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Biomedical subjects

E Fleck

Publications and source records attributed to E Fleck.

At least 181 records · Page 10Linked to original sources

Diagnosis of coronary artery disease and viable myocardium by stress echocardiography. Diagnostic accuracy of different stress modalities.

Stress echocardiography is being used more commonly for routine clinical diagnosis of coronary artery disease. In addition to physical treadmill or bicycle exercise echocardiography, pharmacological stress echocardiography with dobutamine and dipyridamole has also gained increasing significance over the past few years. Numerous studies have proven that these methods diagnose coronary artery disease accurately (exercise echocardiography: sensitivity 71 to 98%, specificity 64 to 100%, dobutamine echocardiography; sensitivity 54 to 96%, specificity 66 to 95%; dipyridamole echocardiography: sensitivity 57 to 74%, specificity 80 to 100%), but no direct comparison has hitherto been able to prove the superiority of any one of these protocols. However it is recognized that the skill and experience of the echocardiographer performing this study has an influence on the accuracy of the technique.

Coronary Disease↗

Intravascular ultrasound imaging in patients with acute myocardial infarction.

Myocardial infarction is the result of acute thrombotic occlusion of a coronary artery secondary to rupture of an atherosclerotic plaque. Intracoronary ultrasonic examinations (ICUS) were performed in patients with acute myocardial infarction in order to describe intraluminal ultrasonic findings at the site of an acute coronary occlusion. Coronary angiography and ICUS studies were performed consecutively within 6 h after the onset of chest pain in 50 patients with acute myocardial infarction (AMI) prior to percutaneous coronary angioplasty (PTCA). Following angiographic documentation of a proximal occlusion, a 3.5 mechanical ultrasound catheter (30 MHz) was advanced successfully through the lesion in 42 of 50 patients (84%). In 37 of the 42 patients (88.1%), ICUS differentiated between pulsatile, low echogenic, intraluminal material suggesting thrombus, and mural more highly echogenic atherosclerotic plaque. A negative imprint of the ICUS catheter was documented within the low echogenic material in 25 of 42 (60%) patients with AMI. Low echogenic intraluminal material was found in 31 of 42 (73.4%) segments proximal to the highly echogenic plaque and in 28 of 42 (66.7%) segments distal to it, indicating pre- and post-stenotic thrombus in AMI. The plaque appeared eccentric in 32 of 42 patients (76.2%) with AMI. Cross-sectional area stenosis due to highly echogenic plaque averaged 48 +/- 14%. Calcification of plaque was evident in 35 of 42 patients (83.3%) and the surface of the plaque was rough in 30 of 42 (42.4%). Fissures were found in 10 (23.8%) and a dissection was detected in four (9.5%) cases.

Adult↗

Changes of fluid-dynamic parameters in peripheral stenoses with transcutaneous interventions.

UNLABELLED: Peripheral vessels provide a useful in vivo haemodynamic model allowing evaluation of local intravascular fluid dynamics. Velocity measurements using a 0.018 inch Doppler-tipped angioplasty guidewire, quantitative angiography and laboratory data were gathered from 45 patients with a total of 48 percutaneous transluminal laser assisted angioplasties (PTLA) in the superficial femoral, in the iliac, in the popliteal artery and in the peroneal artery. From these data, blood flow, whole blood viscosity, Reynold's numbers, Womersley numbers and shear stress were calculated, evaluated as to their changes post PTLA and correlated with clinical improvement at early follow-up. The clinical result was quantified as categorial improvement according to the American Heart Association guidelines. The primary angiographic results of angioplasty were satisfactory in all patients. Clinically 17/45 patients showed a marked, 6/45 a moderate, 18/45 a minimal, and 4/45 no improvement. The mean values of maximal peak velocity at stenosis decreased from 235 +/- 28 cms-1 to 84 +/- 8 cms-1 after PTLA (P < 0.01). The minimal intrastenotic cross section increased from 7.7 +/- 0.9 to 21.9 +/- 1.6 mm2 (P < 0.01). Mean trans-stenotic flow increased after intervention by about 50% (P < 0.01) and improved further by 135% after administration of adenosine triphosphosphate i.a. (P < 0.01). Reynold's numbers were elevated intrastenotically (1285 +/- 198) pre-intervention as compared to values proximal (564 +/- 81) and distal (449 +/- 66) to the stenosis and were reduced significantly (P < 0.05) at stenosis by PTLA, whereas values proximally and distally increased significantly (P < 0.01) post PTLA (proximal 829 +/- 84, intra 773 +/- 107, distal 676 +/- 98). Shear stress, reflecting mechanical interaction between flow and vessel wall, was elevated at stenosis pre-intervention to 44 +/- 8.9 Pa and reduced at post-stenoric vessel sites to 2.4 +/- 0.5 Pa. PTLA caused a decrease in stenosis to 6.3 +/- 1 Pa (P < 0.01) and an increase distally to 4.6 +/- 1 Pa (P < 0.01). Whereas in single stenoses removal of the obstruction was associated with a significant (P < 0.05) increase in trans-stenotic flow and shear stress distally, there was only auenuated increase in trans-stenotic flow in multiple lesions despite an angiographically good PTLA result. Shear stress distally remained low in those patients. Velocities and Reynold's numbers were lower in these vessels even pre PTLA. Residual flow, Reynold's number and minimal cross-section pre-intervention correlated significantly with clinical outcome. Pooling cases with no or minimal, as opposed to those with marked or moderate improvement, 81% of patients were correctly classified using the Reynold's numbers pre- and post-PTLA. CONCLUSION: Peak velocity monitoring is feasible and safe during angioplasty. Velocity provides clinically relevant physiological information in addition to angiography. Combining quantitative angiography, velocity measurements and laboratory data allow the calculation of blood flow, Reynold's numbers and shear stress, thereby providing complex fluid dynamic information. Thus the evaluation of haemo-dynamics in single and multiple obstructions before and after intervention is improved. Fluid dynamic parameters pre-and post-PTLA are significantly correlated with clinical short-term result.

Adult↗

Effects of angiotensin receptor antagonists in heart failure: clinical and experimental aspects.

In addition to inhibition of the circulating renin-angiotensin system, specific inhibition of the cardiac effects of angiotensin II (Ang II) represents an important therapeutic goal in the treatment of clinical heart failure. Subtype 1-specific Ang II receptor (AT1) antagonists have been developed to overcome potential limitations of angiotensin converting enzyme inhibitors, e.g. insufficient control of tissue Ang II production and bradykinin-related side effects. Clinical studies have demonstrated beneficial effects of AT1 antagonists. In a single-dose study, the AT1 antagonist losartan decreased the mean arterial pressure and pulmonary arterial pressure while increasing the cardiac index. Effects were dose dependent. Haemodynamic effects were greater with higher doses, but neurohormonal counter-regulation probably also increased, leading to relatively high levels of circulating Ang II with the 150-mg dose, A decrease in plasma levels of noradrenaline, atrial natriuretic factor, and aldosterone reached partial significance. Administration of multiple doses of losartan for 12 weeks also led to favourable haemodynamic and clinical results. Arterial blood pressure, pulmonary capillary wedge pressure, and systemic vascular resistance decreased. The neurohormonal effects of 12 weeks' administration of AT1 antagonists consisted in a decrease in plasma aldosterone concentrations. Whereas AT1 antagonists may counteract the effects of Ang II on the vasculature, and therefore are effective vasodilators, their direct myocardial effects are less clear. The subtype AT2, which represents the dominant, receptor in both healthy and failing human myocardium, is not blocked by AT1 inhibition. Angiotensin receptors on isolated human cardiac fibroblasts stimulate cellular proliferation via a yet undertermined receptor subtype. AT1 antagonists exert beneficial haemodynamic and neurohormonal effects in human heart failure. Their direct myocardial effects require further investigation.

Angiotensin Receptor Antagonists↗

Tissue- and subtype-specific modulation of angiotensin II receptors by chronic treatment with cyclosporin A, angiotensin-converting enzyme inhibitors and AT1 antagonists.

We wished to determine whether chronic treatment of rats with cyclosporin A (CSA), an angiotensin-converting enzyme inhibitor (ACEI) or angiotensin receptor antagonists modulates the angiotensin receptor density. In rats treated chronically with CSA, the vasoconstrictor response to angiotensin II (AII) is increased and this increase is modulated by ACEI and angiotensin receptor antagonists. Rats were treated for 6 weeks orally with CSA (15 mg/kg/day), the ACE inhibitor lisinopril (10 mg/kg/day), the angiotensin receptor antagonists DUP 753 (10 mg/kg/day), and D 8731 (10 mg/kg/day) and the combinations CSA + lisinopril, CSA + DUP 753, and CSA + D 8731. Olive oil was used as a control. The number of total AII receptors (Bmax) was determined by Scatchard analysis of [125I]Sar1 Ile8 AII binding in kidney, liver, adrenal cortex, and adrenal medulla. The receptor subtypes were analyzed with the specific antagonists DUP 753 (subtype 1) and PD 123319 (subtype 2). CSA upregulated angiotensin receptors in all organs studied. Lisinopril alone downregulated angiotensin receptors and abolished the effect of CSA in liver and adrenal cortex and medulla, but not in the kidney, where it had no effect. DUP 753 alone downregulated the angiotensin receptor subtype 1 in kidney, liver and adrenal cortex; its effect on the adrenal medulla in which 89% of angiotensin receptors are subtype 2, did not quite reach significance. The combination of DUP 753 and cyclosporin CSA abolished the CSA-induced increase in angiotensin receptor density in all four organs. The angiotensin receptor antagonists D 8731 downregulated the angiotensin receptors (subtype 1) in liver and kidney and upregulated angiotensin receptors (subtype 2) in the adrenal medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

Treating poststernotomy mediastinitis by transposition of the greater omentum: late angiographic findings.

Transposition of the greater omentum to the thorax for treatment of severe mediastinal infections due to the anatomical structure and physiological properties of the omental tissue is a proven and safe procedure. From 1987 to 1993, thoracic omentoplasty was performed in 112 cases at our facility. In order to attempt to visualize the vascularization of an omental graft by the right or left gastroepiploic artery via the coeliac trunk, a small group of patients (n = 7) underwent left heart catheterization followed by angiography of the gastroepiploic arteries. Visualization of the gastroepiploic arteries was successful in six patients. Furthermore, anastomoses with adjacent vessels were observed in individual cases. The omental vessels remain open for a long period after transposition to the thorax, and additionally, appear to create anastomoses with surrounding vessels.

Aged↗

Regulation and differential expression of neutral endopeptidase 24.11 in human endothelial cells.

Neutral endopeptidase 24.11, a membrane-bound metallopeptidase, cleaves, and degrades vasoactive peptides such as atrial natriuretic peptide, endothelin, angiotensin I, substance P, and bradykinin. Therefore, the presence of this metallopeptidase may contribute to the regulation of vascular tone and local inflammatory responses in the vascular endothelium and elsewhere. We determined neutral endopeptidase in cultured human endothelial cells from different vascular beds and studied its regulation by protein kinase C. Neutral endopeptidase was detected in all cultured endothelial cell types. Lowest concentrations were measured in human endothelial cells from umbilical veins (360 +/- 14 pg/mg protein), followed by pulmonary and coronary arteries; higher concentrations were found in endothelial cells from the cardiac microcirculation (1099 +/- 73 pg/mg protein). Neutral endopeptidase content increased during cell growth but was not affected by endothelial cell growth factor or modifications of the growth medium. Stimulation of protein kinase C with 1-oleoyl-2-acetyl-rac-glycerol (0.1 to 1 mumol/L) and phorbol 12-myristate 13-acetate (0.01 to 0.1 mumol/L) induced a time- and concentration-dependent increase of endothelial cells that was inhibited by cycloheximide (5 mumol/L), an inhibitor of protein synthesis. Incubation with phospholipase C (1 mumol/L) and thrombin (10 IU/mL) induced upregulation of neutral endopeptidase, resulting in 158 +/- 26% and 150 +/- 22% increases, respectively, compared with controls. The thrombin effect was inhibited by calphostin C (1 mumol/L), an inhibitor of protein kinase C. Endothelial neutral endopeptidase is constitutively expressed in endothelial cells from different origins and is inducible by thrombin via activation of the protein kinase C pathway.

Cell Division↗

Telemedicine in rural areas. Experience with medical desktop-conferencing via satellite.

Cooperation between physicians in hospitals in rural areas can be assisted by desktop-conferencing using a satellite link. For six weeks, medical desktop-conferencing was tested during daily clinical conferences between the Virchow-Klinikum, Berlin, and the Medical Academy, Wroclaw. The communications link was provided by the German Telekom satellite system MCS, which allowed temporary connections to be established on demand by manual dialling. Standard hardware and software were used for videoconferencing, as well as software for medical communication developed in the BERMED project. Digital data, such as computed tomography or magnetic resonance images, were transmitted by a digital data channel in parallel to the transmission of analogue video and audio signals. For conferences involving large groups of people, hardware modifications were required. These included the installation of a video projector, adaptation of the audio system with improved echo cancellation, and installation of extra microphones. Learning to use an unfamiliar communication medium proved to be uncomplicated for the participating physicians.

Germany↗

[Angiotensin receptors--organ and subtype specific regulation in cardiovascular diseases by modulation of the renin-angiotensin system. Studies of the rat model and in human myocardium].

So far, two angiotensin receptor subtypes, called AT1 and AT2, have been described in an animal model and in human. AT1 mediates almost all known effects of angiotensin II and its gene sequence and regulation is well studied. In contrast, only few data on function and regulation of AT2 are available. The complete mRNA sequence of AT2 has only recently been cloned and sequenced. The angiotensin receptors' receptor density and subtype distribution is organ specific. In the rat, lowest densities are found in the myocardium, followed by kidney, liver, adrenal medulla and cortex. The percentage of AT1 in the different organs amounts to 80, 85, 90, 57 and 10%. Angiotensin receptor subtypes have also been quantitated in human myocardium. There, the relatively unknown subtype AT2 dominates (67%). Myocardial receptor density is low, amounting to about 11 fmol/mg protein corresponding to 1/20-1/50 of the density of beta-adrenergic receptors. Angiotensin receptors in the human heart are present on cardiac fibroblasts and induce proliferation of these cells. Blockade of the renin angiotensin system by ACEI and AT1 antagonists in the rat downregulates angiotensin receptors in liver, kidney and adrenals to about 50% in an organ- and subtype specific manner, whereas cyclosporin A upregulates receptors twice. In end-stage human heart failure, but not in early stages, angiotensin receptors are downregulated to 1/3 of control values. Regulator mechanisms at transcriptional level have been elucidated by reporter gene assays; PMA, an activator of proteinkinase C, stimulates the transcription of the AT1 gene. The organ- and subtypespecific regulation of angiotensin receptors by pharmacological agents and/or cardiovascular diseases can contribute to the understanding of these drugs and of the pathophysiology of the corresponding diseases.

Animals↗

Human cardiac fibroblasts express an angiotensin receptor with unusual binding characteristics which is coupled to cellular proliferation.

To assess the cellular localization of angiotensin receptors in human heart, we isolated human cardiac fibroblasts from explanted end-stage failing human hearts. As judged by an immunofluorescence assay, the isolated cells consisted of 96% of fibroblasts. Using receptor binding studies, we could identify a single angiotensin binding site on these cells, with a Kd of 0.6nM and a Bmax of 1.5 fmol/mg protein. Inhibiting concentrations 50 for Ang II and Ang I/II (1-7) were 40nM and 10nM, respectively. Stimulation with Ang II (100 nM) and Ang I/II (1-7) (100nM) led to cellular proliferation which could not be inhibited by Losartan or PD 123319. These results suggest that human cardiac fibroblasts express an as yet unknown angiotensin receptor-subtype.

Angiotensin II↗

Protein composition of the human heart: the construction of a myocardial two-dimensional electrophoresis database.

Molecular changes occurring in myocardial diseases are not well understood. Proteins, as regulatory molecules, should play an important role in the etiology of these diseases. The method of two-dimensional electrophoresis (2-DE) allows the analysis of some thousand proteins with one experiment. An important prerequisite for this kind of investigation is the possibility of identifying the proteins separated by 2-DE. We resolve 3239 proteins of the human myocardium and tried to identify 33 proteins by amino acid analysis and microsequencing. Twenty proteins were identified by search for the protein-chemical data obtained in the Martinsried Institute Protein Sequence Database. Comparisons of 2-DE patterns of different size, which were obtained in different laboratories, were performed with the result that proteins identified on a 2-DE map of one laboratory can be assigned to spots of 2-DE maps produced by another laboratory. Our results show the usefulness of a myocardial 2-DE database; they can be used in different laboratories and make it possible to generate a collection of important human myocardial proteins in a 2-DE database for comparative studies worldwide.

Amino Acid Sequence↗

Preventive effects of diltiazem on cyclosporin A-induced vascular smooth muscle dysfunction.

Cyclosporin A may cause vascular smooth muscle dysfunction due to calcium overload as a consequence of chronically augmented calcium influx. In the present study, the responsiveness to vasocontrictors was investigated in rats after chronic treatment for 6 weeks with placebo, cyclosporin A (30 mg/kg per day), diltiazem (60 mg/kg per day), or cyclosporin A plus diltiazem. Twenty-four hours after the last oral treatment the animals were sacrificed and rings of the thoracic aorta were suspended in organ chambers under isometric conditions in the absence of cyclosporin A or diltiazem. Chronic treatment with cyclosporin A significantly augmented contractions to angiotensin II (10(-9)-10(-5) M). This effect was prevented by cotreatment with diltiazem. Diltiazem did not affect the cyclosporin A-induced reduction in the response to potassium chloride (10-80 mM). The contractions to phenylephrine (10(-9)-10(-6) M) and endothelin-1 (10(-9)-10(-7) M) were not significantly different in the four groups. The preventive effect of diltiazem against the cyclosporin A-induced hypersensitivity to angiotensin II supports the hypothesis of increased calcium influx during cyclosporin A therapy. The results may provide an additional rationale for the use of calcium antagonists in the treatment of the vascular side effects of cyclosporin A.

Animals↗

Acute complications of excimer laser coronary angioplasty: a detailed analysis of multicenter results. Coinvestigators of the U.S. and European Percutaneous Excimer Laser Coronary Angioplasty (PELCA) Registries.

OBJECTIVES: The aim of this study was to document and analyze the incidence and consequences of complications of excimer laser coronary angioplasty. BACKGROUND: Excimer laser coronary angioplasty has been reported to be a safe and feasible alternative or adjunct to conventional balloon angioplasty, but serious and unique complications have been observed. METHODS: Data on 1,595 interventions of excimer laser coronary angioplasty in 1,521 patients were analyzed, using a merged data base from the U.S. and European Percutaneous Excimer Laser Coronary Angioplasty (PELCA) registries. RESULTS: Procedural success was achieved in 89.3% of interventions. Stand-alone laser angioplasty was performed in 17.8% of interventions. Complications included dissection (22.0%), vasospasm (6.1%), filling defects (4.8%), abrupt reclosure (6.1%), embolization (2.3%), perforation (2.4%), arrhythmia (0.7%) and aneurysm formation (0.3%). Major complications were non-Q wave myocardial infarction (2.3%), Q wave myocardial infarction (1.0%), coronary artery bypass grafting (3.1%) and death (0.7%). Logistic regression analysis revealed correlation between dissections and the use of larger catheter size (p = 0.0005), high energy per pulse levels (p = 0.0001 for native vessels), lesion length > 10 mm (p = 0.001) and presence of a side branch (p = 0.01). The incidence of perforations was higher in women (p = 0.004), in treatment of total occlusions (p = 0.02) and in the presence of a side branch (p = 0.03). Fatal complications were correlated with patients with multivessel disease (p < 0.0001), patients with acute myocardial infarction (p = 0.0009) and older patients (> 70 years old, p = 0.004). The incidence of major complications decreased after performance of 50 laser angioplasty procedures at one institution (p = 0.02). CONCLUSIONS: This analysis defines both the learning curve and the profile of complications for excimer laser angioplasty and provides insight into the selection of appropriate patients and proper performance of the procedure.

Acute Disease↗

[Communication and integration of medical documents for the teleconference use. An outcome of the BERMED project].

The collaboration between physicians is supported in the BERMED project by implementing the remote access to distributed patient data and the realisation of computer-based medical conferencing. This requires the integration of the multimedia data in form of a meta-patient record for our medical application systems. These applications are supported by a distributed information management promoting access to different information systems, imaging modalities and digital archival storage systems. The features of image processing are concerned with quantification, segmentation and 3-D-visualisation to obtain additional information. This paper gives an overview of the actual state of the teleconferencing system in radiology.

Computer Communication Networks↗

Genetic polymorphisms of the angiotensin II type 1 (AT1) receptor gene.

Numerous essential, physiological effects on the cardiovascular system are attributable to angiotensin II (Ang II). Because of this we can assume that genetic changes in the specific receptor of Ang II (Ang II type 1 receptor gene, AT1) play a decisive role in the occurrence of cardiovascular disease associated with blood pressure regulation, vascular tone, cardiac and vascular growth process. To test this hypothesis, we examined the presence of polymorphisms within the coding region of the AT1 gene using polymerase chain reaction (PCR) and subsequent non-radioactive sequencing of samples from a control group with no previous history of cardiovascular complaint in individuals or immediate family. Using the Taq-sequencing procedure we found polymorphic sites, especially in the 5' region of the gene (base pair positions 9, 16, 87, 133, 186), two of which led to an exchange of the amino acid (amino acid 6: Ser<==>Pro, amino acid 45: Gly<==>Arg). Together with the silent polymorphism at base pair position 573, which our group established previously, an additional polymorphism in the 3' region of the gene was discovered. This, however, did not confer any changes in amino acid sequence. In a preliminary study we found no association between the distribution of the C/T573 polymorphic site and cardiovascular disease, such as essential hypertension (n = 20) coronary artery disease (n = 16) hypertrophic cardiomyopathy (n = 12) or dilated cardiomyopathy (n = 21). Further studies will be needed to determine to what extent the polymorphisms described are associated with cardiovascular disease.

Amino Acid Sequence↗

Dose-related effects of ACE inhibition in man: quinapril in patients with moderate congestive heart failure. The Study Group on Neurohormonal Regulation in Congestive Heart Failure: Lausanne, Switzerland; Berlin, Düsseldorf, Munich, Germany.

Early treatment with ACE inhibitors of even moderate heart failure is clinically beneficial, even though haemodynamic measurements cannot adequately quantitate such improvement. Neurohumoral assessment is, however, supposed to be more accurate. In 55 patients with moderate heart failure (ejection fraction < or = 35%), we investigated the dose-dependent effects of ACE inhibition with quinapril taken orally (2.5, 5 or 10 mg b.i.d.) following a placebo-controlled, parallel design protocol over 12 weeks. Plasma components of the renin angiotensin system, catecholamines and ANF were measured together with haemodynamics both at rest and during exercise. Before ACE inhibitor treatment, median PRA, Ang I and II and catecholamines were normal, while ANF was increased. All these parameters, including ACE activity, rose during exercise. Chronic inhibition of ACE activity was dose-dependent and the maximal fall in Ang II occurred with quinapril 20 mg.day-1. Humoral changes appeared more assessible than haemodynamic alterations even though many of these changes were reasonably correlated. The effects of chronic ACE inhibition on circulating neurohumoral components in patients with moderate heart failure are small and dose-dependent. Since humoral changes are related to haemodynamics they should account for the clinical benefit. Appropriately high doses of ACE inhibitors should be chosen for treatment of heart failure.

Administration, Oral↗

Characterization of myocardial protein composition in dilated cardiomyopathy by two-dimensional gel electrophoresis.

In order to identify alterations in the myocardial protein pattern that characterize dilated cardiomyopathy (DCM), we compared, by two-dimensional gel electrophoresis, right atrial protein patterns from five patients with DCM and four with normal left ventricular function (two gels per patient). Using computer assisted analysis (PDQUEST, 4.1) we found reproducible protein patterns in the 18 gels (23 x 30 cm, pH 4-9, molecular weight 10-150 kDa). In the two gels from the same patient, 91% of proteins were identical in their position in the pattern and the relative intensities of these protein species correlated with r = 0.85. Three hundred and two +/- 50 protein species were found in several gels, 186 in all 18 gels. Seven proteins in the DCM group were decreased in their relative intensity by > 100%, six were increased by > 100%. Significant quantitative differences between DCM and control patients were found for 25 protein species. Based on seven external marker proteins, a pH and molecular weight value could be calculated for each protein. So far, 30 protein species have been identified by antibodies, amino acid analysis or sequencing procedures. From the 25 proteins that are significantly different between DCM and controls, three have been identified. Expression of the mitochondrial creatine kinase and alpha cristallin B chain was significantly increased in DCM; the malate dehydrogenase family was also significantly decreased in DCM. Two-dimensional electrophoresis appears to be a powerful method for the detection of disease-associated alterations in the myocardial protein pattern.

Adult↗