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T Wichter

Publications and source records attributed to T Wichter.

65 records · Page 4Linked to original sources
PubMed1994

Detection of regional left ventricular asynchrony in obstructive hypertrophic cardiomyopathy by magnetic resonance imaging.

Cine magnetic resonance imaging was used to analyze global and regional left ventricular function in seven patients with obstructive hypertrophic cardiomyopathy (HC) and 10 normal subjects. In patients with HC a 38% higher left ventricular mass index (106.4 +/- 20.2 gm/m2 vs 77.0 +/- 16.1 gm/m2, p < 0.005) associated with a lower end-diastolic volume index (44.9 +/- 8.9 ml/m2 vs 58.3 +/- 9.0 ml/m2, p < 0.005) resulted in an 85% higher mass-to-volume ratio (2.4 +/- 0.52 vs 1.3 +/- 0.57, p < 0.0005). Stroke volume did not differ significantly, whereas ejection fraction was higher (80.4% +/- 6.5% vs 65.4% +/- 7.2%, p < 0.0005) in patients with HC. Although early diastolic filling fraction was smaller in patients with HC (61.0% +/- 22.8% vs 68.4% +/- 14.6%), the difference did not reach significance because of substantial variability. In patients with HC (in contrast to normal subjects) the time to maximal wall thickening was shorter (p < 0.025) in the hypertrophied basal region of the ventricle (223 +/- 42 msec) than in the apical region (267 +/- 35 msec), reflecting asynchrony between these regions. Additionally, in patients with HC the standard deviation of the time to maximal wall thickening in the basal region was significantly higher when compared with that of normal subjects (40.0 +/- 24 msec vs 16.9 +/- 17 msec, p < 0.0005), reflecting asynchrony even within one region. Thus magnetic resonance imaging can detect regional left ventricular asynchrony, an important cause of impaired diastolic function, in patients with HC and normal global systolic function.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

Regional myocardial sympathetic dysinnervation in arrhythmogenic right ventricular cardiomyopathy. An analysis using 123I-meta-iodobenzylguanidine scintigraphy.

BACKGROUND: In patients with arrhythmogenic right ventricular cardiomyopathy (ARVC), the frequent provocation of ventricular tachycardia during exercise, the sensitivity toward catecholamines, and the response toward antiarrhythmic drug regimen with antiadrenergic properties suggest an involvement of the sympathetic nervous system in arrhythmogenesis. METHODS AND RESULTS: To analyze the presence, extent, and location of impaired myocardial sympathetic innervation in ARVC, 123I-meta-iodobenzylguanidine (123I-MIBG) scintigraphy was performed in 48 patients with ARVC. For comparison, 9 patients with idiopathic ventricular tachycardia and a control group of 7 patients without heart disease were investigated. In patients with ARVC, the clinical sustained (n = 25; 52%) or nonsustained (n = 23; 48%) ventricular tachycardia originated in the right ventricular outflow tract in 38 patients (79%), whereas in the remaining 10 patients (21%), the site of origin was the apical (n = 5) or inferior (n = 5) right ventricle. In 33 patients (69%), nonsustained or sustained ventricular tachycardia was provocable by exercise (n = 28 of 48; 58%) and/or by isoproterenol infusion (n = 16 of 37; 43%), whereas programmed ventricular stimulation induced sustained or nonsustained ventricular tachycardia in 16 patients each (33% each). With 123I-MIBG scintigraphy, the right ventricle was not visible in any patient. No areas of intense 123I-MIBG uptake ("hot spots") were observed. All patients of the control group and 7 of 9 patients (78%) with idiopathic ventricular tachycardia showed a uniform tracer uptake in the left ventricle. In contrast, only 8 of 48 ARVC patients (17%) showed a homogeneous distribution of 123I-MIBG uptake, whereas 40 patients (83%) demonstrated regional reductions or defects of tracer uptake. In 3 of 48 patients (6%), the defect area was < 15%; in 21 patients (44%), it was 15% to 30%; and in 16 patients (33%), it was > 30% of the polar map area of the left ventricle (mean, 23 +/- 15%; range, 0% to 57%). In 38 of 40 patients (95%) with an abnormal 123I-MIBG scan, reduced tracer uptake was located in the basal posteroseptal left ventricle, involving the adjacent lateral wall in 10, the anterior wall in 2, and the apex in 12 patients. Only 2 patients demonstrated isolated defects of the anterior or lateral wall; one involved the apex. Perfusion abnormalities in the areas of 123I-MIBG defects were excluded by stress/redistribution 201T1 single-photon emission computed tomography scintigraphy and by normal coronary angiograms in all patients. Abnormalities in 123I-MIBG scintigraphy in patients with ARVC correlated with the site of origin of ventricular tachycardia, demonstrating a regionally reduced tracer uptake in 36 of 38 patients (95%) with right ventricular outflow tract tachycardia compared with only 4 of 10 patients (40%) with other right ventricular origins of tachycardia. There was no correlation between the results of 123I-MIBG scintigraphy and the extent of right ventricular contraction abnormalities, right ventricular ejection fraction, biopsy results, coronary anatomy, or left ventricular involvement in ARVC. CONCLUSIONS: In patients with ARVC, regional abnormalities of sympathetic innervation are frequent and can be demonstrated by 123I-MIBG scintigraphy. Sympathetic denervation appears to be the underlying mechanism of reduced 123I-MIBG uptake and may be related to frequent provocation of ventricular arrhythmias by exercise or catecholamine exposure in ARVC. Therefore, in patients with ARVC, the noninvasive detection of localized sympathetic denervation by 123I-MIBG imaging may have implications for the early diagnosis and for the choice of antiarrhythmic drugs in the treatment of arrhythmias.

3-Iodobenzylguanidine↗
PubMed1994

[The pro-arrhythmic effects of anti-arrhythmia agents].

Proarrhythmia is defined as the provocation of new cardiac arrhythmias or the aggravation of preexisting arrhythmias by antiarrhythmic drugs. The possible types of manifestation of proarrhythmia are manifold. With respect to prognosis, drug-induced ventricular tachyarrhythmias seem to be of particular importance. Monomorphic ventricular tachycardia and ventricular tachycardias of the torsade de pointes type have to be distinguished. The former seem to be mainly based on reentrant mechanisms, while the later is supposed to result from triggered activity. Drug-induced monomorphic tachycardia is most often observed during therapy with drugs which slow conduction (class I agents, proarrhythmic potency: IC > IA > IB). Patients with depressed left ventricular function and previously documented life-threatening tachyarrhythmias are the most susceptible candidates. Torsade de pointes can be preferentially observed during therapy with antiarrhythmic drugs which prolong myocardial repolarization (i.e. class IA and class III agents). Electrolyte abnormalities and/or bradycardia are factors which often predispose to the development of this particular type of proarrhythmia. The physician who prescribes antiarrhythmic drugs must be aware of the different types and clinical manifestations of proarrhythmia. This is necessary to assess the degree of proarrhythmic risk and to determine the benefit/risk ratio before the start of drug therapy.

Anti-Arrhythmia Agents↗
PubMed1993

Sympathetic innervation of the left ventricle is impaired in arrhythmogenic right ventricular disease.

Arrhythmogenic right ventricular disease (ARVD) is a disease of unknown origin that primarily affects the right ventricle and is characterized by ventricular tachyarrhythmias which may lead to syncope and even, though rarely, sudden cardiac death. In 25 patients with ARVD, sympathetic innervation of the left ventricle was assessed by iodine-123 metaiodobenzylguanidine single photon emission tomography (123I-MIBG SPET). In addition, thallium-201 SPET was performed. The diagnosis of ARVD was made by an electrophysiological study and right and left heart catheterization including right ventricular endomyocardial biopsy. Ischaemic heart disease was excluded by coronary angiography. A group of seven patients without any evidence of heart disease served as a control group. Twenty-two of the 25 patients showed reduced uptake of 123I-MIBG. The abnormal areas were located predominantly in posterior and posteroseptal segments of the heart. No focus of increased 123I-MIBG activity could be demonstrated. No patient had signs of left ventricular involvement on left ventricular angiography. In contrast to the results of the 123I-MIBG SPET, those of 201T1 SPET were normal in 16 patients. The remaining nine patients showed areas of slight hypoperfusion not correlated with the reduced 123I-MIBG uptake. 123I-MIBG scintigraphy allows detection of left ventricular adrenergic dysinnervation in ARVD patients without morphological or functional abnormalities of the left ventricle.

3-Iodobenzylguanidine↗
PubMed1993

The signal-averaged ECG: time-domain analysis.

During the past decade, the high-resolution electrocardiogram as a non-invasive technique for the detection of ventricular late potentials has developed from an experimental method into a routinely applied non-invasive method for risk stratification of patients after myocardial infarction. Meanwhile, several approaches have been developed for the detection of ventricular late potentials including time-domain analysis, frequency-domain analysis and spectrotemporal mapping. Clinical applications are no longer limited to patients after myocardial infarction, but cover a wider spectrum of different cardiac diseases. This review focuses on some methodological aspects as well as on the results and current clinical applications of the analysis of the signal-averaged ECG in the time domain.

Action Potentials↗
PubMed1993

Arrhythmogenic right ventricular disease: MR imaging vs angiography.

OBJECTIVE: Arrhythmogenic right ventricular disease (ARVD) is increasingly found in young adults with ventricular arrhythmias and is characterized by ventricular tachycardia originating within the right ventricle and regional or diffuse abnormalities in the contraction of the right ventricle. Until now, the gold standard for the detection of global and regional abnormalities of the right ventricular wall has been angiography combined with biopsy. The purpose of the current study was to compare MR imaging with angiography for assessing the location and extent of morphologic and functional abnormalities in patients with ARVD. SUBJECTS AND METHODS: Electrocardiographically gated spin-echo and cine gradient-echo MR imaging of the heart was performed in 36 consecutive patients with biopsy-proved ARVD. Patients were prospectively separated into two groups according to the results of invasive electrophysiologic tests (18 with inducible ventricular tachycardia during invasive electrophysiologic studies [ARVD 1] and 18 without inducible ventricular tachycardia [ARVD 2]) and compared with 11 control subjects. Global and regional morphology and function of the right ventricle were assessed with MR imaging, and those findings were compared with angiographic findings. RESULTS: Right ventricular ejection fraction was significantly lower in patients with ARVD 1 than in patients with ARVD 2 or in control subjects. Regional abnormalities of the right ventricular wall also were more pronounced in patients with ARVD 1 than in patients with ARVD 2. Signal-intensity increases corresponding to fatty replacement shown by biopsy were seen in 33% of patients with ARVD 1 and in 11% of patients with ARVD 2. Abnormal regions of the right ventricular wall seen on MR images corresponded to angiographic findings in 86% of patients. Comparison with control subjects showed that patients with ARVD 1 had a significant delay in diastolic relaxation of the right ventricle. CONCLUSION: Our results show that MR imaging can be used to assess morphologic alteration, tissue abnormalities, and global as well as regional dysfunction of the right ventricle in patients with ARVD. It may become a useful clinical tool for diagnosing and grading ARVD and a worthy substitute for angiography and biopsy in the follow-up of patients with ARVD.

Adolescent↗
PubMed1993

[Diagnostic and therapeutic problems in idiopathic prolonged QT syndrome. A case report].

The case of a 36-year-old woman with suspected idiopathic long QT syndrome is reported. Diagnosis was made late after syncopal attacks and several episodes of resuscitation had occurred. Although therapy with a beta-blocking agent was initiated and a cardioverter/defibrillator was implanted, the patient died, due to a hydrocephalus internus resulting in cerebral damage. Diagnostic and therapeutic problems in idiopathic long QT syndrome are discussed.

Adult↗
PubMed1992

Efficacy of antiarrhythmic drugs in patients with arrhythmogenic right ventricular disease. Results in patients with inducible and noninducible ventricular tachycardia.

BACKGROUND: Ventricular tachyarrhythmias are the major clinical manifestation of arrhythmogenic right ventricular disease. Although antiarrhythmic therapy has been widely advocated, there is only limited information available on the efficacy of antiarrhythmic drugs in these patients. METHODS AND RESULTS: The short- and long-term efficacies of various antiarrhythmic agents were retrospectively and prospectively analyzed in 81 patients (mean age, 39 +/- 14 years; range, 16-68 years; 61.7% males) with arrhythmogenic right ventricular disease. In 42 patients with inducible ventricular tachycardia during programmed ventricular stimulation, the following efficacy rates were obtained: class Ia and Ib drugs (n = 18), 5.6%; class Ic drugs (n = 25), 12%; beta-blockers (n = 8), 0%; sotalol (n = 38), 68.4%; amiodarone (n = 13), 15.4%; verapamil (n = 5), 0%; and drug combinations (n = 26), 15.4%. Only one of the 10 patients not responding to sotalol was treated effectively by amiodarone, whereas the remaining nine patients proved to be drug refractory toward all other drugs tested (3.8 +/- 2.3 drugs, including amiodarone in five cases) and underwent nonpharmacological therapy. During a follow-up of 34 +/- 25 months, three of the 31 patients (9.7%) discharged on pharmacological therapy had nonfatal recurrences of ventricular tachycardia after 0.5, 51, and 63 months, respectively. In 39 patients with noninducible ventricular tachycardia during programmed ventricular stimulation, the following efficacy rates were observed: class Ia and Ib drugs (n = 16), 0%; class Ic agents (n = 23), 17.4%; beta-blockers (n = 7), 28.6%; sotalol (n = 35), 82.8%; amiodarone (n = 4), 25%; verapamil (n = 24), 50%; and drug combinations (n = 11), 9.1%. During a follow-up of 14 +/- 13 months, four of 33 patients (12.1%) discharged on antiarrhythmic drugs had nonfatal relapses of their clinical ventricular arrhythmia. CONCLUSIONS: Thus, in arrhythmogenic right ventricular disease, sotalol proved to be highly effective in patients with inducible as well as noninducible ventricular tachycardia. Patients with inducible ventricular tachycardia not responding to sotalol are likely to not respond to other antiarrhythmic drugs and should be considered for nonpharmacological therapy without further drug testing. Amiodarone did not prove to be more effective than sotalol and may not be an alternative because of frequent side effects during long-term therapy, especially in young patients. Verapamil and beta-blockers were effective in a considerable number of patients with noninducible ventricular tachycardia and may be a therapeutic alternative in this subgroup. Class I agents appear to be rarely effective in the treatment of both inducible and noninducible ventricular tachycardia in arrhythmogenic right ventricular disease.

Adolescent↗
PubMed1991

[Arrhythmogenic right ventricular disease].

In patients with syncope, ventricular tachyarrhythmias, and sudden death, in the absence of coronary artery disease or dilative and hypertrophic cardiomyopathy, arrhythmogenic right ventricular disease is a common underlying heart disease. It is marked by ventricular tachyarrhythmias of left bundle branch block pattern, often induced by exercise; negative T-waves in the right precordial leads of the surface-ECG, and localized or diffuse right ventricular contraction abnormalities detected by various imaging techniques in a young, apparently healthy population. Congenital disposition with progressive fibrous and lipomatous tissue infiltration of the right ventricular myocardium with hypertrophy and degeneration of surviving myocytes is the pathogenetic factor leading to modification of conduction and resulting in the development of arrhythmogenic zones. This review contains the current knowledge about arrhythmogenic right ventricular disease on the basis of our own experience, and also a review of the literature. Controversial hypotheses concerning etiology and prognosis are discussed. Variant forms and stages of the disease are described, taking differential diagnostic aspects into consideration. Non-invasive and invasive diagnostic methods are evaluated with regard to their diagnostic accuracy, feasibility, and limitations. Pharmacological and alternative therapeutic concepts are presented, including catheter ablation and surgical intervention.

Bundle-Branch Block↗
PubMedDate not supplied

Multislice cardiac spiral CT evaluation of atypical hypertrophic cardiomyopathy with a calcified left ventricular thrombus.

We report a case of a 43-year-old male patient with an atypical nonobstructive hypertrophic cardiomyopathy and a calcified left ventricular thrombus, and present results of multislice computed tomography (MSCT) using retrospective electrocardiograph gating, which is a new modality in cardiac imaging. Obtaining virtually motion-free images with a temporal resolution of 250 ms in an optimized heart scan MSCT allows functional imaging with evaluation of impaired systolic and diastolic left ventricular wall motion.

Adult↗