PDGF-B gene single-nucleotide polymorphisms are not predictive for disease onset or progression of IgA nephropathy.

BACKGROUND: Few genetic factors have been identified that determine susceptibility to and progression of IgA-nephropathy (IgAN). Given that IgAN is usually characterized by mesangioproliferative glomerulonephritis and that PDGF-B is of central pathophysiological relevance in this process, we analyzed four single-nucleotide polymorphisms (SNPs) of the PDGF-B gene to evaluate a possible association of these SNPs with disease onset and progression, histological grading and responses to ACE inhibitor (ACEi) therapy. METHODS: The total study population consisted of 195 IgAN patients (127 from southern Italy and 68 from northern Germany) and 200 healthy controls (100 from each region). All four SNPs were in Hardy-Weinberg equilibrium and genotype distributions did not differ between patients and controls in either region. RESULTS: SNP distribution in Italian patients reaching end-stage renal disease (n=45) also was not significantly different from patients maintaining a serum creatinine below 1.2 mg/dl (n=60) during 5.6 +/- 5.5 years of follow-up. Furthermore, we failed to detect significant effects of any SNP on the slope of 1/serum creatinine, proteinuria level or the antiproteinuric response to ACEi. Additionally, particular PDGF-B genotypes did not correlate with histological grading using the Lee classification. CONCLUSION: We conclude that none of the four PDGF-B SNPs is related to the onset of IgAN in two different populations and that none of them has a major influence on the course of IgAN.

Electromechanical assessment of left ventricular function following successful percutaneous coronary revascularization.

Percutaneous electromechanical mapping was applied to evaluate the impact of coronary revascularization on electrical and mechanical parameters in patients with prior myocardial infarction. In 15 patients with prior (> or = 4 weeks) myocardial Q-wave infarction and regional wall motion abnormalities, left ventricular endocardial mapping was performed immediately prior to percutaneous coronary revascularization. Patients underwent repetitive mapping during 6-month follow-up angiography with good revascularization results in all patients. Mean regional unipolar electrogram (UP) amplitude of all regions remained unchanged (10.4 +/- 4.2 mV prerevascularization vs. 10.2 +/- 4.4 mV postrevascularization), whereas mean local shortening (LS) of all regions increased from 6.0% +/- 5.8% to 9.7% +/- 5.3% (P < 0.001). The percentage of electromechanical match regions (LS < 6% and UP < 9 mV) remained unchanged after revascularization (15% vs. 10%; NS), whereas the percentage of mismatch regions (LS < 6% and UP > 9 mV) declined from 38% to 10% (P < 0.0001). We conclude that electromechanical mapping allows the sensitive detection of improved mechanical function after successful revascularization. Electrical activity remains unchanged 6 months after revascularization and the number of regions with an electromechanical mismatch decrease.

Myocardial viability assessment by endocardial electroanatomic mapping: comparison with metabolic imaging and functional recovery after coronary revascularization.

OBJECTIVES: The objective of this study was to compare electroanatomic mapping for the assessment of myocardial viability with nuclear metabolic imaging using positron emission computed tomography (PET) and with data on functional recovery after successful myocardial revascularization. BACKGROUND: Animal experiments and first clinical studies suggested that electroanatomic endocardial mapping identifies the presence and absence of myocardial viability. METHODS: Forty-six patients with prior (> or =2 weeks) myocardial infarction underwent fluorine-18 fluorodeoxyglucose (FDG) PET and Tc-99m sestamibi single-photon emission computed tomography (SPECT) before mapping and percutaneous coronary revascularization. The left ventricular endocardium was mapped and divided into 12 regions, which were assigned to corresponding nuclear regions. Functional recovery using the centerline method was assessed in 25 patients with a follow-up angiography. RESULTS: Regional unipolar electrogram amplitude was 11.0 mV +/- 3.6 mV in regions with normal perfusion, 9.0 mV +/- 2.8 mV in regions with reduced perfusion and preserved FDG-uptake and 6.5 mV +/- 2.6 mV in scar regions (p < 0.001 for all comparisons). At a threshold amplitude of 7.5 mV, the sensitivity and specificity for detecting viable (by PET/SPECT) myocardium were 77% and 75%, respectively. In infarct areas with electrogram amplitudes >7.5 mV, improvement of regional wall motion (RWM) from -2.4 SD/chord +/- 1.0 SD/chord to -1.5 SD/chord +/- 1.1 SD/chord (p < 0.01) was observed, whereas, in infarct areas with amplitudes <7.5 mV, RWM remained unchanged at follow-up (-2.3 SD/chord +/- 0.7 SD/chord to -2.4 SD/chord +/- 0.7 SD/chord). CONCLUSIONS: These data suggest that the regional unipolar electrogram amplitude is a marker for myocardial viability and that electroanatomic mapping can be used for viability assessment in the catheterization laboratory.