.56 for exercise test performance and 0.16 to 0.54 for anginal symptoms). CONCLUSIONS: Different measures of ischemia, specifically ambulatory ischemia assessed by ambulatory ECG monitoring, exercise performance on exercise test and anginal symptoms, are independent. Efficacy for each clinical end point must be assessed separately when considering response to drug treatment.

Aged↗
PubMed1997

A detailed angiographic analysis of patients with ambulatory electrocardiographic ischemia: results from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study angiographic core laboratory.

OBJECTIVES: The purpose of this Asymptomatic Cardiac Ischemia Pilot (ACIP) data bank study was to characterize angiographic features of coronary pathology of patients enrolled in the ACIP study. BACKGROUND: Ischemia during ambulatory electrocardiographic (AECG) monitoring is associated with increased morbidity and mortality. Reports relating AECG ischemia to severity or complexity of coronary artery disease are few in number and small in size and have produced conflicting results. METHODS: Coronary angiograms from patients with asymptomatic AECG ischemia enrolled in the ACIP study were reviewed at a central core laboratory. Quantitative measurement of percent stenosis and Thrombolysis in Myocardial Infarction flow grades were used to assess the severity of coronary artery disease. Lesions were also evaluated for the presence of intracoronary thrombus, ulceration and lumen contour as indicators of stenosis complexity. In addition, comparisons were made with 27 patients screened for the ACIP study, but who were found ineligible because they did not have AECG ischemia on 48-h Holter monitoring. RESULTS: A total of 329 (75%) of 439 patients with AECG ischemia had multivessel coronary artery disease. Proximal stenoses > or = 50% diameter reduction were common in patients with AECG ischemia (62.2%), as were proximal stenoses > or = 70% (38.7%). Features suggesting complex plaque were found in 50.1% of patients with AECG ischemia. CONCLUSIONS: Multivessel coronary artery disease, severe proximal stenoses and features of complex plaque were observed frequently in patients who exhibited AECG ischemia. The presence of severe and complex coronary artery disease may explain, in part, the increased risk for adverse outcome associated with ischemia during activities of daily life.

Coronary Angiography↗
PubMed2005

Ischemia-modified albumin improves the usefulness of standard cardiac biomarkers for the diagnosis of myocardial ischemia in the emergency department setting.

We studied the role of ischemia-modified albumin (IMA) with standard biomarkers (myoglobin, creatine kinase-MB [CK-MB], troponin I [TnI]) in assessment of 200 patients with suspected myocardial ischemia admitted to the emergency department. Every case was reviewed by a cardiologist. A clinical diagnosis of ischemia was assigned and correlated with biomarker test results. Of the patients, 25 (13.0%) had myocardial ischemia. Receiver operating characteristic curves demonstrated IMA as highly sensitive but somewhat poorly specific for the presence of ischemia (area under curve, 0.63; P = .01). With a cut point of 90 U/mL, the Albumin Cobalt Binding Test had 80% sensitivity and 31% specificity for diagnosing ischemia and a negative predictive value of 92%. IMA was positive in 4 of 5 patients with electrocardiographic (ECG) evidence of ischemia and 16 of 20 patients with coronary ischemia but negative ECG. Among the same patients, the myoglobin-CK-MB-TnI triad had a sensitivity of 57%. The combination of IMA-myoglobin-CK-MB-TnI increased the sensitivity for detecting ischemia to 97%, with a negative predictive value of 92%. IMA is highly sensitive and has a high negative predictive value, which might improve the usefulness of standard biomarkers of myocardial ischemia.

Adult↗
PubMed1996

Calcium movement in ischemia-tolerant hippocampal CA1 neurons after transient forebrain ischemia in gerbils.

Hippocampal CA1 neurons exposed to a nonlethal period (2 min) of ischemia, acquired tolerance to a subsequent lethal 5-min period of ischemia, which usually causes delayed-type neuronal death. Intracellular Ca2+ movements before and after the 5 min of forebrain ischemia were evaluated in gerbil hippocampal CA1 pyramidal neurons, had acquired tolerance in comparison with nonischemia-tolerant CA1 neurons. Evaluation was performed by observing the ultrastructural intracellular Ca2+ distribution and the Ca2+ adenosine triphosphatase (Ca(2+)-ATPase) activity using electron microscopic cytochemistry. In comparison with nonischemia-tolerant CA1 neurons, mitochondria of ischemia-tolerant CA1 neurons sequestered more Ca2+ from the cytosomal fraction 15 min after the 5-min period of ischemia, and Ca2+ deposits in these mitochondria were rapidly decreased. Plasma membrane Ca(2+)-ATPase activities were already significantly elevated before the 5 min of ischemia, and remained at a higher level subsequently compared to nonischemia-tolerant CA1 neurons. Changes in the mitochondrial Ca2+ distribution and Ca(2+)-ATPase activities in ischemia-tolerant CA1 neurons after the 5-min period of ischemia showed a strong resemblance to those in CA3 neurons, which originally possess resistance to such periods of ischemia. These findings suggest that enhanced or maintained activities of mitochondrial Ca2+ sequenstration and plasma membrane Ca(2+)-ATPase reduced Ca2+ toxicity following 5-min ischemia in terms of time, resulting in escape from delayed neuronal death.

Animals↗
PubMed1995

Preconditioning with a single short episode of global ischemia in the isolated working rat heart: effect on structure, mechanical function, and energy metabolism for various durations of sustained global ischemia.

PURPOSE: Preconditioning in the setting of global ischemia, using functional recovery during reperfusion as the endpoint, has recently been demonstrated in the isolated perfused rat heart. It has been suggested that its beneficial actions have a metabolic basis. The isolated rat heart has not been fully characterized with respect to the metabolic, functional, and structural changes associated with this phenomenon in the setting of global ischemia. The purpose of this study was to determine (1) the time course of protection conferred by a single episode (5 minutes) of preconditioning; (2) changes in tissue high energy phosphates, lactate, and glycogen levels at different time intervals; and (3) morphological appearance of the heart at the end of ischemia as well as after reperfusion. METHODS: Isolated perfused working rat hearts were used. Preconditioning consisted of a single episode of 5 minutes of global ischemia and 15 minutes of reperfusion. Preconditioned and non-preconditioned hearts were subjected to global ischemia of 20-35 minutes duration. Functional recovery, energy metabolism (high energy phosphates, lactate, and glycogen), and structural appearance were studied at different stages. RESULTS: The functional recovery of the preconditioned hearts was significantly higher than in the corresponding nonpreconditioned group during reperfusion for all durations of ischemia longer than 25 minutes. The degree of protection observed was less than reported previously. A minor degree of energy sparing was reflected by differences in the rate of depletion of glycogen and accumulation of tissue lactate during the sustained episode of ischemia. Semiquantitative light microscopy evaluation revealed that ischemia-induced structural damage was less in the preconditioned hearts, both at the end of the sustained ischemic episode as well as after reperfusion. CONCLUSIONS: A single episode of global ischemia successfully preconditions the isolated working rat heart. The protection elicited was demonstrated on a functional and structural level, and was accompanied by a small energy-sparing effect.

Animals↗
PubMed1993

Asymptomatic and electrically silent myocardial ischemia during upright leg cycle ergometry and treadmill exercise (clandestine myocardial ischemia).

The frequency of "clandestine" (electrically silent and asymptomatic, but scintigraphically evident) myocardial ischemia during treadmill and upright leg cycle ergometric studies was compared in 38 patients with coronary artery disease and reversible ischemia on both thallium-201 scintigraphy and exercise radionuclide angiography. A similar peak double product was attained in both studies. Angina pectoris was significantly more frequent with treadmill exercise than with leg cycling (29 vs 5%, p = 0.0079). An interpretable and positive exercise electrocardiogram occurred in 53% of treadmill tests, but in only 19% of leg cycle tests (p = 0.0025); in a group of 22 patients without scintigraphic ischemia, leg cycle testing had greater specificity (95 vs 64%, p = 0.0248). Ischemia was manifest by symptoms or an abnormal electrocardiogram in 59% of treadmill tests, but in only 18% of leg cycle tests (p = 0.0003). There were no differences between the exercise variables or the degree of scintigraphic abnormalities of the 22 patients with manifest ischemia and the 16 with clandestine ischemia. However, patients with previous coronary artery bypass surgery experienced clandestine ischemia more frequently than did those without bypass surgery (80 vs 33%, p = 0.0103). Thus, clandestine ischemia occurs more frequently during symptom-limited upright leg cycle ergometry (82%) than during treadmill exercise (42%). The symptomatic and electrical manifestations of exercise-induced ischemia have a critical dependence on the type of exercise used.

Adult↗
PubMed1995

Asymptomatic Cardiac Ischemia Pilot (ACIP) study: impact of anti-ischemia therapy on 12-week rest electrocardiogram and exercise test outcomes. The ACIP Investigators.

OBJECTIVES: This report from the Asymptomatic Cardiac Ischemia Pilot (ACIP) study examines differences in the magnitude of reduction of myocardial ischemia as determined by exercise treadmill testing in patients randomized to three different treatment strategies: angina-guided medical therapy, ischemia-guided medical therapy and coronary revascularization. BACKGROUND: No prospective randomized clinical trials in patients with exercise electrocardiographic (ECG) abnormalities and asymptomatic cardiac ischemia on ambulatory ECG monitoring have compared the impact of different treatment strategies, including coronary revascularization, in terms of reducing myocardial ischemia. METHODS: The ACIP exercise protocol was used. Exercise variables measured included final exercise stage; presence of exercise-induced angina or ischemia; time to angina; time to 1-mm ST segment depression; number of exercise ECG leads with abnormalities; maximal depth of ST segment depression in any lead; sum of ST segment depression; ST/HR index; and rate-pressure product at time to angina, at time to 1-mm ST segment depression and at peak exertion. RESULTS: Peak exercise time was increased by 0.5, 0.7 and 1.6 min in patients assigned to the angina-guided, ischemia-guided and coronary revascularization strategies, respectively, from the qualifying visit to the 12-week visit (p < 0.001). At the qualifying visit, the sum of exercise-induced ST segment depression was 9.4 +/- 5.0 (mean +/- SD), 9.6 +/- 4.7 and 9.9 +/- 5.5 mm (p = NS) in the three treatment strategies, respectively. At the 12-week visit, the sum of exercise-induced ST segment depression was 7.4 +/- 5.7, 6.8 +/- 5.3 and 5.6 +/- 5.6 mm (p = 0.02) in the three treatment strategies, respectively. Each treatment strategy resulted in a significant reduction in all exercise-induced variables of myocardial ischemia measured at 12 weeks. CONCLUSIONS: Coronary revascularization significantly reduced the extent and frequency of exercise-induced myocardial ischemia compared with either medical strategy. The prognostic impact of these observations should be evaluated in a large-scale multicenter clinical trial.

Analysis of Variance↗
PubMed1999

Associations between different status of myocardial ischemia and ischemia-related negative or positive epicardial U-waves: observations during coronary angioplasty.

This study examined the relationships between the polarity of the U wave on intracoronary electrocardiogram (ECG) and the status of myocardial ischemia during angioplasty. The ECG features of ischemia-related U waves were also evaluated. Among 63 patients with intracoronary ECGs adequate for analysis of U waves, there were 26 patients showing a change of the U wave to a negative direction and 18 patients showing a change to a positive direction from baseline to coronary occlusion. Among these patients, 10 of the former showed a distinct change in polarity of the U wave from positive to negative (group A), and 7 of the latter patients showed the opposite change (group B). Patients in group B had a higher incidence of prior myocardial infarction (86% vs 30%; P < .05), presence of an abnormal Q wave on intracoronary ECG (71% vs 20%; P < .05), poor wall motion in the angioplasty-related area (100% vs 30%; P < .01), and lower left ventricular ejection fraction (55.7% +/-8.1% vs 66.6% +/- 4.5%; P < .01) than patients in group A. The remaining patients (other than groups A and B) showing U wave change in a negative (n = 16) or positive (n = 11) direction presented with similar features to those in groups A or B, respectively. The ECG features of several types of ischemia-related U wave were determined by analysis of intracoronary ECG obtained from the patients in groups A and B. In group A, the Bazett-corrected Q (positive U) interval measured at baseline (myocardial state; near normal) was significantly shorter than the Q-(negative U) interval measured during coronary occlusion (acute ischemia) (0.518 +/- 0.031 s vs 0.579 +/- 0.046 s; P < .01). In group B, the Q-(negative U) interval measured at baseline (chronic ischemia) was longer than the Q-(positive U) interval measured during angioplasty (acute-on-chronic ischemia) (0.582 +/- 0.034 s vs 0.501 +/- 0.027 s; P < .001). Thus, intracoronary ECG recorded during angioplasty in the present study revealed physiologic U wave, two types ("acute" and "chronic") of ischemia-related negative and one type ("pseudonormal") of ischemia-related positive U waves, each of which appeared in a different status of myocardial ischemia and possessed characteristic ECG features in its appearance.

Adult↗
PubMed1998

Attenuation of ischemia-induced activation of cardiac sympathetic afferents following brief myocardial ischemia in cats.

OBJECTIVE: We have previously shown that brief myocardial ischemia impairs neural conduction in cardiac sympathetic efferent fibers. However, attenuation of the activity of afferent sympathetic nerves, which may contribute to impaired ischemic nociception and reflex hemodynamic responses, is not well understood. Therefore, we studied the electrophysiological effects of brief myocardial ischemia on the mechano-, chemo- and ischemia-sensitive properties of cardiac sympathetic afferent fibers. METHODS: Single unit activity of sympathetic afferent A delta and C fibers innervating the left ventricle (LV) was recorded from the thoracic chain or rami communicantes in 16 anesthetized cats. We tested the response of impulse activity to (1) mechanical LV probing, (2) epicardial application of bradykinin (10 microg), H2O2 (1.5%) or adenosine (500 microg), and (3) 1 min of coronary occlusion. Repeat tests were performed in 11 of 16 fibers after 15 min of coronary occlusion and 15 min of reperfusion. Control responses were measured in five fibers before and after a 30-min interval without ischemia. RESULTS: Afferent fibers responded with increased activity to LV probing (16/16 fibers), bradykinin (13/16 fibers), H2O2 (7/11 fibers), adenosine (1/11 fibers), and to a 60 s period of coronary occlusion (11/16 fibers). The unit impulse activity to 1 min of coronary occlusion was markedly attenuated after 15 min of myocardial ischemia and 15 min of reperfusion (P < 0.05). This attenuation was associated with reduced sensitivity to mechanical and chemical stimuli, while in separate time-control studies (n = 5) no attenuation was observed in absence of ischemia. CONCLUSION: A brief period of myocardial ischemia is capable of attenuating mechano-, chemo- and ischemia-sensitive activity of cardiac afferent sympathetic nerves. This may have important implications for the mechanism of silent myocardial ischemia.

Adenosine↗
PubMed1997

Relation between ambulatory electrocardiographic monitoring and myocardial perfusion imaging to detect coronary artery disease and myocardial ischemia: an ACIP ancillary study. The Asymptomatic Cardiac Ischemia Pilot (ACIP) Investigators.

OBJECTIVES: This study sought to explore the relation between markers of ischemia detected by ambulatory electrocardiographic (AECG) monitoring and stress myocardial perfusion single-photon emission computed tomography (SPECT). BACKGROUND: Stress myocardial SPECT and AECG monitoring are both utilized in evaluating patients with coronary artery disease. However, information is limited regarding the relation between the presence and extent of ischemia as detected by these two modalities. METHODS: This was an ancillary study of the Asymptomatic Cardiac Ischemia Pilot (ACIP) trial. One hundred six patients with previous coronary angiography underwent AECG monitoring and stress SPECT within a close temporal time period. The frequency and duration of ischemia as assessed by AECG monitoring and the total and ischemic stress-induced myocardial perfusion defect sizes as assessed by SPECT were quantified in separate core laboratories. Multivariate logistic regression and linear regression analysis were used to determine associations between AECG and SPECT abnormalities with regard to angiographic, demographic and treadmill exercise variables. RESULTS: Seventy-four percent of patients with significant (> or = 50%) coronary artery stenosis had SPECT abnormalities, whereas 61% had ischemia by AECG monitoring. The most important predictors of SPECT abnormalities were severity (p < 0.001) of coronary artery stenosis, followed by total exercise duration (p = 0.016) and patient age (p = 0.04). The only predictor of AECG abnormalities was the presence of ST segment depression on the initial exercise treadmill test (p = 0.021). Only a 50% concordance for normalcy or abnormalcy was observed between the SPECT and AECG results, and no relation was observed between the frequency or duration of AECG ischemia and the quantified total or ischemic myocardial perfusion defect size as assessed by SPECT. CONCLUSIONS: Ischemia as detected by AECG monitoring does not correlate with the presence and extent of ischemia as quantified by stress SPECT. Because these techniques appear to detect different pathophysiologic manifestations of ischemia, they may be complementary in more fully defining the functional significance of coronary artery disease and, in particular, which patients are at highest risk for adverse cardiac events.

Adult↗