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Biomedical subjects

B Eber

Publications and source records attributed to B Eber.

At least 55 records · Page 3Linked to original sources
PubMed2001

[Acute coronary syndromes: an update. I. Pathogenesis and drug therapy].

BACKGROUND: Unstable angina accounts for more than one million hospital admissions annually. 6-8% of patients with this condition have non-fatal myocardial infarction or die within the first year after diagnosis. Recently, the term "acute coronary syndromes" has been used to describe the spectrum of conditions that includes unstable angina, non-Q-wave myocardial infarction (which generally presents without ST-segment elevation), and Q-wave myocardial infarction (which generally presents with ST-segment elevation). PATHOGENESIS: Disruption of a formed plaque is a complex pathologic process that is central to the initiation of the acute coronary syndromes. Local thrombosis occurring after plaque disruption results from complex interactions among the lipid core, smooth-muscle cells, macrophages, and collagen. TREATMENT: Multiple huge clinical trials confirmed that aspirin reduces the risk of death from cardiac causes and fatal and non-fatal myocardial infarction by about 50-70% in patients presenting with unstable angina. Ticlopidine may be substituted for aspirin in patients with hypersensitivity to aspirin or gastrointestinal intolerance. Clopidogrel acts similarly to ticlopidin but has fewer side effects than ticlopidine and has not been reported to cause neutropenia. High-risk patients with refractory unstable angina and elevated troponin levels may have substantial benefit of glycoptotein (GP) IIb/IIIa inhibition. Current practice guidelines support the use of the combination of unfractionated heparin and aspirin for the treatment of unstable angina. Clinical studies have demonstrated that the incidence of the composite end point of death, myocardial infarction, or recurrent angina was lower with enoxaparin than with unfractionated heparin. Beta-blockers, nitrates, and calcium-channel blockers are useful for antiischemic therapy in patients with acute coronary syndromes.

Acute Disease↗
PubMed2001

Headache as a manifestation of fatal myocardial infarction.

Cardiac ischemia typically causes chest pain, variously radiating elsewhere. Convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. A 47-year-old man was admitted to the emergency room of our hospital with a 2-hour history of occipital headache. Routine electrocardiography revealed monophasic ST-segment elevation in leads I and aVL and ST-segment depression in leads II, III, and aVF. During recording of lead VI, ventricular fibrillation occurred. Advanced life support was started immediately but failed to restore rhythm and cardiac function. Autopsy showed two-vessel disease with a ruptured plaque and total thrombotic occlusion of the proximal left anterior descending artery and 80% stenosis of the right coronary artery. In this patient, headache was the only symptom of myocardial ischemia. Anatomic convergence of cardiac nerve fibers on central pathways receiving somatic afferents from the head is likely to be responsible for the perception of cardiac ischemic pain as headache. Owing to the very rare occurrence of headache as a symptom of myocardial ischemia, diagnosis is difficult and requires a high degree of suspicion.

Coronary Artery Disease↗
PubMed2001

[Coronary artery bypass graft dysfunction--clinical presentation, laboratory and electrocardiographic parameters].

The recurrence of symptoms after coronary artery bypass surgery is often caused by bypass-dysfunction. In this study we tried to determine factors related to the long-term patency of arterial and venous bypass grafts. We evaluated all patients with bypass grafts undergoing coronary angiography in the year 1998 at our hospital (163 patients, mean age 67 years, mean interval since the operation 79 months, a total of 341 venous bypasses (VBP), 386 peripheral venous anastomoses and 85 arterial (LIMA = left internal mammarial artery) bypasses. The data were collected by a retrospective analysis of the hospital records. Statistics were performed using the Wilcoxon-Mann-Whitney-U test. After an interval of 53 months LIMA-bypasses were patent without stenosis in 92%. Symptoms were caused in only 2% by a dysfunction of the LIMA-graft. The patency of venous bypass grafts decreased with time (5 years after the operation 74% were patent without stenosis, 5-10 years 56%, more than 10 years 35%, p < 0.01). We found clear relations between the function of the venous grafts and the clinical presentation (patent grafts without stenosis in 43% with acute coronary syndromes, in 57% with stable angina [p = 0.08] and in 86% with atypical angina [p < 0.0001 for the difference between each of the first two and the last syndrome]), the resting-ECG (65% patent VBP without stenosis with normal ST-segments and 49% with abnormal ST-segments, p < 0.01), the body-mass-index (70% patent VBP without stenosis with a BMI < 25 and 56% with a BMI > 30, p = 0.05) and the erythrocyte sedimentation rate after 2 hours (79% patent VBP with an ESR < or = 20 mm vs. 64% with an ESR > 49 mm, p = 0.02). The function of VBP after coronary artery bypass graft (CABG)-procedure depends primarily upon the interval since the operation. In addition, we found correlations with clinical presentation, resting-ECG, body-mass-index and erythrocyte-sedimentation rate as a possible marker of inflammation in bypass-atherosclerosis. Therefore, inflammatory processes seem to play an important role in the development of venous graft dysfunction.

Aged↗
PubMed2001

[Pathophysiology and therapeutic aspects of left ventricular "remodeling" in the post-infarct phase].

Left ventricular remodeling is the process by which ventricular size, shape, and function are regulated by mechanical, neurohormonal, and genetic factors. Remodeling may be physiological and adaptive during normal growth or pathological due to myocardial infarction, cardiomyopathy, hypertension, or valvular heart disease. Postinfarction remodeling has been divided into an early phase within 72 hours and a late phase beyond 72 hours. The early phase involves expansion of the infarct zone, which may result in early ventricular rupture or aneurysm formation. Late remodeling involves the left ventricle globally and is associated with time-dependent dilatation, the distortion of ventricular shape, and mural hypertrophy. Hypertrophy and collagen degradation are adaptive responses during postinfarction remodeling. Myocardial repair is triggered by cytokines released from injured myocytes. Ventricular remodeling is influenced most by infarct artery patency. Once infarct evolution has occurred, pharmacological intervention, like ACE inhibition and beta-adrenoreceptor blocking agents, may minimize infarct expansion and ventricular dilatation and improve the long-term prognosis.

Humans↗
PubMed2001

Subclinical hyperthyroidism as a risk factor for atrial fibrillation.

OBJECTIVES: Atrial fibrillation is a well-known manifestation of hyperthyroidism. We studied whether subclinical hyperthyroidism with low serum thyrotropin concentrations and free thyroid hormone concentrations within the normal range in clinically euthyroid persons is a risk factor for subsequent atrial fibrillation. METHODS: We studied 23,638 persons. The subjects were classified according to their serum thyrotropin concentrations: group 1 comprised those with normal values of serum thyrotropin concentration (>0.4-5.0 mU/L) and free tri-iodothyronine and free thyroxine concentrations were within the normal range (22,300 subjects), group 2 comprised those with both low serum thyrotropin values (</=0.03 mU/L) and elevated free tri-iodothyronine and free thyroxine concentrations (725 subjects), and group 3 comprised those with low values of serum thyrotropin (<0.4 mU/L) and free triiodothyronine and free thyroxine concentrations were within the normal range (613 subjects). RESULTS: Atrial fibrillation was present in 513 persons (2.3%) in group 1 with normal values for serum thyrotropin, 100 (13.8%) in group 2 with overt hyperthyroidism, and 78 (12.7%) in group 3 with subclinical hyperthyroidism. The prevalence of atrial fibrillation in patients with low serum thyrotropin concentrations (<0.4 mU/L) was 13.3% compared with 2.3% in patients with normal values for serum thyrotropin (P <.01). The relative risk of atrial fibrillation in subjects with low serum thyrotropin and normal free tri-iodothyronine and free thyroxine concentrations, compared with those with normal concentrations of serum thyrotropin, was 5.2 (95% CI 2.1-8.7, P <.01). CONCLUSION: A low serum thyrotropin concentration is associated with a >5-fold higher likelihood for the presence of atrial fibrillation with no significant difference between subclinical and overt hyperthyroidism.

Atrial Fibrillation↗
PubMed2001

Perspectives-- Focus on statins: lipid-lowering mechanisms and beyond.

Recent large-scale clinical trials have confirmed that statin-induced lipid modification can significantly reduce cardiovascular morbidity and mortality. Statins are now the drugs of choice in lipid management but fail to meet the criteria for an ideal therapy in several respects. Therefore, the search continues for lipid modifying treatments that meet even higher standards. Lipid-lowering drugs currently in development may meet these more exacting standards and together with complementary methods could ultimately form ideal combination therapy. (c) 2001 by CHF, Inc.

Journal Article↗
PubMed2001

[Pharmacologic interventions in primary prevention: lipid lowering drugs, aspirin, antiobesity drugs, and antihypertensive agents].

Heart disease, particularly coronary heart disease is a major cause of morbidity and mortality in developed countries. Cardiovascular disease accounts for more than 50% of deaths. Drug therapy is highly effective for treatment of patients after a first cardiovascular event (secondary prevention). In contrast, introduction of drug therapy for lowering cardiovascular risk before a first cardiovascular event (primary prevention) is discussed controversially. The number of persons who need to be treated for prevention of one cardiovascular event is high and drug therapy in more or less "healthy" people is justified only after accurate assessment of potential risks and possible beneficial effects. Drug therapy combined with non-pharmacological treatment strategies is considered to be appropriate in selected high-risk persons for primary prevention. The following article describes potential indications of several drugs, in particular cholesterol-lowering therapy, aspirin, drug therapy of obesity and hypertension, for use in primary prevention of cardiovascular disease.

Anti-Obesity Agents↗
PubMed2001

[Homocysteine and cardiovascular risk].

Homocysteine is an amino acid that plays a key role in methionine- and homocysteine metabolism. Homocystinuria has been described about four decades ago to be an inherited (autosomal recessive) disorder with rapid progressive atherosclerosis. Thus, homocysteine has been investigated intensively with respect to vascular wall injury and atherogenesis. Folic acid and vitamin B12 are cofactors of methioninsynthase, a key enzyme in homocysteine metabolism. Plasma levels of homocysteine are higher in patients with coronary artery disease documented by coronary angiography than in individuals with normal coronary arteries. Supplementation of folic acid is the treatment of choice to lower plasma homocysteine concentrations. Improvement in endothelial function could be documented in patients with folic acid supplementation. Large scaled clinical trials investigating folic acid supplementation in secondary prevention are now in progress. Today, homocysteine and its association with atherosclerosis raise a lot of questions to be answered. A distinct pathophysiological model linking hyperhomocysteinaemia and atherosclerosis is still not available. The presence of hyperhomocysteinemia in atherosclerotic vascular disease as a surrogate with no pathophysiological relevance itself cannot be ruled out. Routine testing of homocysteine levels is not yet recommended. Treatment of patients with folic acid or vitamin B for primary and secondary prevention of atherosclerotic vascular disease cannot be recommended today, because large scaled intervention trials on homocysteine lowering by vitamin B or folic acid are not available yet. Possible effects of these interventions on acute vascular events are not known.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗
PubMed2001

[Commentary on primary prevention].

In this brief review current guidelines on prevention of atherosclerotic diseases and latest results as well as personal views are presented. It is not my purpose to give a complete overview on this subject; however, some important aspects will be discussed to keep this subject in the forefront of interest.

Arteriosclerosis↗
PubMed2001

A clinical focus on statins.

Clinical trials have demonstrated that inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase (statins) significantly reduce cardiovascular-related morbidity and mortality in patients with and without coronary artery disease. Furthermore, statins are currently the most potent cholesterol-lowering drugs available. Subanalyses of the LIPID study have shown that patients suffering from unstable angina pectoris had at least the same benefit from statin therapy as did patients after myocardial infarction. Studies, recently published (AVERT or MIRACL) provide more information on the topic of therapy with statins in the early phase of acute coronary syndromes.

Angina Pectoris↗
PubMed2001

[Neuromodulation as an alternative method in the treatment of refractory angina pectoris].

Epidural stimulation of the spinal cord affects the activation of afferent nerve fibres. Patients refractory to conventional therapy of angina pectoris can be treated with epidural stimulation since 1985. The stimulation electrode is inserted by a small incision to the skin at Th4-Th5 and positioned to the epidural space at Th1-C7. The impulse generator is implanted to the lateral abdominal wall and connected to the stimulation electrode. This treatment should be restricted to patients refractory to--or not suited for--surgical and catheter-based coronary revascularisation. Clinical trials demonstrated increased exercise tolerance, reduction in severity of exertional angina and ST-depression and reduction of nitrate dosage. No impairment of overall prognosis by neuromodulation has been shown in several clinical studies. Epidural spinal cord stimulation represents an alternative therapy for the treatment of selected patients with angina pectoris refractory to conventional therapy.

Angina Pectoris↗