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T Meinertz

Publications and source records attributed to T Meinertz.

At least 91 records · Page 5Linked to original sources
PubMed2000

Induction of atrial fibrillation with rapid high voltage ventricular pacing for ventricular fibrillation conversion testing. The Ventak AV II DR Study.

OBJECTIVE: To assess whether rapid high voltage ventricular pacing can also induce atrial fibrillation, and whether the induction of atrial fibrillation during ventricular fibrillation conversion testing is related to the patient's heart disease. DESIGN: Prospective study of 50 patients who received the dual chamber implantable cardioverter-defibrillator (ICD) Ventak AV II DR (Guidant) as a first implant. This device can record atrial activity even during a ventricular fibrillation episode and can induce atrial fibrillation by rapid atrial bursts. MAIN OUTCOME MEASURES: Frequency of atrial fibrillation after induction of ventricular fibrillation; clinical characteristics of patients with and without induced atrial fibrillation; frequency of atrial fibrillation induced by rapid atrial bursts during predischarge testing. RESULTS: Atrial fibrillation was observed in 40 of the 217 ventricular fibrillation episodes (18%) that could be detected immediately after delivery of high voltage pacing. The biphasic ICD shock for termination of ventricular fibrillation also terminated the atrial fibrillation in all cases. The 40 episodes of simultaneous atrial and ventricular fibrillation occurred in 18 patients (36%). The distribution of the clinical characteristics of the patients and the inducibility of atrial fibrillation during predischarge testing were similar in those with and without induced atrial fibrillation. CONCLUSIONS: Rapid high voltage ventricular pacing frequently induces atrial fibrillation, which was terminated by the subsequent biphasic ICD shock. The induction of atrial fibrillation seems to be a non-specific phenomenon, unrelated to the clinical status of the patient.

Adult↗
PubMed2000

Acute effects of a class IA antiarrhythmic drug on the ventricular evoked response amplitude in patients with cardiac pacemakers.

Some newer cardiac pacemakers are able to control the efficacy of the ventricular pacing pulse beat by beat and to adjust the ventricular output to the actual pacing threshold. This capture verification is based on the detection of the ventricular evoked response amplitude, which has to be detected immediately after the pacing pulse. The sensitivity of the pacemaker to detect the evoked response amplitude must be adjusted individually to avoid the simultaneous detection of lead polarization. The aim of the present study was to evaluate the acute effects of a class IA antiarrhythmic drug on the evoked response amplitude and polarization in 13 pacemaker patients. The implanted pacemaker was the VVIR pacemaker Regency (St. Jude Medical), which provides the automatic capture verification algorithm Autocapture. The patients received 50 mg of ajmaline intravenously within 1 min. The evoked response amplitude and polarization were measured before and 2, 4, 6 and 8 min after ajmaline injection. The evoked response amplitude significantly decreased from 8.0 +/- 4.0 mV to a minimum value of 6.4 +/- 3.1 mV 2 min after drug administration. The decrease remained significant from the end of the application up to 6 min. The recommended sensitivity setting for the evoked response significantly (p < 0.05) decreased from 4.0 +/- 2.3 mV before to 3.1 +/- 1.3 mV 2 min after administration. No significant changes were observed for polarization. After the ajmaline application in 2 patients, the pacemaker recommended the deactivation of Autocapture for 9 min in 1 patient and 12 min in the other. The reasons were a decrease in the evoked response amplitude from 3.1 to 1.9 mV and from 9.0 to 5.7 mV, respectively, with a polarization ranging to about 3.0 mV. In conclusion, the ajmaline injection decreased the evoked response amplitude for some minutes. These findings indicate that antiarrhythmic drugs can alter the automatic capture verification function.

Aged↗
PubMed2000

[Endocardial mapping and high frequency catheter ablation of ventricular tachycardia after myocardial infarction].

Recurrent ventricular tachycardia in the setting of remote myocardial infarction are frequently resistant to antiarrhythmic drug treatment. Endocardial mapping and ablation is feasible in case of hemodynamically tolerable and reproducibly inducible forms. Identification of critical components of the reentrant circuit is mainly guided by entrainment mapping and the analysis of the post-pacing interval. The emergence of multiple types of ventricular tachycardia is a common limitation of the procedure. Ventricular tachycardia can be acutely abolished by radiofrequency current ablation in 60-70% of cases when only single forms are present. This success rate is substantially lower in case of multiple tachycardia morphologies. The incidence of tachycardia recurrences varies from 20-30%. The overall mortality during follow-up is increased due to progressive heart failure and the occurrence of rapid ventricular tachyarrhythmias. Catheter ablation has been shown to be a useful tool for the treatment of clusters of ventricular tachycardia following implantation of a cardioverter-defibrillator. Furthermore, this method can be life-saving in the setting of incessant forms. Currently, catheter ablation represents an adjunctive treatment to antiarrhythmic drugs and the implantation of a cardioverter-defibrillator. Improvement of mapping and ablation technologies may help to further increase the efficacy of this treatment strategy in the near future.

Catheter Ablation↗
PubMed1999

[Elective percutaneous tracheotomy in long-term ventilation in a coronary intensive care unit].

BACKGROUND AND OBJECTIVE: Long-term mechanical ventilation presents a problem in an intensive care unit (ICU). If done via oral intubation it brings the danger of bacterial contamination and the development of pressure lesions of the gums and tongue. Furthermore, the tube is usually tolerated for only a short time during the weaning phase. Nasal intubation is associated with an increased incidence of nasal necroses and sinusitis. Tracheal intubation has the advantage that the dead space is reduced, it is more comfortable for the patient and the weaning period is shortened, thus decreasing the duration of bed confinement. Percutaneous tracheostomy (PT) was introduced as an alternative to conventional surgical tracheostomy. It was the aim of this study to present the authors' experience with PT. PATIENTS AND METHODS: PT was performed under bronchoscopic control with the aid of dilators or dilatating forceps in 78 patients in a cardiological ICU (13 women, 68 men; average age 64 +/- 14 years) with heart failure (n = 34 [44%]), cerebral problems post-resuscitation (n = 32)[41%]), pulmonary infection (9[11%]) or other conditions (n = 3[4%]). RESULTS: Because of contraindications PT was not done in 12 patients (15%). Percutaneous emphysema developed in one woman as a result of injury to tracheal cartilage. There were no other complications. Two patients with thrombocytopenia were given platelet concentrates during the PT. At the end of the period of ventilation the tracheostomy tube was removed. Spontaneous closure of the stoma occurred within 3 to 5 days. CONCLUSIONS: PT is a minimally invasive alternative to surgical tracheostomy. It has few complications and can be performed in a cardiological ICU.

Aged↗
PubMed1999

Role for NADPH/NADH oxidase in the modulation of vascular tone.

The endothelium modulates vascular tone by producing vasodilator and vasconstrictor substances. Of these, the best characterized and potentially most important are nitric oxide (NO.) and O2-.. These small molecules exhibit opposing effects on vascular tone and chemically react with each other in a fashion that negates their individual effects and leads to the production of potentially toxic substances, such as peroxynitrite (ONOO-). These dynamic interactions may likely have important implications, altering not only tissue perfusion but also contributing to the process of atherosclerosis. The precise O2-. source within vascular tissue remains to be determined. Recent work demonstrated that in endothelial cells as well as in vascular smooth muscle cells, a membrane-associated NAD(P)H-dependent oxidase represents the most significant O2-. source. Interestingly, this oxidase is activated upon stimulation with angiotension II, suggesting that under all conditions of an activated circulating and/or local renin-angiotensin system endothelial dysfunction secondary to increased vascular O2-. production is expected.

Angiotensin II↗
PubMed1999

Increased NADH-oxidase-mediated superoxide production in the early stages of atherosclerosis: evidence for involvement of the renin-angiotensin system.

BACKGROUND: Angiotensin II activates NAD(P)H-dependent oxidases via AT1-receptor stimulation, the most important vascular source of superoxide (O2*-). The AT1 receptor is upregulated in vitro by low-density lipoprotein. The present study was designed to test whether hypercholesterolemia is associated with increased NAD(P)H-dependent vascular O2*- production and whether AT1-receptor blockade may inhibit this oxidase and in parallel improve endothelial dysfunction. METHODS AND RESULTS: Vascular responses were determined by isometric tension studies, and relative rates of vascular O2*- production were determined by use of chemiluminescence with lucigenin, a cypridina luciferin analogue, and electron spin resonance studies. AT1-receptor mRNA was quantified by Northern analysis, and AT1-receptor density was measured by radioligand binding assays. Hypercholesterolemia was associated with impaired endothelium-dependent vasodilation and increased O2*- production in intact vessels. In vessel homogenates, we found a significant activation of NADH-driven O2*- production in both models of hyperlipidemia. Treatment of cholesterol-fed animals with the AT1-receptor antagonist Bay 10-6734 improved endothelial dysfunction, normalized vascular O2*- and NADH-oxidase activity, decreased macrophage infiltration, and reduced early plaque formation. In the setting of hypercholesterolemia, the aortic AT1 receptor mRNA was upregulated to 166+/-11%, accompanied by a comparable increase in AT1-receptor density. CONCLUSIONS: Hypercholesterolemia is associated with AT1-receptor upregulation, endothelial dysfunction, and increased NADH-dependent vascular O2*- production. The improvement of endothelial dysfunction, inhibition of the oxidase, and reduction of early plaque formation by an AT1-receptor antagonist suggests a crucial role of angiotensin II-mediated O2*- production in the early stage of atherosclerosis.

Acetylcholine↗
PubMed1999

Influence of stent length and heparin coating on platelet activation: a flow cytometric analysis in a pulsed floating model.

Platelets are involved in acute and subacute thrombotic occlusions of coronary stents and also may play a role in the pathophysiology of in-stent restenosis. This study sought to investigate the expression of activation dependent glycoproteins on platelets by flow cytometry and time until stent thrombosis in an in vitro model of stent thrombosis. Coronary stents were placed in parallel silicon tubings with circulating citrated platelet rich plasma to measure 1) influence of stent length on platelet antigens; 2) influence of heparin coating on platelet antigens; and 3) time until stent thrombosis. After recalcification aliquots of platelet-rich plasma were taken over 10 minutes in 2-minute intervals and immediately fixed and stabilized. For flow cytometric analysis monoclonal antibodies to CD41a (glycoprotein IIb/ IIIa), CD42b (glycoprotein Ib-V-IX), CD62p (P-selectin), and CD63 (glycoprotein 53) were used. Within 2 minutes after start of circulation, the expression of CD62p and CD63 increased. Longer stents resulted in more platelet activation than shorter stents (25 mm vs. 15 mm; p<0.001. Time until stent thrombosis was reduced (25 mm vs. 15 mm; p<0.05). Heparin coating did not significantly influence flow cytometry detectable platelet activation but prolonged time until stent thrombosis (coated vs. uncoated; p<0.005). In control tubing systems without stents platelet activation was less pronounced (p<0.0001). Antibodies to CD41a and CD42b did not show significant changes. In this model platelet activation detected by flow cytometry and time until stent thrombosis were dependent on stent length and coating. In vitro testing could be useful to optimize stent design and material.

Adult↗
PubMed1999

Validation of lucigenin as a chemiluminescent probe to monitor vascular superoxide as well as basal vascular nitric oxide production.

Lucigenin has been widely used as a chemiluminescent substrate to monitor vascular superoxide (O*-2) formation. The validity of lucigenin for detection of O*-2 has been questioned because O*-2 is generated by lucigenin itself. It has been shown that the concentration of lucigenin is a critical parameter affecting the validity of this assay. In the present studies we evaluated a reduced concentration of lucigenin (5 microM) as a tool to quantify O*-2 production in vascular tissue. Lucigenin-induced effects on endothelial function were assessed by isometric tension recording of isolated aortic rings suspended in organ baths. The effects of lucigenin on O*-2 production were studied using spin trapping and electron spin resonance spectroscopy. Lucigenin at 250 microM but not at 5 microM caused a significant attenuation of endothelium-dependent relaxations to acetylcholine, which was prevented by pretreatment with superoxide dismutase. Spin-trapping studies revealed that lucigenin at 250 microM increased vascular O*-2 production several fold while 5 microM lucigenin did not stimulate O*-2 production. Inhibition of NO synthase by NG-momomethyl-l-arginine as well as the removal of the endothelium almost doubled lucigenin-derived chemiluminescence (LDCL), indicating that basal production of endothelium-derived NO depresses the baseline chemiluminescence signal. Thus, lucigenin at a concentration of 5 microM seems to be a sensitive and valid probe for assessing O*-2 in vascular tissue. It can also be used as an indirect probe to estimate basal vascular NO release.

Acetylcholine↗
PubMed1999

Prospective evaluation of the coronary sinus anatomy in patients undergoing electrophysiologic study.

BACKGROUND: Previous retrospective studies could find a predominant incidence of coronary sinus (CS) anomalies in patients with accessory pathways and a characteristic anatomy of the CS ostium in patients with atrioventricular nodal reentrant tachycardias (AVNRT). HYPOTHESIS: In the present prospective study, CS angiograms were prospectively performed to analyze the incidence of CS anomalies and to measure the diameters of the CS ostium. METHODS: The study included patients referred for electrophysiologic study and catheter ablation of various tachyarrhythmias. The anatomy of the CS and its side branches was visualized [left anterior oblique (LAO) 30 degrees, right anterior oblique (RAO) 30 degrees] by retrograde angiography in 204 consecutive patients (82 women, 122 men, age 45 +/- 15 years); of these, 120 presented with 123 accessory pathways (45 left-sided, 33 right-sided, 45 septal). The diagnosis in the remaining patients was atrioventricular nodal reentrant tachycardia in 43 cases, atrial tachycardia or atrial fibrillation in 12, and ventricular tachycardia in 15. In 14 patients, the indication for the electrophysiologic study was an unexplained syncope. The CS angiogram was evaluated for anomalies and the size of the CS ostium was manually measured in both projections. RESULTS: Anomalies of the CS defined as diverticula, persistent left superior vena cava, or enlarged CS ostia were found in 18 patients (9%). Of those, CS diverticula were found in nine patients, all with a posteroseptal or left posterior manifest accessory pathway, which was abolished within the neck of the diverticulum in seven patients and at the posteroseptal tricuspid annulus in two patients. Persistence of the left superior vena cava was found in five patients, four had atrioventricular reentrant tachycardia secondary to five accessory pathways (left free wall in four, right midseptal in one), and one patient had atrioventricular nodal reentrant tachycardia (AVNRT). Enlargement of the CS ostium of > 25 mm width was detected in nine patients (5%), of whom four had AVNRT. However, the width of the CS ostium generally did not differ significantly between patients with AVNRT (LAO: 14.4 +/- 5.6; RAO 9.3 +/- 2.4 mm) compared with the control group (LAO 13.4 +/- 4.1; 8.2 +/- 1.9 mm). CONCLUSIONS: Anomalies of the CS as diverticula, persistent superior vena cava, or enlargement of the CS ostium are predominantly found in patients with accessory pathway-related tachycardias. Diverticula of the proximal CS were found in 7% of patients with accessory pathways; in these cases, ablation succeeded mostly by radiofrequency (RF) current delivery in the neck of the diverticulum. Enlargement of the CS ostium was more often seen in patients with AVNRT than in all other patients. However, in general the measurements of the coronary sinus ostium did not significantly differ in patients with AVNRT compared with the control group.

Adult↗
PubMed1999

[Medicamentous prevention of symptomatic paroxysmal atrial fibrillation/flutter onset. Goals and design of the SOPAT Study. Executive committee of the investigators representing trial physicians].

The indication to treat symptomatic paroxysmal atrial fibrillation is discussed controversely. Successful medical treatment may result in the reduction of symptoms by improving hemodynamics in a reduction of thromboembolic events. However, several antiarrhythmic drugs are also known to increase the risk of proarrhythmic events. A randomized, double-blind, and placebo-controlled multicenter trial with 1000 patients to be recruited was designed to compare the effects of two antiarrhythmic drugs frequently used in Germany for the treatment of atrial fibrillation, Sotalol and the fixed combination of chinidin and verapamil (Cordichin). Patients with symptomatic paroxysmal atrial fibrillation/atrial flutter will be observed for a period of one year. The occurrence of paroxysmal atrial fibrillation is documented by transtelephonic ECG monitoring. Patients with document an ECG once daily, and recording is mandatory in case of symptoms. ECGs are transmitted to a central data base for analysis. This clinical trial is designed to answer the following questions: (1) What is the average rate of spontaneous events of symptomatic atrial fibrillation? (2) Is it possible to reduce the frequency of symptomatic events by chronic antiarrhythmic drug administration? (3) What is the long-term frequency for the occurrence of severe side-effects under antiarrhythmic medication? The primary endpoint is defined as the time to first recurrence of symptomatic arrhythmia after reaching steady-state plasma concentrations of the study medication. The trial started in November 1997 and is planned to be finished by the end of 1999.

Anti-Arrhythmia Agents↗
PubMed1999

[Comparison of permanent and paroxysmal atrial fibrillation on the clinical outcome following radiofrequency AV node catheter ablation].

UNLABELLED: The aim of the study was to compare the clinical outcome after AV node radiofrequency current ablation and pacemaker implantation in patients with permanent and paroxysmal atrial fibrillation. The study consecutively included 19 patients with permanent (male n = 15; 55 +/- 13 years) and 45 patients with paroxysmal atrial fibrillation (male n = 31; 60 +/- 13 years). Clinical evaluation before and 1 year after ablation included the symptoms and the self-assessed state of health. Before ablation, both groups reported with a similar frequency about tachycardia (permanent n = 15; paroxysmal n = 2) and palpitations (permanent n = 5; paroxysmal n = 19). Patients with permanent (n = 7) atrial fibrillation had more often breathlessness than patients with paroxysmal atrial fibrillation (n = 2), whereas dizziness/syncope was more often reported by patients with paroxysmal (n = 35) than with permanent arrhythmia (n = 8). Ablation improved symptoms in patients with permanent (89%) as well as with paroxysmal atrial fibrillation (84%). The self-assessed state of health described as good had not patient before ablation and 63% patients with permanent and 47% with paroxysmal atrial fibrillation after ablation. There were no differences for the studied parameters between patients with permanent and paroxysmal atrial fibrillation. CONCLUSION: AV node ablation and pacemaker implantation improved the symptoms and the state of health in with paroxysmal and paroxysmal atrial fibrillation. No differences were detected between patients with permanent and paroxysmal atrial fibrillation.

Adult↗
PubMed1999

[Role of Chlamydia pneumoniae in the pathogenesis of coronary disease].

Several studies have demonstrated an association Chlamydia pneumoniae with coronary artery disease, suggesting that infection with C. pneumoniae increases the risk for coronary artery disease by factor 2 or more. Since atherosclerosis is considered to be a chronic inflammatory process, these data would fit into the response-to-injury hypothesis of atherosclerosis rather than representing a completely novel concept. Several pathomechanisms as increased cytokine synthesis, proliferative and proaggregatory effects could transmit the effects of chronic C. pneumoniae infection. Animal models and first clinical trials using antibiotic therapy seem to support an etiological role of C. pneumoniae in coronary artery disease. In this paper the current knowledge of the role of C. pneumoniae in coronary artery disease is reviewed and possible pathomechanisms are discussed.

Adolescent↗
PubMed1999

Prehospital testing for troponin T in patients with suspected acute myocardial infarction.

BACKGROUND: Cardiac troponin T (TnT) is a highly sensitive and specific marker for myocardial damage and can be detected early after myocardial injury. Our hypothesis was to use TnT as an objective marker to verify acute myocardial infarction before hospital admission. METHODS AND RESULTS: We evaluated the sensitivity of a rapid qualitative assay for serum TnT for the detection of acute myocardial infarction in the ambulance and assessed the predictive value of a positive prehospital TnT test for death and myocardial infarction during 6-months of follow-up. The study, conducted in an urban area, included 158 consecutive patients with suspected acute myocardial infarction (93 men aged 69 +/- 13 years). A myocardial infarction was confirmed in 40 and excluded in 118 patients. The prehospital TnT test was positive in 11 patients, of whom 7 had acute myocardial infarction. Fifty-three patients had a positive test result at hospital admission, with evidence of myocardial infarction in 39 of them. The sensitivity to acute myocardial infarction was 18% for the prehospital and 98% for the in-hospital test with 78% and 88% specificity, respectively. During follow-up, patients with a positive prehospital TnT test result had cardiac events more often (9 of 11) than patients with a negative result (26 of 147; P <.0001). CONCLUSIONS: In areas with short transport times to the patient the rapid TnT test performed at the point of care identified only a minority of the patients with acute myocardial infarction. A positive prehospital TnT test result seems to be an objective marker for a worse outcome in patients presenting with suspected acute myocardial infarction.

Aged↗
PubMed1999

Increased NAD(P)H oxidase-mediated superoxide production in renovascular hypertension: evidence for an involvement of protein kinase C.

BACKGROUND: Angiotensin II infusion has been shown to cause hypertension and endothelial dysfunction and to increase superoxide (O-.2) production in vascular tissue, mainly via an activation of nicotinamide adenine dinucleotide (phosphate) [NAD(P)H]-dependent oxidase, the most significant O-.2 source in endothelial and/or smooth muscle cells. With these studies, we sought to determine whether endothelial dysfunction in renovascular hypertension is secondary to an activation of these oxidases. METHODS: Endothelial function in aortas from rats with two kidney-one clip (2K-1C) hypertension and age-matched controls was assessed using isometric tension studies in organ chambers. Changes in vascular O-.2 production were measured using lucigenin-enhanced chemiluminescence and electron spin resonance spectroscopy. RESULTS: In hypertensive animals, relaxation to endothelium-dependent (acetylcholine) and endothelium-independent nitrovasodilators (nitroglycerin) was impaired. Constriction to a direct activator of protein kinase C (PKC) phorbol ester 12,13 dibutyrate (PDBu) was enhanced, and vascular O-.2 was significantly increased compared with controls. Vascular O-.2 was normalized by the PKC inhibitor calphostin C, by the inhibitor of flavin-dependent oxidases, diphenylene iodonium, and recombinant heparin-binding superoxide dismutase, whereas inhibitors of the xanthine oxidase (oxypurinol), nitric oxide synthase (NG-nitro-l-arginine) and mitochondrial NADH dehydrogenase (rotenone) were ineffective. Studies of vascular homogenates demonstrated that the major source of O-.2 was a NAD(P)H-dependent oxidase. Incubation of intact tissue with PDBu markedly increased O-. 2, the increase being significantly stronger in vessels from hypertensive animals as compared with vessels from controls. Endothelial dysfunction was improved by preincubation of vascular tissue with superoxide dismutase and calphostin C. CONCLUSIONS: We therefore conclude that renovascular hypertension in 2K-1C rats is associated with increased vascular O-.2 leading to impaired vasodilator responses to endogenous and exogenous nitrovasodilators. Increased vascular O-.2 is likely secondary to a PKC-mediated activation of a membrane-associated NAD(P)H-dependent oxidase.

Acetylcholine↗