This prospective study evaluated the accuracy of electrocardiogram-gated blood-pool SPECT (GBPS) for the assessment of left ventricular (LV) and right ventricular (RV) ejection fraction (EF), end-diastolic volume (EDV), and end-systolic volume (ESV) in patients with dilated cardiomyopathy (DCM), using cardiac magnetic resonance (CMR) imaging as the reference standard. Methods: Thirty-two patients (24 men and 8 women; mean age, 51 y) with a diagnosis of idiopathic DCM underwent GBPS and CMR. LV and RV parameters including EDV, ESV, and EF from GBPS were calculated using fully automated gradient software and compared with those obtained by CMR. Results: Biventricular volumes were underestimated by GBPS, compared with CMR (P , 0.001). We found no statistical difference between these 2 methods in the assessment of LV EF (P 5 0.23), whereas RV EF was overestimated by GBPS (P , 0.001 vs. CMR). Regression analysis yielded significant correlations between GBPS and CMR in the assessments of biventricular parameters (r 5 0.83 for LV EDV, 0.88 for LV ESV, 0.89 for LV EF, 0.86 for RV EDV, 0.86 for RV ESV, and 0.62 for RV EF; all P , 0.001). Comparison of the deviations of RV indices between GBPS and CMR with the ratio of RV EDV to LV EDV showed that there was a statistically significant trend for RV volumes to be underestimated and for RV EF to be overestimated as the biventricular volumetric ratio decreased (r 5 0.61 for RV EDV, 0.68 for RV ESV, and 20.55 for RV EF; all P , 0.001). Conclusion: For patients with DCM, GBPS correlated well with CMR for the assessment of biventricular parameters, but RV indices should be cautiously interpreted.
Purpose The goals were to explore the correlation of 18F-labeled fibroblast activation protein inhibitor (FAPI) and cardiovascular magnetic resonance (CMR) parameters in ST-elevation myocardial infarction (STEMI) patients with successful primary percutaneous coronary intervention (PPCI) and to investigate the value of FAPI imaging in predicting cardiac functional recovery. Methods Fourteen first-time STEMI patients (11 men, mean age: 62 ± 11 years) after PPCI were prospectively recruited. All patients underwent baseline FAPI imaging (6 ± 2 days post-MI) and CMR (8 ± 2 days post-MI). Ten patients had convalescent CMR (84 ± 4 days post-MI). Myocardial FAPI activity was analyzed on extent (the percentage of FAPI uptake volume over the left ventricular volume, FAPI%), intensity (target-to-background uptake ratio, TBRmax), and amount (FAPI%×TBRmax). Serum biomarkers during the acute phase, late gadolinium enhancement (LGE), T2-weighted imaging (T2WI), extracellular volume (ECV), microvascular obstruction (MVO), and cardiac function from CMR imaging were analyzed. Results Localized but inhomogeneous FAPI uptake was observed, which was larger than the edematous and infarcted myocardium. The MVO area showed lower FAPI uptake compared with the surrounding myocardium. FAPI activity was associated with myocardial injury biomarkers, T2WI, LGE, and ECV at both per-patient and per-segment levels (all p < 0.05). Among the CMR parameters, T2WI had the greatest correlation coefficient with both FAPI% and FAPI%×TBRmax. Baseline TBRmax was correlated with convalescent left ventricular ejection fraction (LVEF)(r = −0.73, p = 0.02). Conclusion FAPI imaging detects more involved myocardium than CMR in reperfused STEMI, and was associated with myocardial damage and convalescent LVEF.
Purpose: To investigate the effect of retinol on cardiac fibroblast proliferation in vitro and on fibrosis formation in mice in vivo. Methods: Proliferative potential of fibroblasts was determined using cell counting kit-8 assay. Acute myocardial infarction (AMI) was induced in mice via ligation of the left side coronary artery. In myocardial tissues, concentration of TNF-α was determined using enzyme-linked immunosorbent assay (ELISA) assay. Results: Exposure to retinol significantly suppressed cardiac fibroblast proliferation under ischemia, when compared to untreated fibroblasts (p < 0.05). However, exposure of cardiac fibroblasts to retinol did not produce toxicity at a dose of 10 μM under normal conditions. In contrast, exposure to normal levels of oxygen, glutamine and glucose significantly reversed the inhibitory potential of retinol against fibroblasts during ischemia (p < 0.05). Treatment of mice with retinol at a dose of 5 mg/kg reversed the AMI-mediated increase in hydroxyproline level in myocardial tissues. Retinol treatment of AMI mice caused significant elevation in the number of CD31+ capillaries in myocardial tissues. Increase in TNF-α by AMI in cardiac tissues of mice was reversed by treatment with retinol at a dose of 5 mg/kg. The retinol treatment also caused significant reversal of AMI-induced down-regulation of Cx43 protein (p < 0.05). Conclusion: Retinol enhanced the proliferation of fibroblasts under ischemic conditions and prevented fibrosis in mice with AMI. Moreover, retinol targeted TNF-α production and upregulated Cx43 expression in myocardial tissues of mice with AMI. Thus, retinol may be useful for the management of myocardial infarction.
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