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Biomedical subjects

U Wiegand

Publications and source records attributed to U Wiegand.

At least 19 recordsLinked to original sources
PubMed2003

Plasma catecholamines and N-terminal proBNP in patients with acute myocardial infarction undergoing primary angioplasty. Relation to left ventricular function and clinical outcome.

BACKGROUND: Neither profiles nor prognostic values of neurohormonal markers have been prospectively evaluated in patients with acute myocardial infarction (AMI) undergoing primary angioplasty. METHODS AND RESULTS: In 118 consecutive patients with AMI undergoing successful reperfusion (TIMI 2 and 3) by primary angioplasty, plasma concentrations of norepinephrine, epinephrine and N-terminal proBNP (NT-proBNP) were measured before, 60 min and 10 days after angioplasty. Catecholamine concentrations (mean+/-SEM) rose to a maximum in the first hour after angioplasty (norepinephrine: 602+/-44 ng/L, epinephrine: 213+/-24 ng/L) and returned to normal at day 10. Conversely, NT-proBNP levels maintained a further increase from 799+/-44 pmol/L at baseline to 924+/-54 pmol/L at day 10. A NT-proBNP concentration above median at 60 min post-angioplasty predicted major adverse cardiac events (n=27) during the 18-36 month follow-up with an odds ratio of 5.9 (1.7-20.3) and was superior to catecholamines, to left ventricular ejection fraction and to other established postinfarction risk markers. CONCLUSIONS: In a low-risk cohort of patients with AMI undergoing successful reperfusion therapy, plasma NT-proBNP concentrations are elevated for at least ten days. The prognostic value of early plasma NT-proBNP should be further evaluated concerning its ability to facilitate risk stratification of infarct patients.

Aged↗
PubMed2001

Admission troponin T level predicts clinical outcomes, TIMI flow, and myocardial tissue perfusion after primary percutaneous intervention for acute ST-segment elevation myocardial infarction.

BACKGROUND: In ST-segment elevation myocardial infarction, a troponin T >/=0.1 microg/L on admission indicates poorer prognosis despite early reperfusion. To evaluate the underlying reason, we studied the value of cardiac troponin T (cTnT) for prediction of outcomes, epicardial blood flow, and myocardial reperfusion after primary percutaneous intervention. METHODS AND RESULTS: Patients (n=140) admitted within 12 hours after onset of symptoms were stratified by admission cTnT. Epicardial and myocardial reperfusion were graded by the TIMI score and by measurement of relative increases of myoglobin, cTnT, and creatine kinase (CK)-MB 60 minutes after recanalization, respectively. cTnT was positive in 64 patients (45.7%) and was associated with longer median time intervals to admission (5.5 versus 3.5 hours, P<0.001) and higher mortality rates after 30 days (12.5% versus 3.9%, P=0.06) and 9 months (14% versus 3.9%, P=0.005). cTnT independently predicted a 3.2-fold risk for incomplete epicardial reperfusion (P=0.03). In addition, cTnT >/=0.1 microg/L was associated with more severely impaired myocardial perfusion despite normal epicardial flow, as indicated by lower 60-minute ratios of myoglobin (2.6 versus 7.6, P=0.007), cTnT (6.6 versus 29.2, P<0.001), and CK-MB (3.5 versus 21.4, P=0.002) and a tendency for less resolution of ST-segment elevations (54% versus 60%, P=0.08). CONCLUSIONS: cTnT predicts poorer clinical outcomes, lower rates of postprocedural TIMI 3 flow, and more severely compromised myocardial perfusion despite normal epicardial flow. Thus, a cTnT-positive patient may require more aggressive adjunctive therapy when treated by percutaneous coronary intervention. The impact of preexisting or evolving microvascular dysfunction and the effect of therapies that target myocardial perfusion require further prospective evaluation.

Aged↗
PubMed2001

Troponin T elevation after successful directional atherectomy.

BACKGROUND: The incidence and correlates of postinterventional cardiac troponin T (cTnT) elevation have not been evaluated in patients with successful directional atherectomy (DCA). METHODS: Total creatine kinase (CK) activity, CK-MB mass concentrations and cTnT levels were measured in 36 patients before, and serially 4, 24, 48 and 72 hours after successful DCA. Patients were followed for death, Q-wave infarction, need for emergency bypass surgery, periprocedural vascular complications (transient in-lab vessel closure, side branch compromise, large dissection), and non-Q-wave infarction on ECG. Patients were followed for clinical outcomes and angiographic restenosis for 6 months. Vascular correlates were studied by coronary angiography and intravascular ultrasound before, immediately after and 4 hours after elective and successful DCA. RESULTS: 25 patients (69.4%) had elevated levels of cTnT, whereas CK-MB mass > or = 6 ng/ml and mild elevations of total CK activity were present in only 36.1 and 5.6%, respectively. Elevated cTnT was related to vascular complications in 44% of cases. Inapparent microembolization of platelets or plaque debris was considered responsible for most of the remaining micronecroses. During 6 month follow-up rates of clinical restenosis (44 vs 9%, p = 0.059) tended to be higher in patients with as compared to patients without cTnT release after DCA. CONCLUSION: Successful DCA is associated with postprocedural elevations of cTnT which relate to minor vascular complications and presumably microembolization of platelets or plaque debris. The superior diagnostic performance of cTnT compared to CK-MB mass may relate to more sensitive identification of microinfarction. Further studies are mandatory to confirm the association between elevation of cTnT and risk of restenosis and TVR.

Atherectomy, Coronary↗
PubMed2001

Angiographic correlates of a positive troponin T test in patients with unstable angina.

OBJECTIVE: To study the angiographic correlates of cardiac troponin T (cTnT)-positive and -negative patients with unstable angina pectoris. BACKGROUND: A positive cTnT test identifies a high-risk subgroup of unstable angina pectoris patients. Only the high-risk cTnT-positive patients seem to benefit from a more aggressive antithrombotic treatment regimen. The underlying coronary pathology in cTnT-positive and -negative patients that explains the predictive power of cTnT on prognosis and response to antithrombotic therapy is largely unknown. METHODS: A total of 197 subsequently admitted patients with unstable angina pectoris underwent cTnT testing by a rapid bedside assay and early qualitative and quantitative angiography. Long-term follow-up was 12 months. RESULTS: Patients with cTnT-positive tests revealed more critical stenoses of culprit lesions (p =.041), more severe reductions of thrombolysis in myocardial infarction flow grades (p <.037), a higher prevalence of intracoronary thrombus (p =.079), and a poorer left ventricular function (p =.047). The odds ratio of cTnT was 5.8 (p <.0001) for presence of thrombus, reduced thrombolysis in myocardial infarction flow, and/or critical stenosis (>90%), and was 3.1 (p =.005) for presence of three-vessel disease, left main disease, and/or reduced left ventricular ejection fraction. Coronary bypass grafting was more frequently performed in the cTnT-positive group. However, event-free survival was not different in our cohort characterized by a high rate of percutaneous coronary interventions. CONCLUSIONS: A positive cTnT test in patients with unstable angina pectoris indicates presence of more severe coronary artery disease and poorer left ventricular function. This finding could explain the differences in short- and long-term outcome and treatment responses to antithrombotic regimens.

Aged↗
PubMed2000

Independent prognostic value of cardiac troponin T in patients with confirmed pulmonary embolism.

BACKGROUND: Cardiac troponin T (cTnT) is a sensitive and specific marker, allowing the detection of even minor myocardial cell injury. In patients with severe pulmonary embolism (PE), myocardial ischemia may lead to progressive right ventricular dysfunction. It was therefore the purpose of this study to test the presence of cTnT and its prognostic implications in patients with confirmed PE. METHODS AND RESULTS: Fifty-six consecutive patients with confirmed PE were enrolled in this prospective study. PE was confirmed by pulmonary angiography, lung scan, or echocardiography and subsidiary analyses. Severity of PE was assessed by a clinical scoring system, and cTnT was measured within 12 hours after admission. cTnT was elevated (>/=0.1 microg/L) in 18 (32%) patients with massive and moderate PE but not in patients with small PE. In-hospital death (odds ratio 29. 6, 95% CI 3.3 to 265.3), prolonged hypotension and cardiogenic shock (odds ratio 11.4, 95% CI 2.1 to 63.4), and need for resuscitation (odds ratio 18.0, 95% CI 2.6 to 124.3) were more prevalent in patients with elevated cTnT. cTnT-positive patients more often needed inotropic support (odds ratio 37.6, 95% CI 5.8 to 245.6) and mechanical ventilation (odds ratio 78.8, 95% CI 9.5 to 653.2). After adjustment, cTnT remained an independent predictor of 30-day mortality (odds ratio 15.2, 95% CI 1.22 to 190.4). CONCLUSIONS: cTnT may improve risk stratification in patients with PE and may aid in the identification of patients in whom a more aggressive therapy may be warranted.

Aged↗
PubMed2000

Clinical and angiographic outcome of patients with acute inferior myocardial infarction.

OBJECTIVES: This study sought to determine the procedural success and the in-hospital outcome after primary coronary angioplasty in patients with acute inferior myocardial infarction and right ventricular involvement (RVI). BACKGROUND: RVI represents an easily detectable, highly prevalent subset of acute inferior infarction associated with poor outcome even in the era of thrombolysis. Primary PTCA may offer advantages in patients with inferior infarction involving the right ventricle. METHODS: Primary coronary angioplasty with optimal stenting was performed in 87 of 88 consecutive patients presenting within 24 hours after onset of acute inferior myocardial infarction. On the basis of right precordial ST segment elevations at admission, patients were classified into those without (n=61) and those with RVI (n=27). The patients were followed prospectively for angiographic success at 10 days and for in-hospital clinical outcome. RESULTS: Baseline characteristics including age, severity of coronary artery disease, proportion of stent implantation, and occurrence of cardiogenic shock were comparable. Patients with RVI had larger infarct sizes (lactate dehydrogenase level: 962 vs 580 U/l, P=0.03), developed more often complete atrioventricular block (18.5 vs. 2%, p=0.0038), needed more often parasympatholytics (48.1 vs 18.8%, p<0.001), and had a substantially higher incidence of the Bezold-Jarisch reflex (29.6 vs 6.6%, p<0.01) following reperfusion. Success of recanalization therapy acutely and at 10 days, as well as in hospital mortality were similar in patients with and without RVI (88.5 vs. 85.2%, 79.3 vs. 84.7%, 7.4 vs 9.8%). However, patients with RVI revealed a greater lumen gain acutely after PTCA (2.49 vs. 2.13 mm, p=0.025) and experienced less frequently major cardiac events (14.8 vs. 36.1%, p=0.04) which included reinfarction, re-ischemia, coronary bypass grafting, stent thrombosis, and cardiac death. In addition, procedural success was established more rapidly (fluoroscopy time: 10 vs 15 min., p=0.032) and with less contrast material (242 vs 295 ml, p=0.015) in patients with RVI. This is probably due to the more proximal location (84.6 vs 6.6%, p<0.0001) and the larger reference diameter (3.17 vs. 2.79 mm, p=0.03) of the occluded right coronary artery. CONCLUSIONS: Primary PTCA is an appropriate reperfusion strategy in patients with RVI. Further comparative studies are required to compare the effectiveness of primary PTCA with early thrombolytic therapy in this high risk setting.

Aged↗
PubMed2000

Soluble L-selectin and neutrophil derived oxidative stress after pacing induced myocardial ischemia in chronic stable coronary artery disease.

We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L-selectin (sL-selectin) and generation of neutrophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and stable angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lactate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL-selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL-selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 +/- 80 vs 836 +/- 82 ng/mL, P = 0.03). At peak pacing, nine of ten patients with CAD developed myocardial ischemia (lactate extraction ratio at rest 28% +/- 7%, at peak pacing -16% +/- 6%). In these patients, luminol-enhanced chemiluminescence (CL, 0.88 +/- 0.45 vs 1.9 +/- 0.9 cpm x 10(5), P = 0.09) and levels of sL-selectin (547 +/- 80 vs 764 +/- 86 ng/mL, P = 0.03) from naive neutrophils increased significantly in CS blood suggesting a potent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL-selectin levels. In conclusion, myocardial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic stable coronary artery disease leading to increased generation of ROS and shedding of L-selectin into the coronary circulation.

Adult↗
PubMed2000

Relationship of cardiac troponin T and procoagulant activity in unstable angina.

OBJECTIVE: The present study sought to determine the incidence of increased procoagulant activity in patients with unstable angina (UAP), and to evaluate the relationship between cardiac troponin T (cTnT) and molecular markers of hemostatic activation. Method. We studied 44 patients with UAP further classified by plasma cTnT levels. All patients received an antithrombotic therapy consisting of therapeutic doses of unfractionated heparin and acetylsalicylic acid. Quantitative levels of cTnT and plasma concentrations of fibrin monomers (FM), prothrombin fragments F1+2, thrombin antithrombin III complexes (TAT), plasminogen and alpha2-antiplasmin were sampled serially within the first 48 h. RESULTS: Increased plasma concentrations of FM were detected in 45.5% of patients and were more frequently present among those with cTnT concentrations > or =0.1 ng/ml (13 of 18 vs 7 of 26 patients, p = 0.003). In these patients, mean plasma concentrations of FM were significantly higher than in patients with cTnT <0.1 ng/ml (7.93 +/- 2.3 vs 3.12 +/- 0.6 microg/ml, p = 0.02). There was a close relationship between plasma levels of cTnT and FM (r = 0.74, p <0.004), prothrombin fragments F1+2 (r = 0.71, p = 0.046) and a trend to significance was noted for TAT (r = 0.42, p = 0.055). No significant correlation was observed with markers of the fibrinolytic system (plasminogen and alpha2-anti-plasmin). Plasma levels of cTnT > or =0.1 ng/ml identified a concomitant increase of hemostatic markers with a sensitivity, specificity and positive predictive value of 65, 79, and 72% for FM, 63, 76, and 67% for prothrombin fragments F1+2, and 58, 66, and 39% for TAT, respectively. CONCLUSIONS: In patients with UAP, cTnT identifies patients with increased procoagulant activity and is closely related to plasma levels of molecular markers of hemostatic activation. Therefore, cTnT alone or in combination with one of these markers may be helpful to identify patients requiring more potent antithrombin or antiplatelet therapy.

Aged↗
PubMed1999

Prothrombin fragments F1+2, thrombin-antithrombin III complexes, fibrin monomers and fibrinogen in patients with coronary atherosclerosis.

We determined the plasma levels of prothrombin fragment F1+2, thrombin-antithrombin III complexes (TAT), fibrin monomers (FM), D-dimers (DD) and fibrinogen in 57 patients with angiographically verified graded coronary artery disease (CAD) free of concomitant peripheral atherosclerosis, cerebrovascular disease or diabetes mellitus and a group of 21 apparently healthy controls. Blood was collected from the antecubital vein through atraumatic venipuncture prior to the angiographic procedure. Plasma levels of hemostatic markers were related to the presence and graded severity of CAD. The levels of prothrombin fragment F1+2 (1.74+/-0.11 vs. 1.0+/-0.07 nmol/l, P<0.001), FM (41.6+/-5.5 vs. 7.42+/-3.05 nmol/l, P<0.001), TAT (15.6+/-2.7 vs. 2.96+/-0.32 microg/l, P<0.001) and fibrinogen (3.64+/-1.3 vs. 3.08+/-0.33 g/l, P<0.01) were significantly higher in patients with CAD compared to controls, while there was no difference regarding the fibrinolytic system represented by DD (441.6+/-58.9 vs. 337.4+/-42.05 microg/l, n.s.). Within the CAD group, patients with extensive coronary atherosclerosis (> or =2 vessel disease) had significantly higher values for prothrombin fragment F1+2 (1.89 vs. 1.57 nmol/l, P = 0.04), FM (50.7 vs. 29.8 nmol/l, P = 0.03), and a trend to significance was noted for fibrinogen (3.9 vs. 3.3 g/l, P = 0.07) suggesting that blood coagulability was related to the severity of the disease and that hemostatic markers of thrombin activity represent a useful tool to identify patients with a latent hypercoagulable state with a higher susceptibility to sustain coronary thrombosis.

Antithrombin III↗
PubMed1999

Inhibition of ventricular stimulation in patients with dual chamber pacemakers and prolonged AV conduction.

Episodes of repetitive P wave undersensing have been described in dual chamber pacemakers due to automatic extension of the postventricular atrial refractory period (PVARP). Pacemaker stimulation was completely inhibited despite the presence of adequate P waves. This study sought to determine whether cycles of repetitive P wave undersensing occur even in the absence of PVARP extension. Two-hundred fifty-five patients were investigated after DDD or VDD pacemaker implantation for intermittent atrioventricular (AV) block. Forty-six episodes of repetitive atrial undersensing were found during 24-hour Holter ECG in nine patients. Pacemaker syndrome-like symptoms occurred. Episodes were elicited by atrial or ventricular premature contractions when (1) native AV conduction was present but considerably prolonged, (2) intrinsic sinus rate exceeded pacemaker intervention rate, and (3) native AV interval plus PVARP exceeded sinus cycle length. Programming of a particularly short AV interval and PVARP helped to reduce the incidence of repetitive P wave undersensing. Patients with dual chamber devices and prolonged native AV conduction are prone to develop episodes of output inhibition. Standard timing cycles may be inappropriate in these patients.

Atrioventricular Node↗
PubMed1998

An optimized AV delay algorithm for patients with intermittent atrioventricular conduction.

Detection and promotion of an intermittent atrioventricular (AV) conduction is the objective of an AV delay hysteresis algorithm in dual chamber pacemaker (DDD) pacing. The AV delay following an atrial event is automatically extended by a programmable interval (AV hysteresis interval) if the previous cycle showed spontaneous AV conduction, i.e., a ventricular event was detected within the previous AV delay. An automatic search mode scans for spontaneous ventricular events during the hysteresis interval: a single AV delay extension (equal to the programmed AV delay hysteresis) will occur after a successive, programmable number of AV cycles with ventricular pacing. If a spontaneous AV conduction is present, the AV delay will remain extended by the hysteresis interval. Our first results in 17 patients with intermittent AV block disclosed a satisfactorily working algorithm with effective reduction of ventricular stimuli. In relation to the underlying conduction disturbance and pacemaker settings, the majority of our patients showed a reduction of ventricular pacing events up to 90% without any adverse hemodynamic or electrophysiological changes. Based on clinical (promotion of a physiological activation and contraction sequence) and technical (reduction of power consumption) advantages, the AV hysteresis principle could be of incremental value for future dual chamber pacing in patients with intermittent complete heart block.

Aged↗
PubMed1998

Neutrophil-derived oxidative stress after myocardial ischemia induced by incremental atrial pacing.

We studied the effect of atrial pacing-induced myocardial ischemia on the generation of oxygen free radicals (OFR) in 8 patients with verified coronary artery disease (CAD) and in a control group of 4 patients without coronary atherosclerosis. Myocardial ischemia was measured metabolically by simultaneous lactate sampling from coronary sinus (CS) and arterial blood. Generation of OFR from purified viable polymorphonuclear neutrophils (PMN) was assessed by means of the chemiluminescence (CL) method. At peak pacing, 7 of 8 patients with CAD exhibited transient myocardial ischemia (mean lactate extraction ratio at rest: 23.6 +/- 7.7 vs 5.21 +/- 5.1% at peak pacing, p = 0.012). In these patients, unstimulated PMN harvested from the CS depicted a significant increase of luminol-enhanced CL (from 1.06 +/- 0.54 to 2.15 +/- 1.28 cpm x 10(5), p = 0.012) after atrial pacing. There was no additional effect from further ex vivo stimulation with phorbol myristate acetate. This finding underscores the role of myocardial ischemia as a potent endogenous activator of PMN function and may have implications in the pathogenesis and progression of atherosclerosis.

Cardiac Pacing, Artificial↗
PubMed1998

Differential effects of defibrillation on systemic and cardiac sympathetic activity.

OBJECTIVE: To assess the effect of defibrillation shocks on cardiac and circulating catecholamines. DESIGN: Prospective examination of myocardial catecholamine balance during dc shock by simultaneous determination of arterial and coronary sinus plasma concentrations. Internal countershocks (10-34 J) were applied in 30 patients after initiation of ventricular fibrillation for a routine implantable cardioverter defibrillator test. Another 10 patients were externally cardioverted (50-360 J) for atrial fibrillation. MAIN OUTCOME MEASURES: Transcardiac noradrenaline, adrenaline, and lactate gradients immediately after the shock. RESULTS: After internal shock, arterial noradrenaline increased from a mean (SD) of 263 (128) pg/ml at baseline to 370 (148) pg/ml (p = 0.001), while coronary sinus noradrenaline fell from 448 (292) to 363 (216) pg/ml (p = 0.01), reflecting a shift from cardiac net release to net uptake. After external shock delivery, there was a similar increase in arterial noradrenaline, from 260 (112) to 459 (200) pg/ml (p = 0.03), while coronary sinus noradrenaline remained unchanged. Systemic adrenaline increased 11-fold after external shock (p = 0.01), outlasting the threefold rise following internal shock (p = 0.001). In both groups, a negative transmyocardial adrenaline gradient at baseline decreased further, indicating enhanced myocardial uptake. Cardiac lactate production occurred after ventricular fibrillation and internal shock, but not after external cardioversion, so the neurohumoral changes resulted from the defibrillation process and not from alterations in oxidative metabolism. CONCLUSIONS: A dc shock induces marked systemic sympathoadrenal and sympathoneuronal activation, but attenuates cardiac sympathetic activity. This might promote the transient myocardial depression observed after electrical discharge to the heart.

Adult↗
PubMed1998

Cardiomyopathic lentiginosis/LEOPARD syndrome presenting as sudden cardiac arrest.

A 26-year-old apparently healthy man with numerous pigmented skin lesions collapsed during an evening party and was resuscitated from ventricular fibrillation. Hypertrophic cardiomyopathy and subaortic tunnel were disclosed by angiocardiography. A diagnosis of cardiomyopathic lentiginosis/lentigines (multiple), electrocardiographic abnormalities, ocular hypertelorism, pulmonary stenosis, abnormalities of the genitalia, retardation of growth, and deafness (sensorineural) syndrome was made. The patient then underwent treatment with an implantable pacer-cardioverter-defibrillator device. Further evaluation revealed several well-established features of the disorder. This is the first reported case of survival from ventricular fibrillation associated with this rare and little known multifaceted syndrome. Disseminated lentiginosis must prompt clinicians to evaluate such cases further since underlying disorders may be associated with considerable morbidity and, apparently, sudden death.

Abnormalities, Multiple↗
PubMed1997

Priming of neutrophils after elective percutaneous transluminal coronary angioplasty is unrelated to accompanying brief myocardial ischemia.

OBJECTIVE: The purpose of this study was to investigate the effect of brief myocardial ischemia and vascular trauma induced by elective percutaneous transluminal coronary angioplasty on in vivo 'priming' and activation of neutrophils. PATIENTS AND METHODS: We studied 16 patients undergoing elective coronary angioplasty for symptomatic coronary artery disease and a control group of seven patients undergoing diagnostic cardiac catheterization. Free radical production from purified neutrophils (Ficoll-Hypaque density gradient method) was measured indirectly by the chemiluminescence method. Myocardial ischemia during balloon inflation was assessed by serial lactate determinations from coronary sinus and arterial blood. The degree of transient angioplasty-related myocardial ischemia was related to the oxidative response of activated neutrophils. RESULTS: Mean (+/-S.E.M.) oxidative response, i.e. the lucigenin- and luminol-enhanced-chemiluminescence (counts per minute) of neutrophils sampled from the coronary sinus increased significantly after percutaneous transluminal coronary angioplasty (Lucigenin-chemiluminescence: pre-angioplasty 3.69+/-0.64x10(5) vs. post-angioplasty 7.08+/-1.2x10(5), P<0.01; Luminol-chemiluminescence: pre-angioplasty 2.81+/-0.67x10(6) vs. post-angioplasty 5.2+/-0.92x10(6), P<0.01). Twelve of 16 patients developed transient cardiac lactate production (mean coronary sinus lactate excess: +0.12 mmol/l) and three disclosed a lactate extraction ratio <10%, both suggestive of myocardial ischemia. However, there was no correlation between the cardiac lactate production and the increased oxidative response after coronary angioplasty (r2 (Lucigenin-chemiluminescence)=0.02, n.s.; r2 (Luminol-chemiluminescence)=0.06, n.s.). CONCLUSION: 'Priming' of neutrophils, as reflected by increased oxidative response, is likely to occur after coronary angioplasty, but not after the angiographic procedure itself. However, 'priming' seems to be unrelated to the transient brief period of myocardial ischemia and rather depends on an alternative mechanism.

Adult↗