Background: Layer-specific speckle-tracking echocardiography (STE) is a noninvasive approach that assesses subclinical left ventricular dysfunction. We aimed to investigate the (I) alteration of layer-specific STE parameters and the dyssynchrony index; and (II) the disease parameters associated with layer-specific STE change in drug-naïve patients with new-onset systemic lupus erythematosus (SLE) without cardiac symptoms.Methods: Thirty-five drug-naïve patients with new-onset SLE and twenty-five healthy controls were enrolled. All individuals received both conventional echocardiographic and two-dimensional STE assessment. The data of layer-specific global longitudinal strain (GLS), global circumferential strain (GCS), and peak systolic dispersion (PSD) were acquired in layer-specific STE.Results: All patients had a normal left ventricular ejection fraction (LVEF)(mean LVEF: 58%) and conventional echocardiographic parameters were comparable between patients and controls. Decreased layer-specific GLS and elevated PSD were observed in SLE patients (whole layer GLS:
Abstract. Alterations in vascular or myocardial structure and function have been demonstrated in offspring subjected to prenatal nicotine exposure (PNE), however, limited data are available on how these changes interact. The present study assessed the hypothesis that prenatal nicotine exposure induced gender-specific alterations of left ventricular-arterial coupling indices in adult offspring. Female Sprague-Dawley rats were exposed to either nicotine (8 mg/kg/day) or saline via subcutaneous osmotic mini-pumps throughout gestation. Male and female offspring, aged 12 months, underwent non-invasive echocardiography and invasive left ventricular cannulation. Left ventricular-arterial coupling was analysed as the ratio of effective arterial elastance (Ea) to ventricular end-systolic elastance (Ees). The left ventricular myocardium and aorta were stained with hematoxylin and eosin and the myocardial cell cross-sectional area was calculated. Simultaneously, the ratio of medium thickness to internal diameter in the aorta and mesenteric artery was determined. The fibrosis component of left ventricle myocardium was analyzed by Sirius-red staining and further confirmed by hydroxyproline determination. The elastic properties of the aortic wall were analyzed by van Gieson staining. PNE caused significant increases in pulse pressure (56.36±7.41 vs. 50.16±4.94 mmHg; P<0.05) and left ventricular meridional wall stress (78.25±9.12 vs. 69.64±7.58 kdyne/cm 2 ; P<0.05) in male offspring compared with the control. Conversely, no similar effect was observed in female offspring. An elevated augmentation index was noted in male and female pups. Additionally, Ea/Ees was reduced in PNE males compared with control males, due to a disproportionate increase in Ees vs. Ea whereas in females, Ea/Ees did not differ significantly due to tandem increase in Ea and Ees. In addition, collagen cross-linking was markedly higher in male offspring, whereas it was unaltered in females compared with their respective controls. Fragmentation of the elastic network in the aorta and the increased ratio of medial thickness to internal diameter in the mesenteric artery were more evident in male offspring when compared with female offspring. PNE caused combined ventricular-arterial stiffening in male and female offspring, with lower Ea/Ees in males, while Ea/Ees was preserved in females. Enhanced collagen cross-linking in the myocardium, underdeveloped elastic fibers in the aorta and remodeled resistance vessels were associated with pathological ventricular arterial mismatching. The results of the present study indicated that male offspring were more susceptible to the development of ventricular and arterial dysfunction in response to PNE compared with female offspring.
To clarify the effect of prenatal nicotine exposure (PNE) on vascular endothelial function (VEF) in offspring rats, and to explore whether these effects are long-lasting and sex-dependent. Pregnant Sprague-Dawley rats were randomized into two groups and exposed to either 102 mg/mL nicotine (experimental group) or normal saline (control group) through a subcutaneously implanted osmotic micropump. Vascular rings from the thoracic aorta were collected from offspring rats at 1, 4, and 12 months of age. The specimens were used to determine VEF using functional tests and to observe morphologic and pathologic changes of blood vessels in hematoxylin and eosin-stained samples with light microscopy. The percentage of acetylcholine-induced endothelium-dependent vasorelaxation (EDV) of the thoracic aorta was significantly higher in the experimental group than in the control group in 1-, 4-, and 12-month-old female offspring rats (18.68±2.32 vs. 13.85±6.10, 17.44±3.91 vs. 10.77±5.77, and 30.96±22.26 vs. 18.94±13.61, respectively; P <0.05). The percentage of acetylcholine-induced EDV was significantly lower in the experimental group than in the control group in 1-, 4-, and 12-month-old male offspring rats (10.31±4.05 vs. 16.05±14.80, 5.57±2.81 vs. 12.12±5.62, and 11.98±7.24 vs. 58.87±32.43, respectively; P <0.05). The hematoxylin & eosin-stained vascular rings of the offspring rats displayed an uneven lumen, scattered intimal thickening, partial shedding and vacuolar degeneration of endothelial cells, and inflammatory cell infiltration and phagocytosis in the experimental group. In addition, overt smooth muscle atrophy in tunica media, disordered cell arrangement, and unclear structure of the elastic fiber layer was observed. None of these histopathologic changes were found in the control group. In adult offspring rats, PNE not only affected the VEF of the thoracic aorta but also led to pathologic changes in the vascular structure. Additionally, the effects of PNE on VEF were sex-specific, manifesting primarily as significantly improved VEF in female offspring rats and significantly impaired VEF in male offspring rats, lasting into adulthood.
Background Layer-specific speckle-tracking echocardiography (STE) is a noninvasive approach assessing subclinical left ventricular (LV) dysfunction. We aimed to investigate: (I) layer‐specific strain and dyssynchrony index alteration; (II) disease parameters associated with layer-specific STE change; (III) effects of hydroxychloroquine (HCQ) therapy on layer-specific STE parameters in drug-naïve patients with new-onset systemic lupus erythematosus (SLE) without cardiac symptoms. Methods 35 drug-naïve patients with new-onset SLE and 25 age-and-sex-matched healthy controls were enrolled. All individuals received both conventional echocardiographic and two-dimensional STE assessment. Layer-specific global longitudinal strain (GLS), global circumferential strain (GCS) and peak systolic dispersion (PSD) were acquired in layer-specific STE. The effect of HCQ monotherapy on GLS parameters and PSD was assessed in 7 SLE patients with stable disease. Results All patients had normal left ventricular ejection fraction (LVEF). Conventional echocardiographic parameters were comparable between patients and controls. Decreased layer-specific GLS and elevated PSD were observed in SLE patients. In contrast, there’s no difference of layer-specific GCS at the basal level, papillary muscle level and apical level between patients and controls. More severely impaired GLS was observed in patients with higher disease activity, high-risk aPL profile or renal involvement. PSD increased in patients with higher disease activity or high-risk aPL profile. Correlational analysis showed that GLS at three layers and PSD correlated with high-sensitivity CRP (hsCRP) levels. PSD correlated with epicardial GLS, when treating hsCRP level, renal involvement, profile of aPL and disease activity as control variables. Multivariate regression showed hsCRP level and epicardial GLS are the predictors of layer-specific GLS impairment and elevated PSD, respectively. No change of GLS at three layers or PSD was observed in the first 6 months of HCQ treatment, compared with baseline. During the second 6 months of HCQ treatment, increase of endocardial GLS and whole layer GLS, and decrease of PSD were detected. There was no change of epicardial GLS during follow-up. Conclusion Drug-naïve patients with new-onset SLE, even having normal LVEF, are likely to have subclinical GLS impairment and LV dyssynchrony. SLE-related risk factors are associated with these dysfunctions. Continuous use of HCQ may provide beneficial effects to the silent cardiac impairment.
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