Indication and implementation of lipidapheresis, rheopheresis, or immunoadsorption (lessons learnt from Germany's largest apheresis center).

Efficient modes of extracorporeal blood purification are available today for apheresis treatment of progressive atherosclerosis, autoimmune disease, or for improving hemorheology. Advanced technology and sophisticated care render apheresis treatment selective, safe and tolerable. Our task is to constantly update indications for apheresis based on best evidence available and good clinical practice, as well as, to determine how apheresis therapy can be made available to those in need or with otherwise refractory disease. Presenting examples of lipid apheresis, rheopheresis, or immunoadsorption for treatment of hypercholesterolemia, hyperlipoproteinemia (a), acute hearing loss, refractory or exacerbating multiple sclerosis, we highlight real world obstacles for implementation of treatment, resulting in still too many patients with proven or recommended indication left untreated. Based on the experience of the largest apheresis center in Germany, with more than 3,300 treatments per year, we depict the necessary structure for identification of patients, defining indication, referral, implementation of therapy, and reimbursement. Apheresis is unfamiliar to most patients and many practitioners or consultants. Nephrologists, performing >90% of apheresis treatments in Germany, have to form a network for referral comprising all regional care-givers, general practitioners as well as the respective specialists (mainly, cardiologists, endocrinologists, diabetologists, ORL specialists, neurologists, ophthalmologists, or rheumatologists), and insurances or other cost-bearing parties for offering a scientifically approved therapeutic regimen and comprehensive care. We have realized this concept in a high volume apheresis center acting in a closely knit network characterized by an unrelenting effort at ongoing medical education. As a consequence, we include approximately 10 times more patients with appropriate diagnoses in our apheresis program as compared to the national average.

Energetic differences between viable and non-viable myocardium in patients with recent myocardial infarction are not an effect of differences in wall thinning- a multivoxel (31)P-MR-spectroscopy and MRI study.

To evaluate multivoxel (31)P-MR spectroscopy (MRS) for assessment of energy metabolism in patients with myocardial infarction (MI) in correlation to left ventricular (LV) wall thickness and the outcome of revascularization. Thirty patients with subacute anterior myocardial infarction and planned revascularization were enrolled. 3D-chemical shift imaging was applied to determine PCr/ATP ratios in two areas: infarcted/anterior and noninfarcted/septal myocardium. MRI was used to evaluate LV function and wall thickness, and was repeated 6 months after revascularization to assess myocardial viability. Fifteen volunteers were controls. Fifteen patients showed normalization of wall motion abnormalities after revascularization (Group 1; viable), 15 not (Group 2; non-viable). Regarding infarcted/anterior myocardium, Group 2 had lower PCr/ATP ratios (0.81 +/- 0.60 vs 1.17 +/- 0.25), and PCr/ATP ratios were reduced in both groups compared to controls (1.45 +/- 0.29). Regarding noninfarcted/septal myocardium, again Group 2 had lower ratios (0.93 +/- 0.53 vs 1.31 +/- 0.38); however, compared to controls (1.51 +/- 0.32) a reduction of PCr/ATP ratios was only found in Group 2. For both myocardial regions, no correlations between PCr/ATP ratios and LV wall thickness were detected. The more severe energetic alteration in irreversibly damaged myocardium is not an effect of differences of wall thinning. Additional alterations of noninfarcted, adjacent myocardium can be detected.

Absolute concentrations of high-energy phosphate metabolites in normal, hypertrophied, and failing human myocardium measured noninvasively with (31)P-SLOOP magnetic resonance spectroscopy.

OBJECTIVE: The purpose of the present study was to measure absolute concentrations of phosphocreatine (PCr) and adenosine triphosphate (ATP) in normal, hypertrophied, and failing human heart. BACKGROUND: Conflicting evidence exists on the extent of changes of high-energy phosphate metabolites in hypertrophied and failing human heart. Previous reports using phosphorus-31 magnetic resonance spectroscopy ((31)P-MRS) have quantified metabolites in relative terms only. However, this analysis cannot detect simultaneous reductions. METHODS: Four groups of subjects (n = 10 each), were studied: volunteers and patients with hypertensive heart disease (HHD), aortic stenosis, and dilated cardiomyopathy (DCM). Left ventricular (LV) function and mass were measured by cine magnetic resonance imaging. Absolute and relative concentrations of PCr and ATP were determined by (31)P-MRS with spatial localization with optimum point spread function. RESULTS: Left ventricular ejection fraction remained normal in HHD and aortic stenosis, but was severely reduced to 18% in DCM; LV mass was increased by 55%, 79%, and 68% respectively. In volunteers, PCr and ATP concentrations were 8.82 +/- 1.30 mmol/kg wet weight and 5.69 +/- 1.02 mmol/kg wet weight, and the PCr/ATP ratio was 1.59 +/- 0.33. High-energy phosphate levels were unaltered in HHD. In aortic stenosis, PCr was decreased by 28%, whereas ATP remained constant. In DCM, PCr was reduced by 51%, ATP by 35%, and reduction of the PCr/ATP ratio by 25% was of borderline significance (p = 0.06). Significant correlations were observed among energetic and functional variables, with the closest relations for PCr. CONCLUSIONS: In human heart failure due to DCM, both PCr and ATP are significantly reduced. Ratios of PCr to ATP underestimate changes of high-energy phosphate levels.

Effect of additional temporary glycoprotein IIb/IIIa receptor inhibition on troponin release in elective percutaneous coronary interventions after pretreatment with aspirin and clopidogrel (TOPSTAR trial).

OBJECTIVES: The Troponin in Planned PTCA/Stent Implantation With or Without Administration of the Glycoprotein IIb/IIIa Receptor Antagonist Tirofiban (TOPSTAR) trial investigated: 1) the amount of troponin T (TnT) release after nonacute, elective percutaneous coronary intervention (PCI) in patients pretreated with aspirin and clopidogrel; and 2) the effect of additional glycoprotein (GP) IIb/IIIa receptor inhibiton on postinterventional TnT release. BACKGROUND: No data are available yet as to whether additional administration of a GP IIb/IIIa receptor antagonist might be beneficial in patients undergoing elective PCI already pretreated with aspirin and clopidogrel. METHODS: After bolus application of the study medication (tirofiban [T] or placebo [P]), PCI was performed followed by an 18-h continuous infusion of T/P. Primary end point of the study was incidence and amount of TnT release after elective PCI after 24 h. RESULTS: A total of 12 h after PCI troponin release was detected in 63% of the patients receiving P and in 40% of the patients receiving T (p < 0.05), after 24 h in 69% (P) and 48% (T) (p < 0.05) and after 48 h in 74% (P) versus 58% (T) (p < 0.08) of the patients. No differences were observed regarding major bleeding, intracranial bleeding or nonhemorrhagic strokes. After nine months a reduction of combined death/myocardial infarction/target vessel revascularization could be observed in the tirofiban group ([T] 2.3% vs. [P] 13.04%, p < 0.05). CONCLUSIONS: Troponin T release occurs after successful intervention in 74% of the patients undergoing elective PCI after 48 h even after pretreatment with aspirin and clopidogrel. The GP IIb/IIIa receptor antagonist tirofiban is able to decrease the incidence of troponin release significantly in this patient population.

Cardiac systolic rotation and contraction before and after valve replacement for aortic stenosis: a myocardial tagging study using MR imaging.

OBJECTIVE: Aortic stenosis leads to the derangement of cardiac function and contraction mode because of chronic pressure overload that is relieved after surgical valve replacement. The purpose of this study was to determine the changes in left ventricular systolic rotation and contraction using MR tagging in patients with aortic stenosis before and after surgical valve replacement compared with age-matched healthy volunteers. MATERIALS AND METHODS: Twelve patients with aortic stenosis were examined with an electrocardiographically triggered two-dimensional tagging sequence at 1.5 T before and 12 months after surgical valve replacement for the evaluation of wall function of the apical, mid ventricular, and basal levels. Eight healthy volunteers in the same age group served as the control group. RESULTS: Before surgery, all patients showed a significant increase of apical rotation (22.2 degrees +/- 5.9 degrees vs 10.3 degrees +/- 2.5 degrees, p < 0.0001) and overall left ventricular torsion (25.1 degrees +/- 6.6 degrees vs 14.5 degrees +/- 3.7 degrees, p < 0.001); basal rotation was not significantly different (-2.9 degrees +/- 2.1 degrees vs -4.2 degrees +/- 1.9 degrees, p = not significant) compared with the volunteer group. Apical rotation and torsion were negatively correlated with left ventricular mass (r = -0.73, p < 0.01, and r = -0.61, p < 0.05, respectively) and end-diastolic volume (r = -0.73, p < 0.01 and r = -0.64, p < 0.03, respectively). One year after surgery, basal rotation was reduced in the patients with aortic stenosis compared with the patients in the control group (-1.9 degrees +/- 1.8 degrees, p < 0.01). In comparison with preoperative values, apical rotation (14.2 degrees +/- 3.6 degrees, p < 0.01) also decreased but was still elevated, and this resulted in a normalization of left ventricular torsion (16.1 degrees +/- 3.7 degrees, p < 0.01). CONCLUSION: Surgical valve replacement for aortic stenosis leads to normalization of the left ventricular torsion 1 year after surgery. Pressure overload before surgery is associated with an increase of systolic left ventricular wringing motion, possibly serving as a compensatory mechanism. This mechanism declines with increasing left ventricular hypertrophy and dilatation.