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T Meinertz

Publications and source records attributed to T Meinertz.

At least 127 records · Page 7Linked to original sources

[Risk assessment in coronary heart disease: ventricular arrhythmias, myocardial ischemia and sudden cardiac death].

There is increasing evidence for a fatal interaction of myocardial ischemia, ventricular arrhythmias, and sudden cardiac death in some patients with coronary artery disease. Evidence comes from autoptic studies, from the evaluation of patients who survived an episode of sudden cardiac death, from follow-up data of these patients either treated or not by revascularization therapy and/or an implantable cardioverter-defibrillator and indicate that reducing the individual ischemic burden will be beneficial to reduce the incidence of sudden cardiac death. Studies in patients with stable and especially with unstable angina using Holter monitoring could demonstrate that there is a close and causal relationship between myocardial ischemia inducing or aggravating life-threatening ventricular arrhythmias and sudden cardiac death particularly in patients with unstable and postinfarction status. This review summarizes some of our clinical knowledge on this topic and indicates that preventive strategies for myocardial ischemia are the antiarrhythmic treatment of choice in patients with severe coronary artery disease and evidence or at risk for ischemic proarrhythmia.

Coronary Disease↗

Enhanced coagulation activation in troponin T-positive unstable angina pectoris.

Intracoronary thrombus formation and systemic activation of coagulation have been demonstrated in unstable angina pectoris. Circulating troponin T as a marker of minor myocardial cell injury is associated with adverse outcome in this condition. Little information exists about the interrelation of coagulation activation and myocardial cell injury in unstable angina. We quantitatively assessed systemic activation of coagulation and myocardial cell injury in serial blood samples obtained up to 10 days from 22 patients with angiographically documented coronary heart disease and unstable angina pectoris at rest. In the nine patients with increased maximal levels of serum troponin T, maximal concentrations of fibrin monomers during the first 48 hours were higher than those in patients with persistently normal troponin T concentrations (6.3+/-4.8 vs. 2.9+/-2.3 mg/L; p = 0.04). The proportion of patients with at least one blood sample showing an increased concentration of plasma fibrin monomer was also higher in the group with increased troponin T (67% vs. 15%; p = 0.04). Plasma prothrombin fragment F1+2 levels showed a nonsignificant trend toward higher values in troponin T-positive patients. Enhanced activation of coagulation in patients with troponin T-positive unstable angina may contribute to the adverse outcome associated with this condition.

Aged↗

Long-term nitroglycerin treatment is associated with supersensitivity to vasoconstrictors in men with stable coronary artery disease: prevention by concomitant treatment with captopril.

OBJECTIVES: We examined whether long-term nitroglycerin (NTG) treatment leads to an increase in sensitivity to vasoconstrictors. To assess a potential role of the renin-angiotensin system in mediating this phenomenon, we treated patients concomitantly with the angiotensin-converting enzyme (ACE) inhibitor captopril. BACKGROUND: The anti-ischemic efficacy of organic nitrates is rapidly blunted by the development of nitrate tolerance. The underlying mechanisms are most likely multifactorial and may involve increased vasoconstrictor responsiveness. METHODS: Forearm blood flow and vascular resistance were determined by using strain gauge plethysmography. The short-term responses to intraarterial angiotensin II (1, 3, 9 and 27 ng/min) and phenylephrine (an alpha-adrenergic agonist drug, 0.03, 0.1, 0.3 and 1 microg/min) were studied in 40 male patients with stable coronary artery disease. These patients were randomized into four groups receiving 48 h of treatment with NTG (0.5 microg/kg body weight per min) or placebo with or without the ACE inhibitor captopril (25 mg three times daily). RESULTS: In patients treated with NTG alone, the maximal reductions in forearm blood flow in response to angiotensin II and phenylephrine were markedly greater (-64 +/- 3% and -53 +/- 4%, respectively) than those in patients receiving placebo (-41 +/- 2% and -42 +/- 2%, respectively). Captopril treatment completely prevented the NTG-induced hypersensitivity to angiotensin II and phenylephrine (-33 +/- 3% and -35 +/- 3%, respectively) but had no significant effect on blood flow responses in patients without NTG treatment (-34 +/- 2% and -37 +/- 3%, respectively). CONCLUSIONS: We conclude that continuous administration of NTG is associated with an increased sensitivity to phenylephrine and angiotensin II that is prevented by concomitant treatment with captopril. The prevention of NTG-induced hypersensitivity to vasoconstrictors by ACE inhibition indicates an involvement of the renin-angiotensin system in mediating this phenomenon.

Adult↗

Several unsuccessful internal and external defibrillations during active can ICD implantation in a patient with pneumothorax.

During implantable cardioverter defibrillator (ICD) implantation of an active can ICD several defibrillations with 20 J and 34 J as well as 360 J externally were ineffective. The implant criteria were finally met with a second defibrillation lead and reversed polarity. A left-sided pneumothorax due to subclavian vein puncture was detected soon after ICD implantation. It is assumed that especially in the active can alignment the developing pneumothorax made defibrillation current flow more difficult. In case of several unsuccessful defibrillations during active can ICD implantation in which the subclavian vein was punctured, the possibility of a pneumothorax should be considered.

Defibrillators, Implantable↗

A prospective randomized comparison between fixed rate response programming and automatic rate response optimization in activity-triggered DDDR pacemakers. Thera Pacemaker Study Group.

Activity rate response programming depends on the physician's experience and on the limited knowledge of patient's daily activities. The present investigation compares a new continuous automatic adjustment of the activity rate response called rate response optimization (OPT) with fixed activity rate response programming (FIXED). At hospital discharge 37 patients with Thera DR pacemakers (Medtronic) were randomized either to FIXED (n = 20; 65 +/- 12 years, male n = 12) or to OPT (n = 17; 65 +/- 12 years, male n = 13). After 1 month's follow-up occurrence of complaints related to rate-responsive pacing and the percentage of pacing were assessed. Other activity sensor parameters were programmed according to clinical judgement and similarly distributed in the two groups. Activity rate response was 7.1 +/- 1.4 (FIXED) and 7.2 +/- 1.7 (OPT), activity threshold was medium in 9 (FIXED) and 8 (OPT), and medium/low in 11 (FIXED) and 9 (OPT) patients, respectively. No patient with FIXED had any complaints with respect to activity-triggered rate response. One patient with OPT reported palpitations due to rapid changes in the pacing rate leading to reprogramming of the pacemaker. Atrium and ventricle were paced in 56 +/- 31% (FIXED) and in 58 +/- 35% (OPT; not significant) and the atrium only in 4 +/- 10% (FIXED) and 0% (OPT; not significant), respectively. In the 17 patients programmed to OPT the pacemaker increased activity rate response in 5 and decreased activity rate response in 3 patients. In conclusion, as only 1 (3%) patient had complaints related to the activity rate response and fixed rate response programming according to clinical judgement already resulting in symptom-free DDDR pacing, no differences could be detected between the fixed rate response programming and rate response optimization.

Aged↗

[Electrophysiologic study and endocardial ECG mapping in the detection of causes of heart rhythm disorders].

Accessory pathways and ectopic heart focuses tachycardias are often cause of tachycardias. AV reentry tachycardias are great diagnostic and therapeutic problems. Using the electrophysiological investigation and ECG mapping, there is possibility to find out abnormal pathways and ectopic atrial and ventricular focuses. In electrophysiological investigations we can use bipolar, threepolar and multipolar electrodes and mapping electrodes, as well. The ablation catheter is introduced by transveins way in electrophysiological investigation of right atrium and ventricle, and via the femoral artery to the left atrium and ventricle. We investigated 45 patients, who are hospitalised at the Cardiology clinic Ependorf, of the University in Hamburg Accessory pathways were found out in 37 (82.22%) patients. Successful RF catheter ablation was done in 34 (91.89%) patients and unsuccessful in 3 (8.10%). Ectopic focuses were found out in patients with left ventricle aneurysm. It was indication for aneurysmectomia in two cases and for implantation of antitachycardia pacemaker in one case.

Adult↗

Emergency room triage of patients with acute chest pain by means of rapid testing for cardiac troponin T or troponin I.

BACKGROUND: Evaluation of patients with acute chest pain in emergency rooms is time-consuming and expensive, and it often results in uncertain diagnoses. We prospectively investigated the usefulness of bedside tests for the detection of cardiac troponin T and troponin I in the evaluation of patients with acute chest pain. METHODS: In 773 consecutive patients who had had acute chest pain for less than 12 hours without ST-segment elevation on their electrocardiograms, troponin T and troponin I status (positive or negative) was determined at least twice by sensitive, qualitative bedside tests based on the use of specific monoclonal antibodies. Testing was performed on arrival and four or more hours later so that one sample was taken at least six hours after the onset of pain. The troponin T results were made available to the treating physicians. RESULTS: Troponin T tests were positive in 123 patients (16 percent), and troponin I tests were positive in 171 patients (22 percent). Among 47 patients with evolving myocardial infarction, troponin T tests were positive in 44 (94 percent) and troponin I tests were positive in all 47. Among 315 patients with unstable angina, troponin T tests were positive in 70 patients (22 percent), and troponin I tests were positive in 114 patients (36 percent). During 30 days of follow-up, there were 20 deaths and 14 nonfatal myocardial infarctions. Troponin T and troponin I proved to be strong, independent predictors of cardiac events. The event rates in patients with negative tests were only 1.1 percent for troponin T and 0.3 percent for troponin I. CONCLUSIONS: Bedside tests for cardiac-specific troponins are highly sensitive for the early detection of myocardial-cell injury in acute coronary syndromes. Negative test results are associated with low risk and allow rapid and safe discharge of patients with an episode of acute chest pain from the emergency room.

Acute Disease↗

Treatment of in-stent coronary restenosis by excimer laser angioplasty.

We evaluated the efficacy and safety of excimer laser angioplasty (ELCA) with adjunctive balloon angioplasty in patients with restenotic or occluded coronary stents. ELCA was performed in 70 patients (60 +/- 9 years), who had previously been treated with Micro Stents (n = 65), Palmaz-Schatz (n = 38), Wiktor, NIR, Freedom, and Multi-Link stents (n = 1 each). Restenosis (> or =50% diameter stenosis) was documented in 90 stents, another 17 stents were occluded. Laser energy was delivered to the lesions with catheters 1.4, 1.7 (eccentric), and 2.0 mm in diameter. Procedural success was controlled by intravascular ultrasound in a subgroup. Laser catheters crossed all restenotic or occluded stents and decreased diameter stenosis from 80 +/- 13% to 44 +/- 11% (p <0.001). Adjunctive balloon angioplasty further reduced diameter stenosis to 13 +/- 13% (p <0.001). In 13 patients with 21 stents, serial intravascular ultrasound imaging revealed a reduction of plaque area within the stent by 34 +/- 22% (from 4.2 +/- 1.8 mm2 to 2.7 +/- 1.1 mm2) after ELCA and a reduction by 65 +/- 16% (to 1.5 +/- 0.7 mm2) after balloon angioplasty (p <0.01). There were 4 patients with an increase of creatine kinase levels, 8 patients with major dissections (in 7 patients they were related to adjunctive balloon angioplasty), 1 patient with distal embolization, 2 with minor perforations, and 1 patient with stent dislocation. Reintervention during hospitalization was necessary in 3 patients. ELCA is an efficient and safe technique to debulk tissue in restenotic lesions and total occlusions within stents. The incidence of procedure related complications was low.

Adult↗

[The effect of a lower stimulation frequency on the AV synchronicity of VDD pacemakers].

BACKGROUND AND OBJECTIVE: Implantation of a VDD pacemaker (ventricular pacing; dual sensing [atrial and ventricular]; dual response [triggered + inhibited]) together with a single VDD electrode catheter restores synchronous AV ventricular stimulation in patients with higher-grade AV block and intact sinus function. If higher-frequency stimulation occurs it may be a sign of pacemaker malfunction or of inadequate pacemaker programming. This study was undertaken to determine, at first follow-up examination, in how many patients with a VDD pacemaker VVI stimulation occurred more than 5% of the time; how such patients differed from those with 5% or fewer VVI stimulations; and whether a changed program reduced the proportion of VVI stimulations. PATIENTS AND METHODS: 67 consecutive patients were tested 1 to 3 months after implantation of the Unity VDD pacemaker (Sulzer Intermedics). The frequency of VVI stimulations was determined via a diagnostic pacemaker memory store. After intermediate analysis, programming was optimized and the patients then re-tested 12 months after the initial implantation. RESULTS: At the first follow-up examination 54 patients had VVI stimulations of < or = 5% (0.5 +/- 0.9%) and 13 had > 5% of the time (19.8 +/- 10.7%). The two groups differed significantly from one another in their lower intervention frequency (< or = 5% VVI stimulations: 47 +/- 6/min; > 5% VVI stimulations: 58 +/- 5/min). In particular, the pacemakers in patients with > 5% VVI stimulations had been significantly more often programmed to values of > 50/min. As a result, the pacemakers of these patients were reprogrammed to a lower frequency. A year after implantation there was no longer any difference in the lower intervention frequency, 44 +/- 4/min, between patients with initially > 5% VVI stimulations and those with initially < or = 5% stimulations. At the same time, the proportion of VVI stimulations fell to 4 +/- 6%, with 67% of patients having AV synchronicity of > 95%. INTERPRETATION: At first follow-up, patients with > 5% VVI stimulations differed from those with < or = 5% stimulations with regard to an increased lower intervention frequency. In most of these patients the proportion of AV stimulations was increased to > 95% by reducing the lower intervention frequency to < or = 50/min.

Aged↗

[Resuscitation in ventricular fibrillation as the first manifestation of Bland-White-Garland syndrome in adulthood].

CASE REPORT: This case presents a 31-year-old male patient with anomalous origin of the left coronary artery from the pulmonary trunc. First symptom of the disease was a survived sudden cardiac death. Subsequent angiographic and echocardiographic studies demonstrated the anomalous origin of the left coronary artery from the pulmonary artery. There were no signs of prior myocardial infarction. After reimplantation of the anomalous originating left coronary artery no myocardial ischemia could be detected in the thallium-201 myocardial imaging, which was present before surgical correction. In this case myocardial ischemia was the only potential triggering mechanism responsible for the sudden cardiac death, which was no longer detectable after surgical correction. Therefore no additional pharmacological and nonpharmacological antiarrhythmic treatment was initiated. CONCLUSION: In rare cases the first manifestation of Bland White Garland syndrome in the adult patient could be sudden cardiac death due to ventricular fibrillation.

Adult↗

[Change in therapy of cardiac arrhythmias. Current studies--initial results].

Treatment of Arrhythmias in Development-Recent Trials, First Results When dealing with preliminary or brand new results of large randomised trials, the requirement should be the assessment of the data by experts in the arrhythmia field. This holds especially true for studies addressing the complex problem of the prevention of sudden cardiac death. During recent years a number of controlled randomised trials have been published showing no or a harmful effect of antiarrhythmic drugs on the prognoses of patients at risk of sudden cardiac death. The results of these studies have clearly changed the scenario of preventive antiarrhythmic drug treatments. Some newer studies-published only in a preliminary form-seem to indicate that some Class III antiarrhythmics can have a positive effect. Studies are under way to compare the preventive effect of this antiarrhythmic drug therapy against sudden cardiac death with that of the implantable cardioverter/defibrillator. The improvement of prognosis remains the ultimate goal of antiarrhythmic therapy.

Anti-Arrhythmia Agents↗

Flow cytometric analysis of coronary stent-induced alterations of platelet antigens in an in vitro model.

One of the limitations of coronary stenting is the subacute thrombotic occlusion. In an in vitro model, we examined the effects of tantalum wire stents (n = 12) on platelet antigens. Platelet-rich plasma (PRP) was circulated in PVC tubing systems. At fixed intervals over a 10-min time course, aliquots of PRP were drawn, stained with monoclonal antibodies (CD41a, CD42b, CD62p, and CD63), and analyzed by flow cytometry. Within 2 minutes of the onset of circulation, expression of the activation-dependent antigens CD62p and CD63 increased in all tubing systems with stents. This early increase was followed by a progressive rise in fluorescence intensity of these neoantigens over the course of 10 minutes (p < 0.05 vs.. control system without stent). Antigens CD41a and CD42b did not show significant changes in either system. The artificial surfaces and shear forces of stent meshes induce alterations in platelet antigens. Flow cytometry provides a sensitive technique for in vitro testing of the thrombogenicity of coronary stents, and may be useful in further improving stent biocompatibility.

Adult↗

Propafenone during acute myocardial ischemia in patients: a double-blind, randomized, placebo-controlled study.

OBJECTIVES: The proarrhythmic risk of class I antiarrhythmic agents in combination with myocardial ischemia is mainly the result of their effects on ventricular repolarization. This study was designed to evaluate the effect of class Ic antiarrhythmic agents on QT dispersion during myocardial ischemia. BACKGROUND: QT interval dispersion on the 12-lead electrocardiogram (ECG) has been suggested as a noninvasive marker of inhomogeneous ventricular repolarization and susceptibility to ventricular arrhythmias. METHODS: In a randomized, double-blind study, 98 patients undergoing percutaneous transluminal coronary angioplasty (PTCA) were pretreated with propafenone or placebo. QT dispersion was defined as a maximal minus minimal QT interval on the 12-lead ECG before and after PTCA. The power of the study to detect clinically meaningful differences in QT dispersion was 0.75, and a twofold increase in QT dispersion in the propafenone group compared with the placebo group was considered clinically relevant. RESULTS: The QT and corrected QT (QTc) intervals increased significantly during occlusion of the left anterior descending coronary artery (LAD) (9% and 11%, respectively, p < 0.05), whereas occlusion of the circumflex and right coronary arteries had no effect. QTc dispersion increased significantly in the propafenone group during ischemia (+52%, p = 0.002, vs. +23%, p = 0.15). The most considerable effect on QT dispersion was observed during LAD occlusion and ischemia of the anterior wall (+74%, p = 0.025). Corrected JT dispersion (+57%, p = 0.017, vs. +24%, p = 0.23) and the QT dispersion ratio (+1.6%, p = 0.031, vs. 0.9%, p = 0.34) showed similar effects. Plasma levels of propafenone (522 +/- 165 micrograms/liter) did not influence the results. CONCLUSIONS: During myocardial ischemia, particularly during LAD occlusion, propafenone results in a significant increase in QT dispersion. The results indicate that QT interval prolongation and enhanced QT dispersion reflect inhomogeneous ventricular repolarization generated by the ischemic anterior wall of the myocardium. These observations may demonstrate a clinically important interaction between myocardial ischemia, repolarization variables and propafenone.

Adult↗

[Magnesium deficiency and magnesium substitution. Effect on ventricular cardiac arrhythmias of various etiology].

During recent years there has been an increasing but still controversial discussion on the antiarrhythmic effects and overall benefit of magnesium when directed to patients with various types of ventricular tachyarrhythmias. While magnesium is considered to be a simple, safe and cost-effective approach and many casuistic and empiric reports have indicated antiarrhythmic properties of magnesium in patients with suspected or manifest ventricular arrhythmias, controlled studies proving the antiarrhythmic and overall benefit and justifying a broader use of magnesium in treating various types of ventricular arrhythmias are missing or rare. At present, antiarrhythmic properties and clinical benefit of magnesium application has only been established in patients with torsade de pointes and digitalis-induced ventricular tachyarrhythmias. In perioperative patients at risk for ventricular tachyarrhythmias and in patients suffering from manifest heart failure, data may also indicate some antiarrhythmic properties of magnesium, however, in this case with a wide consensus that the prevention of magnesium deficit is more effective and preferred in most patients over the therapeutic application of magnesium. Another group of patients who may profit from such a therapeutic approach are patients with frequent ventricular arrhythmias and stable underlying heart disease, in whom a recently published double-blind, randomized study documented an antiarrhythmic effect of a 3 week treatment with potassium and magnesium. For all other types of ventricular tachyarrhythmias, the therapeutic use of magnesium can be considered as not harmful, but also as not proven to be effective.

Anti-Arrhythmia Agents↗