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1.
Int J Cardiol Heart Vasc ; 50: 101349, 2024 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-38322018

RESUMO

Quantitative flow ratio (QFR) is a novel, software-based noninvasive method for the quantitative evaluation of coronary physiology. QFR results correlate with invasive FFR measurements in the three main epicardial coronary arteries. However, QFR data for the evaluation of coronary side branches (SB) are scarce. The evaluation of QFR-performance of SB was retrospective and prospective. Eighty-seven patients with suspected chronic coronary syndrome, who received angiography using routine core lab projections, were retrospectively analyzed. On the second part 37 patients, who received angiography using recommended standardized coronary angiography projections, were prospectively analyzed. Quantitative analysis was performed for SB with a maximum lumen diameter proximal of ≥2 mm based on quantitative coronary angiography (QCA) by two certified experts with the software QAngio XA 3D 3.2. Using routine projections, QFR computation in 55 % of the SB were obtained (123 out of 224). Using standardized projections, 85 % of SB were computed by QFR (64 out of 75; p < 0.001 vs routine projections). The fluoroscopy time for recommended projections was not significantly different as opposed to routine projections (3.75 ± 2.2 vs. 4.58 ± 3.00 min, p = 2.6986). Using the standardized projections was associated with a higher amount of contrast medium (53.44 ± 24.23 vs. 87.95 ± 43.73 ml, p < 0.01), longer overall procedure time (23.23 ± 16.35 vs. 36.14 ± 17.21 min, p < 0.01) and a higher dose area product (1152.28 ± 576.70 vs. 2540.68 ± 1774.07 cGycm2, p < 0.01). Our study shows that the blood flow of the vast majority of coronary SB can be determined non-invasively by QFR in addition to the main epicardial coronary arteries when standardized projections are used.

3.
Cytokine ; 13(6): 342-8, 2001 Mar 21.
Artigo em Inglês | MEDLINE | ID: mdl-11292317

RESUMO

OBJECTIVE: The mechanism underlying exercise intolerance in chronic heart failure is still unclear. An increased concentration of inflammatory cytokines could be detected in the serum of patients with chronic heart failure (CHF) exhibiting a correlation with the severity of the disease. The variety of molecular alterations triggered by these cytokines in the skeletal muscle is almost unknown. The study was designed to analyze the differential gene expression in skeletal muscle myoblasts after stimulation with inflammatory cytokines. METHODS: L6 rat skeletal muscle myoblasts were incubated for 24 h with a combination of IL-1beta/IFN-gamma and the differential gene expression profile was determined by a PCR-based subtractive hybridization method. RESULTS: Out of 173 picked clones 141 different sequences could be identified. By comparison with Genebank, the identity of 73 genes (51.7%) could be confirmed, whereas the rest did not show a homology to any known gene. Some of the identified genes are known to be altered in patients with CHF. CONCLUSION: In summary, the results of this study provide information about changes in gene expression after exposure of skeletal muscle cells to inflammatory cytokines. This information may yield a new gene pool, worthwhile to be analyzed in skeletal muscle of patients with chronic heart failure.


Assuntos
Citocinas/metabolismo , Músculos/citologia , Proteínas Nucleares , Fatores de Transcrição , Animais , Apoptose , Northern Blotting , Western Blotting , Células Cultivadas , Clonagem Molecular , DNA Complementar/metabolismo , Proteínas de Ligação a DNA/biossíntese , Bases de Dados Factuais , Eletroforese em Gel de Ágar , Matriz Extracelular/metabolismo , Insuficiência Cardíaca/genética , Insuficiência Cardíaca/metabolismo , Interferon gama/farmacologia , Interleucina-1/farmacologia , Proteínas Quinases Ativadas por Mitógeno/biossíntese , Músculo Esquelético/metabolismo , Óxido Nítrico Sintase/biossíntese , Óxido Nítrico Sintase Tipo II , Hibridização de Ácido Nucleico , Plasmídeos/metabolismo , RNA Mensageiro/metabolismo , Ratos , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Tempo , Ubiquitina-Proteína Ligases , Proteínas Quinases p38 Ativadas por Mitógeno
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