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Biomedical subjects

U C Hoppe

Publications and source records attributed to U C Hoppe.

At least 19 recordsLinked to original sources
PubMed2005

[Levosimendan].

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3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2005

[Everolimus].

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Everolimus↗
PubMed2005

[How to detect impending cardiac insufficiency].

The characteristic leading symptoms of heart failure are a reduction in physical performance, dyspnea and the development of edema. At this point, such examinations as an ECG and determination of various laboratory parameters become mandatory. For the differential diagnostic exclusion of a pulmonary cause of respiratory distress, lung function tests and chest X-rays are needed. If heart failure is suspected clinically, echocardiography is the most important noninvasive method for identifying a cardiac functional disorder. With the aid of this examination, systolic function, diastolic filling, myocardial thickness and valve function can be evaluated. Cardiac catheterization is emportant to determine the underlying causes of heart failure and to plan therapy.

Cardiac Catheterization↗
PubMed2005

[Dilated cardiomyopathy in tachycardiac atrial flutter].

HISTORY AND CLINICAL FINDINGS: We present a 38-year-old male patient with progressive exertional dyspnoea and intermittent palpitations. The initial examination detected a regular tachycardia with a heart rate of 160 bpm. EXAMINATIONS, DIAGNOSIS: In association with intermittent palpitations the 12-lead ECG detected a typical type of atrial flutter. A transthoracic echocardiography and cardiac catheterization revealed a left ventricular dilation and marked systolic dysfunction (EF 39 %) with normal coronaries. The diagnosis of dilated cardiomyopathy was made on these findings. TREATMENT AND COURSE: On the basis of this diagnosis, we treated our patient by radiofrequency catheterablation, which successfully terminated atrial flutter. Three month after ablation the echocardiography was normal with an increase of the shortening fraction from 18 to 37 % and the patient was asymptomatic. Retrospectively the diagnosis of tachycardia-induced cardiomyopathy was made. CONCLUSION: Tachycardia-induced cardiomyopathy is a rare, but reversible form of dilated cardiomyopathy. The cornerstone in the management of these patients is to achieve a normal ventricular beating rate. Radiofrequency catheterablation is a curative therapeutic option that can terminate tachyarrhythmias and lead to significant improvement of left ventricular diameters, systolic function and symptoms in patients with tachycardia-induced cardiomyopathy.

Adult↗
PubMed2005

Digitalis in heart failure! Still applicable?

In patients with heart failure and atrial fibrillation cardiac glycosides, generally in combination with beta-blockers, are indicated to control ventricular rate. In systolic heart failure and sinus rhythm, however, the use of digitalis continues to be debated. There are special concerns that cardiac glycosides might lead to an increased mortality rate in women. Retrospective analyses, however, do not indicate any sex-based differences in the effectiveness of cardiac glycosides. Beneficial effects of cardiac glycosides in heart failure seem to be related to the attenuation of sympathetic activation and neurohumoral alterations, which is already obtained at low digoxin serum concentrations, while high serum levels are associated with increased mortality. Therefore, in patients with sinus rhythm who remain symptomatic under an optimized therapy with ACE inhibitors, beta-blockers and diuretics in addition to digitalis should be considered regardless of the gender. However, target serum digoxin concentrations should be low in a range of 0.5 to 0.8 ng/ml.

Adrenergic beta-Antagonists↗
PubMed2005

Hypereosinophilic syndrome associated with acute necrotizing myocarditis and cardiomyopathy.

We report the rare case of a 55-year-old female with massive eosinophilic myocarditis and severe, however reversible, impairment of left ventricular function. The patient presented with reduced physical condition, progressive dyspnea on exertion and peripheral edema. The white blood count revealed a leukocytosis and markedly elevated peripheral blood eosinophilics (48.8%). An endomyocardial biopsy demonstrated massive myocardial infiltration with eosinophilic granulocytes and necrosis. The symptoms and laboratory parameters indicate the presence of a hypereosinophilic syndrome. The differential diagnosis of a Churg-Strauss syndrome is discussed. Medical heart failure treatment according to international guidelines and an immunosuppressive treatment with prednisolone (Decortin H) 1.5 mg/kgBW) were initiated. This therapy led to a dramatic reduction of the eosinophilic granulocyte count and normalization of the peripheral blood count, which correlated with a significant improvement of clinical symptoms. Consistently, an increase of left-ventricular function was observed. Upon successive dose reduction to a maintenance dosage of 10 mg prednisolone, the patient's clinical status and peripheral blood count remained stable.

Acute Disease↗
PubMed2004

[Recurrent syncope after blunt trauma of the thorax].

HISTORY AND ADMISSION FINDINGS: A 35-year-old patient presented with a non-penetrating chest trauma due to an automobile accident. Examinations showed a trauma of the left shoulder (reversed Hill-Sachs lesion). After diagnostic procedures, he underwent surgery four weeks later. During the hospital stay, the patient developed angina pectoris, dizziness and syncopes. INVESTIGATIONS AND DIAGNOSIS: When the patient was transferred to our institution a 12-leads electrocardiogram and blood analysis were unremarkable. Cardiac catheterization revealed a relaxation disorder of the left ventricular anterior wall with normal coronaries. The Holter-ECG detected with occasional attacks of dizziness and recurrent syncopes concurrent with intermittent episodes of high-degree atrioventricular block and supraventricular tachycardias. This led to the diagnosis of myocardial contusion with long term symptomatic arrhythmias. TREATMENT AND COURSE: Since syncopes and arrhythmias persisted over several weeks following myocardial contusion a combined therapy with a dual chamber pacemaker and beta-blocker was initiated. CONCLUSION: ECG monitoring after blunt chest trauma in the early period and after several days is mandatory to screen and prevent potentially life threatening posttraumatic arrhythmias.

Accidents, Traffic↗
PubMed2001

Functional consequences of the arrhythmogenic G306R KvLQT1 K+ channel mutant probed by viral gene transfer in cardiomyocytes.

IKs, the slow component of the delayed rectifier potassium current, figures prominently in the repolarization of heart cells. The K+ channel gene KvLQT1 is mutated in the heritable long QT (LQT) syndrome. Heterologous coexpression of KvLQT1 and the accessory protein minK yields an IKs-like current. Nevertheless, the links between KvLQT1 and cardiac IKs are largely inferential. Since the LQT syndrome mutant KvLQT1-G306R suppresses channel activity when coexpressed with wild-type KvLQT1 in a heterologous system, overexpression of this mutant in cardiomyocytes should reduce or eliminate native IKs if KvLQT1 is indeed the major molecular component of this current. To test this idea, we created the adenovirus AdRMGI-KvLQT1-G306R, which overexpresses KvLQT1-G306R channels. In > 60 % of neonatal mouse myocytes, a sizable IKs could be measured using perforated-patch recordings (8.0 +/- 1.6 pA pF-1, n = 13). IKs was increased by forskolin and blocked by clofilium or indapamide but not by E-4031. While cells infected with a reporter virus expressing only green fluorescent protein (GFP) displayed IKs similar to that in uninfected cells, AdRMGI-KvLQT1-G306R-infected cells showed a significantly reduced IKs (2.4 +/- 1.1 pA pF-1, n = 10, P < 0.01) when measured 60-72 h after infection. Similar results were observed in adult guinea-pig myocytes (5.9 +/- 1.2 pA pF-1, n = 9, for control vs. 0.1 +/- 0.1 pA pF-1, n = 5, for AdRMGI-KvLQT1-G306R-infected cells). We conclude that KvLQT1 is the major molecular component of IKs. Our results further establish a dominant-negative mechanism for the G306R LQT syndrome mutation.

1-Methyl-3-isobutylxanthine↗
PubMed2001

Distinct gene-specific mechanisms of arrhythmia revealed by cardiac gene transfer of two long QT disease genes, HERG and KCNE1.

The long QT syndrome (LQTS) is a heritable disorder that predisposes to sudden cardiac death. LQTS is caused by mutations in ion channel genes including HERG and KCNE1, but the precise mechanisms remain unclear. To clarify this situation we injected adenoviral vectors expressing wild-type or LQT mutants of HERG and KCNE1 into guinea pig myocardium. End points at 48-72 h included electrophysiology in isolated myocytes and electrocardiography in vivo. HERG increased the rapid component, I(Kr), of the delayed rectifier current, thereby accelerating repolarization, increasing refractoriness, and diminishing beat-to-beat action potential variability. Conversely, HERG-G628S suppressed I(Kr) without significantly delaying repolarization. Nevertheless, HERG-G628S abbreviated refractoriness and increased beat-to-beat variability, leading to early afterdepolarizations (EADs). KCNE1 increased the slow component of the delayed rectifier, I(Ks), without clear phenotypic sequelae. In contrast, KCNE1-D76N suppressed I(Ks) and markedly slowed repolarization, leading to frequent EADs and electrocardiographic QT prolongation. Thus, the two genes predispose to sudden death by distinct mechanisms: the KCNE1 mutant flagrantly undermines cardiac repolarization, and HERG-G628S subtly facilitates the genesis and propagation of premature beats. Our ability to produce electrocardiographic long QT in vivo with a clinical KCNE1 mutation demonstrates the utility of somatic gene transfer in creating genotype-specific disease models.

Action Potentials↗