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Biomedical subjects

E Fleck

Publications and source records attributed to E Fleck.

At least 91 records · Page 5Linked to original sources
PubMed2000

Reproducibility of serial intravascular ultrasound measurements in patients with angiographically silent coronary artery disease after heart transplantation.

BACKGROUND: Intracoronary ultrasound (ICUS) imaging is the most sensitive method for the early detection and serial evaluation of vasculopathy of transplants. Both lack of agreement between observers and lack of agreement between serial, independent pullback procedures (repeatability), which can result in a variable intraluminal catheter position may limit the reproducibility of ICUS measurements. OBJECTIVE: To evaluate the reproducibility of serial measurements of standard linear and area cross-sectional coronary dimensions in patients with non-obstructive transplant vasculopathy. METHODS: We performed ICUS imaging of patients without angiographic evidence of obstructive epicardial coronary artery disease after heart transplantation. A 30 MHz phased-array transducer was used. Two independent pullbacks of the left anterior descending coronary artery were performed and recorded on CD-ROM for off-line quantitative analysis of the most severely diseased site. Agreement of observers and repeatability of serial measurements were calculated by the use of linear regression analysis and Bland-Altman plots. RESULTS: Regarding agreement of observers, correlation coefficients for intra-observer agreement ranged from r = 0.98 to r = 0.99; those for interobserver agreement ranged from r = 0.87 to r = 0.98. Serial measurements of the identical coronary artery cross-section within independent catheter pullback procedures were possible for 104 of 112 target lesions (92.90/%). Correlation coefficients ranged from r = 0.91 to r = 0.97 (for lumen diameter r = 0.91, for lumen area r = 0.93, for vessel diameter r = 0.91, for vessel area r = 0.97, for thickness of plaque r = 0.96 and for area of plaque 0.94). The mean difference of measurements was around zero for all parameters with SD from 0.13 to 0.4 mm for linear parameters and from 1.53 to 1.82 mm2 for area parameters. CONCLUSION: Serial intravascular ultrasound measurements are highly reproducible without any evidence of systematic error and a SD of differences of measurements beyond the maximal spatial resolution of currently available intravascular ultrasound catheters.

Coronary Angiography↗
PubMed2000

Coronary arterial stents: safety and artifacts during MR imaging.

PURPOSE: To investigate the safety and imaging artifacts with different coronary arterial stents and magnetic resonance (MR) imaging sequences. MATERIALS AND METHODS: The heating, artifacts, and ferromagnetism with different stents were studied with a 1.5-T MR tomograph with ultrafast gradients by using turbo spin-echo, turbo gradient-echo, and echo-planar imaging sequences. Nineteen stents, which were 8-25 mm in length and 3.0-4.5 mm in diameter, were evaluated. Stent deviation induced by the magnetic field and during MR imaging, migration, and heating caused by the radio-frequency pulses were examined. The size of imaging artifacts was measured with all the stents under standardized conditions and with six stents after their implantation into the coronary arteries of freshly explanted pig hearts. RESULTS: All except two types of stents showed minimal ferromagnetism. No device migration or heating was induced. Turbo spin-echo images had minimal artifacts; larger artifacts were seen on the turbo gradient-echo and echo-planar images. With ultrafast gradients, the artifacts on the echo-planar images were substantially reduced. CONCLUSION: The studied coronary stents were not influenced by heating or motion during 1.5-T MR imaging. Artifact size differed according to the type and size of the stent and the MR imaging sequence used. Thus, patients with these stents can be safely examined.

Angioplasty, Balloon, Coronary↗
PubMed2000

Doxazosin inhibits retinoblastoma protein phosphorylation and G(1)-->S transition in human coronary smooth muscle cells.

Previous studies have demonstrated that the alpha(1)-adrenergic receptor antagonist doxazosin (Dox) inhibits multiple mitogenic signaling pathways in human vascular smooth muscle cells. This broad antiproliferative activity of Dox occurs through a novel mechanism unrelated to its blocking the alpha(1)-adrenergic receptor. Flow cytometry demonstrated that Dox prevents mitogen-induced G(1)-->S progression of human coronary artery smooth muscle cells (CASMCs) in a dose-dependent manner, with a maximal reduction of S-phase transition by 88+/-10.5% in 20 ng/mL platelet-derived growth factor and 1 micromol/L insulin (P+I)-stimulated cells (P<0.01 for 10 micromol/L Dox versus P+I alone) and 52+/-18.7% for 10% FBS-induced mitogenesis (P<0.05 for 10 micromol/L Dox versus 10% FBS alone). Inhibition of G(1) exit by Dox was accompanied by a significant blockade of retinoblastoma protein (Rb) phosphorylation. Hypophosphorylated Rb sequesters the E2F transcription factor, leading to G(1) arrest. Adenoviral overexpression of E2F-1 stimulated quiescent CASMCs to progress through G(1) and enter the S phase. E2F-mediated G(1) exit was not affected by Dox, suggesting that it targets events upstream from Rb hyperphosphorylation. Downregulation of the cyclin-dependent kinase inhibitory protein p27 is important for maximal activation of G(1) cyclin/cyclin-dependent kinase holoenzymes to overcome the cell cycle inhibitory activity of Rb. In Western blot analysis, p27 levels decreased after mitogenic stimulation (after P+I, 43+/-1.8% of quiescent cells [P<0.01 versus quiescent cells]; after 10% FBS, 55+/-7.7% of quiescent cells [P<0. 05 versus quiescent cells]), whereas the addition of Dox (10 micromol/L) markedly attenuated its downregulation (after P+I, 90+/-8.3% of quiescent cells [P<0.05 versus P+I alone]; after 10% FBS, 78+/-8.3% of quiescent cells [P<0.05 versus 10% FBS alone]). Furthermore, Dox inhibited cyclin A expression, an E2F regulated gene that is essential for cell cycle progression into the S phase. The present study demonstrates that Dox inhibits CASMC proliferation by blocking cell cycle progression from the G(0)/G(1) phase to the S phase. This G(1)-->S blockade likely results from an inhibition of mitogen-induced Rb hyperphosphorylation through prevention of p27 downregulation.

Adrenergic alpha-Antagonists↗
PubMed2000

Angiotensin II and PDGF-BB stimulate beta(1)-integrin-mediated adhesion and spreading in human VSMCs.

beta(1)-Integrins play an important role for adhesion and spreading of human smooth muscle cells. In the present study we examined the influence of angiotensin II and platelet-derived growth factor (PDGF)-BB on beta(1)-integrin-dependent functions of human smooth muscle cells obtained from iliac arteries. Treatment of these cells with PDGF-BB (20 ng/mL) and Angiotensin II (1 micromol/L) did not change beta(1)-integrin expression up to 48 hours as analyzed by flow cytometry and reverse transcription polymerase chain reaction. beta(1)-integrins predominantly mediated adhesion of human smooth muscle cells to collagen I (79.7+/-4.4%, P<0.01) and fibronectin (66. 6+/-2.4%, P<0.01). Treatment of smooth muscle cells with Angiotensin II (1 micromol/L) and PDGF-BB (20 ng/mL) significantly increased the adhesion to collagen I by 56.5% and 44.3%, respectively, and to fibronectin by 49.6% and 36.4%, respectively (all P<0.05). Angiotensin II-induced effects were mediated by the AT(1) receptor. The PDGF-BB mediated increase of adhesion was inhibited in the presence of genestein, a tyrosine-kinase inhibitor and by protein kinase C downregulation with phorbol 12-myristate 13-acetate. Spreading of smooth muscle cells also was beta(1)-integrin dependent on collagen I and alpha(5)beta(1)-integrin dependent on fibronectin. Angiotensin II and PDGF-BB increased cell spreading on fibronectin up to 276% and 318%, respectively, and on collagen I up to 133% and 138% (all P<0.05). These increases were significantly inhibited by blocking antibodies against beta(1)-integrin, alpha(5)-integrin on fibronectin, the AT(1) receptor blocker irbesartan, and genestein. The present data demonstrate that angiotensin II and as well PDGF-BB enhance beta(1)-integrin-dependent adhesion and spreading of human vascular smooth muscle cells. Furthermore, the experiments with PDGF suggest an involvement of protein kinase C activation leading to these enhanced effects.

Angiotensin II↗
PubMed2000

Angiotensin II and alpha(v)beta(3) integrin expression in rat neonatal cardiac fibroblasts.

We recently demonstrated that alpha(v)beta(3) integrins are involved in the mechanisms of angiotensin II (Ang II)-induced DNA synthesis and collagen gel contractions in rat cardiac fibroblasts (CFBs), cellular mechanisms that are relevant for cardiac remodeling. The aim of the present study was to elucidate the effect of Ang II and other growth factors on the regulation of the alpha(v)beta(3) integrins in fibroblasts from neonatal rat hearts. The alpha(v)beta(3) integrin receptor expression was significantly increased (P<0.05) at the mRNA level after treatment with Ang II, transforming growth factor-beta(1) (TGF-beta(1)), and platelet-derived growth factor (PDGF) for 8 and 16 hours. The surface expression of the alpha(v) and beta(3) integrin subunits was elevated after 32 and 48 hours (P<0.05) as determined with flow cytometry. To investigate fibroblast motility, we performed chemotaxis experiments with transwell chambers. Ang II was chemotactic for CFBs, as tested with checkerboard experiments. The chemotactic effect was concentration dependent and was completely blocked by Ang II type 1 receptor blockers but not by Ang II type 2 receptor blocker PD 123319. Ang II- and PDGF-BB-mediated chemotaxis could be significantly inhibited by RGD peptides and the blocking antibodies against alpha(v)beta(3) integrin (both P<0.01). Adhesion of CFBs to vitronectin was partially inhibited by an antibody to alpha(v)beta(3) integrin but was mainly mediated by an alpha(v)beta(5) integrin. Relevant in vivo expression of alpha(v)beta(3) integrin by CFBs was confirmed with in situ hybridization with probes for alpha(v) and beta(3) mRNA in rat hearts. The present study demonstrates that the expression of alpha(v)beta(3) integrin is augmented by Ang II, PDGF, and TGF-beta(1) in neonatal CFBs. Furthermore, this integrin is involved in the chemotaxis, motility, and adhesion of CFBs. The present findings support the current concept that integrins participate in the control of fibroblast behavior during cardiac remodeling mechanisms.

Angiotensin II↗
PubMed2000

Magnetic resonance real-time imaging for the evaluation of left ventricular function.

New ultrafast gradient systems and hybrid imaging sequences make it possible to acquire a complete image in real time, without the need for breathholding or electrocardiogram (ECG) triggering. In 21 patients, left ventricular function was assessed by the use of a turbo-gradient echo technique, an echo-planar imaging (EPI) technique, and a new real-time imaging technique. End-diastolic and end-systolic volumes, left ventricular muscle mass, and ejection fraction of the ultrafast techniques were compared with the turbo-gradient echo technique. Inter- and intraobserver variability was determined for each technique. Image quality was sufficient for automated contour detection in all but two patients in whom foldover occurred in the real-time images. Results of the ultrafast imaging techniques were comparable with conventional turbo-gradient echo techniques. There was a tendency to overestimate the end-diastolic volume by 3.9 and 1.3 ml with EPI real-time imaging, the end-systolic volume by 0.9 and 5.0 ml, and the left ventricular mass by 2.6 and 23.8 g. Ejection fraction showed a tendency to be overestimated by 1.1% with EPI and underestimated by 4.5% with real-time imaging. Correlation between EPI real-time imaging and turbo-gradient echo were 0.94 and O.95, respectively, for end-diastolic volumes, 0.98 and 0.96, respectively, for end-systolic volumes, and 0.96 and 0.89, respectively, for left ventricular mass. Inter- and intraobserver variability was low with all three techniques. Real-time imaging allows an accurate determination of left ventricular function without ECG triggering. Scan times can be reduced significantly with this new technique. Further studies will have to assess the value of real-time imaging for the detection of wall motion abnornmalities and the imaging of patients with atrial fibrillation.

Analysis of Variance↗
PubMed1999

Troglitazone inhibits angiotensin II-induced extracellular signal-regulated kinase 1/2 nuclear translocation and activation in vascular smooth muscle cells.

The thiazolidinedione troglitazone inhibits angiotensin II-induced extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase activity in vascular smooth muscle cells. Activation of extracellular signal-regulated kinase 1/2 by angiotensin II is a multistep process involving both its phosphorylation by mitogen-activated protein kinase extracellular signal-regulated kinase kinase in the cytoplasm and a subsequent translocation to the nucleus. The cytoplasmic activation of extracellular signal-regulated kinase 1/2 in vascular smooth muscle cells proceeds through the protein kinase Czeta --> mitogen-activated protein kinase extracellular signal-regulated kinase kinase --> extracellular signal-regulated kinase pathway. Troglitazone did not affect the angiotensin II-induced activation of protein kinase Czeta or its downstream signaling kinases extracellular signal-regulated kinase 1/2 in the cytosol. In contrast, angiotensin II-induced activation of protein kinase Czeta and extracellular signal-regulated kinase 1/2 in the nucleus were both inhibited by troglitazone. Nuclear translocation of extracellular signal-regulated kinase 1/2 induced by angiotensin II was completely blocked by troglitazone. Protein kinase Czeta, however, did not translocate upon angiotensin II stimulation. Troglitazone, therefore, inhibits both angiotensin II-induced nuclear translocation of extracellular signal-regulated kinase 1/2 and the nuclear activity of its upstream signaling kinase protein kinase Czeta. Since extracellular signal-regulated kinase 1/2 nuclear translocation may be a critical signaling step for multiple growth factors that stimulate vascular smooth muscle cells proliferation and migration, troglitazone may provide a new therapeutical approach for the prevention and treatment of atherosclerosis and restenosis.

Angiotensin II↗
PubMed1999

Efficient transcription of the human angiotensin II type 2 receptor gene requires intronic sequence elements.

To investigate mechanisms of human angiotensin II type 2 receptor (hAT2) gene regulation we functionally characterized the promoter and downstream regions of the gene. 5'-Terminal deletion mutants from -1417/+100 to -46/+100 elicited significant but low functional activity in luciferase reporter gene assays with PC12W cells. Inclusion into the promoter constructs of intron 1 and the transcribed region of the hAT2 gene up to the translation start enhanced luciferase activity 6.7+/-1.6-fold and 11.6+/-1.7-fold (means+/-S.E.M.) respectively, whereas fusion of the promoter to the spliced 5' untranslated region of hAT2 cDNA did not, which indicated an enhancement caused by intronic sequence elements. Reverse transcriptase-mediated PCR confirmed that the chimaeric hAT2-luciferase mRNA was regularly spliced in PC12W cells. A Northern blot analysis of transfected cells showed levels of luciferase mRNA expression consistent with the respective enzyme activities. Mapping of intron 1 revealed that a 12 bp sequence in the centre of the intron was required for the increase in promoter activity, whereas the 5' adjacent intronic region mediated a decrease in luciferase activity. Mutation of the 12 bp region led to altered protein binding and markedly decreased luciferase activity. Cloned into a promoterless luciferase vector, a 123 bp intron 1 fragment was able to direct reporter gene expression to the same activity as occurred in conjunction with the 5' flanking region. These results indicate that sequence elements in intron 1 are necessary for efficient transcription of hAT2. In reporter gene assays, intron 1 might by itself function as a promoter and initiate transcription from an alternative start point.

5' Untranslated Regions↗
PubMed1999

Noninvasive diagnosis of ischemia-induced wall motion abnormalities with the use of high-dose dobutamine stress MRI: comparison with dobutamine stress echocardiography.

BACKGROUND: The analysis of wall motion abnormalities with dobutamine stress echocardiography (DSE) is an established method for the detection of myocardial ischemia. With ultrafast magnetic resonance tomography, identical stress protocols as used for echocardiography can be applied. METHODS AND RESULTS: In 208 consecutive patients (147 men, 61 women) with suspected coronary artery disease, DSE with harmonic imaging and dobutamine stress magnetic resonance (DSMR) (1.5 T) were performed before cardiac catheterization. DSMR images were acquired during short breath-holds in 3 short-axis views and a 4- and a 2-chamber view (gradient echo technique). Patients were examined at rest and during a standard dobutamine-atropine scheme until submaximal heart rate was reached. Regional wall motion was assessed in a 16-segment model. Significant coronary heart disease was defined as >/=50% diameter stenosis. Eighteen patients could not be examined by DSMR (claustrophobia 11 and adipositas 6) and 18 patients by DSE (poor image quality). Four patients did not reach target heart rate. In 107 patients, coronary artery disease was found. With DSMR, sensitivity was increased from 74.3% to 86.2% and specificity from 69.8% to 85.7% (both P<0.05) compared with DSE. Analysis for women yielded similar results. CONCLUSIONS: High-dose dobutamine magnetic resonance tomography can be performed with a standard dobutamine/atropine stress protocol. Detection of wall motion abnormalities by DSMR yields a significantly higher diagnostic accuracy in comparison to DSE.

Aged↗
PubMed1999

Functional MRI in ischemic heart disease based on detection of contraction abnormalities.

Even though several non-invasive techniques are available for the assessment of coronary artery disease and the detection of myocardial ischemia, many coronary angiograms yield negative results, thus, warranting higher accuracy for non-invasive tests. The detection of obstructive coronary artery disease is only possible during physical or pharmacological stress. Currently, the assessment of wall motion abnormalities by echocardiography is clinically the most widely used method. However, a significant number of patients yield suboptimal or non-diagnostic images despite improvements with harmonic imaging. Cardiovascular magnetic resonance (CMR) imaging allows a non-invasive visualization of the heart with high spatial and temporal resolution. Gradient echo CMR images permit an exact and reproducible determination of global and regional left ventricular function, wall thickness and wall thickening and identical pharmacological stress protocols, as currently used for dobutamine stress echocardiography, can be implemented for CMR imaging. A review of the literature on dobutamine stress CMR for the detection of stress induced wall motion abnormalities is presented and the safety of CMR stress examinations is discussed. The results show, that especially in those patients with suboptimal echocardiographic image quality dobutamine stress CMR is superior in comparison with dobutamine stress echocardiography and may replace echocardiography in these patients. Further possibilities by the use of myocardial tagging or intravascular contrast agents are outlined.

Cardiotonic Agents↗
PubMed1999

Noninvasive determination of coronary blood flow velocity with magnetic resonance imaging: comparison of breath-hold and navigator techniques with intravascular ultrasound.

The aim of this study was to evaluate two different magnetic resonance (MR) techniques for the noninvasive assessment of intracoronary blood flow. Coronary blood flow velocities were measured invasively in 26 angiographically normal segments of 12 patients. Noninvasive measurements were performed in identical segments with two MR techniques using a 1.5 T MR tomograph (ACS NT, Philips). A single breath-hold technique (temporal resolution: 140 msec) and a similar non-breath-hold technique with prospective navigator correction and improved temporal resolution (45 msec) were used. Maximal coronary flow velocities determined by MR correlated closely with invasive measurements (breath-hold: r = 0.70; navigator: r = 0.86); however, a significant underestimation of the MR measurements was found (slope = 0.33 and 0.37). The relative difference from the invasive method was lower for the navigator technique compared with the breath-hold technique (P<0.02). Both MR techniques allow the determination of coronary blood flow velocities. The higher temporal resolution and shorter acquisition window of navigator-corrected non-breath-hold techniques lead to increased accuracy. This approach is a further step toward the diagnostic use of MR flow measurements in coronary artery disease.

Aged↗
PubMed1999

Optimization of realtime adaptive navigator correction for 3D magnetic resonance coronary angiography.

Breathing motion artifacts reduce the quality of MR coronary artery images. Real-time adaptive navigator correction with different correction factors (0%, 30%, 60%, 80% of diaphragmatic displacement) was used to correct for respiratory motion in 3D coronary artery imaging. Significant improvements of image quality were achieved by adaptive motion correction in comparison with conventional navigator gating. A close correlation between the correction factor, which yielded optimal image quality, and cardiac displacement relative to diaphragmatic displacement was found. The quality of coronary artery imaging can be improved using real-time adaptive navigator correction. Correction factors have to be adjusted for each segment of the coronary arteries and for each patient. Magn Reson Med 42:408-411, 1999.

Adult↗
PubMed1999

Analysis and functional characterization of alternatively spliced angiotensin II type 1 and 2 receptor transcripts in the human heart.

Expression levels of angiotensin II type 1 and type 2 receptors (AT1, AT2) vary at different cardiac localizations and are regulated in cardiac diseases. Differential splicing of the 5' untranslated exons of the primary AT1 mRNA transcripts may modulate translational efficiency and thus receptor expression. We therefore searched for AT1 and AT2 mRNA splice patterns specific to chamber localization or to cardiac performance and analyzed their effect on protein expression in transfection experiments. The exon composition of the AT1 and AT2 mRNA transcripts in normal and diseased human hearts were analyzed using a reverse transcription polymerase chain reaction followed by HPLC quantitation of the amplificates. We compared atrial (n=18) and ventricular (n=28) samples and endomyocardial biopsies (n=10) from patients with normal and severely impaired cardiac function and one donor heart, which was not used for transplantation. AT1 transcripts with the exon composition 1/2/5 and 1/5 represented about 93-98% of all AT1 mRNAs; transcript 1/2/3/5 represented 8% in the atria and 2% in ventricles. Since exon 2 reduces translational efficiency in vitro, the ratios of transcripts with and without exon 2, (1/2/5+1/2/3/5) to (1/5), were compared. These were 1.24+/-0.07 in normal atria, 0.96+/-0.09 in atria from failing hearts (P<0.05), 0.68 in the left ventricle of the donor heart, and 0.58+/-0.03 in failing left ventricles. Endomyocardial biopsy specimens showed significant differences between controls and heart failure (controls 0.63+/-0.04 vs. heart failure 0.52+/-0.02, P<0.05). Of the two identified AT2 transcripts, mRNA 1/2/3 was the most abundant in the human heart (92%). Luciferase reporter gene assays were performed to test the effect of the various 5' untranslated regions (5' UTRs) on protein expression. Among the constructs which contained the AT1 promoter/AT1 5' UTRs the plasmid Ex 1/2/5 exhibited 27% lower luciferase activity than Ex 1/5 (n=24, P<0.001), and Ex 1/2/3/5 expressed only 35.9% of Ex 1/5 activity (P<0.001). Among the reporter gene plasmids with the AT2 promoter/AT2 5' UTRs the construct Ex 1/2/3 expressed a 31% lower luciferase activity than Ex 1/3 (n=20, P<0.001). In conclusion, alternative splicing may represent a mechanism of ATR regulation in vivo. In the human heart, AT1 splice patterns differ distinctly between atria and ventricles and to a lesser degree between controls and failing hearts. This may lead to differences in AT1 mRNA translation into protein in the various cardiac areas and under different pathophysiological conditions.

Animals↗
PubMed1999

Expression of ACE mRNA in the human atrial myocardium is not dependent on left ventricular function, ACE inhibitor therapy, or the ACE I/D genotype.

The activity of the cardiac renin-angiotensin system is altered in human heart failure, but the regulatory mechanisms are unknown. We analyzed whether angiotensin-converting enzyme (ACE) mRNA expression in heart failure is altered in the atrial myocardium, and whether a correlation exists between atrial ACE mRNA expression and the parameters of left ventricular function. We also investigated whether the use of ACE inhibitors or the ACE I/D genotype modulates the atrial ACE mRNA content. For this purpose patients who were to undergo routine cardiac surgery were selected in a prospective manner according to left ventricular function and ACE inhibitor therapy. Samples of atrial myocardium were taken, and ACE mRNA expression was determined by internally standardized reverse transcription polymerase chain reaction. Atrial ACE mRNA expression did not differ in patients with left ventricular ejection fraction higher than 55% (2423+/-199 copies/ng RNA) and those with a value less than 45% (2661+/-143 copies/ng RNA, n.s.). ACE mRNA expression also did not differ in patients using ACE inhibitors (2585+/-175 copies/ng RNA) and those not using ACE inhibitors (2476+/-185 copies/ng RNA). Furthermore, atrial ACE mRNA expression was not affected by the ACE genotype (DD 2573+/-203, ID 2472+/-215, II 2563+/-249 copies/ng RNA). We conclude that the regulation of atrial ACE mRNA expression occurs predominantly by local mechanical or para- or autocrine factors.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1999

[Long-term outcome of therapy of recurrent myocardial ischemia after surgical revascularization].

UNLABELLED: Although there are randomized data for CABG vs. medical therapy and CABG vs. PTCA in primary therapy of CAD, there is few evidence on the appropriate therapy of recurrent angina after prior CABG. We analyzed data from 1265 consecutive patients (pts.) presenting for recurrent angina after previous CABG who required either re-CABG (n = 67), PTCA (n = 768) or medical therapy alone (medRx) (n = 430) at our institution during 1986 through 1996. Outcome after index therapy is monitored during 45 +/- 34 months. The 3 therapeutic groups were similar with respect to gender (84% male), age at therapy (60 years), prevalence of diabetes (22%), and time to first ischemic event after primary CABG (37 months). Actuarial survival was significantly higher in the PTCA-group at 1, 5 and 10 years after therapy of recurrent angina, despite the freedom from subsequent re-intervention was significantly lower (1-year-survival 95% [37%] vs. 95% [3%] medRx vs. 79% [4%] re-CABG, 5-year-survival 87% [57%] vs. 78% [17%] medRx vs. 50% [4%] re-CABG and 10-year-survival 72% [65%] vs. 63% [31%] medRx vs. 50% [15%] re-CABG resp., p < 0.0001, [numbers in brackets represent corresponding values for incidence of re-intervention, p < 0.0001]). These findings were similar after adjustment for different baseline characteristics. Following this adjustment multivariate Cox-analysis identified age beyond 70 years, diabetes mellitus and therapy: redo-CABG as independent correlates for mortality for the entire group. THERAPY: angioplasty was identified as an independent correlate for survival. In contrast, therapy: angioplasty was an independent correlate for re-intervention after therapy. CONCLUSIONS: In this nonrandomized series of patients with recurrent angina after previous CABG, an initial strategy of angioplasty resulted in a significant higher overall survival, although this regimen is associated with a greater need for subsequent revascularization procedures.

Adult↗
PubMed1999

[Influence of image quality on the diagnostic accuracy of dobutamine stress magnetic resonance imaging in comparison with dobutamine stress echocardiography for the noninvasive detection of myocardial ischemia].

The analysis of wall motion abnormalities with dobutamine stress echocardiography is an established method for the detection of myocardial ischemia. With ultrafast magnetic resonance tomography, the application of identical stress protocols as used for echocardiography is possible. In 208 consecutive patients (147 M, 61 F) with suspected coronary artery disease, dobutamine stress echocardiography partially using harmonic imaging and dobutamine stress magnetic resonance tomography (DSMR) were performed prior to cardiac catheterization. DSMR images were acquired during short breath holds in 3 short axis-, a 4-, and a 2-chamber view using a turbo gradient echo technique. Patients were examined at rest and during a standard dobutamine-atropine scheme until submaximal heart rate was reached. Regional wall motion was assessed in a 16 segment model. Significant coronary heart disease was defined as angiographic >/=50% diameter stenosis. With DSMR, significantly more patients yielded very good (69%) or good (13%) image quality in comparison with dobutamine stress echocardiography (20% and 31%, p<0. 05). Moderate image quality occurred in 16% with MR and 41% with dobutamine stress echocardiography (p<0.05), 2% and 8% were non-diagnostic. With each technique 18 patients could not be examined (DSE: emphysema: 10, adipositas: 8, DSMR: claustrophobia: 11, adipositas: 6, contraindication: 1). Four patients did not reach target heart rate. In 107 patients, significant coronary artery disease was found. With DSMR sensitivity was 88.7% (dobutamine stress echocardiography: 74.3%; p<0.05) and specificity 85.7% (dobutamine stress echocardiography: 69.8%; p <0.05). This difference was most pronounced in the group with moderate echocardiographic image quality. High dose DSMR is superior to dobutamine stress echocardiography and can replace this technique especially in patients with moderate echocardiographic image quality.

Adult↗