Citations

Introduction: Serum creatinine (sCr) is routinely used to calculate estimated glomerular filtration rate (eGFR) in heart failure (HF) pts. However, changes in muscle mass may limit the accuracy of sCr as marker of renal function in this population. Cystatin C (CysC) is independent of muscle mass and provides an alternative measure of eGFR. In prior studies, higher sCr/CysC ratio has been associated with higher muscle mass. Herein, we compared CysC- and sCr-based eGFR at serial time points among pts admitted with HF. We hypothesized that muscle mass would decline during HF admission and this would result in a decrease of sCr/CysC ratio. Methods: We pooled pts from 3 trials performed in pts admitted with HF (DOSE, ROSE and CARRESS-HF). eGFR was calculated using CKD-EPI-CysC equation (eGFRCysC) and sCr-based MDRD equation (eGFRsCr). The relative difference between eGFRCysC and eGFRsCr (ΔeGFR) was calculated as follows: (eGFRCysC-eGFRsCr)/ eGFRsCr. To control for confounders, we analyzed changes in sCr/CysC ratio and in ΔeGFR among pts with samples available at both admission and a subsequent time point. Results: A total of 2849 samples were available in 841 pts (age 68 ± 13, 26% female, left ventricular ejection fraction 36 ± 17%). Compared with eGFRsCr, eGFRCysC reclassified 50% of the samples to different GFR categories, mainly to more advanced renal dysfunction (Fig. A). eGFRCysC was significantly lower than eGFRsCr at all time points (Fig. B). From time of admission to all subsequent time points, sCr/CysC ratio declined while ΔeGFR widened (all p-values<0.001). At time of enrollment in CARRESS-HF, each additional day of HF admission was associated with a decline in sCr/CysC ratio of 1.5% (p=0.04). Conclusions: The use of CysC reclassifies a large proportion of pts admitted with HF to more advanced renal dysfunction when compared to sCr-based assessment. The discrepancy between CysC- and sCr-based eGFR appears to widen during HF admission, likely due to muscle mass wasting.

Introduction: Spontaneous coronary artery dissection (SCAD) is a rare but life threatening cause of acute coronary syndrome and a common etiology of pregnancy-associated myocardial infarction (PAMI). Hypothesis: We aimed to examine the clinical presentation, treatment, and outcomes of the largest pregnancy associated-SCAD (P-SCAD) patient cohort to date. Methods: A total of 128 women enrolled in the Mayo Clinic SCAD Registry between 2010-2020 who were pregnant or up to 1 year postpartum at time of P-SCAD were identified. We subdivided P-SCAD in an “early” group with <12 weeks of delivery and a “late” group presenting between >12 weeks -12 months following delivery. Results: Among the 128 women with P-SCAD, 7(5%) occurred during pregnancy (2/7 first trimester, 5/7 third trimester). Of the 121 women with postpartum P-SCAD, 88/121(72%) occurred <12 weeks of delivery and 33/121(27%) at 12 weeks to 1 year postpartum. The mean age of P-SCAD was 35.3 +/- 4 years (26-48). The most common symptom on presentation was chest pain 118/128(92%); 62/128(48%) presented with ST elevation MI and 58/128(45%) presented with non-ST elevation MI. Multivessel involvement occurred in 40/128(31%), left anterior descending artery (LAD) in 88/128(69%), and left main (LM) in 28/128(22%) of all P-SCAD. Percutaneous coronary intervention (PCI) was performed in 52/128(41%) with a success rate of 81%. Coronary artery bypass grafting was performed in 24/128(19%) of which 6/24 patients had an unsuccessful PCI, 14/24 had proximal or multivessel SCAD, and 4/24 had persistent or extension of initial SCAD. Of those treated conservatively 52/128(40%), 11/52(21%) had LM and LAD. Among all the P-SCAD patients, 84/128 (66%) were screened for an underlying arteriopathy, of whom 44 (52 %) were diagnosed with fibromuscular dysplasia. At a median follow up of 3 years (IQR 1 to 6), 12/128 (9%) of all P-SCAD survivors had a recurrent SCAD event and 7/12 (58%) were within 1 year postpartum. There were no deaths. Conclusions: P-SCAD most commonly presents with ST-elevation MI and multivessel involvement within the initial 12 weeks postpartum. Clinicians need to be familiar with this etiology of PAMI to avoid delay in diagnosis and appropriate management.

Dysfunction of the left ventricle (LV) with impaired contractility following chronic ischemia or acute myocardial infarction (AMI) is the main cause of ischemic mitral regurgitation (IMR), leading to moderate and moderate-to-severe mitral regurgitation (MR). The site of AMI exerts a specific influence determining different patterns of adverse LV remodeling. In general, inferior-posterior AMI is more frequently associated with regional structural changes than the anterolateral one, which is associated with global adverse LV remodeling, ultimately leading to different phenotypes of IMR. In this narrative review, starting from the aforementioned categorization, we proceed to describe current knowledge regarding surgical approaches in the management of IMR.

Computational fluid dynamics (CFD) has grown as a tool to help understand the hemodynamic properties related to the rupture of cerebral aneurysms. Few of these studies deal specifically with aneurysm growth and most only use a single time instance within the aneurysm growth history. The present retrospective study investigated four patient-specific aneurysms, once at initial diagnosis and then at follow-up, to analyze hemodynamic and morphological changes. Aneurysm geometries were segmented via the medical image processing software Mimics. The geometries were meshed and a computational fluid dynamics (CFD) analysis was performed using ANSYS. Results showed that major geometry bulk growth occurred in areas of low wall shear stress (WSS). Wall shape remodeling near neck impingement regions occurred in areas with large gradients of WSS and oscillatory shear index. This study found that growth occurred in areas where low WSS was accompanied by high velocity gradients between the aneurysm wall and large swirling flow structures. A new finding was that all cases showed an increase in kinetic energy from the first time point to the second, and this change in kinetic energy seems correlated to the change in aneurysm volume.