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Biomedical subjects

E Erdmann

Publications and source records attributed to E Erdmann.

At least 127 records · Page 7Linked to original sources
PubMed1998

Calcium content of the sarcoplasmic reticulum in isolated ventricular myocytes from patients with terminal heart failure.

Systolic [Ca2+]i-transients have been shown to be depressed in isolated ventricular myocytes from patients with terminal heart failure compared to controls. Experiments were performed in human ventricular cells to investigate whether this reduced systolic [Ca2+]i-transient may be due to a decreased Ca(2+)-content of the sarcoplasmic reticulum (SR). Single myocytes were isolated from left ventricular myocardium of patients with terminal heart failure undergoing cardiac transplantation. These results were compared to those obtained from cells of healthy donor hearts that were not suitable for transplantation for technical reasons. [Ca2+]i-transients were recorded from isolated cells under voltage clamp perfused internally with the Ca(2+)-indicator fura-2. The Ca(2+)-content of the SR was estimated by rapid extracellular application of caffeine (10 mM) to open the Ca(2+)-release channel of the SR and comparison of the caffeine-induced [Ca2+]i-transients in cells from patients with heart failure and from controls without heart failure. Upon steady-state depolarizations to +10 mV (maximum of the Ca(2+)-current), [Ca2+]i-transients in cells from patients with heart failure were significantly smaller than in myocytes from undiseased hearts (333 +/- 26 v 596 +/- 80 nM, P < 0.05). Application of caffeine caused a [Ca2+]i-transient that was always larger than during depolarization. Caffeine-induced [Ca2+]i-transients were significantly smaller in cells from diseased hearts compared with controls (970 +/- 129 v 2586 +/- 288 nM, P < 0.01). A positive correlation was found between left ventricular ejection fraction and caffeine-induced [Ca2+]i-transients in these cells. It is concluded, that depressed [Ca2+]i-transients in myocytes from patients with heart failure may be caused by a decreased Ca(2+)-content of the SR possibly due to an altered Ca(2+)-ATPase activity in these hearts. It is not necessary to postulate an additional defect of the Ca(2+)-release function of the SR to account for the alterations of intracellular (Ca2+]i-handling.

Adult↗
PubMed1998

Digitalis therapy--relevance of heart rate reduction.

Although digitalis is of limited antiarrhythmic value in patients with atrial fibrillation, it does control ventricular heart rate in the majority of patients at rest. It may be necessary, to add a beta-blocking agent or a calcium antagonist to control ventricular heart rate during exercise. This therapeutic approach should be controlled by exercise testing. In heart failure patients with sinus rhythm digitalis decreases heart rate, has antiadrenergic effects, and restores baroreceptor and parasympathetic activity. These actions are seen only in patients with severe heart failure due to left ventricular enlargement and low ejection fraction. In mild heart failure as well as in diastolic heart failure or cor pumonale, digitalis does not seem to be of clinical value. Thus, the use of digitalis in patients with sinus rhythm should be restricted to those with severe heart failure.

Anti-Arrhythmia Agents↗
PubMed1998

Dobutamine magnetic resonance imaging predicts contractile recovery of chronically dysfunctional myocardium after successful revascularization.

OBJECTIVES: This study sought to evaluate whether myocardial viability, as assessed by magnetic resonance imaging (MRI), reliably predicts postrevascularization left ventricular (LV) recovery. BACKGROUND: Compared with positron emission tomographic findings, MRI has proved to be a reliable technique for the identification of residual myocardial viability. However, the predictive accuracy of MRI-assessed preserved end-diastolic wall thickness (DWT) and dobutamine-induced systolic wall thickening (SWT) for LV functional recovery has not yet been evaluated. METHODS: Rest and low dose dobutamine MRI was performed in 43 patients with a chronic infarct (> or =4 months since ischemic event) and LV dysfunction who had undergone revascularization of the infarct-related vessel. On the basis of segmental evaluation of corresponding short-axis tomograms, infarct regions were graded viable by MRI if 1) DWT was > or =5.5 mm, and 2) dobutamine-induced SWT was > or =2 mm in > or =50% of dysfunctional segments related to the infarct region. Functional recovery was defined as SWT > or =2 mm in > or =50% of infarct-related segments at rest 4 to 6 months after successful revascularization. RESULTS: Recovery of regional SWT could be observed in 27 (63%) of 43 patients. Comparison MRI grading before and after revascularization indicated that dobutamine-induced SWT was a better predictor of LV functional recovery (sensitivity 89%, specificity 94%) than was preserved DWT (sensitivity 92%, specificity 56%). Segments that remained akinetic after revascularization had significantly lower DWT (6.0+/-3.1 mm [n = 219] vs. 9.8+/-2.6 mm [n = 188], p < 0.001) than those with improved SWT. Left ventricular ejection fraction increased significantly in patients with dobutamine-induced SWT than in those with no contractile reserve (14+/-9% vs. 3+/-9%, p < 0.0002), and the magnitude of this increase was correlated with the number of dobutamine-responsive segments per infarct region (r = 0.68, p < 0.0001). CONCLUSIONS: Quantitative assessment of dobutamine-induced SWT in chronic infarcts by MRI is a highly accurate predictor of LV functional recovery, and the presence of significantly reduced DWT reliably indicates irreversible myocardial damage. Therefore, dobutamine stress testing for the assessment of myocardial viability can be restricted to patients with preserved DWT.

Adult↗
PubMed1998

Significance of rest technetium-99m sestamibi imaging for the prediction of improvement of left ventricular dysfunction after Q wave myocardial infarction: importance of infarct location adjusted thresholds.

OBJECTIVE: The value of rest technetium-99m (Tc-99m) sestamibi scintigraphy under oral nitrate medication to predict myocardial viability was examined in patients with chronic infarcts. BACKGROUND: The value of rest Tc-99m sestamibi to predict viability in infarct regions has not been fully established because significant underestimation of viability, especially in the inferior myocardial wall, has been reported. METHODS: Forty patients with Q wave myocardial infarction underwent Tc-99m sestamibi single-photon emission computed tomography under nitrate medication before revascularization of the infarct-related artery. Wall motion was quantified from paired angiograms before and 4 months after revascularization. Tracer uptake was quantified in the central infarct region identified on the angiogram. RESULTS: The average Tc-99m sestamibi uptake in the central infarct region of patients with anterior infarcts and improvement of left ventricular function was significantly higher (68+/-12%, mean+/-SD) than in patients without improvement of function (40+/-14%, p < 0.02). The average Tc-99m sestamibi uptake in the central infarct region of patients with improvement of function and inferior infarcts was significantly lower (43+/-7%) than in patients with anterior infarcts (68+/-12%, p < 0.003), but was significantly higher than in patients with inferior infarction and no improvement of function (31+/-7%, p < 0.02). Using an infarct location adjusted optimal threshold (50% for anterior infarcts, 35% for inferior infarcts), Tc-99m sestamibi had a positive predictive value of 90% and a negative predictive value of 91% for improvement of left ventricular function. CONCLUSION: Quantitative rest Tc-99m sestamibi scintigraphy after oral nitrates reliably predicts improvement of left ventricular function after revascularization if infarct location adjusted thresholds are used.

Aged↗
PubMed1998

Methods of assessment and clinical relevance of myocardial hibernation and stunning. Assessment of myocardial viability.

During the past decade there has been intense clinical interest in the differentiation between scar tissue and postischemic viable myocardium and its relevance to patient treatment and outcome. Frequently used paradigms of myocardial viability are hibernation and stunning which both refer to reversible left-ventricular contraction impairment. Hibernation describes the concomitant reduction of myocardial perfusion and contractility, whereas stunning characterizes contractile impairment persisting for some time after perfusion has been restored. In the clinical setting ischemia, stunning, hibernation, and necrosis may coexist. A variety of imaging techniques encompassing a wide range of physiologic entities such as contractile function, perfusion, membrane integrity and cell metabolism are currently in use to differentiate between these conditions, and they allow an accurate decision making with respect to revascularization procedures or conservative management. This article reviews current concepts and diagnostic methods to assess viable myocardium, and it attempts to address the clinical relevance of revascularization procedures in patients with coronary artery disease harboring dysfunctional but viable myocardium.

Cell Survival↗
PubMed1998

Chronic eosinophilic pneumonia with atypical radiographic presentation.

Chronic eosinophilic pneumonia (CEP) is a rare disease characterized by a progressive symptomatic deterioration of more than 1 month, pulmonary infiltrates with eosinophils, and a dramatic response to corticosteroid treatment. We describe a patient with CEP who presented with right upper lung infiltrates with evidence of cavitation.

Anti-Inflammatory Agents↗
PubMed1997

[Contusio cordis--too seldom diagnosed?].

BACKGROUND: Myocardial contusion is the most common injury caused by blunt chest trauma. Cardiac contusion often does not produce significant symptoms and, thus, remains unrecognized. CASE REPORT: A 29-year-old professional ice-hockey player presented with a tachyarrhythmia two days after having suffered a thoracic trauma. Two weeks prior to admission he had an influenza-like infection. Non-invasive diagnostic methods were normal. However, cardiac catheterization revealed an akinesis of the left ventricular anterior wall in the absence of any coronary artery lesions. Endomyocardial biopsy did not show any evidence of myocarditis but erythrocyte extravasations in the endo- and myocardium, thus, confirming the diagnosis of cardiac contusion. Three months later, left ventriculography and coronary angiography did neither demonstrate any abnormalities of ventricular contraction nor of the coronary vessels. CONCLUSION: Myocardial contusion is still being rarely diagnosed after sporting accidents. Cardiac contusion is a benign disorder in most patients. However, due to its potentially lethal outcome and as sequelae may present late after the trauma, early and precise diagnosis is important, both from the clinical point of view as well as for future insurance requests. Thus, invasive diagnostic techniques should be performed when non-invasive examinations do not provide a conclusive diagnosis.

Adult↗
PubMed1997

[Therapy of heart failure. I. Definition, pathophysiology, therapy of acute heart failure].

Acute cardiac insufficiency is often the result of acute or chronic overloading of the heart due to arterial hypertension, coronary heart disease and/or a reduction in ventricular muscle mass following myocardial infarction. Whenever possible, treatment should be causal (e.g. treatment of hypertension, operative correction of valvular disease). While the incidence of heart failure continues to increase, morbidity and mortality associated with the disease process have remained essentially unchanged. About 30% of the patients die within the first 12 months. The prognosis and outcome of heart failure patients strongly correlate with markers of neuroendocrine activation. While numerous drugs are capable of improving hemodynamics at rest or physical performance, they fall to prolong survival. It is hoped, that new pathophysiological information might lead to the development of new, effective therapeutic approaches.

Cardiotonic Agents↗
PubMed1997

[Therapy of heart failure. II. Therapy of chronic heart failure].

Current medical treatment of chronic heart failure makes use of a combination of diuretics, cardiac glycosides and ACE inhibitors. The latter have improved the chances of survival of patients with chronic cardiac insufficiency. The combination of hydralazine hydrochloride and isosorbide dinitrate also improves survival, but direct comparison of both regimens provided evidence for a less favourable effect than that of the ACE inhibitors. Inhibition of neuroendocrine activation has been demonstrated only for ACE inhibitors and cardiac glycosides. The use of beta blockers represents a new therapeutic strategy that over the long term improves cardiomyocyte function, cardiac output at rest, and physical performance. For this indication, however, beta blockers should be used with extreme caution and at very low initial doses. New approaches in the area of clinical research are, for example, calcium sensitizers, modulators of intracellular calcium and/or sodium homeostasis, imidazolin receptor antagonists with an action on the central nervous system and AT1 receptor antagonists.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Changes in essential myosin light chain isoform expression provide a molecular basis for isometric force regulation in the failing human heart.

We investigated the effects of the expression of myosin light chain (MLC) isoforms on the Ca2+ sensitivity of isometric force production of demembranated (skinned) fibers of papillary muscle from the left ventricle of three groups: patients with ischemic cardiomyopathy, patients with dilated cardiomyopathy (NYHA IV) and normal human hearts. Expression and phosphorylation of the phosphorylatable MLC isoforms (MLC-2) was equal within all three groups. However, 72% of the patients investigated in this study expressed the atrial essential MLC (ALC-1) in addition to the essential ventricular MLC (VLC-1) ranging between 2.4% and 10.3%. Using fibers from failing hearts, we observed a significant positive correlation between ALC-1 and Ca2+ sensitivity in that the higher the ALC-1 expression the higher the Ca2(+)-sensitivity: pCa50 (Ca2+ required for half-maximal force production) was 5.87 without ALC-1 and 6.08 with 10.3% ALC-1. Fibers from a normal heart (no ALC-1) revealed a pCa50 of 5.85. Isoform and phosphorylation patterns of tropomyosin and troponin I remained unchanged in the patients and normal hearts. Our results suggest that Ca2+ responsiveness and force development of the human heart is regulated by the expression of different MLC-1 isoforms.

Calcium↗