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P Taggart

Publications and source records attributed to P Taggart.

At least 19 recordsLinked to original sources
PubMed2005

Evidence of a breakdown of corticostriatal connections in Parkinson's disease.

Dendritic spines are important structures which receive synaptic inputs in many regions of the CNS. The goal of this study was to test the hypothesis that numbers of dendritic spines are significantly reduced on spiny neurones in basal ganglia regions in Parkinson's disease as we had shown them to be in a rat model of the disease [Exp Brain Res 93 (1993) 17]. Postmortem tissue from the caudate and putamen of patients suffering from Parkinson's disease was compared with that from people of a similar age who had no neurological damage. The morphology of Golgi-impregnated projection neurones (medium-sized spiny neurones) was examined quantitatively. The numerical density of dendritic spines on dendrites was reduced by about 27% in both nuclei. The size of the dendritic trees of these neurones was also significantly reduced in the caudate nucleus from the brains of PD cases and their complexity was changed in both the caudate nucleus and the putamen. Dendritic spines receive crucial excitatory input from the cerebral cortex. Reduction in both the density of spines and the total length of the remaining dendrites is likely to have a grave impact on the ability of these neurones to function normally and may partly explain the symptoms of the disorder.

Aged↗
PubMed2002

Physiological changes in ventricular filling alter cardiac electrophysiology in patients with abnormal ventricular function.

OBJECTIVE: To explore the hypothesis that patients with abnormal ventricular function have an altered electrophysiological response to physiological changes in ventricular filling which is not evident in people with normal ventricles. DESIGN: The influence of an acute alteration in ventricular filling on dispersion of repolarisation, measured as QT dispersion, was examined in subjects with normal (n = 9) and abnormal ventricles (n = 9). A physiological reduction in ventricular filling was achieved using dual chamber atrioventricular (AV) pacing in two different modes-AV pacing: atrial activation 120 ms before ventricular activation such that atrial contraction occurred normally in late diastole; and VA (ventriculoatrial) pacing: atrial activation 50 ms after ventricular activation, such that atrial contraction occurred after closure of the AV valves. The absence of effective atrial contraction was confirmed by echocardiography. Ventricular cycle length and sequence of excitation through the ventricle was constant throughout both VA and AV sequences within each patient. RESULTS: During AV pacing (normal ventricular filling) there was no significant difference in QT dispersion between the two groups. In contrast during VA pacing, when the atrial component to ventricular filling was abolished, there was an immediate and consistent increase in QT dispersion compared with baseline in subjects with abnormal ventricular function (p < 0.001) but not in those with normal ventricles. CONCLUSIONS: An abrupt change in ventricular filling, within the physiological range, increased QT dispersion in subjects with abnormal ventricular function but not in subjects with normal ventricles. The findings suggest an altered electrophysiological response to ventricular load in patients with abnormal ventricular function.

Echocardiography↗
PubMed2001

Transmural repolarisation in the left ventricle in humans during normoxia and ischaemia.

BACKGROUND: Studies in isolated tissues and myocytes show different repolarisation properties in subepicardium, midmyocardium and subendocardium. Whether these differences are present in vivo and are relevant to humans has been the subject of controversy. Our objectives were (1) to ascertain whether transmural repolarisation gradients are present in humans, (2) to determine whether the greater sensitivity of subepicardial cells to ischaemia in vitro is manifest during early ischaemia in humans in vivo. METHODS AND RESULTS: We studied 21 patients during routine coronary artery surgery. Unipolar activation recovery intervals (ARI) were recorded from five transmural locations between subepicardium and subendocardium in the left ventricular wall. A pacing protocol spanned a range of cycle lengths from a cycle length of 300 ms to the maximum permitted by the intrinsic atrial activity. Following the onset of cardiopulmonary bypass recordings were obtained before (control) and during a 3-min period of global ischaemia. During control transmural ARIs were homogeneous between 300 and 1500 ms (ventricular pacing) and 750 and 1500 ms (atrial spontaneous beats). During ischaemia, ARIs shortened similarly at all transmural electrode sites and transmural homogeneity was maintained. CONCLUSIONS: Transmural repolarisation differences within the ventricular wall of the human heart were absent at cycle lengths within the physiological range but also during prolonged cycles. During early (global) ischaemia repolarisation changed equally in subepicardial and subendocardial regions and transmural homogeneity of repolarisation was preserved.

Adult↗
PubMed2001

Coronary artery disease in patients with chest pain who have low-risk clinical characteristics and negative cardiac troponin I.

Patients who have low-risk clinical features and negative cardiac troponin levels may be suitable for early discharge after a brief period of observation in the emergency department (ED). Little is known about the prevalence and severity of coronary artery disease in such patients, although this has implications for follow-up. Subjects included 570 patients who were at < or =7% risk of acute myocardial infarction (AMI), remained clinically stable (defined as the absence of new ischemic changes on their electrocardiograph, signs or symptoms of heart failure, the development of a cardiac arrhythmia or hypotension requiring either inotropes or volume repletion) and had cardiac troponin I (cTnI) levels <0.2 microgl(-1) during the initial 12 hours of hospitalization. Clinical features were documented and those undergoing stress tests and/or coronary angiograms had these graded by 2 independent observers. Overall, 190 (33.3%) of this population, who might be considered suitable for early discharge, had objective evidence of coronary artery disease. Patients with chest pain who are at low risk of AMI, remain clinically stable and have negative cTnI over the initial 12 hours of observation are a heterogeneous population, some of who have threatening coronary disease. This does not preclude early discharge from the ED but emphasizes the need for careful assessment and follow-up.

Aged↗
PubMed2001

Soluble intercellular adhesion molecule-1 as a predictor of early adverse events in patients with chest pain compatible with myocardial ischemia.

STUDY OBJECTIVE: Inflammation plays an important role in acute coronary syndromes, and some evidence indicates that patients with a more pronounced vascular inflammatory response have a poorer outcome. Soluble intercellular adhesion molecule-1 (sICAM-1) is a specific marker for vascular endothelial cell activation. The aim of this study was to investigate the prognostic value of plasma sICAM-1 levels in patients with acute chest pain compatible with myocardial ischemia. METHODS: This prospective study was conducted at 2 urban university medical centers. The study cohort consisted of 119 consecutive patients with chest pain in whom myocardial ischemia was suspected clinically at presentation. Patients with conditions that affect sICAM-1 levels were ineligible. Cardiac troponin I (cTnI), C-reactive protein, and sICAM-1 levels were assayed at presentation to the emergency department. The primary end point was the occurrence of a serious cardiac event (death, nonfatal acute myocardial infarction, coronary revascularization) in the hospital. RESULTS: Although sICAM-1 levels tended to be higher in patients with a serious cardiac event, there was no significant association. In contrast, a cTnI level greater than 0.2 ng/mL was a powerful predictor of an in-hospital serious cardiac event (odds ratio 16.3, 95% confidence interval [CI] 4.7 to 55.9; P <.0001). Soluble ICAM-1 levels of more than 260 ng/mL at presentation had a sensitivity for predicting a serious cardiac event of 63% (95% CI 46% to 81%) but a specificity of only 47% (95% CI 38% to 57%). CONCLUSION: In a heterogeneous population of patients with chest pain compatible with myocardial ischemia, elevated sICAM-1 levels are poor predictors of an individual patient suffering a serious cardiac event in the hospital.

Adult↗
PubMed2001

The expression of the CD18 leucocyte integrin in a rabbit model of acute myocardial infarction: a pilot study of temporal changes and relationship to infarct size.

CD18 integrins mediate leucocyte adhesion to vascular endothelium. This represents the initial step in inflammatory cell infiltration following myocardial necrosis. The current study assessed whether the expression of these rapidly activated and readily measured adhesion receptors on circulating neutrophils would reflect the extent of cardiac damage in a rabbit model of acute myocardial infarction. Myocardial ischaemia/infarction was induced in anaesthetised adult male New Zealand white rabbits (n = 8) by ligation of the circumflex or marginal coronary artery. To control for the effects of anaesthesia and surgery, 4 rabbits underwent identical procedures without the induction of infarction. Absolute infarct size (in mg) and infarct size as a percentage of total left ventricular mass (relative infarct size) were calculated by differential staining and weighing of necrotic myocardium. Flow cytometry was used to determine cell surface expression of CD18 at six time points (baseline, 20 and 45 min of ischaemia and 20, 60 and 180 min of reperfusion). Absolute neutrophil CD18 expression and changes in expression over baseline were correlated with absolute and relative infarct size. Mean neutrophil CD18 expression increased significantly (from 2.42 +/- 0.20 to 3.07 +/- 0.29; p = 0.04) within 20 min of ischaemia. CD18 expression at 3 h did not predict absolute or relative infarct size (r = 0.40 and 0.37, respectively). The percentage change in cell surface CD18 expression (above baseline levels) was, however, correlated with both measures of infarct size (r = 0.76, p = 0.03, and r = 0.92, p = 0.001, respectively). In conclusion, in this rabbit model of myocardial infarction, neutrophil CD18 expression rises within 20 min of the induction of ischaemia but absolute values after 3 h of reperfusion are poor indicators of infarct size. Although percentage change in neutrophil CD18 levels over baseline correlates with infarct size there is considerable variation between individuals, limiting any clinical application.

Animals↗
PubMed2000

Inhomogeneous transmural conduction during early ischaemia in patients with coronary artery disease.

Electrical inhomogeneity and conduction slowing are critical factors in the initiation and maintenance of ventricular arrhythmias during early ischaemia. Studies in animal models have shown delay in epicardial activation compared to endocardial activation. Epicardial activation delay has been attributed to either enhanced sensitivity of epicardium to ischaemia or to mid-myocardial conduction delay. No information is available in humans and in particular in patients with chronic ischaemia due to coronary artery disease who may have altered electrophysiological properties. Twenty-three patients undergoing routine coronary surgery were studied. All had severe two or three vessel coronary artery disease and a documented history of angina for a mean of 2.4 years. On cardiopulmonary bypass a 3 min period of ischaemia was created by cross clamping the aorta between the input from the pump oxygenator and the coronary arteries. During atrial pacing (normal endocardial to epicardial activation) intramyocardial activation time within the left ventricular free wall between subendocardial and subepicardial plunge electrode terminals, increased from 12.7+/-1.5 ms (control) to 28.2+/-3.2 ms after 3 min ischaemia at the base. At the apex, the activation time increase (over the same distance) was less (19.5+/-2 ms at 3 min ischaemia). This difference in increase in activation time at the base and apex was significant (P<0.05). At the apex the ischaemia induced activation delay occurred primarily over the endocardial half of the wall, whereas the opposite was observed at the base of the heart. Using an epicardial electrode array stimulation along the long axis of the epicardial fibres showed minimal conduction delay during ischaemia whereas stimulation transverse to the epicardial fibres resulted in substantial conduction time prolongation, as was the case with intramural conduction. Intramural conduction during ischaemia was similar in non-infarcted regions of infarcted hearts compared to hearts with no previous MI. To conclude, in patients with coronary artery disease epicardial activation delay early during ischaemia is caused primarily by intramural delay and not by delay along the epicardium. Moreover, the ischaemia-induced transmural activation delay is inhomogeneous.

Aged↗
PubMed2000

Acute psychological stress and the propensity to ventricular arrhythmias; evidence for a linking mechanism.

AIMS: This study was designed to test the hypothesis that acute psychological stress is capable of inducing an increase in the dispersion of repolarization in patients with underlying coronary artery disease. METHODS AND RESULTS: Twenty four patients undergoing elective coronary angiography were studied, 17 with significant coronary artery disease and seven with normal coronary arteries. Following coronary angiography they were subjected to a series of timed cognitive tests, well known to induce acute psychological stress. An individual's perception of stress was assessed by visual analogue scales. Serial ECGs were recorded during the cognitive tests and QT, QRS and JT intervals measured from which QT, QRS and JT dispersion were calculated. Psychological stress was reported by the seven patients with normal coronaries and 14 of the 17 with coronary artery disease. In patients who experienced stress a marked increase in QT dispersion, reflecting JT dispersion, was observed in those with coronary artery disease (F=22.4, P=0.0001) but not in those without. At baseline there was no difference in QT dispersion between those with and without coronary artery disease (27-57 ms, 17-53 ms, P > or = 0.5). CONCLUSION: Acute psychological stress induces an increase in QT dispersion in patients with underlying coronary artery disease due to changes in JT dispersion (rather than QRS dispersion). This suggests that psychological stress modifies the dispersion of repolarization through ischaemia related changes in action potential duration.

Acute Disease↗
PubMed2000

Repolarisation and refractoriness during early ischaemia in humans.

OBJECTIVES: To determine whether effective refractory period (ERP) shortens or lengthens in the first minutes of ischaemia in humans, and the relation between ERP changes and action potential duration (APD). METHODS: ERP and monophasic action potential duration (MAPD) were measured from a single left ventricular epicardial site in 26 patients undergoing coronary artery surgery. Cardiopulmonary bypass was instituted and normothermia maintained. Refractory period was determined by the extrastimulus technique at a basic cycle length of 500 ms, at four times (group 1, 15 patients) or two times (group 2, 11 patients) the preischaemic diastolic threshold. A three minute period of ischaemia was instituted by aortic cross clamping between the input from the pump oxygenator and the heart. RESULTS: After three minutes of ischaemia, mean (SEM) ERP lengthened from 232 (5) ms (control) to 246 (7) ms (p < 0.005) in group 1, and from 256 (10) ms (control) to 348 (25) ms (p < 0.005) in group 2. In the same time MAPD shortened from 256 (5) ms (control) to 189 (9) ms (p < 0.001) with no difference between groups. Thus postrepolarisation refractoriness developed during ischaemia. Before ischaemia, ERP showed a good correlation with APD (R(2) = 0.64) but by one minute of ischaemia the correlation was poor (R(2) = 0.29). CONCLUSIONS: These results show that during the first three minutes of global ischaemia in patients with coronary artery disease: (1) ERP lengthened in response to both a low and a high stimulus strength; and (2) there was a good correlation between ERP and APD before ischaemia, which was lost by one minute as APD decreased and ERP increased. These findings may have important implications in arrhythmogenesis.

Action Potentials↗
PubMed2000

Prevalence of cocaine use and its impact on asthma exacerbation in an urban population.

OBJECTIVES: To assess the prevalence of cocaine use, and its impact on severity of presentation, among adults presenting to the emergency department (ED) with asthma. A secondary aim was to assess the use of various asthma treatment modalities, with reference to the 1997 National Asthma Education and Prevention Program (NAEPP) guidelines. METHODS: All adults aged 18 to 55 years who presented to the ED of this institution with an asthma attack, were approached about participating in the study, which required giving informed consent, answering a facilitated questionnaire, and giving a urine sample for drug screening. RESULTS: Patients were enrolled during a 7-month period. A total of 163 patients were approached to enter the study; 116 patients consented to participate in the study, with 103 submitting complete urine samples. Thirty-seven patients refused to participate, and 10 were excluded. Sixty-eight percent of the patients were women, with a mean age of 33 years. African-Americans made up 89% of the total group. Thirty-five percent were cigarette smokers. Urine cocaine tests were positive in 13 of 103 (13%); 6 of 103 (5.8%) were positive for opiates. In the cocaine-positive group, 5 of 13 patients (38%) were admitted to the hospital, including two patients requiring intubation and mechanical ventilation. Of the total group, 23 of 103 patients (22%) were admitted, and 5 of those 23 admitted patients (22%) were cocaine-positive. Length of stay was significantly longer (5 vs 2.5 days, p < 0.05) in the cocaine-positive admitted patients. Forty-six percent of all patients reported using inhaled corticosteroids (ICS), with 39% of admitted patients using them. Thirty-two percent of all patients had obtained three or more refills of their beta(2)-agonist inhaler in the previous month. CONCLUSIONS: The prevalence of cocaine use may be much higher than the 13% shown in this study, because of patients' refusal to participate in the study. Second, the severity of exacerbation appears to be worse in the cocaine-positive group. Finally, the majority of patients presenting did not use ICS in accordance with the NAEPP guidelines.

Adolescent↗
PubMed1999

Cardiac mechano-electric feedback in man: clinical relevance.

Clinical conditions associated with sudden cardiac death due to arrhythmia are frequently accompanied by abnormalities of mechanical loading and wall stretch. These arrhythmias may result from several mechanisms including secondary depolarisations during or following the action potential or from a combination of conduction slowing and action potential shortening. Mechanical perturbations have been shown to reproduce these electrophysiological effects experimentally. However the effect of mechanical intervention is complex depending on the timing and intensity of the stimulus and the interplay between effects mediated via stretch activated channels and calcium cycling. Studies in patients during cardiac catheterisation or cardiac surgery using monophasic action potentials have shown alteration in the time course and shape of action potential repolarisation in response to changes in ventricular loading. Although stretch in experimental preparations has been shown to be arrhythmogenic, particularly in pathological conditions, the role of mechanically induced electrophysiological changes in important clinical ventricular arrhythmias remains to be established.

Animals↗
PubMed1999

Research fundamentals VI: misconduct in biomedical research.

The goal of medical research is the acquisition and application of new knowledge for the benefit of individual patients and society as a whole. Achieving this goal requires excellence in scientific methodology, honesty in data collection and interpretation, and realistic assessment of the implications of the findings. Underlying all steps in the acquisition of new knowledge is the absolute need for application of the highest ethical standards for research. Occasionally, ethical principles of research are breached because of lack of understanding or the carelessness of researchers. However, researchers have the obligation to know and apply basic principles of research ethics in order to avoid, prevent, or recognize deviations from ethical scientific behavior. When intentional violations of the principles of ethical research occur, the impact to the scientific and lay community can be profound. Misconduct can be prevented if the ethical principles of research are understood and consistently applied. This paper describes the sources and detection of misconduct in the production of science in order to provide emergency researchers with the knowledge needed to prevent misconduct from occurring at all.

Bias↗
PubMed1999

Utility of cardiac troponin I, creatine kinase-MB(mass), myosin light chain 1, and myoglobin in the early in-hospital triage of "high risk" patients with chest pain.

OBJECTIVE: To evaluate the use of cardiac troponin I (cTnI), creatine kinase-MB(mass) (CK-MB(mass)), myosin light chain 1 (MLC 1), and myoglobin in identifying "high risk" patients with chest pain who will experience serious cardiac events (SCEs) in hospital. DESIGN: Prospective study. SETTING: University affiliated medical centre in Philadelphia, USA. PATIENTS: 208 patients with chest pain, at > 7% risk of acute myocardial infarction (MI), but without new ST segment elevation on their presenting ECG. INTERVENTIONS: cTnI, CK-MB(mass), MLC 1, and myoglobin concentrations were obtained on admission (0 hour) and at 4, 8, 16, and 24 hours. MAIN OUTCOME MEASURES: The sensitivity, specificity, positive and negative predictive value, and pre- and post-test probabilities of patients suffering an SCE in hospital were determined. SCEs included cardiac death, acute MI, cardiac arrest, life threatening cardiac arrhythmia, cardiogenic shock, and urgent coronary revascularisation. RESULTS: Admission concentrations of all markers were poor predictors of SCEs in hospital but improved substantially at subsequent timepoints. cTnI and CK-MB(mass) were consistently the most useful prognostic indicators. If both were negative at 0, 4, and 8 hours, then 99% (95% confidence interval 96% to 100%) of patients remained free from SCEs. The only SCEs not thus predicted were revascularisation procedures and associated complications. Additional tests after 8 hours, or the inclusion of additional markers, did not improve predictive accuracy further. CONCLUSIONS: Patients with high risk clinical features on admission who have negative cTnI and CK-MB(mass) concentrations at 0, 4, and 8 hours later have a favourable in-hospital prognosis and could be considered for early triage out of coronary care units.

Biomarkers↗
PubMed1998

Plasticity of synapses in the rat neostriatum after unilateral lesion of the nigrostriatal dopaminergic pathway.

In the 6-hydroxydopamine model of Parkinson's disease in the rat, there is a significant reduction in the number of dendritic spines on the principal projection neurons in the neostriatum, presumably attributable to loss of the nigrostriatal dopamine input. These spines invariably receive input from terminals forming asymmetric synapses that originate mainly from the cortex. The object of the present study was to determine the fate of those terminals after the loss of dendritic spines. Unbiased estimates of synaptic density and absolute numbers of synapses in a defined volume of the neostriatum were made using the "disector" and Cavalieri techniques. Numerical synaptic density of asymmetric synaptic contacts was 17% lower in the neostriatum deprived of dopamine innervation and, in absolute terms, there were 3 billion (19%) fewer contacts. The numerical density of a subpopulation of asymmetric contacts on dendritic spines that have complex or perforated synaptic specializations and normally make up 9% of the asymmetric population was 44% higher on the experimental side. Asymmetric synapses were found to be enriched in glutamate using postembedding immunogold labeling. The present observations demonstrate that the loss of spines previously reported after 6-hydroxydopamine lesions is accompanied by a loss of asymmetric synapses rather than by the movement of synapses from spines to other postsynaptic targets. The study also demonstrates that there is an increase in complex synaptic interactions that have been implicated in synaptic plasticity in other regions of the CNS after experimental manipulations.

Animals↗
PubMed1997

The role of Na(+)-Ca2+ exchange current in electrical restitution in ferret ventricular cells.

1. The mechanisms underlying electrical restitution (recovery of action potential duration after a preceding beat) were investigated in ferret ventricular cells. The time to 80% recovery (t80) of action potential duration was approximately 204 ms. 2. At a holding potential of -80 mV, the Ca2+ current (ICa) reactivated and the delayed rectifier K+ current (IK) deactivated very rapidly (t80: approximately 32 and approximately 93 ms, respectively). The kinetics of both currents are too fast to account for electrical restitution alone. 3. The putative inward Na(+)-Ca2+ exchange current (INa-Ca) produced by the Na(+)-Ca2+ exchanger in response to the intracellular Ca2+ transient reprimed (t80: 189 ms) with the same time course as mechanical restitution (recovery of contraction) and with a similar time course to electrical restitution. 4. Substantial reduction of inward INa-Ca, by buffering intracellular Ca2+ with the acetyl methyl ester form of BAPTA, shortened the action potential and greatly altered the electrical restitution curve. Subsequent addition of nifedipine (to block ICa) or 4-aminopyridine (4-AP) (to block the transient outward current, ITO) further altered the electrical restitution curve. 5. Any time-dependent current that contributes to the action potential is likely to affect the time course of electrical restitution. Although ICa, IK and ITO were previously thought to be the only currents involved in electrical restitution, we conclude that inward INa-Ca also plays an important role.

4-Aminopyridine↗
PubMed1997

Acute ischaemia: a dynamic influence on QT dispersion.

BACKGROUND: The aim of this study was to test the hypothesis that acute myocardial ischaemia increases QT dispersion measured from the 12-lead electrocardiogram. METHODS: Incremental atrial pacing was used to induce myocardial ischaemia in 18 patients with coronary artery disease and QT dispersion was measured. Six patients with normal coronary arteries served as the control group. FINDINGS: All the patients with coronary artery disease developed angina and/or ST depression accompanied by marked increases in QT dispersion (mean increase 38 ms, 95% CI 30 to 45 ms, p < 0.001). In contrast, in the six patients with normal coronary arteries who remained without symptoms and without ST changes, there was no significant change in QT dispersion in response to pacing. Baseline QT dispersion did not distinguish those patients with coronary artery disease from those with normal coronary arteries (44 ms [95% Cl 39-49 ms] vs 40 ms [25-55 ms]), respectively. INTERPRETATION: These results demonstrate that myocardial ischaemia induced by incremental atrial pacing in patients with coronary artery disease causes an acute increase in QT dispersion. Such "inducible" QT dispersion may prove more useful than resting QT dispersion in assessing the individual risk of arrhythmic events in patients with coronary artery disease.

Arrhythmias, Cardiac↗
PubMed1996

Human ventricular action potential duration during short and long cycles. Rapid modulation by ischemia.

BACKGROUND: Mechanisms underlying the initiation of ventricular arrhythmias in ischemia by a premature beat or after a pause remain unclear. The kinetics of electrical restitution, which is the modulation of action potential duration (APD) by an abrupt alteration in cycle length, may be important. METHODS AND RESULTS: We recorded one or two simultaneous monophasic action potentials (MAPs) from the right ventricular septum during balloon occlusion of the left anterior descending coronary artery (LAD) (14 patients), which is expected to induce ischemia at the recording site, and during occlusion of the right coronary artery (RCA) (7 patients), which is not expected to induce ischemia at the recording area. The latter acted as a control. A test pulse sequence was incorporated whereby during steady-state pacing, test beats of altered cycle length were interpose. During LAD occlusion, APD for basic beats shortened from 260 +/- 4 to 236 +/- 4 ms (P < .0001), whereas the control group (RCA occlusion) showed no significant change (251 +/- 7 to 249 +/- 9 ms; P = NS). LAD occlusion resulted in flattening of the slope relating APD of test beats to diastolic interval (P = .001), whereas in the control group (RCA occlusion) the slope remained unchanged. Similar results were obtained during a second occlusion. CONCLUSIONS: LAD occlusion in patients during balloon angioplasty shortened MAP duration of basic beats and minimized, abolished, or reversed the normal APD/diastolic-interval relation of test beats of altered cycle length at sites served by the occluded vessel. The results suggest that ischemia flattens the electrical restitution curve in the human endocardium. These findings may have important implications in arrhythmogenesis.

Action Potentials↗