Clinical characteristics, risk factors, and prognostic analyses of coronary small vessel disease: a retrospective cohort study of 986 patients

Coronary small vessel disease (CSVD) is often associated with significant percutaneous coronary intervention (PCI) related complications, complex lesions, complex PCI, and poor long-term prognosis. We designed this retrospective study to clarify the characteristics, risk factors, and prognostic analyses of CSVD in Chinese populations A total of 986 patients who underwent coronary angiography and stent implantation at the First Affiliated Hospital of Zhejiang University School of Medicine were evaluated. Patients were grouped into CSVD or non-small vessel disease (non-CSVD) according to stent diameter. Clinical data, coronary angiography, and long-term follow-up were recorded. Multivariate logistic regression, the Kaplan–Meier method, Log-rank Test, and Cox regression model were used for statistical analysis. Alcohol consumption (OR = 0.420, 95% CI: 0.299–0.588, P P P P P P P = 0.008), stroke (1.9% vs. 0.3%, P = 0.007), target lesion revascularization (5.8% vs. 2.9%, P = 0.029), target vessel revascularization (6.8% vs. 3.4%, P = 0.016), and non-target vessel revascularization (7.8% vs. 4.0%, P = 0.012) were all substantially higher in CSVD patients. Troponin I level (OR = 1.008, 95% CI: 1.004–1.012, P P P  Compared to non-CSVD, CSVD was associated with more complex lesions, had worse revascularization efficacy, and a poorer prognosis.</p

Additional file 1 of Single cell and lineage tracing studies reveal the impact of CD34+ cells on myocardial fibrosis during heart failure

Additional file 1. Figure S1. Quality control of single-cell RNA sequencing and comparison of single-cell RNA sequencing data of different normal heart. Figure S2. GO and trajectory analysis of selected subclusters of fibroblasts. Figure S3. Construction and verification of CD34-CreERT2; Rosa26-tdTomato lineage tracing mouse. Figure S4. Top five genes expressed and GO analysis of subclusters of fibroblasts in CD34 lineage cells. Figure S5. Schematic depicting of bone marrow transplantation and confirmation of the reconstitution of bone marrow cells. Figure S6. Characterization of EC clusters of different stages of pathological cardiac hypertrophy by ScRNA-seq. Figure S7. Characterization of MF/Mo/DC clusters of different stages of pathological cardiac hypertrophy by ScRNA-seq. Figure S8. Characterization of Lymphocytes clusters of different stages of pathological cardiac hypertrophy by ScRNA-seq. Figure S9. Cell communication between different cell types at different stages of pathological cardiac hypertrophy. Figure S10. Cell communication between different cell types at different stages of pathological cardiac hypertrophy. Figure S11. Effect of depletion of CD34+ cells on myocardial fibrosis. Figure S12. Heart-derived CD34+ cells can be directed into fibroblasticcells. Figure S13. Quality control of human heart single-cell RNA sequencing and the respective molecular signatures of each subcluster. Figure S14. Top five genes of each cluster and the expression of selected cell marker gene in CD34+ cells ofhuman heart