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T Meinertz

Publications and source records attributed to T Meinertz.

At least 199 records · Page 11Linked to original sources

Comparison in acute myocardial infarction of anisoylated plasminogen streptokinase activator complex versus heparin evaluated by simultaneous thallium-201/technetium-99m pyrophosphate tomography.

In a subgroup of 45 patients with acute myocardial infarction (AMI) from the German multicenter trial of anisoylated plasminogen streptokinase activator complex (APSAC) (n = 20) versus heparin (n = 25), simultaneous thallium (TI)-201 technetium (Tc)-99m pyrophosphate (PYP) tomography was initiated to elucidate a possible benefit of APSAC over heparin. Findings in the 2 treatment groups were similar with respect to TI-201 defect score, relative scintigraphic infarct size, and in keeping with the main group coronary artery patency, global ejection fraction and maximal creatine kinase level. However, 2 different TI-201/Tc-99m PYP accumulation patterns within the area of infarction (homogeneous, group A; inhomogeneous, group B) were identified. Both treatment groups were similar with regard to the frequency of the homogeneous and inhomogeneous pattern. In comparing the 2 accumulation patterns, creatine kinase peaked earlier in group A than in group B, and global left ventricular ejection fraction was significantly higher in group A than in group B. In Group A, 30 of 31 patients and in group B 7 of 11 patients had a patent infarct-related vessel (p < 0.025). TI-201 defect score was lower in group A than in group B. Likewise, relative size of the infarction as determined from Tc-99m PYP images was significantly lower in group A than in group B. Fifteen patients experienced cardiogenic shock or severe heart failure. Patients in group B had a higher incidence of these in-hospital complications than patients in group A (92 vs 12%, p < 0.0005). Scintigraphic infarct size and TI-201 defect score were greater in patients with the aforementioned clinical events.(ABSTRACT TRUNCATED AT 250 WORDS)

Anistreplase↗

Distinguishing between acute and subacute massive pulmonary embolism by conventional and Doppler echocardiography.

OBJECTIVE: To determine the ability of conventional and Doppler echocardiography to distinguish between minor, acute massive, and subacute massive pulmonary embolism in patients with confirmed pulmonary embolism. DESIGN: Prospective study of a consecutive series of 47 patients with confirmed pulmonary embolism. SETTING: Department of internal medicine, university clinic. PATIENTS: 11 patients (23%) had minor, 23 patients (49%) had acute massive, and 13 patients (28%) had subacute massive pulmonary embolism. RESULTS: Dilatation of the right ventricular cavity (33 (92%)) and asynergy of the right ventricular free wall (29 (81%)) were seen only in patients with acute and subacute massive pulmonary embolism (n = 36). 23 (64%) with pulmonary hypertension had tricuspid regurgitation. The velocity of the tricuspid regurgitant jet correlated with the pulmonary arterial pressure (r = 0.88, SEE = 11.6 mm Hg) and was significantly lower in patients with acute massive pulmonary embolism (3.0 (0.4) m/s, n = 12) than in patients with subacute massive pulmonary embolism (4.2 (0.6) m/s; n = 11) (p < 0.001). The use of predefined indices (right ventricular free wall thickness > 5 mm; tricuspid regurgitant jet velocity > 3.7 m/s; and the occurrence of both a dilated right ventricular cavity with normal interventricular septal motion, or an inspiratory collapse of the inferior vena cava, or both) correctly identified 11 of 13 patients (85%) with subacute massive pulmonary embolism. CONCLUSION: Conventional and Doppler echocardiography were successful in evaluating the haemodynamic consequences of pulmonary embolism.

Acute Disease↗

[Transesophageal echocardiography in patients with systemic arterial embolism].

The percentage of ischemic strokes or peripheral arterial embolism attributed to cardiogenic embolism is about 30% and 75%, respectively. Diagnostic work-up in patients with prior arterial embolism is of prognostic importance, because embolic events are often recurrent. Cardioembolic sources with major risk of embolism are atrial fibrillation, mechanical or biological heart valve prosthesis, left ventricular or left atrial thrombi, left atrial myxomas, bacterial endocarditis, nonbacterial thrombotic endocarditis and nonischemic dilative cardiomyopathies. Cardioembolic sources with minor risk of embolism are mitral valve prolapse, isolated mitral annular calcification, patent foramen ovale, atrial septal aneurysm and calcific aortic valve stenosis. Studies have shown that two-dimensional transthoracic echocardiography yields little useful information in patients with arterial embolism. The advent of transesophageal echocardiography in the late 1980s allowed a more reliable identification of potential cardioembolic sources. The close contact of the echoprobe in the esophagus to the heart allows better resolution of intracardiac structures, particularly when cardiovascular abnormalities at the atrial level, the base of the heart and the thoracic aorta are sought. We studied 153 patients with clinically suspected arterial embolism by transthoracic and transesophageal echocardiography. Patients with extracranial carotide occlusive disease and patients older than 60 years were excluded from the study. In 88 out of 153 patients (58%) a cardioembolic mechanism could be detected by the combination of transthoracic and transesophageal echocardiography. Using the transthoracic method alone, a cardioembolic source could only be found in 55 patients (36%). Valvular heart disease and regional or global wall motion abnormalities could be visualized by both methods with similar results. However, only two out of 22 left atrial thrombi detected by transesophageal echocardiography could be documented also with the transthoracic approach. Transesophageal echocardiography was superior in the evaluation of valvular vegetations, intracardiac tumors, diseases of the thoracic aorta and abnormalities of the interatrial septum. Only left ventricular thrombi could be better evaluated by the transthoracic method, because visualization of the left ventricular apex by the transesophageal approach is problematic. In patients with systemic arterial embolism the combination of transthoracic and transesophageal echocardiography is the diagnostic method of choice to detect a cardioembolic source. Randomized studies in the future must prove, whether the echocardiographic findings can lead to better therapeutic strategies to improve the prognosis of patients with embolic disease.

Adult↗

Diagnostic value of transesophageal echocardiography in atrial septal aneurysm.

Transthoracic and transesophageal echocardiography was performed in 40 consecutive adult patients with an atrial septal aneurysm. In 11 (27%) of 40 patients transthoracic echocardiography failed to demonstrate the lesion and the diagnosis was established by the transesophageal approach only. Interatrial shunting, assessed by echocardiographic contrast study and/or color flow mapping, was detected in 13 (54%) of 24 patients on transthoracic imaging and in 29 (76%) of 38 patients during transesophageal echocardiography. Identification of multiple fenestrations (n = 9) and thrombi within the aneurysm (n = 2) could be achieved only by transesophageal ultrasound. A cerebrovascular event of suspected embolic origin occurred in 20 (50%) of 40 patients; 11 (55%) of the 20 patients had repeated cerebral events. Except for mitral valve prolapse in 2 patients and spontaneous left atrial contrast phenomenon in 1 patient no other potential cardiac source of embolism could be identified by transesophageal echocardiography. A marked thickening of the aneurysm was present in 14 (70%) of 20 patients with a cerebrovascular event versus only 4 (20%) of 20 patients without a cerebrovascular event (p less than 0.01). The mechanism of embolization may be both primary thrombus formation within the aneurysm and paradoxical embolization through an interatrial communication as suggested by the findings on transesophageal ultrasound in 2 patients. Although the patients of this study represent a highly selected group it may be concluded that atrial septal aneurysm is a cardiac abnormality with embolic potential. Transesophageal echocardiography has to be regarded the imaging method of choice for evaluation of this lesion.

Adult↗

Percutaneous mitral balloon valvuloplasty--a comparative evaluation of two transatrial techniques.

The efficacy and safety of two different percutaneous transfemoral mitral balloon valvuloplasty procedures were evaluated in 45 patients. A double-balloon technique with Mansfield balloons was applied in the first 22 patients (group A), and an Inoue single-balloon technique was used in the subsequent 23 patients (group B). Mean diastolic gradient decreased from 17 +/- 7 mm Hg to 8 +/- 3 mm Hg (p < 0.001) in group A and from 13 +/- 4 mm Hg to 8 +/- 3 mm Hg (p < 0.001) in group B. The mitral orifice area increased from 1.1 +/- 0.3 cm2 to 2.2 +/- 0.8 cm2 (p < 0.001) in group A and from 1.2 +/- 0.4 cm2 to 1.7 +/- 0.7 cm2 (p < 0.001) in group B. The length of the total procedure and the total fluoroscopy time were considerably shorter in group B (86 +/- 24 minutes and 18 +/- 7 minutes) compared with group A (128 +/- 38 minutes and 35 +/- 14 minutes; p < 0.001). Mitral regurgitation (grade 3/4) was observed after the procedure in two patients in group A but in nine patients in group B. Cardiac tamponade occurred in two patients in group A, but no major complications were seen in group B. The Inoue single-balloon technique seemed to be safe, easier to perform, and equally effective.

Adult↗

Effects of amiodarone versus quinidine and verapamil in patients with chronic atrial fibrillation: results of a comparative study and a 2-year follow-up.

Rapid, reliable and safe reestablishment of sinus rhythm is the major aim of pharmacologic treatment in patients with chronic atrial fibrillation. The mainstay of therapy in this arrhythmia has been quinidine. More recently, amiodarone was shown in non-comparative studies to be superior to class IA agents under certain conditions. In 40 patients with atrial fibrillation persisting for 4 weeks up to 2 years, the efficacy and safety of either quinidine and verapamil (days 1 to 3, quinidine 1,500 mg/day; days 4 to 6, quinidine 1,500 mg + verapamil 240 mg/day) or amiodarone therapy (days 1 to 3, amiodarone 1,200 mg/day intravenously; days 4 to 14, amiodarone 800 mg/day orally) were randomly examined. Responders continued on their effective medication for 3 months. Thereafter, all patients were treated with a fixed regimen of quinidine (480 mg/day) plus verapamil (240 mg/day) for up to 2 years. During atrial fibrillation, quinidine reduced mean ventricular cycle length by 40 ms (-5%), quinidine and verapamil increased mean cycle length by 57 ms (8%) and amiodarone by 192 ms (28%, p less than 0.01). In addition, quinidine and verapamil had a characteristic "rate-smoothing" effect on atrioventricular conduction during atrial fibrillation. The rhythm was converted to sinus rhythm after quinidine in 5 (25%) of 20 patients and after the combination of quinidine and verapamil in 11 (55%) of 20 patients. Amiodarone restored sinus rhythm in 12 (60%) of 20 patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Amiodarone↗

Short-term and long-term treatment with propafenone: determinants of arrhythmia suppression, persistence of efficacy, arrhythmogenesis, and side effects in patients with symptoms.

OBJECTIVE: To assess the clinical criteria predicting the short and long-term efficacy of propafenone, an agent with class IC antiarrhythmic activity and a broad pharmacological profile. DESIGNS: Prospective study of propafenone at doses of 450 to 900 mg/day during a six week dose titration period (including a placebo phase with two separate 24 Holter recordings). Responders to treatment were followed for one year. PATIENTS: One hundred patients with frequent ventricular arrhythmias (greater than 30 extrasystoles/h) of Lown class III and IVA/B and without evidence of myocardial infarction within the past six months. ANALYSIS: Multivariate regression analysis of spontaneous arrhythmia variability and of different clinical variables to determine the short and long-term efficacy and safety of propafenone. MEASUREMENTS AND MAIN RESULTS: Propafenone 450 mg/day was effective in 30/100 patients (30%), and at 600 mg/day another 14 responded. The efficacy of propafenone correlated with a low spontaneous arrhythmia variability and, as shown by multivariate analysis, with a lower patient age (p less than 0.05). When the dose was increased to 900 mg/day a further six (12%) patients responded. However, with increasing doses of propafenone, the one year probability of effective treatment decreased from 86% (450 mg/day) to 67% (600 mg/day) and to 44% (900 mg/day). After restudying the patients at three, six, and 12 months and after dose adjustment in 11/44 patients (25%), 31 patients (70%) remained responders. Loss of permanent antiarrhythmic efficacy was best predicted by the initial dose that achieved a response. No patient died suddenly or had arrhythmogenic effects during Holter monitoring. Side effects occurred in 36% of patients but these rarely limited long-term treatment. CONCLUSIONS: A younger age, low spontaneous arrhythmia variability, and particularly a low titration dose were the best predictors of the short and long term efficacy of propafenone. All other responders should have repeated Holter recordings during the first year of treatment.

Adult↗

Prevalence, circumstances, mechanisms, and risk stratification of sudden cardiac death in unipolar single-chamber ventricular pacing.

BACKGROUND: Permanent cardiac pacing is well established for the improvement of prognosis and quality of life in patients with severe bradycardia. However, sudden cardiac death still remains an unresolved problem, as it occurs in approximately 20-30% of paced patients. This 2-year follow-up study was directed at prospectively assessing prevalence, circumstances, and mechanisms of sudden death in 2,021 permanently paced patients. METHODS AND RESULTS: During the observation period, 220 patients (11%) died (mean pacing interval, 50.5 +/- 7 months). Lethal cerebrovascular events in 66 of 220 patients (30%) and sudden death in 49 of 220 patients (23%) were the two most frequently reported modes of death. Nonsudden (first year, 20%; subsequent years, 6.9%; p less than 0.01) and sudden death mortality rate (4% versus 1.8%, p less than 0.05) were highest during the first year. Mortality was unrelated to the patient's activity status at the time of death. Sudden cardiac death occurred more often in male patients (increased risk, 1.7 versus female patients; p less than 0.001) and patients younger than 60 years of age (5.2 versus patients older than 60 years, p less than 0.001). Patients with severe bradycardia (sudden death rate, 28%), severe atrioventricular block (25%), or atrial fibrillation with low ventricular rate (25%) before pacemaker implantation were more likely to suffer from sudden cardiac death than patients with previous syncopal attacks (sudden death rate, 15%) or sick sinus syndrome (17%). The highest incidence of sudden death was observed in patients with bifascicular and trifascicular bundle branch block. In this group, 35% of patients died suddenly during the follow-up period compared with 18% of patients without bundle branch block. In a subsequent study in 90 consecutive patients with various types of bundle branch block, undersensing of up to 13% of ectopic ventricular beats occurred in patients with bifascicular block. Pacing-induced tachyarrhythmias and ventricular fibrillation were documented in 10% of undersensed ectopic ventricular beats as well as in the setting of atrial fibrillation associated with ventricular arrhythmias. CONCLUSIONS: Young age, male sex, and a severely diseased heart indicated by the presence of bifascicular and trifascicular bundle branch block are the strongest predictive clinical parameters for sudden cardiac death, especially in the first year after pacemaker implantation.

Aged↗

Prevalence of circadian variations and spontaneous variability of cardiac disorders and ECG changes suggestive of myocardial ischemia in systemic arterial hypertension.

BACKGROUND: Systemic hypertension is a well-known risk factor for coronary artery disease and sudden cardiac death. Recent interest focused on the presence of malignant ventricular arrhythmias (VA) and myocardial ischemia in hypertensive patients and provided a potential link for fatal tachyarrhythmic events. METHODS AND RESULTS: We studied 150 untreated normokalemic hypertensive patients (56 +/- 9 years; 56 women and 94 men) without manifest coronary artery disease to determine prevalence, severity, and interaction of VA and significant ST segment changes induced by daily activities. One third of the patients were randomized to 4 weeks of placebo and restudied for spontaneous variability of the two parameters. All patients were included in a 3-year follow-up study. VA were observed in 129 of 150 hypertensive patients (86%) and peaked in the early morning and late afternoon. Twenty-two patients (15%) had ventricular pairs, and 20 patients (13%) had nonsustained ventricular tachycardia. Transient ST segment depression observed in 47 patients (33%; mean incidence, 2.7 +/- 0.8 episodes/24 hr) showed a characteristic circadian variation similar to VA and were asymptomatic in 93% of the episodes. At the time of transient ST segment depression, VA increased 4.6 times (p less than 0.01). After 4 weeks of placebo, marked variations in the incidence of VA (VA suppression rate -100%, or increase greater than 400%) were observed in 29% of the patients, and in 60% of all patients repetitive VA were present in only one of the two Holter recordings. Day-and-night variations of VA and transient ST segment changes were highly reproducible during the placebo period. After 3 years of follow-up, eight of 146 patients (5%) had suffered myocardial infarction, and five patients had died from cardiac events (three patients died from sudden cardiac death). Logistic regression analysis revealed left ventricular hypertrophy (relative risk, 6.1; p less than 0.01) and transient ST segment abnormalities during daily activities (relative risk, 4.4; p less than 0.05) to be of independent prognostic significance to predict cardiac events during follow-up instead of repetitive VA (relative risk, 1.3; NS). CONCLUSIONS: VA associated with a high spontaneous variability and predominantly asymptomatic transient ST segment changes are common in hypertensives; the interaction of both risk factors may provide an important link for fatal VA. Antiarrhythmic therapy is not to be recommended in the majority of patients. Presence of left ventricular hypertrophy and transient ST segment changes were the most powerful predictors of cardiac events during the follow-up.

Adult↗

Clinical implications of new insights into mechanism of antiarrhythmic drug action.

A classification system of antiarrhythmic drugs should help the clinician to select the optimal antiarrhythmic drug for a particular arrhythmia in an individual patient. This goal cannot be achieved by the Vaughan Williams classification system. Other important goals of this classification system were to provide the clinician with some information about proarrhythmic effects and about the possibility of combining particular antiarrhythmic agents. To date, a subdivision of class III antiarrhythmic agents has not been accomplished.

Animals↗

Efficacy of intravenously administered amiodarone for short-term control of serious arrhythmias.

Intravenously administered amiodarone exerts substantial antiarrhythmic activity that is based on several different electrophysiologic mechanisms. Of these, the most important consists of an antitachycardic effect together with a significant prolongation of repolarization. The acute intravenous administration of amiodarone has been found to be effective in supraventricular and ventricular tachyarrhythmias resistant to conventional antiarrhythmic agents. Because amiodarone is free of detrimental hemodynamic effects in the majority of patients, intravenous administration of this compound seems to be particularly suitable in patients with serious arrhythmias in the setting of compromised left ventricular function.

Action Potentials↗

Exercise-induced symptomatic and asymptomatic myocardial ischemia in patients with severe coronary artery disease: focus on the efficacy and safety of gallopamil.

Symptomatic and asymptomatic episodes of transient myocardial ischemia are well-known risk factors in patients with coronary artery disease. In a single-blind, randomized, and placebo-controlled study, the efficacy and safety of gallopamil was studied during a 1-week treatment period in 25 patients with high-grade coronary artery stenosis and frequent, exercise-induced episodes of myocardial ischemia. Eighteen patients were men, and seven patients were women; the mean age +/- SD was 59 +/- 7 years. After a 1-week run-in period (days 1-7), all patients were treated with gallopamil 50 mg t.i.d. (days 8-14) and placebo t.i.d. (days 15-21) or vice versa. Twenty-four-hour Holter monitoring, exercise testing, and adverse effects were controlled at days 7, 14, and 21. During the run-in period, all patients suffered a mean of 5.9 +/- 2.9 episodes of transient myocardial ischemia, mean ischemic duration was 38 +/- 29 min/day. Gallopamil increased exercise tolerance from 7.9 to 9.8 min (+24%, p < 0.05) and resulted in reduction of the weekly usage of short-acting nitrates by 45% compared to placebo. During 24-h Holter monitoring, mean heart rate at the onset of ST-segment depression increased from 106 to 118 beats/min (p < 0.05). The frequency of daily ischemic episodes was reduced after gallopamil administration from 6.1 to 3.9 episodes/day (-37%, p < 0.05), the total ischemic burden decreased for symptomatic episodes by -54% (p < 0.05) and for asymptomatic episodes by 29% (p < 0.05). Gallopamil modified the circadian distribution of ischemic episodes by modifying the morning peak of transient myocardial ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

[Clinical evaluation of new anti-arrhythmia drugs after the CAST (Cardiac Arrhythmia Suppression Trial) study].

The results of the Cardiac Arrhythmia Suppression Trial (CAST) are of great importance for the development and clinical evaluation of new antiarrhythmic agents. Today, the development of a new antiarrhythmic drug is only justified, if the benefit risk ratio is superior compared to those agents already available in clinical practice. The primary criterion of therapeutic efficacy is the prevention of tachyarrhythmic sudden cardiac death and/or the prevention of sustained ventricular tachycardia.

Anti-Arrhythmia Agents↗

[Immunoscintigraphy using 111In-antimyosin-antibodies in the clinical diagnosis of myocarditis].

Thirty patients suspected of having acute myocarditis underwent examination with 111In-labeled antimyosin antibodies. The heart/lung ratio was used for scintigraphic evaluation, with a value of > 1.5 being regarded as positive. The values were correlated with a score based on typical clinical parameters, separating myocarditis into categories "unlikely", "possible" and "highly probable". There was complete correlation in the category "myocarditis highly probable"--with a heart/lung ratio > 1.5 (11 patients)--and in the category of "myocarditis unlikely"--with a heart/lung ratio of < or = 1.5 (5 patients). The category "myocarditis possible" included 2 cases with a scintigraphic vote for the presence of myocarditis and 12 cases against. Immunoscintigraphy with antimyosin antibodies has shown itself to be a valuable non-invasive tool in the investigation of suspected myocarditis.

Acute Disease↗

[Risk stratification and long-term therapy with amiodarone in patients with idiopathic dilated cardiomyopathy].

Patients with cardiomyopathy are known to suffer from a high prevalence of tachyarrhythmic complications and sudden cardiac death. In a prospective study, 30 patients (25 men, 5 women, mean age: 52 +/- 12 years) with dilated cardiomyopathy underwent 48-h-Holter monitoring and programmed electrical stimulation and, independent from the results of the diagnostic work-up, were then randomized either to amiodarone or to a conventional or no antiarrhythmic therapy. At baseline, frequent ventricular arrhythmias (> 30 ventricular premature beats/h) were observed in 15/30 patients (50%), 13 patients (43%) had repetitive ventricular arrhythmias, additionally. Four patients suffered spontaneous sustained tachyarrhythmias. During programmed electrical stimulation, sustained monomorphic ventricular tachycardia was induced in 3/3 patients with and in 1/25 patients (4%) without a history of sustained tachycardia. Sustained monomorphic ventricular tachycardia was induced with one to two extrastimuli; three extrastimuli only increased the incidence of inducible ventricular fibrillation (8 patients, 28%). During a mean follow-up of 28 +/- 6 months 10/30 patients (33%) died for cardiac reasons (sudden cardiac death: 4/10 patients). Cardiac death was most likely in patients with a left-ventricular ejection fraction < 35% (5/18 patients, 28% versus 1/12 patients with ejection fraction > 35%, 8%) and further increased in the presence of reduced exercise tolerance and frequent and repetitive ventricular arrhythmias (4/7 patients, 57%). In the amiodarone group 4/15 patients died (27%, sudden cardiac death: one patient), while in patients not treated by amiodarone 8/15 patients died (54%; sudden cardiac death: three patients). Amiodarone therapy was well tolerated in all but one patient.

Adult↗

[Sudden cardiac death: can individual risk be predicted?].

Only 30-40% of all victims of sudden cardiac death could so far be classified as risk patients during their lifetime. Risk factors for sudden death have little predictive value in an asymptomatic population: for example, the typical risk profile for the presence of coronary heart disease and changes in the surface-ECG at rest and especially in the surface-ECG under stress. Usually, the victims of sudden cardiac death among top performance athletes have been suffering from a heart disease of which they knew nothing beforehand: below 40 years of age, mostly from hypertrophic cardiomyopathy; beyond 40, predominantly from coronary heart disease. Among the heart diseases, sudden cardiac death is the cause of death most often in hypertrophic cardiomyopathy, in dilatative cardiomyopathy and in certain types of coronary heart disease. Notwithstanding the employment of fully update cardiological diagnostics the risk patients cannot be identified with reliable precision among those suffering from these diseases. It is only clinically manifest persistent ventricular tachycardia or successful reanimation in case of ventricular fibrillation that will definitely pinpoint the patient as being at risk of sudden cardiac death also in the future.

Cardiomyopathy, Dilated↗