Cardiac function in fetal and infants born to mothers with gestational diabetes

Background The intraventricular pressure differences (IVPD) IVPD using color M-mode is a specific marker in infants of mothers with gestational diabetes mellitus (GDM). (Circulation R 2019, 378–388). Purpose This study investigated the myocardial performance of fetuses in mothers with GDM under the new GDM definition. Method The study population comprised of 27 mothers with GDM and the fetus. Women with GDM were defined as those with a glucose metabolism abnormality that existed before or began during the current pregnancy and was diagnosed using OGTTs. The 5 mothers with type 1 or type 2 DM were receiving insulin before their pregnancy. Fetal echo measurements were performed about median gestational age 35 weeks. The primary outcomes were comparisons of the fetal myocardial performance of GDM with insulin administration and without administration using echocardiography with IVPD, and IVPG. The secondary outcome has investigated the relationships between echocardiography parameters, IVPD, and IVPG, and maternal factors. For all statistical analyses, P<0.05 was considered significant. Result In the insulin group was higher RV output (Fig. 2A). Maternal max HbA1c was observed to have a positive correlation with fetal RV output, significantly (Fig. 2B). Maternal max fasting blood glucose was observed to have a negative correlation with the Total, Basal and Mid to apical IVPD, significantly, respectively. Serial change of LV Total IVPD from fetal to after birth shown in Slide. In both groups, LV Total IVPD was increasing from fetal and after birth significantly. Conclusion The mechanism associated with the favorable systolic and diastolic performances in IGDMs is suggested to involve metabolic adaptations in the heart. In diabetic mice, these adaptations seem to prevent the heart from failing during conditions of pressure overload, suggesting a restoration of the balance between glucose and fatty acid utilization is beneficial for cardiac function. In fetal LV and RV-IVPD might be interacted the mother's blood sugar control. These indexes can predict the sensitive fetal and infant's cardiac dysfunction for GDM. FUNDunding Acknowledgement Type of funding sources: None.

Abstract 12984: Long-term Prognostic Value of the Serial Change of Acute Hemodynamic Index During Hospitalization in Patients Admitted for Acute Decompensated Heart Failure

Backgrounds: Controlled heart rate (HR) and increased pulse pressure (PP) are related to better outcomes in stable heart failure. Hemodynamic response to stress evaluated by an acute hemodynamics index (AHI), the product of HR and PP, has been reported to be associated with poor outcomes in patients admitted for acute decompensated heart failure (ADHF). However, there is no information available on the long-term prognostic value of the serial change of AHI during hospitalization in patients admitted for ADHF. Methods and Results: We studied 259 patients admitted for ADHF and discharged with survival. We measured AHI (HR x PP/1000) at admission and discharge. AHI significantly decreased from admission to discharge (6.98±3.04 to 3.81±1.21 bpm·mmHg, p<0.0001). During a mean follow-up period of 5.0±3.2 yrs, 53 patients had cardiac death. The change [ad-dis] of AHI from admission to discharge (AHI[ad-dis]) was significantly less in patients with than without cardiac death (1.98±2.17 vs 3.47±2.87 bpm·mmHg, p=0.0005). Multivariate Cox regression analysis revealed that AHI[ad-dis], but not PP[ad-dis], was significantly associated with cardiac death, independently of prior heart failure hospitalization, body mass index, estimated glomerular filtration rate, hemoglobin level and left ventricular end-diastolic dimension. ROC analysis revealed that AUC in AHI[ad-dis](0.668[0.588-0.749]) was greater than that in PP[ad-dis](0.637[0.572-0.717]). Patients with less AHI[ad-dis] (≤1.79 bpm·mmHg by ROC analysis) had a significantly higher risk of cardiac death than those with greater AHI[ad-dis] (adjusted hazard ratio: 3.19[1.77 to 5.76], 30% vs 13%, p<0.0001). Conclusions: Cardiac death was frequently observed in ADHF patients who had less degree of the decrease in AHI during hospitalization. The change of AHI during hospitalization would be a simple and useful marker for risk stratification in patients admitted for ADHF.

Pirfenidone plus inhaled N-acetylcysteine for idiopathic pulmonary fibrosis: a randomised trial

BackgroundA randomised controlled trial in Japan showed that inhaled N-acetylcysteine monotherapy stabilised serial decline in forced vital capacity (FVC) in some patients with early idiopathic pulmonary fibrosis (IPF). However, the efficacy and tolerability of combination therapy with an antifibrotic agent and inhaled N-acetylcysteine are unknown.MethodsThis 48-week, randomised, open-label, multicentre phase 3 trial compared the efficacy and tolerability of combination therapy with pirfenidone plus inhaled N-acetylcysteine 352.4 mg twice daily with the results for pirfenidone alone in patients with IPF. The primary end-point was annual rate of decline in FVC. Exploratory efficacy measurements included serial change in diffusing capacity of the lung for carbon monoxide (DLCO) and 6-min walk distance (6MWD), progression-free survival (PFS), incidence of acute exacerbation, and tolerability.Results81 patients were randomly assigned in a 1:1 ratio to receive pirfenidone plus inhaled N-acetylcysteine (n=41) or pirfenidone (n=40). The 48-week rate of change in FVC was −300 mL and −123 mL, respectively (difference −178 mL, 95% CI −324–−31 mL; p=0.018). Serial change in DLCO, 6MWD, PFS and incidence of acute exacerbation did not significantly differ between the two groups. The incidence of adverse events (n=19 (55.9%) for pirfenidone plus N-acetylcysteine; n=18 (50%) for pirfenidone alone) was similar between groups.ConclusionsCombination treatment with inhaled N-acetylcysteine and pirfenidone is likely to result in worse outcomes for IPF.

P1478 Evaluation of reversibility of alcoholic cardiomyopathy using doubaimine stress echocardiography

Alcoholic cardiomyopathy (CM) is known as a reversible CM. Appropriate medications with cessation of alcohol may lead to full recovery of chamber size and contractility. But there is not much information about morphologic and hemodynamic changes over the course of treatment, and predictors of reversibility. We experienced the patient with alcoholic CM who was admitted with heart failure and recovered over 1 year and 5 months. He consumed daily 180g alcohol for 6 months before admission. On initial echocardiography, left atrial (LA) dimension, left ventricular (LV) systolic dimension (SD) and diastolic dimension (DD), inferior vena cava (IVC) size, and ejection fraction (EF) were 50 mm, 69 mm, 78 mm, 27 mm and 22%, respectively. Doppler examination revealed a restrictive pattern in tansmitral flow, and a systolic peak velocity/diastolic peak velocity (S/D) ratio of less than 1 in pulmonary vein flow (PVF). Pressure gradient through tricuspid regurgitation was 29 mmHg. Coronary angiogram confirmed no significant stenosis. Within 1 week after medications, LVEF increased mainly by decrease of enlarged LVSD which might be partly caused by volume overload, evidenced by respiratory variation of transmitral flow. On 8th day, we performed dobutamine stress echocardiography (DSE) to evaluate reversibility because LVEF slightly decreased despite decrease of LVDD. During dobutamine infusion, both LVDD and LVSD decreased along with increase of LVEF according to dose escalation. From 1 to 2 months, LVEF slightly increased with decrease of LVDD and LVSD. Afterwards, LVEF was normalized mainly with decrease of LVSD, and LVEF was completely normalized at 1 year and 5 month after initiation of treatment. Initial increase of LVEF might reflect decrease of LVSD by relief of volume overload rather than improving LV contractility. Based on this observation of serial change of chambers and LVEF, we speculate that increased LV wall tension, which is induced by increase of preload as a compensating mechanism for increasing stroke volume, might aggravate LVEF in later stage of heart failure with reduced EF. The sequence of normalization in chamber size was IVC, and then LA, and then LVDD. Transmitral flow as an indicator of diastolic dysfunction changed from restrictive (transiently existed only for 1 week) to abnormal relaxation pattern (no change since that time). PVF pattern showed S/D ratio &lt; 1 until 1 week, and then triphasic pattern at 1 month, finally biphasic pattern at 8 month after initiation of medications. We observed a serial change of echocardiographic findings in patient with alcoholic CM, which might provide an insightful information to understand reverse of LV or LA remodeling associated with hemodynamic parameters, and DSE might be helpful to evaluate reversibility of LV systolic function and convince patients who are reluctant to medications.