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Biomedical subjects

Gert Baumann

Publications and source records attributed to Gert Baumann.

At least 55 records · Page 3Linked to original sources
PubMed2004

Reduction of morbidity by immunoadsorption therapy in patients with dilated cardiomyopathy.

BACKGROUND: In patients with dilated cardiomyopathy (DCM) and severe congestive heart failure, immunoadsorption (IA) and subsequent IgG substitution leads to an acute and prolonged hemodynamic improvement. Goal of this study was to investigate the long-term effect of immunoadsorption on morbidity. METHODS: In a retrospective analysis of 34 patients (17 patients who have received immunoadsorption therapy and 17 control patients) were included. Inclusion criteria were DCM, left ventricular ejection fraction less than 35%, NYHA classes II-III. The average time after immunoadsorption was 3.0 years (median 2.3 years). Both groups did not differ concerning sex, age, duration of disease, medication, baseline ejection fraction and NYHA class. RESULTS: In patients who have received immunoadsorption (IA) the days of hospitalisation for congestive heart failure per year could be significantly reduced in contrast to the control patients (17.2 days prior to IA, 4.3 days after IA). Even if the procedural days for immunoadsorption were included there was still a significant reduction of hospitalisation if IA therapy was longer than 2.5 years ago. The days of hospitalisation increased gradually with time during the follow up period. IA induced an acute increase in EF (19.8-25.7%, p<0.01 vs. baseline). CONCLUSION: IA not only leads to an acute hemodynamic improvement in patients with DCM but may also reduce morbidity in these patients during the next 3 years.

Adrenergic beta-Antagonists↗
PubMed2004

Immunoadsorption in idiopathic dilated cardiomyopathy, a 3-year follow-up.

OBJECTIVE: Recent studies have shown that immunoadsorption (IA) leads to improvements in left ventricular function and in functional status in selected patients with idiopathic dilated cardiomyopathy (DCM) and circulating autoantibodiesautoantibod. Most of the few studies dealing with this topic describe only short-term results. The aim of this study was to ascertain the prolonged effects of IA over a period of 3 years. MATERIALS AND METHODS: Our study included nine patients with circulating beta1-adrenoreceptor antibodies who suffered from idiopathic DCM (left ventricular ejection fraction <30%). IA was performed using an adsorber against immunoglobulins (Ig Therasorb, Baxter). During therapy and after 3 months, hemodynamic parameters were monitored using a Swan-Ganz thermodilution catheter. All patients were monitored under clinical and echographical examinations over a period of at least 3 years. RESULTS: During IA hemodynamic measurements show increases in both cardiac and stroke volume index (from 2.0 (S.E.M. 0.16) to 3.0 (S.E.M. 0.32) l min(-1) m(-2), and from 26.1 (S.E.M. 2.63) to 38.9 (S.E.M. 3.56) ml/m2, respectively). Hemodynamic stabilization was observed after the following 3 months (CI 2.6 (S.E.M. 0.14) l min(-1) m(-2), SVI 37.9 (S.E.M. 2.14) ml/m2). After 36 months five patients were still alive. Antibody titers increased in patients who deteriorated. The five patients who are still alive show an increase in left ventricular ejection fraction and no significant increase in antibody titers. CONCLUSION: Immunoadsorption may improve short-term hemodynamics as well as long-term follow-up of patients with severe idiopathic dilated cardiomyopathy. Increase in antibody titers is accompanied by deterioration of cardiovascular function.

Autoantibodies↗
PubMed2004

Long-term up-regulation of eNOS and improvement of endothelial function by inhibition of the ubiquitin-proteasome pathway.

The ubiquitin-proteasome system is the major pathway for intracellular protein degradation in eukaryotic cells. Endothelial nitric oxide synthase (eNOS) is the key enzyme of vascular homeostasis involved in the pathophysiology of several cardiovascular diseases. The aim of our study was to investigate whether eNOS expression and activity are regulated by the proteasome. Bovine pulmonary artery endothelial cells (CPAE cells) were treated with the proteasome inhibitor MG132. MG132 (50-250 nmol/L) dose-dependently increased mRNA and protein levels of eNOS. Comparable results were obtained with other specific proteasome inhibitors, whereas the nonproteasomal calpain and cathepsin inhibitor ALLM had no effect. Efficacy of proteasome inhibition was evidenced by accumulation of poly-ubiquitinylated proteins and by measuring proteasomal activity in cell extracts. Cycloheximide prevented up-regulation of eNOS protein, indicating that post-translational stabilization of eNOS is not involved. eNOS activity was increased up to 2.8-fold (MG132 100 nmol/L, 48 h). Incubation of rat aortic rings with MG132 significantly enhanced endothelial-dependent vasorelaxation. Single MG132 treatment (100 nmol/L) induced long-term effects in CPAE cells, with increases of eNOS protein and activity for up to 10 days. Our results indicate that low-dose proteasome inhibition enhances eNOS expression and activity, and improves endothelial function.

Animals↗
PubMed2004

Detection of acute myocardial ischemia during percutaneous transluminal coronary angioplasty by endocardial acceleration.

The first heart sound is generated by vibrations from the myocardium during isovolumic contraction. Peak endocardial acceleration (PEA) has been used previously to measure these vibrations in humans and correlates with myocardial contractility during inotropic interventions. It is unknown if changes in PEA can be used to characterize a reduction in contractility during ischemic episodes. This study was designed to evaluate the use of an endocardial accelerometer for the detection of acute myocardial ischemia. Thirteen patients undergoing routine percutaneous transluminal coronary angioplasty (PTCA) consented to having a single-axis, lead-based accelerometer positioned in the right ventricular apex. PEA was defined as the maximum peak-to-peak amplitude during a window 50 ms before to 200 ms following the peak R wave. Time of endocardial acceleration (TEA) was defined as the time from the peak R wave to the maximum accelerometer signal within this window. To obtain a more robust estimate of the strength of vibrations, a 100-beat template of the accelerometer signal was constructed at baseline and applied as a matched filter during ischemia. The peak magnitude of the filtered endocardial accelerometer signal (Max Filtered EA) was used as an index of signal intensity. Median baseline PEA, TEA, and Max Filtered EA were 0.91 +/- 0.35 g, 75.2 +/- 16.2 ms, and 0.40 +/- 0.20 g, respectively. PEA and Max Filtered EA significantly decreased by 7% during ischemia (0.91 to 0.85 g and 0.40 to 0.37 g, both P < 0.05, respectively). TEA did not significantly change from baseline (77.0 ms, P = ns). The results of this study suggest that acute ischemia can be detected with an endocardial accelerometer in humans.

Acceleration↗
PubMed2004

Detection of a novel sense-antisense RNA-hybrid structure by RACE experiments on endogenous troponin I antisense RNA.

Conformational changes in the troponin/tropomyosin complex significantly alter the mechanical properties of cardiac muscle. Phosphorylation of cardiac troponin I, part of the troponin/tropomyosin complex, reduces calcium affinity, which leads to increased relaxation of cardiac muscle. Because cardiac troponin I plays a central role in tuning the heart to different work demands, detailed knowledge of troponin I protein regulation is required. Our group previously detected naturally occurring antisense RNA for troponin I in human and rat hearts, and here, attempt to unravel the structure of rat cardiac troponin I antisense RNA. We performed rapid amplification of cDNA ends (RACE) experiments and discovered antisense sequences identical to a copy of the sense mRNA, which led us to conclude that the antisense RNA must be transcribed from troponin I mRNA in the cytoplasm. Moreover, we isolated RNA structures comprising sense and antisense sequences in one continuous molecule. As we found no homolog structures described in the literature, we called this "hybrid RNA." Because a duplex formation was demonstrated previously we concluded that hybrid RNA is a consequence of a tight interaction between sense and antisense troponin I RNA in vivo, which we discuss in the article.

Animals↗
PubMed2003

Coronary artery disease: new insights and their implications for radiology.

Coronary artery disease (CAD) diminishes local, regional, or global blood supply to the heart and is most commonly caused by coronary atherosclerosis. New insights into the etiology of atherosclerosis suggest that CAD is an inflammatory disorder that responds well to modulation rather than an unchangeable chronic process. Since 75% of all acute coronary syndromes result from rupture of atherosclerotic plaques, factors causing rupture have a crucial role. Magnetic resonance imaging and CT have the potential to visualize the composition of coronary artery plaques and thus to identify plaques at risk. Considering the new insights into stunning and hibernation, myocardial late enhancement on MRI might provide pivotal information for therapeutic decision making among lysis therapy, catheter intervention, and bypass surgery. Exercise electrocardiography without or with right precordial leads, stress echocardiography, and stress scintigraphy are simple clinical procedures to identify CAD with high sensitivities of 67, 92, 76, and 88%, respectively. The MRI and CT have to be compared with these good results. Nevertheless, we are expecting that MRI and CT will replace the conventional diagnostic modalities, gain a central role in diagnosing patients with suspected CAD, and prove to be cost-effective in this regard.

Coronary Disease↗
PubMed2003

A constituent of green tea, epigallocatechin-3-gallate, activates endothelial nitric oxide synthase by a phosphatidylinositol-3-OH-kinase-, cAMP-dependent protein kinase-, and Akt-dependent pathway and leads to endothelial-dependent vasorelaxation.

Epidemiological studies suggest that tea catechins may reduce the risk of cardiovascular disease, but the mechanisms of benefit have not been determined. The objective of the present study was to investigate the effects of epigallocatechin-3-gallate (EGCG), the major constituent of green tea, on vasorelaxation and on eNOS expression and activity in endothelial cells. EGCG (1-50 microm) induced dose-dependent vasodilation in rat aortic rings. Vasodilation was abolished by pretreatment with Ng-nitro L-arginine methyl ester. In bovine aortic endothelial cells, EGCG increased endothelial nitric oxide (eNOS) activity dose-dependently after 15 min. Treatment with EGCG induced a sustained activation of Akt, ERK1/2, and eNOS Ser1179 phosphorylation. Inhibition of extracellular signal-regulated kinase (ERK)1/2 had no influence on eNOS activity or Ser1179 phosphorylation. Simultaneous treatment of cells with selective inhibitors for cAMP-dependent protein kinase (PKA) and Akt completely prevented the increase in eNOS activity by EGCG after 15 min, indicating that both kinases act in concert. Specific phosphatidylinositol-3-OH-kinase inhibitors yielded identical results. Akt inhibition prevented eNOS Ser1179 phosphorylation, whereas inhibition of PKA did not influence Akt and eNOS Ser1179 phosphorylation. Pretreatment of endothelial cells with EGCG for 4 h markedly enhanced the increase in eNOS activity stimulated by Ca-ionomycin, suggesting that Akt accounts for prolonged eNOS activation. Treatment of cells for 72 h with EGCG did not change eNOS protein levels. Our results indicate that EGCG-induced endothelium-dependent vasodilation is primarily based on rapid activation of eNOS by a phosphatidylinositol 3-kinase-, PKA-, and Akt-dependent increase in eNOS activity, independently of an altered eNOS protein content.

Animals↗
PubMed2003

Interaction of CA repeat polymorphism of the endothelial nitric oxide synthase and hyperhomocysteinemia in acute coronary syndromes: evidence of gender-specific differences.

We have recently shown that high CA repeat copy numbers (> or = 34 repeats) in intron 13 of the endothelial nitric oxide (eNOS) gene are associated with excess risk of coronary artery disease. Hyperhomocysteinemia interacts by several mechanisms with the NO system, thereby favoring endothelial dysfunction. Since hyperhomocysteinemia evidently promotes prothrombotic activation, we investigated a possible interaction among hyperhomocysteinemia, the eNOS CA repeat polymorphism, and acute coronary syndromes. The median value of homocysteine in our study population was 9.4 micromol/l. We accordingly determined the relative risk of acute coronary syndromes for homocysteine values higher than 9.4 micromol/l and 9.4 micromol/l or lower in the entire coronary artery disease group, and at different CA repeat cutoff values (34, 35, 36, 37, 38 CA repeats). For the entire coronary artery disease group ( n=1000), homocysteine levels higher than 9.4 micromol/l were not significantly associated with acute coronary syndromes. Although the CA repeat copy numbers were not associated with acute coronary syndromes in the overall group, the relative risk among women with homocysteine higher than 9.4 micromol/l for developing acute coronary syndromes increased nonsignificantly from 0.98 at cutoff 34 CA repeats to 1.68 at 35 CA repeats and significantly to 4.89 at 36 CA repeats, 11.20 at 37 CA repeats, and 18.32 at 38 CA repeats. This effect modification was not observed in men. These data suggest gender-specific gene-environment interaction between the CA repeat eNOS polymorphism and homocysteine in acute coronary syndromes.

Acute Disease↗
PubMed2003

Relaxin, a pregnancy hormone, is a functional endothelin-1 antagonist: attenuation of endothelin-1-mediated vasoconstriction by stimulation of endothelin type-B receptor expression via ERK-1/2 and nuclear factor-kappaB.

We have recently demonstrated that relaxin (RLX) acts as compensatory mediator in human heart failure. RLX inhibits the stimulation of endothelin-1, the most potent vasoconstrictor in heart failure. Upregulation of the endothelin type-B receptor (ET(B)), which mediates endothelin-1 clearance and endothelial release of NO, represents a pivotal mode of RLX action. However, signal transduction and abundance of this phenomenon are unknown. Therefore, we investigated RLX-induced regulation of ET(B) in human umbilical vein endothelial, epithelial (HeLa), and vascular smooth muscle cells. In human umbilical vein endothelial cells and HeLa cells, but not in human vascular smooth muscle cells, RLX upregulated ET(B) expression and activated extracellular signal-regulated kinase-1/2 (ERK-1/2) and nuclear factor-kappaB (NF-kappaB), a transcription factor. PD-98059, a selective inhibitor of the mitogen-activated protein kinase kinase-1 (MEK-1)-ERK-1/2 pathway, abolished ERK-1/2 and NF-kappaB activation and ET(B) upregulation. NF-kappaB inhibition also prevented RLX-mediated ET(B) stimulation. In NF-kappaB-luciferase reporter assays, we demonstrated complete inhibition of RLX-induced NF-kappaB activation in cells transfected with dominant-negative Raf-1, MEK-1, or ERK-1/2 constructs, whereas dominant-negative Ras had no effect. In rat aorta and mesenteric artery, RLX pretreatment, in an ET(B)-dependent fashion, mitigated the maximum contractile response to endothelin-1, by 38+/-4% and 43+/-6%, and the endothelin-1 sensitivity (-log[EC(50)]: aorta, 8.2+/-0.2 for vehicle versus 7.2+/-0.2 for RLX; mesenteric artery, 8.0+/-0.2 for vehicle versus 7.1+/-0.1 for RLX). RLX pretreatment augmented the dilator effect of the ET(B) agonist endothelin-3 by 100+/-8% and 133+/-13%. In conclusion, RLX stimulates endothelial and epithelial ET(B) via a Ras-independent Raf-1-MEK-1-ERK-1/2 pathway that activates NF-kappaB. On vascular smooth muscle cells, ET(B), a contributor to endothelin-mediated vasoconstriction, remains unaffected. This renders RLX a functional endothelin-1 antagonist.

Animals↗
PubMed2003

Long-term results after partial left ventriculectomy.

BACKGROUND: Long-term clinical, echocardiographic and hemodynamic effects after partial left ventriculectomy (PLV) and predictors of outcome have been determined. METHODS: Between January 1995 and July 1999, PLV was performed in 39 patients. In 15 patients the etiology of heart failure was idiopathic dilated cardiomyopathy (DCMP), 19 patients had ischemic cardiomyopathy (ICMP) and five patients had valvular cardiomyopathy. Concomitant procedures included coronary artery bypass grafting in 16 patients, mitral valve repair in 33 patients and aortic valve replacement in five patients. All patients belonged in New York Heart Association (NYHA) functional class III or IV. Mean follow-up was 663+/-514 days. Clinical, echocardiographic and hemodynamic assessments and metabolic stress testing were performed preoperatively, within 30 days postoperatively and 6, 12 and 24 months after the operation. RESULTS: Actuarial survival was 64% after 1 year, 55% after 2 years and 44% 3 years after the operation. In patients with ICMP as well as in patients with DCMP actuarial 1 year survival was 60%. At 2-year follow-up NYHA functional class was improved significantly (P<0.05), but LV ejection fraction, LV end-diastolic diameter, cardiac index and peak oxygen consumption did not differ significantly from preoperative values. Analysis of factors influencing postoperative outcome indicated that decreased left ventricular wall thickness and a failure to increase the stroke volume index as a response to preoperative dobutamine administration were associated with postoperative mortality. CONCLUSIONS: PLV is associated with considerable postoperative mortality and lacking long-term improvement of cardiac performance.

Adult↗
PubMed2003

Hemodynamic improvement and removal of autoantibodies against beta1-adrenergic receptor by immunoadsorption therapy in dilated cardiomyopathy.

The removal of beta(1)-adrenergic receptor (beta(1)AR) autoantibodies by immunoadsorption (IA) has been proposed as a potential mechanism for the improvement of the left ventricular function in dilated cardiomyopathy (DCM). In the present study, the possible association between removal of the autoantibodies against the human beta(1)AR with the hemodynamic improvement induced by IA was investigated.IA was performed in 22 DCM patients (n=22; NYHA III-IV, EF<30%, stable medication). The beta(1)AR autoantibodies from column eluents (CE) were detected by enzyme-linked immunosorbent assay (ELISA) and BIAcore methods. CE of 32% (7/22) of the patients was found to be antibody-positive with ELISA or BIAcore. In addition, a bioassay system was also used for the detection of this autoantibody. Seventy-three percent (16/22) of the patients were found to be antibody-positive by this method. However, independent of the beta(1)AR antibody detection method, both antibody-positive and antibody-negative groups showed similar acute and prolonged hemodynamic improvements during IA therapy. Furthermore, antibody-positive and -negative groups received a comparable improvement of left ventricular ejection fraction. These results suggest that different mechanisms are involved in the hemodynamic improvement induced by IA. The beneficial hemodynamic effects induced by IA are not directly associated with the removal of beta(1)AR autoantibodies.

Autoantibodies↗
PubMed2003

Apical tissue tracking echocardiography for characterization of regional left ventricular function: comparison with magnetic resonance imaging in patients after myocardial infarction.

OBJECTIVE: The purpose of this study was to characterize the normal pattern of apical tracking and to investigate whether tissue tracking imaging is more useful for evaluation of regional left-ventricular function than noncontrast harmonic echocardiography in patients after myocardial infarction. BACKGROUND: Left ventricular longitudinal shortening plays an important role in cardiac contraction, and can be evaluated online by a new Doppler tissue imaging method. METHODS: We included 40 healthy participants and 40 patients after myocardial infarction. They underwent tissue tracking imaging and noncontrast harmonic imaging by an experienced and an inexperienced observer. Diagnostic accuracy of semiquantitative evaluation of left ventricular function was compared using magnetic resonance imaging as reference method. RESULTS: Velocity-time integrals decreased from basal to apical segments in healthy participants. Tissue tracking imaging has a higher diagnostic sensitivity than noncontrast imaging for the diagnosis of regional wall-motion abnormalities (expert, 78% vs 97%, P <.01; beginner, 63% vs 91%, P <.001), whereas specificity remained unchanged (expert, 99% vs 97%, not significant; beginner, 91% vs 92%, not significant). CONCLUSIONS: Tissue tracking imaging is feasible and evaluates regional systolic myocardial function quantitatively with high diagnostic accuracy compared with magnetic resonance imaging in patients after myocardial infarction, and is more accurate than noncontrast harmonic echocardiography.

Aged↗
PubMed2003

Prevalence of malnutrition in hospitalized medical patients: impact of underlying disease.

BACKGROUND/AIMS: Malnutrition is common among hospitalized patients. We investigated whether certain diseases predispose more frequently for malnutrition than others. METHODS: Nutritional state was assessed by clinical scores, anthropometry and bioimpedance analysis in 502 consecutively admitted patients in the departments of internal medicine in two hospitals in Berlin (n = 300, university hospital; n = 202, district hospital). The prevalence of malnutrition was compared in patient groups with a different diagnosis. RESULTS: Malnutrition was present in 24.2% of all patients. A clear association between diagnoses and malnutrition was found: the prevalence of malnutrition was significantly higher in malignant than in non-malignant diseases (50.9 vs. 21.0%, p < 0.0001). High prevalence rates >30% were observed in subgroups of patients with inflammatory bowel diseases, chronic heart failure and benign lung diseases. Patients with gastrointestinal diseases, however, were not more frequently malnourished than other medical patients (28.8 vs. 22.0%). Malnourished patients were significantly older (70.0 +/- 13.6 vs. 58.3 +/- 15.6 years, p < 0.0001) and had a 40% longer hospital stay (13.1 +/- 8.1 vs. 9.3 +/- 6.8 days, p < 0.0001) than well-nourished patients. CONCLUSIONS: Patients with malignancies, inflammatory bowel disease, chronic heart failure and benign lung diseases need special attention due to the high prevalence of malnutrition.

Age Factors↗
PubMed2002

Plasma levels and cardiovascular gene expression of urotensin-II in human heart failure.

The peptide urotensin-II (U-II) has been described as most potent vasoconstrictor identified so far, but plasma values in humans and its role in cardiovascular pathophysiology are unknown. We investigated circulating urotensin-II and its potential role in human congestive heart failure (CHF). We enrolled control individuals (n=13; cardiac index [CI], 3.5+/-0.1 l/min/m2; pulmonary wedge pressure [PCWP], 10+/-1 mm Hg), patients with moderate (n=10; CI, 2.9+/-0.3 l/min/m2; PCWP, 14+/-2 mm Hg) and severe CHF (n=11; CI, 1.8+/-0.2 l/min/m2; PCWP, 33+/-2 mm Hg). Plasma levels of urotensin-II differed neither between controls, patients with moderate and severe CHF nor between different sites of measurement (pulmonary artery, left ventricle, coronary sinus, antecubital vein) within the single groups. Hemodynamic improvement by vasodilator therapy in severe CHF (CI, +78+/-3%; PCWP, -55+/-3%) did not affect circulating U-II over 24 h. Preprourotensin-II mRNA expression in right atria, left ventricles, mammary arteries and saphenous veins did not differ between controls with normal heart function and patients with end-stage CHF. In conclusion, urotensin-II plasma levels and its myocardial and vascular gene expression are unchanged in human CHF. Circulating urotensin-II does not respond to acute hemodynamic improvement. These findings suggest that urotensin-II does not play a major role in human CHF.

Adult↗
PubMed2002

Potential role of autoantibodies belonging to the immunoglobulin G-3 subclass in cardiac dysfunction among patients with dilated cardiomyopathy.

BACKGROUND: Immunoadsorption capable of removing circulating autoantibodies represents an additional therapeutic approach in dilated cardiomyopathy (DCM). The role played by autoantibodies belonging to the immunoglobulin (Ig) subclass G-3 in cardiac dysfunction remains to be elucidated. METHODS AND RESULTS: Patients with DCM (left ventricular ejection fraction <30%) participated in this case-control study. Nine patients underwent immunoadsorption with protein A (low affinity to IgG-3), and 9 patients were treated with anti-IgG, which removes all IgG subclasses. Immunoadsorption was performed in 4 courses at 1-month intervals until month 3. In the 2 groups, immunoadsorption induced comparable reduction of total IgG (>80%). IgG-3 was effectively eliminated only by anti-IgG adsorption (eg, during the first immunoadsorption course; protein A, -37+/-4%; anti-IgG, -89+/-3%; P<0.001 versus protein A). The beta1-receptor autoantibody was effectively reduced only by anti-IgG (P<0.01 versus protein A). Hemodynamics did not change in the protein A group. In the anti-IgG group during the first immunoadsorption course, cardiac index increased from 2.3+/-0.1 to 3.0+/-0.1 L x min(-1) x m(-2) (P<0.01 versus protein A). After 3 months, before the last immunoadsorption course, cardiac index was 2.2+/-0.1 L x min(-1) x m(-2) in the protein A group and 3.0+/-0.2 L x min(-1) x m(-2) in the anti-IgG group (P<0.01 versus protein A). Left ventricular ejection fraction increased only in the anti-IgG group (P<0.05 versus protein A). CONCLUSIONS: Autoantibodies belonging to IgG-3 may play an important role in cardiac dysfunction of DCM. The removal of antibodies of the IgG-3 subclass may represent an essential mechanism of immunoadsorption in DCM.

Adrenergic beta-Antagonists↗
PubMed2002

Effect of partial left ventriculectomy on left and right ventricular volumes and function as assessed with electron beam tomography: preliminary results.

Our objective was to determine if left ventricular reduction surgery affects left and right ventricular volumes and function. Twenty-three patients with end-stage heart failure underwent contrast-enhanced electron beam tomographic function studies before and twice after partial left ventriculectomy (PLV). The PLV was combined with other cardiosurgical procedures in 20 of 23 patients. Left and right ventricular enddiastolic volume (LVEDV, RVEDV), stroke volume (LVSV, RVSV), ejection fraction (LVEF, RVEF), and enddiastolic diameter (LVEDD, RVEDD) were determined by manual tracing of endo- and epicardial borders at enddiastole and endsystole. Patients were scanned 31 days (+/-34) before and 18 days (+/-13) and 8 months (+/-4) after PLV. Mean pre- and early and late postoperative values for LVEDV, LVSV, LVEF, and LVEDD were 387.9 ml (+/-125.5 ml), 255.6 ml (+/-79.3 ml; p<0.01), and 253.7 ml (+/-97.8 ml; p<0.05), 79.7 ml (+/-25.2 ml), 74.8 ml (+/-17.9; n.s.), and 79.1 ml (+/-26.5 ml; n.s.), 21.6% (+/-7.3%), 31.9% (+/-13.4%; p<0.05), and 34.1% (+/-14.1%; p<0.05), and 72.0 mm (+/-10.6 mm), 64.3 mm (+/-8.5 mm; p<0.05), and 63.5 mm (+/-9.4 mm; p<0.05), respectively. Mean pre- and postoperative values for RVEDV, RVSV, RVEF, and RVEDD were 177.7 ml (+/-72.8 ml), 172.4 ml (+/-59.2 ml; n.s.), and 178.9 ml (+/-60.8 ml; n.s.), 60.3 ml (+/-21.6 ml), 68.8 ml (+/-19.9 ml; n.s.), and 78.3 ml (+/-25.3 ml; n.s.), 38.1% (+/-15.4%), 43.7% (+/-16.3%; p<0.05), and 45.1% (+/-11.2%; n.s.), and 50.4 mm (+/-10.9 mm), 48.1 mm (+/-8.7 mm; n.s.), and 48.5 mm (+/-9.8 mm; n.s.), respectively. The PLV may induce a significant early reduction of left ventricular volumes and improvement of biventricular function; however, our results must be judged carefully as the majority of patients in this study underwent additional cardiosurgical procedures, the contributory effect of which on the overall outcome remains unclear.

Aged↗
PubMed2002

The adrenomedullin receptor acts as clearance receptor in pulmonary circulation.

Adrenomedullin (AM) is a powerful pulmonary vasodilator with antimitogenic properties. We investigated the role of the AM receptor (AMR) and the calcitonin gene-related peptide type-1 receptor (CGRP1R) in regulating pulmonary vascular AM levels. The AMR antagonist hAM(22-52) (120 nmol/L) significantly elevated AM release compared with controls to 250% after 2 h in isolated rat lungs and to 830% after 4 h in pulmonary artery endothelial cells (PAEC). CGRP1R blockade had no effect. AMR blockade did not influence prepro-AM mRNA levels nor did inhibition of protein synthesis by cycloheximide (0.01 mg/mL) abolish the effect of the AMR antagonist. Radioligand-binding studies with PAEC membranes revealed a decrease by 44% of the AMR density in response to AMR antagonism. Altogether, the pulmonary vascular AMR represents not only a functionally active, but also a clearance receptor; its expression is constitutively stimulated by basal AM. This identifies a novel mechanism for controlling pulmonary AM levels.

Adrenomedullin↗