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Claudia Stöllberger

Publications and source records attributed to Claudia Stöllberger.

At least 19 recordsLinked to original sources
PubMed2007

Diagnosis of left atrial appendage thrombi by multiplane transesophageal echocardiography: interlaboratory comparative study.

BACKGROUND: Transesophageal echocardiography (TEE) is regarded as the method of choice for imaging left atrial appendage thrombi (LAAT). However, the interobserver variability among 2 independent echocardiographic laboratories in diagnosing LAAT by multiplane TEE has not yet been assessed. METHODS AND RESULTS: The videorecordings of 50 patients in atrial fibrillation (25 from each laboratory) were blindly reviewed by 1 experienced observer from each institution. LAAT were assessed as present, absent or questionable. Indications for TEE were: cardioversion (n=17), valve disease (n=13), endocarditis (n=12), or embolism (n=8). The prevalence of LAAT was 10% (observer 1) vs 12% (observer 2). A questionable LAAT was assessed in 6% vs 12% and a LAAT was excluded in 84% vs 76%, respectively. By head-to-head comparison, disagreement occurred in 11 cases (22%, kappa=0.5). Discrepant results were not related to the echocardiographic equipment. Problems occurred because of reverberation artifacts of the ridge between the left atrial appendage and left upper pulmonary vein (n=5), and in differentiating LAAT from spontaneous echocardiographic contrast (n=4) or an echogenic atrioventricular groove (n=1). The differentiation of pectinate muscles from LAAT was the reason for disagreement in only 1 case. Eliminating the category of questionable thrombi increased the kappa value to 0.65. In 5 patients undergoing cardiac surgery, both observers had agreed on the presence (n=1) or absence (n=4) of LAAT, and intraoperatively the results of TEE were confirmed. CONCLUSION: Even with multiplane TEE, interobserver variability among 2 independent echocardiographic laboratories for diagnosing LAAT remains high because of problems in differentiating LAAT from spontaneous echocardiographic contrast and reverberation artifacts.

Adult↗
PubMed2006

Prognosis of left ventricular hypertrabeculation/noncompaction is dependent on cardiac and neuromuscular comorbidity.

BACKGROUND AND OBJECTIVES: Left ventricular hypertrabeculation/noncompaction (LVHT) is a cardiac abnormality frequently associated with neuromuscular disorders (NMD). The data about long-term prognosis of patients with LVHT are controversial. Aim of the study in a cohort of LVHT patients was to assess the long-term prognosis regarding mortality, cardiac and neuromuscular comorbidity. METHODS AND RESULTS: In 86 patients LVHT was diagnosed echocardiographically between June 1995 and December 2004 (21 female, mean age 52 +/- 14, range 14-94 years). All patients underwent a baseline cardiologic investigation and were invited for a neurologic investigation. A specific NMD was diagnosed in 21, a NMD of unknown etiology in 33, the neurologic investigation was normal in 13 and 19 patients refused. During a mean follow-up of 51 months (range 3-106 months) the mortality rate was 5.3%/year. Predictors for an increased mortality were increased age (p=0.0134), presence of NMD (p=0.0324), exertional dyspnoea (p=0.0329), edema (p=0.0049), heart failure (p=0.0048), left anterior hemiblock (p=0.0078) and a left ventricular fractional shortening <25% (p=0.0648). CONCLUSION: The mortality of LVHT in adult patients depends on cardiac and neurologic comorbidity. Predictors for mortality are increased age, neuromuscular disorder, heart failure, left ventricular dilatation and systolic dysfunction.

Adolescent↗
PubMed2006

Acquired noncompaction associated with myopathy.

In a 40-year-old woman, hospitalised in May 2001 because of heart failure NYHA IV due to dilated cardiomyopathy, echocardiography had shown a normally sized but poorly contracting left ventricle with normal wall thickness. In October 2005, echocardiography in the same patient revealed a dilated left ventricle with extensive trabeculations and deep intertrabecular recesses in the lateral and posterior wall. The ratio of the noncompacted/compacted myocardium was 2. At clinical neurologic examination myopathy was suspected. Left ventricular hypertrabeculation/noncompaction may be associated with neuromuscular disorders and is not a congenital abnormality in each case.

Adult↗
PubMed2006

Non-compaction on autopsy in Duchenne muscular dystrophy.

Left ventricular hypertrabeculation (LVHT)/non-compaction is frequently associated with neuromuscular disorders. Recently, LVHT has been detected in a 28-year patient with Duchenne muscular dystrophy. Here, the patho-anatomic findings of this patient are presented, which showed LVHT located within in the apex and the anterior and lateral wall, being the most demanded segments during systole. The septum and the left ventricular outflow tract were not involved. The patho-anatomic specimen also showed aberrant bands and false tendons, a frequent finding in hearts with LVHT. The patho-anatomic findings were in line with those of LVHT patients with or without neuromuscular disorders.

Adult↗
PubMed2006

Cardiologic and neurologic findings in left ventricular hypertrabeculation/noncompaction relating to echocardiographic indication.

BACKGROUND: Left-ventricular hypertrabeculation/noncompaction (LVHT) is characterized by prominent trabeculations and intertrabecular recesses. LVHT is usually diagnosed if a patient is referred for echocardiography. The study assessed if cardiologic and neurologic findings differ relating to indication for echocardiography. METHODS: Included were patients in whom LVHT was diagnosed in one echocardiographic laboratory between June 1995 and December 2005. All patients underwent a cardiologic examination and were invited for a neurological investigation. RESULTS: LVHT was diagnosed in 93/35,181 patients (26 female, 53+/-15 years). Heart failure was the most frequent indication (n=49), followed by chest pain (n=21), syncope (n=8), search for cardiac involvement in myopathy (n=7), stroke or embolism (n=3), arterial hypertension (n=3) and screening of LVHT patients' relatives (n=2). Patients with the indication "heart failure" were older than patients with other indications (59.4+/-13.1 versus 44.9+/-12.9 years, p<0.001), had more often a neuromuscular disorder of unknown etiology (53% versus 32%, p<0.05), exertional dyspnoea (96% versus 32%, p<0.001), edema (25% versus 7%, p<0.05) and advanced heart failure (NYHA III: 41% versus 11%, p<0.01; NYHA IV: 29% versus 9%, p<0.05), suffered less often from arterial hypertension (22% versus 41%, p<0.05), angina pectoris (14% versus 34%, p<0.05) and palpitations or syncope (10% versus 30%, p<0.05). Patients with the indication "heart failure" had less frequent normal ECG than patients with other indications (2% versus 18%, p<0.01), had more frequent > or = 2 ECG abnormalities (57% versus 36%, p<0.05), left bundle branch block (29% versus 9%, p<0.05), a larger left-ventricular enddiastolic diameter (69.9+/-9.7 versus 57.4+/-12.2 mm, p<0.001), a lower left-ventricular fractional shortening (16.9+/-6.1% versus 31.1+/-11.5%, p<0.001) and more often valvular abnormalities (76% versus 30%, p<0.001). Location and extension of LVHT did not differ between indication groups. CONCLUSION: Echocardiographers should be aware of LVHT in any indication for echocardiography.

Adolescent↗
PubMed2006

Magnetic resonance imaging does not always confirm left ventricular noncompaction.

Left ventricular hypertrabeculation/noncompaction (LVHT) is diagnosed echocardiographically or by other imaging techniques, like cardiac magnetic resonance imaging (CMRI). LVHT was diagnosed echocardiographically in a 48-year-old woman with peripheric embolism and a neuromuscular disorder of unknown etiology. The spongiform trabecular meshwork was located in the ventricular lateral and posterior wall. CMRI failed to visualize LVHT and showed only a homogenously thickened structure. The reason for overlooking LVHT on cardiac magnetic resonance imaging might be poor image quality due to movement and respiration artefacts, the fine meshwork, exceeding the resolution capacity of the technique, and the atypical location of LVHT. CMRI does not confirm LVHT in every case on each occasion. This is most likely due to limitations in image resolution of the technique and movement artefacts of the myocardium.

Echocardiography↗
PubMed2006

Noncompaction in Duchenne muscular dystrophy: frustrated attempt to create a compensatory left ventricle?

The histological workup of the myocardium of a patient with Duchenne muscular dystrophy and left ventricular hypertrabeculation/noncompaction (LVHT) revealed an extremely thin left ventricular wall and a noncompacted layer double in size compared to the compacted layer. Within the compacted layer islets of fibrous tissue predominated, surrounded by areas of myxoid appearance hardly producing collagen, and occasionally normal or dystrophic cardiomyocytes. The noncompacted layer consisted largely of intact cardiomyocytes rarely intermingled with collagen-producing, fibrous tissue. This variant appearance of the compacted and noncompacted layer was found in all areas of noncompaction. These histopathological findings suggest that LVHT represents a compensatory attempt to overcome the failing compacted but dystrophic myocardium.

Adult↗
PubMed2006

Successful heart failure therapy in mitochondrial disorder with noncompaction cardiomyopathy.

OBJECTIVE: Effective heart failure therapy with angiotensin-converting enzyme inhibitors and beta-blockers in a patient with mitochondrial disorder and asymptomatic previously stable hypertrophic cardiomyopathy and left ventricular noncompaction (NCCMP) has not been reported. CASE REPORT: In a 58-year-old male with juvenile seizures, impaired hearing, recurrent pancreatitis, diabetes, recurrent emesis and diarrhea, discrete weakness for hip flexion, general wasting, and reduced tendon reflexes, elevated muscle-enzymes, abnormal lactate-stress-test, and mitochondrial dysfunction on muscle biopsy, mitochondrial disorder was diagnosed at age 51 year. Echocardiography revealed myocardial thickening and NCCMP. Cardiac abnormalities did not progress upon repeated follow-ups. At age 57 year he developed acute heart failure during respiratory infection. Echocardiography additionally revealed reduced left ventricular systolic function, and a restrictive filling pattern. Within seven weeks of therapy with ramipril (2.5 mg/day) and bisoprolol (1.25 mg/day) the restrictive filling pattern disappeared and fractional shortening normalized. CONCLUSION: This case shows that heart failure in a patient with mitochondrial disorder and previously stable hypertrophic cardiomyopathy and NCCMP promptly resolves under therapy with angiotensin-converting enzyme inhibitors and beta-blockers.

Adrenergic beta-Antagonists↗