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Biomedical subjects

Josef Finsterer

Publications and source records attributed to Josef Finsterer.

At least 127 records · Page 7Linked to original sources
PubMed2004

Cardiorespiratory findings in sudden unexplained/unexpected death in epilepsy (SUDEP).

Sudden unexplained/unexpected death in epilepsy (SUDEP), with an incidence of 0.35-9.3/1000 patient-years depending on the severity of epilepsy, remains a diagnostic and therapeutic challenge. Potential pathomechanisms comprise cardiac arrhythmia, due to myocardial ischemia, electrolyte disturbances, arrhythmogenic drugs, or transmission of the epileptic activity via the autonomic nervous system to the heart, and central or obstructive apnea. In most studies on SUDEP, data are lacking about the family and patient's own clinical history, cardiovascular symptoms, concomitant diseases and prior findings. Whether arterial hypertension, diabetes, hypercholesterolemia, other neurologic disorders, lung diseases, smoking or electrolyte disturbances are risk factors for SUDEP is unknown. Whereas cardiac dysfunction during seizures has been documented by electrocardiography, and cardiac abnormalities are found in up to 33% of SUDEP cases autoptically, investigations between seizures found only little cardiac abnormalities. More knowledge about the cardiovascular and pulmonary status of epileptic patients during, immediately after and between seizures is needed, which may contribute to better understand and possibly prevent SUDEP by measures like "cardioprotective" drugs, respiratory therapy or implantation of a cardioverter/defibrillator.

Death, Sudden↗
PubMed2004

Left ventricular hypertrabeculation/noncompaction with and without neuromuscular disorders.

BACKGROUND: Left ventricular hypertrabeculation/noncompaction (LVHT) is frequently associated with neuromuscular disorders (NMD). It is unknown, whether LVHT patients differ according to the presence or absence of NMD. Aim of the study was to assess, if clinical, ECG or echocardiographic findings differ between LVHT patients with and without NMD. METHODS: Included were all patients, in whom LVHT was diagnosed between June 1995 and February 2003 in one echocardiographic laboratory. All patients underwent a cardiologic examination and were invited for a neurologic investigation. RESULTS: Of 77 patients with LVHT (19 female, mean age 52 years), 59 were investigated neurologically. Eleven were neurologically normal, 21 had a definite NMD (metabolic myopathy, n=15; Leber's hereditary optic neuropathy, n=3; myotonic dystrophy, n=2 and Becker muscular dystrophy, n=1). The remaining 27 had a NMD of unknown etiology. Neurologically normal patients had more often anginal chest pain than patients with definite NMD (64% vs. 14%, P=0.0042) or NMD of unknown etiology (64% vs. 26%, P=0.0157). Neurologically normal patients were more often in NYHA class 0 or I than patients with NMD of unknown etiology (64% vs. 26%, P=0.0289) and had a thinner interventricular septum than patients with NMD (10.6 mm vs. 12.8 mm, P=0.0253). CONCLUSIONS: Cardiac abnormalities are hardly different between patients with and without NMD.

Electrocardiography↗
PubMed2004

Effect of needle-EMG on blood-pressure and heart-rate.

Though immediate pain is reported by nearly all patients undergoing needle-EMG, little is known about its cardiovascular risk from changes in blood-pressure or heart-rate. This study was thus conducted to investigate if, and to which degree, blood-pressure and heart-rate are influenced by needle-EMG. In 50 patients, 24 women, 26 men, aged 26-78 years, conventional needle-EMGs from 54 muscles were recorded. Pain was assessed on a verbal analogue pain-scale (1-10) and blood-pressure and heart-rate were measured before, during and after EMG. Mean pain-ratings before, during and after EMG were 0.8, 4.1 and 1.0, respectively. Mean systolic/diastolic blood-pressure was 144/87 mmHg before, 145/86 mmHg during and 144/87 mmHg after EMG. Mean heart-rate before, during and after EMG was 77, 77 and 78 beats/min, respectively. Systolic/diastolic blood-pressure increased above 145/85 mmHg in only 2/6 patients during EMG. The weak affection of blood-pressure and heart-rate by pain from needle-EMG was found in patients with and without hypertension. Mean blood-pressure, heart-rate and pain-ratings before, during and after EMG were independent of age, sex and muscle. The correlation between pain-ratings and blood-pressure and heart-rate was not significant. This study shows that needle-EMG moderately hurts but does not increase blood-pressure or heart-rate, irrespective of known arterial hypertension. Based upon these findings, the cardiovascular risk of needle-EMG from changes in blood-pressure or heart-rate is regarded negligibly low.

Adult↗
PubMed2004

Left ventricular hypertrabeculation/noncompaction.

In normal human hearts the left ventricle (LV) has up to 3 prominent trabeculations and is, thus, less trabeculated than the right ventricle. Rarely, more than 3 prominent trabeculations can be found at autopsy and by various imaging techniques in the LV. For this abnormality, different synonyms are used such as spongy myocardium, LV noncompaction, and LV hypertrabeculation (LVHT). In this review it is stated that: (1) LVHT has a higher prevalence than previously thought and the prevalence of LVHT seems to increase with the improvement of cardiac imaging; (2) because LVHT is most frequently diagnosed primarily by echocardiography, echocardiographers should be aware and trained to recognize this abnormality; (3) LVHT is frequently associated with other cardiac and extracardiac, particularly neuromuscular, disorders; (4) there are indications that the cause of LVHT is usually a genetic one and quite heterogeneous; and (5) controversies exist about diagnostic criteria, nomenclature, prognosis, origin, pathogenesis, and the necessity to classify LVHT as a distinct entity and cardiomyopathy by the World Health Organization.

Cardiomyopathies↗
PubMed2004

Reconsidering idiopathic CK-elevation.

This study investigated the frequency of persisting, idiopathic creatine-kinase (CK)-elevation, how often the cause of idiopathic CK-elevation could be clarified, and the most frequent causes of idiopathic CK-elevation. Among 28 patients with previously idiopathic CK-elevation, CK remained elevated in 32%. The cause of idiopathic CK-elevation could be determined in 46%. Causes were mitochondriopathy (n = 5), seizure (n = 2), stroke (n = 2), myositis (n = 1), intramuscular-injection (n = 1), alcohol myopathy (n = 1), and pravastátin myopathy (n = 1). In 10 of these patients CK was normal at follow-up. CK-elevation remained idiopathic in 54%. Idiopathic CK-elevation should be comprehensively re-evaluated, even if CK is only slightly elevated or normal at follow-up.

Adult↗
PubMed2004

Unilateral compression neuropathy of the hypoglossal nerve due to head suspension orthosis in mitochondriopathy.

An 85-year-old woman with multisystem mitochondriopathy experienced tension headache, cervical pain, torque head-posture, and vertigo since 1980 for which she was continuously wearing a head-suspension-orthosis- since 1990. Since 1996 she developed severe left-sided weakness and wasting of the tongue. Needle-EMG of the left genioglossus muscle revealed abnormal spontaneous activity and reduced interference-pattern. No morphological alterations in the anatomical course of the hypoglossal nerve were found. Severe, unilateral weakness and wasting of the tongue was interpreted due to chronic compression of the hypoglossal nerve by long-standing use of a head-suspension-orthosis for cervical pain from cervical muscle weakness and resulting spinal degeneration.

Aged↗
PubMed2004

Risk-factor profile in severe, generalized, obliterating vascular disease.

A 74-year-old woman had a history over 25 years of endarterectomy of both renal arteries, iliac venous thrombosis, pulmonary embolism, left internal carotid artery endarterectomy, coronary angioplasty, aortocoronary bypass grafting, occlusion of the right axillary artery, lower-limb claudication due to common iliac artery aneurysm, external iliac artery stenosis, multiple femoral artery stenoses, bifurcational stent grafting, occlusion of the left brachial artery and the right external iliac artery, and stroke. Assessment of the risk-factor profile revealed an absence of classic risk factors but the presence of the factor V Leiden mutation, the methylenetetrahydrofolate reductase AI298C mutation, the HFE C282Y mutation, plasminogen activator inhibitor-1 gene mutation, the -455 G/A fibrinogen gene polymorphism, the epsilon3/epsilon4 apolipoprotein E -675 4G gene polymorphism, and hyperhomocysteinemia. This case shows that severe, generalized, occlusive vascular disease may be due to the combination of various genetic risk factors for atherosclerosis and venous thromboembolism.

Aged↗
PubMed2004

Platelet function in mitochondriopathy with stroke and stroke-like episodes.

Stroke and stroke-like episodes are frequent complications in mitochondriopathy, particularly in MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes) which is a disorder of the mitochondrial oxidative metabolism in diverse cell types. To clarify a possible pathological aspect of stroke in these patients, we investigated platelet function before and after physical exercise. Ten patients with mitochondriopathy and stroke and ten healthy sex and age matched controls were investigated in an analyst blinded, prospective cross-sectional trial. Exercise decreased intraplatelet adenosine triphosphate (ATP) concentrations by -22% from baseline in patients with mitochondriopathy (p<0.01 between groups) while exercise increased ATP-levels by 28% healthy controls (p=0.01 vs baseline). Thrombin receptor activating peptide (TRAP) stimulated P-selectin expression increased up to 50% (p<0.05) in healthy subjects following exercise compared to 39% (p>0.05) in patients with mitochondriopathy. Exercise trendwise decreased platelet plug formation under shear stress by 24% in patients as measured by the platelet function analyzer PFA-100(R). Tromboelastography showed firm thrombus formation and delayed lysis in patients following exercise. In conclusion, this trial has shown that ATP depletion during and after exercise probably accounts for a defective oxidative metabolism in platelets of patients with mitochondriopathy and stroke. This might induce decreased platelet function in these patients but fails to explain the increased stroke rate. Therefore other mechanisms seem to be etiologically involved in the pathogenesis of stroke in patients with mitochondriopathy.

Adenosine Triphosphate↗
PubMed2004

Lone noncompaction in Leber's hereditary optic neuropathy.

The association of Leber's hereditary optic neuropathy (LHON) and left ventricular non-compaction in the absence of other neurologic or cardiac abnormalities has not been reported. In a 19-year-old man with deteriorating visual acuity, first in the right and two weeks later also in the left eye, LHON was diagnosed, based upon reduced visual acuity, abnormal visually evoked potentials, hyperaemia of the papilla, hyperaemia of the peripapillary capillaries, peripapillary teleangiectasias, congested peripapillary veins, complete central scotoma and spotted partial defects of the remaining visual field. No other ophthalmologic abnormalities were detected. Because of frequent cardiac involvement in LHON a thorough cardiologic investigation was carried out. The cardiovascular history was uneventful. Clinical cardiologic examination and ECG were normal. Transthoracic echocardiography, however, revealed left ventricular noncompaction in the apex and the lateral wall. No other cardiac abnormalities were found. In conclusion, LHON without other neurological abnormalities may be associated with lone left ventricular noncompaction. Patients with LHON should undergo a cardiologic investigation.

Adult↗
PubMed2004

Thrombi in left ventricular hypertrabeculation/noncompaction--review of the literature.

OBJECTIVE: Left ventricular hypertrabeculation/noncompaction (LVHT) is diagnosed when numerous, excessively prominent trabeculations and deep interventricular recesses are found in the left ventricle. Although it is assumed that the intertrabecular recesses are a location prone to thrombus formation, the prevalence of thrombi in LVHT hearts is unknown. METHODS: A Medline research was carried out looking for reports of pathoanatomical investigations of LVHT hearts. Excluded were reports in which a connection between the coronary arteries with the intertrabecular recesses were described. RESULTS: In 22 articles pathoanatomical findings of 37 hearts were described (9 women, 27 men, 1 not indicated). The age ranged from 26 gestational weeks to 80 years. Twenty-four hearts were investigated by autopsy, 13 as explanted hearts. The left ventricle was dilated in 29 patients. In 9 patients, a previous embolic event had occurred. All 9 patients had additional risk factors for embolism such as atrial fibrillation (n = 1), left ventricular dysfunction (n = 5) or atrial fibrillation and left ventricular dysfunction (n = 3). In only 2 patients, a thrombus was detected pathoanatomically. CONCLUSIONS: Thrombus-formation is a rare event in patients with LVHT. From these data we infer that LVHT in itself is no indication for oral anticoagulation. However, if additional cardiac abnormalities, known to increase the risk of embolism, like atrial fibrillation or left ventricular systolic dysfunction, accompany LVHT, they have to be treated as usual.

Autopsy↗
PubMed2004

Left ventricular hypertrabeculation/noncompaction and neuromuscular disorders in idiopathic dilated cardiomyopathy.

OBJECTIVE: Our aim was to assess 1) the association of idiopathic dilative cardiomyopathy (IDC) and left ventricular hypertrabeculation/noncompaction (LVHT), 2) the use of cardiac magnetic resonance imaging (CMRI) in IDC and 3) the association of IDC and neuromuscular disorders (NMD). METHODS: Patients in whom coronary heart disease had been excluded by coronary angiography and whose left ventricular end diastolic diameter was > 59 mm and fractional shortening < 25% with no other causes of cardiac dysfunction, were invited to participate. RESULTS: Among 25 patients, 18 refused CMRI (claustrophobia n = 13, inability to lie flat n = 5), thus 7 patients (2 female, 47-66 years) were included. LVHT was found in 5/7 cases. In 4/5 patients who were neurologically investigated, a NMD was found. In 2/7 cases echocardiography failed to visualise the ventricular apex. CONCLUSIONS: Patients with IDC should be investigated neurologically. In IDC patients with poor echocardiographic quality CMRI should be applied.

Aged↗