Vessel Pulse Amplitude Mapping in Eyes With Central and Hemi Retinal Venous Occlusion.

Purpose: The purpose of this study was to describe vessel pulse amplitude characteristics in eyes with central retinal vein occlusion (CRVO), hemiretinal vein occlusion (HVO), normal eyes (N1 N1), and the unaffected contralateral eyes of CRVO and HVO eyes (N1 CRVO and N1 HVO), as well as the unaffected hemivessels of HVO eyes (N2 HVO). Methods: Ophthalmodynamometry estimates of blood column pulse amplitudes with modified photoplethysmography were timed against cardiac cycles. Harmonic analysis was performed on the vessel reflectance within 0.25 to 1 mm from the disc center to construct pulse amplitude maps. Linear mixed modeling was used to examine variable effects upon the log harmonic pulse amplitude. Results: One hundred seven eyes were examined. Normal eyes had the highest mean venous pulse amplitude (2.08 ± 0.48 log u). CRVO had the lowest (0.99 ± 0.45 log u, P < 0.0001), followed by HVO (1.23 ± 0.46 log u, P = 0.0002) and N2 HVO (1.30 ± 0.59 log u, P = 0.0005). N1 CRVO (1.76 ± 0.34 log u, P = 0.52) and N1 HVO (1.33 ± 0.37 log u, P = 0.0101) had no significantly different mean amplitudes compared to N1 N1. Arterial amplitudes were lower than venous (P < 0.01) and reduced with venous occlusion (P < 0.01). Pulse amplitude versus amplitude over distance decreased along the N1 N1 vessels, with increasing slopes observed with CRVO (P < 0.01). Conclusions: Pulse amplitude reduction and attenuation characteristics of arteries and veins in venous occlusion can be measured and are consistent with reduced vessel wall compliance and pulse wave transmission. Translational Relevance: Retinal vascular pulse amplitudes can be measured, revealing occlusion induced changes, suggesting a role in evaluating the severity and progression of venous occlusion.

Hidden systolic dysfunction of the right ventricle in patients with increased pulmonary vascular resistance 3 months after COVID-19 pneumonia.

Aim      To study the relationship of echocardiographic right ventricular (RV) structural and functional parameters and indexes of pulmonary vascular resistance (PVR) in patients 3 months after COVID-19 pneumonia.Material and methods  This cross-sectional, observational study included 96 patients aged 46.7±15.2 years. The inclusion criteria were documented diagnosis of COVID-19-associated pneumonia and patient's willing to participate in the observation. Patients were examined upon hospitalization and during the control visit (at 3 months after discharge from the hospital). Images and video loops were processed, including the assessment of myocardial longitudinal strain (LS) by speckle tracking, according to the effective guidelines. The equation [tricuspid regurgitation velocity/ time-velocity integral of the RV outflow tract × 10 + 0.16] was used to determine PRV. Patients were divided into group 1 (n=31) with increased PRV ≥1.5 Wood units and group 2 (n=65) with PRV <1.5 Wood units.Results At baseline, groups did not differ in main clinical functional characteristics, including severity of lung damage by computed tomography (32.7±22.1 and 36.5±20.4 %, respectively. р=0.418). Echocardiographic linear, planimetric and volumetric parameters did not significantly differ between the groups. In group 1 at the control visit, endocardial LS of the RV free wall (FW) (-19.3 [-17.9; -25.8] %) was significantly lower (р=0.048) than in group 2 (-23.4 [-19.8; -27.8] %), and systolic pulmonary artery pressure (sPAP) according to C. Otto (32.0 [26.0; 35.0] mm Hg and 23.0 [20.0; 28.0] mm Hg) was significantly higher than in group 2 (р<0.001). According to the logistic regression, only endocardial RV FW LS (odds ratio, OR, 0.859; 95 % confidence interval, CI, 0.746-0.989; р=0.034) and sPAP (OR, 1.248; 95 % CI, 1.108-1405; р<0.001) were independently related with the increase in PVR. Spearman correlation analysis detected a moderate relationship between PVR and mean PAP according to G. Mahan (r=0.516; p=0.003) and between PVR and the index of right heart chamber functional coupling with the PA system (r=-0.509; p=0.007) in group 1 at the control visit.Conclusion      In patients 3 months after COVID-19 pneumonia, hidden RV systolic dysfunction defined as depressed endocardial RV FW LS to -19.3% is associated with increased PVR ≥1.5 Wood units.

Oral treprostinil improves pulmonary vascular compliance in pulmonary arterial hypertension.

Oral treprostinil has been shown to improve exercise capacity and delay disease progression in patients with pulmonary arterial hypertension (PAH), but its effects on hemodynamics are not well-characterized. The FREEDOM-EV trial was a Phase III, international, placebo-controlled, double-blind, event-driven study in 690 participants with PAH who were taking a single oral PAH therapy. FREEDOM-EV demonstrated a significantly reduced risk for clinical worsening with oral treprostinil taken three times daily and did not uncover new safety signals in PAH patients. Sixty-one participants in the FREEDOM-EV trial volunteered for a hemodynamics sub-study. Pulmonary artery compliance (PAC), a ratio of stroke volume to pulmonary pulse pressure, significantly increased from Baseline to Week 24 in the oral treprostinil group compared with the placebo group (geometric mean 26.4% active vs. -6.0% placebo; ANCOVA p=0.007). There was a significant increase in cardiac output in the oral treprostinil group compared to the placebo group (geometric mean 11.3% active vs. -6.4% placebo; ANCOVA p=0.005) and a corresponding significant reduction in pulmonary vascular resistance (PVR) (geometric mean -21.5 active vs. -1.8% placebo; ANCOVA p=0.02) from Baseline to Week 24. These data suggest that increased compliance contributes to the physiological mechanism by which oral treprostinil improves exercise capacity and delays clinical worsening for patients with PAH.

Hemodynamic response to positive end-expiratory pressure and prone position in COVID-19 ARDS.

BACKGROUND: Use of high positive end-expiratory pressure (PEEP) and prone positioning is common in patients with COVID-19-induced acute respiratory failure. Few data clarify the hemodynamic effects of these interventions in this specific condition. We performed a physiologic study to assess the hemodynamic effects of PEEP and prone position during COVID-19 respiratory failure. METHODS: Nine adult patients mechanically ventilated due to COVID-19 infection and fulfilling moderate-to-severe ARDS criteria were studied. Respiratory mechanics, gas exchange, cardiac output, oxygen consumption, systemic and pulmonary pressures were recorded through pulmonary arterial catheterization at PEEP of 15 and 5 cmH2O, and after prone positioning. Recruitability was assessed through the recruitment-to-inflation ratio. RESULTS: High PEEP improved PaO2/FiO2 ratio in all patients (p = 0.004), and significantly decreased pulmonary shunt fraction (p = 0.012), regardless of lung recruitability. PEEP-induced increases in PaO2/FiO2 changes were strictly correlated with shunt fraction reduction (rho=-0.82, p = 0.01). From low to high PEEP, cardiac output decreased by 18 % (p = 0.05) and central venous pressure increased by 17 % (p = 0.015). As compared to supine position with low PEEP, prone positioning significantly decreased pulmonary shunt fraction (p = 0.03), increased PaO2/FiO2 (p = 0.03) and mixed venous oxygen saturation (p = 0.016), without affecting cardiac output. PaO2/FiO2 was improved by prone position also when compared to high PEEP (p = 0.03). CONCLUSIONS: In patients with moderate-to-severe ARDS due to COVID-19, PEEP and prone position improve arterial oxygenation. Changes in cardiac output contribute to the effects of PEEP but not of prone position, which appears the most effective intervention to improve oxygenation with no hemodynamic side effects.

Renal Resistive Index: Not Only for Kidney Clinics.

Renal Resistive Index (RRI) is a measurement of the resistance of the renal blood flow. A value higher than 0.70 is a marker of increased resistance and is correlated with kidney injury and its severity. Additionally, it may be associated with the mortality rate in the post-surgery population. In COVID-19 subjects, we found that high RRI has been associated with high levels of serum C-reactive protein, a marker of systemic inflammatory reaction syndrome. Finally, we propose RRI not only as a marker of kidney injury, but also as a tool to evaluate the course of critical illness.

Pulmonary Hemodynamics and Ventilation in Patients With COVID-19-Related Respiratory Failure and ARDS.

BACKGROUND: It has been suggested that COVID-19-associated severe respiratory failure (CARDS) might differ from usual acute respiratory distress syndrome (ARDS) due to failing autoregulation of pulmonary vessels and higher shunt. We sought to investigate pulmonary hemodynamics and ventilation properties in patients with CARDS compared to patients with ARDS of pulmonary origin. METHODS: This was a retrospective analysis of prospectively collected data from consecutive adults with laboratory-confirmed severe acute respiratory syndrome coronavirus 2 patients treated in our ICU in 04/2020 and a comparison of the data to matched controls with ARDS due to respiratory infections treated in our ICU from 01/2014 to 08/2019 for whom pulmonary artery catheter data were available. RESULTS: CARDS patients (n = 10) had ventilation characteristics similar to those of ARDS (n = 10) patients. Nevertheless, mechanical power applied by ventilation was significantly higher in CARDS patients (23.4 ± 8.9 J/min) than in ARDS (15.9 ± 4.3 J/min; P < 0.05). COVID-19 patients had similar pulmonary artery pressure but significantly lower pulmonary vascular resistance, as cardiac output was higher in CARDS vs. ARDS patients (P < 0.05). Shunt fraction and dead space were similar in CARDS compared to ARDS (P > 0.05) and were correlated with hypoxemia in both groups. The arteriovenous pCO2 difference (▵pCO2) was elevated (CARDS 5.5 ± 2.8 mmHg vs. ARDS 4.7 ± 1.1 mmHg; P > 0.05), as was the P(v-a)CO2/C(a-v)O2 ratio (CARDS mean 2.2 ± 1.5 vs. ARDS 1.7 ± 0.8; P > 0.05). CONCLUSIONS: Respiratory failure in COVID-19 patients seems to differ only slightly from ARDS regarding ventilation characteristics and pulmonary hemodynamics. Our data indicate microcirculatory dysfunction. More data need to be collected to assure these findings and gain more pathophysiological insights into COVID-19 and respiratory failure.

Maternal and fetal effects of COVID-19 virus on a complicated triplet pregnancy: a case report.

BACKGROUND: Coronavirus disease 2019 (COVID-19), the global pandemic that has spread throughout the world, is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Given the limited scientific evidence on the manifestations and potential impact of this virus on pregnancy, we decided to report this case. CASE PRESENTATION: The patient was a 38 year-old Iranian woman with a triplet pregnancy and a history of primary infertility, as well as hypothyroidism and gestational diabetes. She was hospitalized at 29 weeks and 2 days gestational age due to elevated liver enzymes, and finally, based on a probable diagnosis of gestational cholestasis, she was treated with ursodeoxycholic acid. On the first day of hospitalization, sonography was performed, which showed that biophysical scores and amniotic fluid were normal in all three fetuses, with normal Doppler findings in two fetuses and increased umbilical artery resistance (pulsatility index [PI] > 95%) in one fetus. On day 4 of hospitalization, she developed fever, cough and myalgia, and her COVID-19 test was positive. Despite mild maternal symptoms, exacerbated placental insufficiency occurred in two of the fetuses leading to the rapid development of absent umbilical artery end-diastolic flow. Finally, 6 days later, the patient underwent cesarean section due to rapid exacerbation of placental insufficiency and declining biophysical score in two of the fetuses. Nasopharyngeal swab COVID-19 tests were negative for the first and third babies and positive for the second baby. The first and third babies died 3 and 13 days after birth, respectively, due to collapsed white lung and sepsis. The second baby was discharged in good general condition. The mother was discharged 3 days after cesarean section. She had no fever at the time of discharge and was also in good general condition. CONCLUSIONS: This was a complicated triplet pregnancy, in which, after maternal infection with COVID-19, despite mild maternal symptoms, exacerbated placental insufficiency occurred in two of the fetuses, and the third fetus had a positive COVID-19 test after birth. Therefore, in cases of pregnancy with COVID-19 infection, in addition to managing the mother, it seems that physicians would be wise to also give special attention to the possibility of acute placental insufficiency and subsequent fetal hypoxia, and also the probability of vertical transmission.

Haemodynamic characteristics of COVID-19 patients with acute respiratory distress syndrome requiring mechanical ventilation. An invasive assessment using right heart catheterization.

AIMS: Interstitial pneumonia due to coronavirus disease 2019 (COVID-19) is often complicated by severe respiratory failure. In addition to reduced lung compliance and ventilation/perfusion mismatch, a blunted hypoxic pulmonary vasoconstriction has been hypothesized, that could explain part of the peculiar pathophysiology of the COVID-19 cardiorespiratory syndrome. However, no invasive haemodynamic characterization of COVID-19 patients has been reported so far. METHODS AND RESULTS: Twenty-one mechanically-ventilated COVID-19 patients underwent right heart catheterization. Their data were compared both with those obtained from non-mechanically ventilated paired control subjects matched for age, sex and body mass index, and with pooled data of 1937 patients with 'typical' acute respiratory distress syndrome (ARDS) from a systematic literature review. Cardiac index was higher in COVID-19 patients than in controls [3.8 (2.7-4.5) vs. 2.4 (2.1-2.8) L/min/m2 , P < 0.001], but slightly lower than in ARDS patients (P = 0.024). Intrapulmonary shunt and lung compliance were inversely related in COVID-19 patients (r = -0.57, P = 0.011) and did not differ from ARDS patients. Despite this, pulmonary vascular resistance of COVID-19 patients was normal, similar to that of control subjects [1.6 (1.1-2.5) vs. 1.6 (0.9-2.0) WU, P = 0.343], and lower than reported in ARDS patients (P < 0.01). Pulmonary hypertension was present in 76% of COVID-19 patients and in 19% of control subjects (P < 0.001), and it was always post-capillary. Pulmonary artery wedge pressure was higher in COVID-19 than in ARDS patients, and inversely related to lung compliance (r = -0.46, P = 0.038). CONCLUSIONS: The haemodynamic profile of COVID-19 patients needing mechanical ventilation is characterized by combined cardiopulmonary alterations. Low pulmonary vascular resistance, coherent with a blunted hypoxic vasoconstriction, is associated with high cardiac output and post-capillary pulmonary hypertension, that could eventually contribute to lung stiffness and promote a vicious circle between the lung and the heart.