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Biomedical subjects

E Erdmann

Publications and source records attributed to E Erdmann.

At least 145 records · Page 8Linked to original sources
PubMed1997

[Intracoronary ultrasound changes the therapeutic approach in ambivalent angiography findings].

Despite careful evaluation of multiple projections, coronary angiography may give ambiguous results of lesion severity. The purpose of this study was to analyze the impact of ultrasound imaging on revascularization treatment strategy in angiographically ambiguous findings. We reviewed our experience with such equivocal angiographic findings before intervention in 31 patients (34 lesions) who had additional intravascular ultrasound (IVUS) to clarify coronary anatomy. Intervention was felt to be indicated if area stenosis by IVUS exceeded 50% in the left main or 75% in other major coronary arteries. To evaluate the clinical efficacy of IVUS based management strategies, all patients had clinical follow-up after 1 year. Seven of nine ostial lesions were overestimated by angiography, but two of three left main lesions were found to be significant. Seven lesions in one of the proximal coronary arteries whose significance was difficult to judge by angiography were found not to be significant by IVUS, whereas in the other four severe obstruction was confirmed. Membranes by angiography corresponded to remnants of ruptured plaques by IVUS in all five patients. However, significant narrowing was found in only two patients. Side branch ostial lesions were ruled out by IVUS in all four instances. Two patients with unstable angina but normal angiograms showed complex atherosclerotic plaques in the left coronary artery. IVUS led to a change of therapy in 21 patients (revascularization instead of conservative treatment in two and cancellation of initially intended intervention in 19). At follow-up examination, 17 of these 21 patients were free of cardiac symptoms. Interventions at the site thought not severely diseased by IVUS had to be performed in two patients with persistent angina who were afterwards free of symptoms. One patient with persistent chest pain had a second coronary angiogram during the follow-up period, but conservative therapy was continued. Evaluation was impossible in one patient because of bypass surgery due to another coronary lesion. In conclusion, IVUS was clinically useful in patients with angiographically ambiguous findings and resulted in a change of therapy in 21/31 patients obviating interventions in 19 patients with excellent clinical results.

Adult↗
PubMed1997

A prognostic computer model to predict individual outcome in interventional cardiology. The INTERVENT Project.

It is not yet possible to predict an individual's outcome from percutaneous transluminal coronary angioplasty or alternative/adjunctive coronary interventional techniques. The purpose of the INTERVENT project is to redefine complications associated with coronary interventions, to set up a prognostic computer model to predict individual outcome and to compare the results to those of conventional statistical techniques. 2500 data items were analysed in 455 consecutive patients (mean age: 61.1 +/- 8.3 years; range 33-84 years; 80.4% male, 16.7% unstable angina, 5.1%/10.1% acute/subacute myocardial infarction) undergoing coronary interventions at three university centres. In-lab/out-of-lab complication rates were 0.4%/0.9% (death), 1.8%/0.2% (abrupt vessel closure with myocardial infarction) and 5.5%/4.0% (haemodynamic complications). Computer algorithms derived by applying techniques from artificial intelligence were able (1) to reduce the set of possible relevant risk factors from 2500 to about 40, (2) to predict individual risk with an accuracy of > 95% and (3) to explain the structural relationship between outcome and risk factors. Patient data from two centres were used to construct and test the algorithm. Data from a third centre were used to evaluate the algorithm. The most important predictors-were acute myocardial infarction, heart failure (NYHA class > II), unstable angina, complex lesions, high low density lipoprotein cholesterol and duration of coronary heart disease. Neither age nor gender impaired the percutaneous transluminal coronary angioplasty results in acute ischaemic syndromes; however, for stable angina, procedural risk increased with age. There was little risk from primary percutaneous transluminal coronary angioplasty in acute myocardial infarction in patients with NYHA heart failure classes I-II; however, the risk was high for patients in NYHA classes > II, either with or without additional thrombolysis. Alternative/adjunctive intervention techniques were no predictors for in-lab-, but were predictors for post-procedural complications.

Adult↗
PubMed1997

The effect of positive inotropes on the failing human myocardium.

Heart failure is associated with pathobiochemical changes that can reduce the responsiveness of the myocardium to positive inotropic agents. We studied the contractile effects of a range of inotropic agents on papillary muscle strips from healthy and failing human hearts. Specimens were obtained from patients with different grades of heart failure. These included individuals undergoing mitral valve replacement (New York Heart Association Class II-III) or receiving heart transplantation (New York Heart Association Class IV). Heart failure was associated with attenuation of myocardial contractile responses to dobutamine, histamine, 3-isobutyl-1-methylxanthine, and the phosphodiesterase inhibitors, milrinone and pimobendan. However, pretreatment of the papillary muscle with isoprenaline augmented the positive inotropic effect observed with the phosphodiesterase inhibitors. The contractile response to ouabain was not influenced by the presence of heart failure. We conclude that, unlike beta-adrenoceptors, cardiac glycoside receptors in the myocardium are not down regulated in the presence of heart failure.

1-Methyl-3-isobutylxanthine↗
PubMed1997

Increased oxidation of LDL in patients with coronary artery disease is independent from dietary vitamins E and C.

There is increasing experimental evidence that oxidation of LDL plays a major role in the pathogenesis of coronary artery disease (CAD). However, results from clinical studies on LDL oxidation and CAD are not consistent. In most studies only single plasma factors of LDL oxidation have been determined. We studied 207 patients who underwent coronary angiography. They were divided into subjects with CAD (n = 137) and those without CAD (n = 70). We determined the susceptibility of LDL to in vitro oxidation (lag phase), potential prooxidative and antioxidative plasma factors (plasma vitamin E, LDL vitamin E, ascorbate, iron, copper, ferritin, and ceruloplasmin), and markers of in vivo LDL oxidation (autoantibodies to malondialdehyde-modified LDL, oxidized LDL, and thiobarbituric acid-reactive substances), plasma lipids and lipoproteins, smoking habits, and other coronary risk factors in both groups. The lag phase was significantly shorter in patients with CAD than in patients without CAD (101 +/- 38.6 versus 119 +/- 40.6 minutes, P < .01). There was no correlation between the lag phase and the other oxidation parameters or the coronary risk factors. In multivariate regression analyses the lag phase remained significant in all tested models. Our data suggest that a short lag phase of LDL oxidation might be an independent risk factor of CAD.

Aged↗
PubMed1997

[Value of polymerase chain reaction (PCR) in diagnosis of tuberculosis and mycobacterium infections caused by ubiquitous mycobacteria].

The rise in both incidence and the number of multi-drug-resistant strains has made tuberculosis an alarming health problem even in some developed countries. Moreover, due to the HIV pandemic an increase in mycobacterial diseases caused by ubiquitous mycobacteria has been observed. The microbiological standard procedures are critical diagnostic tools, and a more rapid detection of mycobacteria by new laboratory techniques would be helpful. We investigated the role of the polymerase chain reaction (PCR) in the detection of M. tuberculosis complex and of ubiquitous mycobacteria. 580 clinical specimens obtained from 525 patients were examined. The majority of sampled material was bronchoalveolar lavage fluid. Based on cultural identification of mycobacteria, the incidence of tuberculosis in our patients was 3.4%. For detection of M. tuberculosis complex the insertion sequence IS 6110 was used. Relative to cultural identification, diagnostic specificity of PCR was 99.5%, and sensitivity was 66.7%, respectively. In 3.0% of the total patient group and in 8.8% of HIV-infected patients an infection by ubiquitous mycobacteria was found. Ubiquitous mycobacteria were detected using the hypervariable region of the 16S-rRNA-gene, and species-identification was done by sequence analysis. For ubiquitous mycobacteria, sensitivity of PCR was 60.0% relative to cultural identification and 62.5% relative to a proven disease. PCR is a useful method in the rapid diagnosis of pulmonary tuberculosis with excellent specificity but lack of sensitivity.

AIDS-Related Opportunistic Infections↗
PubMed1997

Effect of cyclopiazonic acid on the force-frequency relationship in human nonfailing myocardium.

The present study investigated the functional role of the sarcoplasmic reticulum Ca++-ATPase in contraction and relaxation, intracellular Ca++-transients, as well as on the force-frequency relationship in human myocardium. The Ca++-ATPase activity of membrane vesicles isolated from sarcoplasmic reticulum (SR) obtained from nonfailing donor hearts (n = 7) was measured in the presence of cyclopiazonic acid (CPA, 0-30 microM), a highly specific inhibitor of the Ca++-ATPase of the SR (SERCA). The effects of CPA on parameters of contraction and relaxation, force-frequency relationship and [Ca++]i transients (with fura-2) were studied on isolated left ventricular muscle strips from human nonfailing myocardium. CPA concentration-dependently inhibited SERCA activity of isolated SR vesicles. In the presence of CPA (30 microM) the former positive force-frequency relationship in human left ventricular nonfailing myocardium became negative. Especially at high frequencies of stimulation, CPA decreased developed tension, peak rate of tension rise and systolic fura-2-light emission, whereas time to peak tension, time to peak [Ca++]i, time to 95% relaxation, diastolic tension and diastolic Ca++ levels were increased. Peak rate of tension decay and time to half-relaxation and half-decay of [Ca++]i were not altered significantly after treatment with CPA. These findings provide evidence that the SERCA plays a functional role in the frequency-dependent increase in force of contraction in human myocardium. Because an impaired function of the SERCA is predominantly followed by alterations of inotropic and to a lesser degree of lusitropic function, other important factors to lower [Ca++]i and influence relaxation may be present in human myocardium to compensate for the reduced SERCA activity, e.g., Na+-Ca++ exchanger.

Adult↗
PubMed1996

Regional expression of sodium pump subunits isoforms and Na+-Ca++ exchanger in the human heart.

Cardiac glycosides exert a positive inotropic effect by inhibiting sodium pump (Na,K-ATPase) activity, decreasing the driving force for Na+-Ca++ exchange, and increasing cellular content and release of Ca++ during depolarization. Since the inotropic response will be a function of the level of expression of sodium pumps, which are alpha(beta) heterodimers, and of Na+-Ca++ exchangers, this study aimed to determine the regional pattern of expression of these transporters in the heart. Immunoblot assays of homogenate from atria, ventricles, and septa of 14 nonfailing human hearts established expression of Na,K-ATPase alpha1, alpha2, alpha3, beta1, and Na+-Ca++ exchangers in all regions. Na,K-ATPase beta2 expression is negligible, indicating that the human cardiac glycoside receptors are alpha1beta1, alpha2beta1, and alpha3beta1. alpha3, beta1, sodium pump activity, and Na+-Ca++ exchanger levels were 30-50% lower in atria compared to ventricles and/or septum; differences between ventricles and septum were insignificant. Functionally, the EC50 of the sodium channel activator BDF 9148 to increase force of contraction was lower in atria than ventricle muscle strips (0.36 vs. 1.54 microM). These results define the distribution of the cardiac glycoside receptor isoforms in the human heart and they demonstrate that atria have fewer sodium pumps, fewer Na+-Ca++ exchangers, and enhanced sensitivity to inotropic stimulation compared to ventricles.

Adult↗
PubMed1996

Comparison of dobutamine transesophageal echocardiography and dobutamine magnetic resonance imaging for detection of residual myocardial viability.

A dobutamine-induced contraction reserve in akinetic but viable myocardium, observed by echocardiography or magnetic resonance imaging (MRI), is a reliable indicator of myocardial viability. However, the comparative diagnostic accuracy of these 2 techniques is unknown. Therefore, 43 patients with myocardial infarction (infarct age > or = 4 months) and regional akinesia underwent dobutamine transesophageal echocardiography (TEE) and dobutamine MRI (10 microg dobutamine/ min/kg). Both imaging techniques were compared with the reference standard 18F-fluorodeoxyglucose positron emission tomography (FDG PET). An infarct region was considered viable if a dobutamine contraction reserve could be assessed visually by TEE or quantitatively by MRI in > or = 50% of segments graded "a" or dyskinetic at rest. Infarct regions were graded viable by PET if FDG uptake was > or = 50% of the maximal FDG uptake in a region with normal wall motion by left ventriculography. A dobutamine contraction reserve was found in 21 of 43 patients (49%) by TEE and MRI. A viable infarct region by FDG PET was diagnosed in 26 of 43 patients (60%). FDG uptake and dobutamine TEE were concordant in 36 of 43 patients (84%) and dobutamine MRI and FDG PET were concordant in 38 of 43 patients (88%). Sensitivity and specificity of dobutamine TEE and dobutamine MRI for FDG PET-defined myocardial viability were 77% versus 81% and 94% versus 100%, respectively. Both imaging techniques yielded similar results for the detection of myocardial viability as defined by FDG uptake, with a slightly higher sensitivity and specificity for the quantitatively evaluated dobutamine contraction reserve by MRI.

Adrenergic beta-Agonists↗
PubMed1996

Altered inotropism in the failing human myocardium.

Beta-adrenoreceptor-cAMP-dependent inotropic interventions lose their effectiveness depending on the degree of myocardial failure. This blunted effect of beta-adrenoreceptor-dependent stimulation might be due to a downregulation of beta-adrenoreceptors and an increase of inhibitory G-proteins leading to decreased intracellular cAMP-concentrations. However, the maximal positive inotropic effect elicited by elevation of the extracellular [Ca2+] does not differ between failing and nonfailing human myocardium, indicating that terminally failing human myocardium is effective to increase force of contraction to the same degree as nonfailing tissue. Agents which increase force of contraction primarily via increasing the intracellular [Na+], e.g., cardiac glycosides and the Na(+)-channel activator BDF 9148, exert a higher potency in failing myocardium than in nonfailing tissue to increase force of contraction. This could result from an enhanced protein expression of the Na+/Ca(2+)-exchanger observed in diseased human hearts. Alterations in the intracellular Ca(2+)-homeostasis reported in failing myocardium lead to a negative force-frequency-relationship and a prolonged relaxation. As the protein expression of SERCA IIa and phospholamban seems to be similar in NYHAIV and nonfailing tissue, the reduced Ca(2+)- uptake may result from an altered regulation of these proteins, e.g., reduced phosphorylation of phospholamban or the SERCA IIa. After inhibition of the Ca(2+)-ATPase of the sarcoplasmic reticulum with the high specific inhibitor cyclopiazonic acid the former positive force-frequency-relationship became significantly less positive even in the nonfailing tissue and twitch course became similar to diseased hearts. These findings may be indicative for the importance of the Ca(2+)-reuptake mechanism into the sarcoplasmic reticulum in addition to the regulatory control at the site of the contractile apparatus for the regulation of contraction and relaxation in human myocardium.

Adrenergic beta-Agonists↗
PubMed1996

Analysis of beta-adrenergic receptor mRNA levels in human ventricular biopsy specimens by quantitative polymerase chain reactions: progressive reduction of beta 1-adrenergic receptor mRNA in heart failure.

OBJECTIVES: This study investigated the relation between the severity of heart failure and the extent of the reduction of beta 1-adrenergic receptor messenger ribonucleic acid (mRNA) levels in biopsy specimens from the ventricular septum obtained during cardiac catheterization of patients with various degrees of heart failure. BACKGROUND: Heart failure is accompanied by desensitization of the beta-adrenergic receptor system, which is in part due to downregulation of beta 1-adrenergic receptors. Downregulation of beta 1-adrenergic receptors has been suggested to be caused by reductions in mRNA levels. METHODS: Because biopsy specimens were small and receptor mRNAs not abundant, mRNA levels were determined by quantitative reverse transcription/polymerase chain reactions. This method was validated by measuring synthetic ribonucleic acid (RNA) standards and samples from explanted hearts by solution hybridization assays. Both methods yielded similar results, but the polymerase chain reaction method was approximately 1,000-fold more sensitive. Sources of variations in the polymerase chain reaction were quantitated and found to be best controlled for by determination of the glyceraldehyde phosphate dehydrogenase mRNA as an endogenous control. RESULTS: Beta 1-adrenergic receptor mRNA levels in the biopsy specimens were decreased by 7% in mild (New York Heart Association functional class II), 26% in moderate (functional class III) and > 50% in severe heart failure (functional class IV). There was a good correlation between hemodynamic indicators of heart failure and beta 1-adrenergic receptor mRNA levels. In contrast, beta 2-adrenergic receptor mRNA levels were apparently unaffected by heart failure. CONCLUSIONS: Reduced beta 1-adrenergic receptor mRNA levels occur early in heart failure and can be detected in septal biopsy specimens during right heart catheterization. The reduction in beta 1-adrenergic receptor expression may contribute to further loss of cardiac function.

Adult↗
PubMed1996

Predictive value of low dose dobutamine transesophageal echocardiography and fluorine-18 fluorodeoxyglucose positron emission tomography for recovery of regional left ventricular function after successful revascularization.

OBJECTIVES: This study was designed to assess the predictive value of myocardial viability diagnosed by dobutamine transesophageal echocardiography and fluorine (F)-18 fluorodeoxyglucose positron emission tomography for left ventricular functional recovery after revascularization in patients with chronic left ventricular dysfunction. BACKGROUND: The identification of akinetic but viable myocardium is of particular importance for the selection of patients with a compromised left ventricle who will benefit from coronary revascularization. METHODS: Multiplane rest and dobutamine transesophageal echocardiography (dobutamine, 5 and 10 microg/min per kg) studies and F-18 fluorodeoxyglucose positron emission tomographic studies at rest were performed in 2 patients with 1) previous myocardial infarction and regional akinesia, 2) a stenosed infarct-related coronary artery, and 3) a patent infarct-related vessel after revascularization. A basally akinetic segment was considered viable by transesophageal echocardiography if dobutamine-induced contractile reserve could be observed. Viability by positron emission tomography was defined as F-18 fluorodeoxyglucose uptake > or = 50% of the maximal uptake in a region with normal wall motion. Recovery of regional left ventricular function 4 to 6 months after revascularization was diagnosed by transesophageal echocardiography if > or = 50% of segments akinetic at baseline had improved wall thickening. RESULTS: Dobutamine transesophageal echocardiography identified viable infarct regions in 25 (59%) of 42 patients, and F-18 fluorodeoxyglucose positron emission tomography in 30 (71%) of 42 patients, yielding diagnostic agreement in 86% of patients. Sensitivity and specificity for prediction of left ventricular functional recovery in individual patients was 92% and 88%, respectively, for dobutamine transesophageal echocardiography versus 96% and 69% for F-18 fluorodeoxyglucose positron emission tomography. Segments remaining akinetic after revascularization had a significantly lower (p < 0.001) F-18 fluorodeoxyglucose uptake (48 +/- 15%) than that (73 +/- 15%) of segments with recovery of regional left ventricular function. CONCLUSIONS: Both dobutamine transesophageal echocardiography and F-18 fluorodeoxyglucose positron emission tomography were highly sensitive in predicting functional recovery of chronically kinetic or dyskinetic myocardium after successful revascularization. Thus, dobutamine transesophageal echocardiography is a clinically valuable alternative to F-18 fluorodeoxyglucose positron emission tomography for assessing residual viability and predicting functional recovery after revascularization.

Adrenergic beta-Agonists↗
PubMed1996

Enhanced sensitivity of the failing human myocardium to cardiac glycosides and Na(+)-channel activators.

Cardiac glycosides and Na+ -channel activators increase intracellular Na+ and thereby enhance the transport rate of the sarcolemmal Na+/Ca2+ exchanger. We tested the hypothesis of whether increased expression of the Na+/Ca2+ exchanger in failing human myocardium is accompanied by enhanced sensitivity of the failing human myocardium toward cardiac glycosides and Na+ -channel activators. We studied the positive inotropic effects of the new Na+ -channel activator BDF and the cardiac glycoside ouabain in human failing (New York Heart Association [NYHA] functional class IV, heart transplants for dilated cardiomyopathy, n = 11) and nonfailing (donor hearts, n = 5) myocardium on electrically driven left ventricular papillary muscle strips (1 Hz, 37 degrees C). The effectiveness of ouabain and BDF to increase force of contraction was similar in human nonfailing and failing myocardium. BDF was more potent to increase force of contraction in failing than in nonfailing tissue (p < 0.05). The time until maximal inotropic effect developed after ouabain was significantly shorter in NYHA IV (mean 150 +/- 16 min) than in nonfailing myocardium (mean 240 +/- 20 min). These results suggest that human failing myocardium exerts and enhanced sensitivity to cardiac glycosides and Na+ -channel activators, possibly because of enhanced expression of the Na+/Ca2+ exchanger or because of an altered intracellular Na+ -homeostasis.

Adolescent↗
PubMed1996

Beta-blocking agents in heart failure. Should they be used and how?

Experience accumulated from several large trials strongly suggests that beta-blockers should be used for the management of chronic heart failure[87]. It is appropriate to add beta-blockade to conventional therapy such as diuretics, ACE inhibitors and digoxin, as this was the approach used in the major trials. It is appropriate to treat patients with mild, moderate and, when stable, severe chronic heart failure. The benefits obtained include improvements in left ventricular function, reductions in symptoms and morbidity, improvement of quality of life, and delay of clinical progression, reflected in a reduced need for cardiac transplantation and, probably, a reduction in mortality. beta-blockers are much better tolerated, when used appropriately in selected patients, than was previously supposed. To confirm the improvement in survival recently reported with carvedilol, further prospective trials using different beta-blockers are warranted. No major comparative trials have been carried out between beta-blockers in chronic heart failure, therefore it is not known whether the differences between them are clinically significant. The optimal dose of beta-blocker and the effect in patient groups excluded from or poorly represented in the clinical trials (e.g. elderly patients) have yet to be determined. Placebo-controlled mortality trials with bucindolol (BEST) and bisoprolol (CIBIS-II) are under way[89,90]. A large study of carvedilol versus metoprolol (COMET), added to conventional treatment, is planned.

Adrenergic beta-Antagonists↗
PubMed1996

[Lumen enlargement in coronary angioplasty: qualitative and quantitative analysis of vascular mechanisms with intravascular ultrasound].

The purpose of this study was to determine the mechanisms by which balloon angioplasty increases luminal patency. Therefore serial examinations with intravascular ultrasound before and after coronary balloon angioplasty were performed. Forty consecutive patients (7 female, 33 male, aged 58 +/- 9 years) with 49 dilated lesions were examined with a 3.5 F, 20 MHz mechanical intravascular ultrasound imaging system before and immediately after coronary balloon angioplasty. Quantitative measurements of lumen area, total arterial area, plaque area and arterial stretch were performed in the dilated vessel segments. Plaque reduction accounted for 65% and vessel wall stretch for 35% of the total increase in luminal patency after angioplasty. In 34/49 (69%) lesions plaque reduction and in 15/49 (31%) arterial stretch contributed most (> 50%) of the overall increase in luminal area post angioplasty. in lesions with an ultrasound area stenosis before PTCA larger than the mean value of the group (> or = 87%) plaque reduction contributed a significantly higher percentage to luminal gain as compared to lesions with an area stenosis < 87% (76.5 +/- 25.0 vs 52.7 +/- 29.9, p < 0.05). Conversely, PTCA resulted in a significantly greater amount of vessel walls stretch in lesions with an area stenosis < 87% (47.3 +/- 29.9 vs. 24.4 +/- 24.2; p < 0.05). In lesions with localized dissections (32/49 (65%)) after PTCA as compared to lesions without dissection a significantly greater relative reduction of stenosis (24% +/- 13% vs. 19% +/- 7%, p < 0.05) was found. Plaque reduction and to a lesser extent vessel wall stretch constitute the principal mechanisms responsible for increased luminal patency after balloon angioplasty. The amount of plaque reduction and vessel wall stretch on the overall luminal gain after PTCA is dependent on the size of area stenosis. The presence of localized dissections after angioplasty correlates favorably with a better result.

Adult↗