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Biomedical subjects

C Stöllberger

Publications and source records attributed to C Stöllberger.

At least 19 recordsLinked to original sources
PubMed2006

Positive troponin-T in noncompaction is associated with neuromuscular disorders and poor outcome.

OBJECTIVES: Though cardiac troponin-T may be positive in hypertrophic and dilated cardiomyopathy, it is not known how often troponin-T is positive in left ventricular hypertrabeculation/ noncompaction (LVHT), an unclassified cardiomyopathy. This retrospective study aimed to assess how often troponin-T is positive in LVHT, is associated with elevated CK, is attributable to cardiac or extra-cardiac causes, in particular neuromuscular disorders (NMDs), or if it is a predictor of poor survival. RESULTS: Among 100 patients, detected over a period of 11 years, troponin-T was determined at least once in 71 (71%) of them. Troponin-T was determined once in 36 patients, twice in 8 cases, three times in 11 patients, and more than three times in 16 cases. Troponin- T was positive at least once in 12 patients (17%). Forty-five of the 71 patients suffered from a NMD (63%). Troponin-T positivity was associated with elevated CK in 6 cases. Troponin-T-positivity was attributable to acute myocardial ischemia in a single case, to chronic renal failure in 5 cases, to dilated cardiomyopathy in 4 cases, to atrial fibrillation in 3 cases, to heart failure in 4 cases, and to NMD in 10 cases. Troponin-T positivity in LVHT patients with NMD was assumed to be due to cardiac involvement in the disease. Among the 22 patients who died during the observational period troponin was determined in 16 and was positive in 4 (25%). CONCLUSIONS: Troponin-T is positive in 17% of the patients with LVHT. Most of these patients suffer from a NMD. Troponin-T positivity in LVHT predicts the presence of NMD and poor survival.

Adult↗
PubMed2006

Pitfalls in the diagnosis of left ventricular hypertrabeculation/non-compaction.

Left ventricular hypertrabeculation/non-compaction (LVHT) is a cardiac abnormality, characterised by >3 trabeculations apically to the papillary muscles and intertrabecular spaces. LVHT may occur with other cardiac abnormalities, heart failure, electrocardiographic abnormalities and neuromuscular disorders. This study gives an overview about (1) patients with LVHT in whom LVHT was initially overlooked and (2) cardiac conditions that may lead to falsely diagnosed LVHT. In 50 reported cases, LVHT has been overlooked and misdiagnosed as dilated (n = 20), hypertrophic (n = 14) or restrictive cardiomyopathy (n = 2), endocardial fibroelastosis (n = 5), endomyocardial fibrosis (n = 1), myocarditis (n = 3), thrombus (n = 2), localised left ventricular hypertrophy (n = 1), left ventricular mass (n = 1) or myocardial/pericardial disease (n = 1). In 14 patients, LVHT was diagnosed only by transoesophageal echocardiography (n = 1), computed tomography (n = 2) ventriculography (n = 2), magnetic resonance imaging (n = 3) or pathoanatomic findings (n = 6). Falsely diagnosed LVHT comprises false tendons, aberrant bands, thrombi, apical hypertrophic cardiomyopathy, fibroma, obliterative processes, intramyocardial haematoma, cardiac metastases and intramyocardial abscesses. Echocardiographers should be more aware of LVHT and consider its differential diagnoses.

Diagnostic Errors↗
PubMed2006

QT prolongation due to aortic aneurysm rupture and amiodarone in a patient with a H558R polymorphism in the cardiac sodium channel gene SCN5A.

The duration of the QT interval is influenced by many pathologic processes and drugs. We report a 74-year-old man who was admitted after syncope. His electrocardiogram (ECG) showed a QT interval of 0.44 s (QTc 0.53 s). After 10 h a ruptured abdominal aortic aneurysm was diagnosed and the patient underwent implantation of an aorto-bi-iliac Y-prosthesis. After surgery QT interval normalized. Under therapy with amiodarone, given because of atrial fibrillation, QT prolongation occurred again and disappeared after discontinuation of amiodarone. The postoperative course was complicated by critical illness polyneuropathy and plexopathy. Whereas amiodarone is a well recognized cause of QT prolongation, aortic aneurysm rupture has not been described previously. Vegetative mechanisms and sudden decrease of cardiac afterload due to the ruptured aneurysm may have altered myocardial repolarisation and thus prolonged QT interval duration. In conclusion in a patient with syncope and QT prolongation, extracardiac causes like rupture or an aortic aneurysm have to be included into the differential diagnosis.

Aged↗
PubMed2005

Tako-tsubo-like left ventricular dysfunction: clinical presentation, instrumental findings, additional cardiac and non-cardiac diseases and potential pathomechanisms.

Tako-tsubo-like left ventricular dysfunction phenomenon (TTP) has primarily been described in Japan and is characterized by transient left ventricular apical ballooning in the absence of coronary artery disease, associated with chest symptoms, electrocardiographic changes and minimal cardiac enzymes release. Aim of the present review is to summarize the current knowledge about TTP. TTP has been described predominantly in females. TTP occurs also outside Japan. Clinical symptoms comprise anginal chest pain, dyspnea and syncope. TTP occurs frequently after acute emotional or physical stress. Electrocardiographic ST- elevations may be present only for several hours. Then, normalization of the ST-segment occurs, followed by negative T waves, which persist for months. Arterial hypertension in TTP is found in up to 76%, hyperlipidaemia in up to 57%, diabetes mellitus in up to 12% and smoking in up to 18% of the patients. Several pathomechanisms have been proposed: myocardial stunning due to increased catecholamine levels, coronary vasospasm, atherosclerotic plaques rupture, myocarditis, catecholamine-induced hyperkinesis of the basal left ventricular segments and genetic. Patients with TTP should be monitored like patients with myocardial infarction. Care should be taken in the application of catecholamines and nitrates. Betablockers should be given in the acute and chronic phase, and possibly indefinitely to prevent recurrences. The prognosis of TTP is assumed to be good, but in the acute phase there are deaths due to multisystem organ failure, cardiogenic shock, ventricular fibrillation and ventricular rupture. The long term prognosis of TTP patients is largely unknown.

Humans↗
PubMed2004

Skeletal muscle involvement in congenital long QT syndrome.

Skeletal muscle involvement in a genetically confirmed congenital long QT syndrome (LQTS) has not been reported. In a 36-year-old male, intracerebral bleeding from a brainstem cavernoma suddenly occurred. His history was noteworthy for congenital LQTS due to a point mutation in the KVLQT1-gene on chromosome 11. The mutation was also found in his two daughters, his sister, her daughter and his mother. His ECG showed sinusrhythm and a QTc-interval of 0.46 ms. Needle-EMG from the right abductor pollicis, left brachial biceps, left extensor digitorum, and right anterior tibial muscle(s), carried out because muscle involvement had been previously reported in clinically diagnosed congenital LQTS, revealed abnormal spontaneous activity, but otherwise normal motor unit architecture. LQTS, due to a KVLQT1 mutation, may manifest not only in the heart, but subclinically also in the skeletal muscle.

Action Potentials↗
PubMed2004

Candida sepsis with intramyocardial abscesses mimicking left ventricular noncompaction.

Left ventricular (LV) noncompaction is a rare abnormality characterized by more than three trabeculations protruding from the LV wall, distal to the papillary muscles and visible in one echocardiographic image plane. The intertrabecular spaces are perfused from the LV cavity, as visualized on color Doppler imaging. Differential diagnoses of LV noncompaction are intraventricular thrombi, false tendons, aberrant bands, intramyocardial hematoma, cardiac metastases and the apical type of hypertrophic cardiomyopathy. Intramyocardial abscesses have not been reported as a differential diagnosis of LV noncompaction. In the patient presented, cardiac microabscesses due to candida sepsis mimicked LV noncompaction and should be considered in the differential diagnosis of LV noncompaction.

Abscess↗
PubMed2004

Histological detection of intramyocardial abscesses in Candida sepsis mimicking left ventricular non-compaction/hypertrabeculation on echocardiography.

Left ventricular non-compaction/hypertrabeculation (LVHT) is a rare cardiac abnormality characterized by more than three trabeculations protruding from the left ventricular wall, apically to the papillary muscles, visible in one echocardiographic image plane and intertrabecular spaces, perfused from the ventricular cavity. LVHT is frequently associated with neuromuscular disorders. Differential diagnoses of LVHT are intraventricular thrombi, false tendons, aberrant bands, intramyocardial hematoma, cardiac metastases and the apical type of hypertrophic cardiomyopathy. Intramyocardial abscesses have not been reported as a differential diagnosis of left ventricular non-compaction. In the presented case, cardiac microabscesses as a result of Candida sepsis mimicked left ventricular non-compaction in a 55-year-old man with hypopharyngeal carcinoma who died 20 days after chemotherapy. These microabscesses were not visible on echocardiography but were detected only at histologic examination of the myocardium. This case shows that intramyocardial abscesses as a result of Candida sepsis are a rare differential diagnosis of LVHT.

Abscess↗
PubMed2003

Left atrial appendage morphology: comparison of transesophageal images and postmortem casts.

BACKGROUND: Aim of the study was to compare 1) transesophageal echocardiographic (TEE) measurements of the left atrial appendage (LAA) with postmortem casts and 2) the TEE with the postmortem diagnosis of LAA thrombi. METHODS: From the TEE images and LAA casts length, orifice, diameter and number of branches were assessed. LAA area was measured by TEE and LAA volume from the cast. RESULTS: In 12 patients who underwent TEE and autopsy, measurements of LAA length and area correlated well with the cast volume ( r=0.6 to r=0.93). The agreement between TEE and LAA casts, concerning the number of branches, was only moderate. In one patient, a false positive diagnosis of a LAA thrombus occurred. CONCLUSIONS: LAA size and orifice diameter can be assessed reliably by TEE. The complex LAA morphology hampers measurements of LAA length, branches, course and diagnosis of thrombi.

Acrylic Resins↗
PubMed2003

Nonsteroidal anti-inflammatory drugs in patients with cardio- or cerebrovascular disorders.

Nonsteroidal anti-inflammatory drugs (NSAIDs) are a frequently prescribed group of highly effective drugs of which the most well-known side effect is gastrointestinal peptic ulcer. However, NSAIDs have additional renal, cardiovascular, hematological, dermatological, and neurological side effects. Although the spectrum of side effects is slightly different between the conventional NSAIDs and the recently developed cyclooxygenase 2 (COX-2) inhibitors, their overall spectrum is quite similar. Aim of this review is to summarize the current knowledge about NSAIDs and their effects on patients with cardio- or cerebrovascular disorders. NSAIDs interact with many drugs which are used in patients with cardio- or cerebrovascular disorders: They attenuate the effects of diuretics, betablockers, ACE inhibitors and AT-2 blockers, thus leading to uncontrolled hypertension or aggravation of heart failure. They increase digoxin levels, potentiate the effect of oral anticoagulants and interact with platelet inhibitors, thus leading to a higher bleeding risk. There are indications that NSAIDs may induce hypertension in normotensives and that COX-2 inhibitors may lead to an increased rate of myocardial infarction and strokes. Based on these data it is recommended that NSAIDs should be avoided in patients with cardio- or cerebrovascular disorders and alternative pharmaceutical, physical or surgical therapy should be applied. If NSAIDs are inevitable, their side effects should be well monitored; they should be prescribed with caution when given in combination with diuretics, betablockers, ACE inhibitors, AT-2 blockers, digitalis, oral anticoagulants and platelet inhibitors. COX- 2 inhibitors should be avoided in patients with known coronary or cerebrovascular disorders. In patients with uncontrolled hypertension or worsening of heart failure, unreported NSAID-use should be considered. Generally, there is a need to develop further analgetic drugs without the described side effects for patients with cardio- and cerebrovascular disorders.

Adrenergic beta-Antagonists↗
PubMed2003

Is left ventricular hypertrabeculation/ noncompaction a cardiac manifestation of Fabry's disease?

BACKGROUND AND OBJECTIVES: Some types of hypertrophic cardiomyopathy are due to cardiac Fabry's disease. Since left ventricular hypertrabeculation/noncompaction (LVHT) is regarded a subtype of hypertrophic cardiomyopathy, we looked for the alpha-galactosidase levels in blood leukocytes of LVHT patients. METHODS: Included were male patients in whom LVHT was diagnosed between June 1995 and September 2002. Echocardiographic criteria for LVHT were 1) >3 trabeculations protruding from the left ventricular wall, apically to the papillary muscles, visible in 1 image plane, and 2) intertrabecular spaces perfused from the ventricular cavity, as visualised on colour Doppler imaging. Trabeculations were defined as structures with the same echogenicity as the myocardium and moving synchronously with the ventricular contractions. Excluded were patients with known neuromuscular disorders. All patients were asked for systemic manifestations of Fabry's disease and blood tests were taken. The alpha-galactosidase-A activity was determined by means of an established fluorometric assay in blood leukocytes. RESULTS: Forty-one patients were invited and 26 accepted the invitation. The remaining patients had died (n=5), lived abroad (n=5) or were unwilling (n=5). Among the 26 patients, aged 28-78 years, who followed the invitation, one had renal failure due to renal shrinkage and one had suffered from a stroke 3 years previously. Leukocyte alpha-galactosidase levels ranged from 70 to 188 nM/mg Prot/h (normal: > or =42 nM/mg Prot/h). In none of the patients was the alpha-galactosidase level reduced. CONCLUSION: LVHT does not seem to be a manifestation of cardiac Fabry's disease. To definitively exclude Fabry's disease, however, endomyocardial biopsy is required.

Adult↗