Prevalence, Clinical Significance, and Management of Peripheral Arterial Disease in Women: Is There a Role for Postmenopausal Hormone Therapy?

Peripheral arterial disease (PAD), like coronary heart disease, is a clinical manifestation of atherosclerosis and is associated with increased mortality. Although atherosclerotic cardiovascular disease is the leading cause of death for women as well as for men, PAD in women has received less attention than coronary heart disease or stroke. This paper reviews the prevalence of PAD, its risk factors, clinical significance, and management in women. One gender-specific therapeutic issue of particular interest to practitioners and the lay public is the role of postmenopausal hormone therapy. Prior to completion of the Heart and Estrogen/Progestin Replacement Study and the Women's Health Initiative Hormone Trials, postmenopausal hormone therapy was believed to exert antiatherosclerotic effects and to thereby reduce coronary heart disease risk in women on the basis of case-control and cohort studies. This review particularly focuses on the role, if any, of postmenopausal hormone therapy for prevention or treatment of PAD, which was a pre-specified secondary outcome for these three randomized trials

Percutaneous management of ostial stenosis of the left internal mammary artery graft

A 61-year-old man, who had undergone coronary artery bypass surgery 10 years earlier, presented with a non-ST segment elevation myocardial infarction. He was treated with medical therapy and taken to the Cardiac Catheterization Laboratory. A left heart catheterization demonstrated an ostial stenosis in the left internal mammary artery graft, which was felt to be the culprit lesion. This was successfully repaired with a drug eluting stent. This case is presented as an unusual location for a de novo coronary stenosis. The pathophysiology of these lesions is not well understood

Immunogenic aspects of stem cell therapy in regenerative medicine

Departamentul de Medicină, Diviziunea de Cardiologie, Diviziunea de Medicină Genomică, Departmentul de Fizioterapie și Științe ale Sănătății, Centrul Medical „George Washington”, Washington, DCUtilizarea celulelor stem pentru regenerarea și repararea țesuturilor deteriorate a fost de interes pentru comunități științifice și profesioniști timp de câteva decenii. Studiile de translație în cercetările de medicină regenerativă au scopul de a facilita transferul cunoștințelor științifice de bază ce țin de biologia celulelor stem în opțiuni terapeutice posibile. Celulele stem au un potențial promițător pentru aplicarea acestora în repararea sau regenerarea organelor și țesuturilor. Totuși, rata de supraviețuire a celulelor stem transplantate nu a fost una optimă și varia în funcţie de metodele de livrare și tipul celulelor. Unul dintre mecanismele de transplantare care au eșuat este reacția imună a gazdei împotriva celulelor stem livrate. În cadrul acestei analize se vor discuta datele disponibile în literatura despre sursele de celule stem, imunogenitatea diferitor tipuri de celule stem și liniile lor descendente, precum și potențialele strategii de îmbunătățire a supraviețuirii și eficacitatea transplantării celulelor stem în medicina regenerativă.Using stem cells to regenerate and repair damaged tissue has been a focus of the scientific communities and medical professionals for the last couple of decades. Translational studies in regenerative medicine research are intended to facilitate the transfer of the basic science knowledge of stem cell biology into potential therapeutic options. Stem cells have a promising potential for application in repair or regeneration of organs and tissues. However, the survival rate of the transplanted stem cells has not been optimal and varies depending on the delivery methods and type of cells. One of the mechanisms of the failed transplantations is the host’s immune reaction against the delivered stem cells. In this review, we will discuss the available data in the literature on sources of stem cells, the immunogenicity of different types of stem cells and their progeny lineages, and the potential strategies to improve the survival and the efficacy of the stem cells transplantation in regenerative medicine.https://stiinta.usmf.md/sites/default/files/2018-09/MJHS%20nr.%201_2014.pd

Estimation of cardiac output and pulmonary vascular resistance by contrast echocardiography transit time measurement: a prospective pilot study

Background Studies with other imaging modalities have demonstrated a relationship between contrast transit and cardiac output (CO) and pulmonary vascular resistance (PVR). We tested the hypothesis that the transit time during contrast echocardiography could accurately estimate both CO and PVR compared to right heart catheterization (RHC). Methods 27 patients scheduled for RHC had 2D-echocardiogram immediately prior to RHC. 3 ml of DEFINITY contrast followed by a 10 ml saline flush was injected, and a multi-cycle echo clip was acquired from the beginning of injection to opacification of the left ventricle. 2D-echo based calculations of CO and PVR along with the DEFINITY-based transit time calculations were subsequently correlated with the RHC-determined CO and PVR. Results The transit time from full opacification of the right ventricle to full opacification of the left ventricle inversely correlated with CO (r = -0.61, p \u3c 0.001). The transit time from peak opacification of the right ventricle to first appearance in the left ventricle moderately correlated with PVR (r = 0.46, p \u3c 0.01). Previously described echocardiographic methods for the determination of CO (Huntsman method) and PVR (Abbas and Haddad methods) did not correlate with RHC-determined values (p = 0.20 for CO, p = 0.18 and p = 0.22 for PVR, respectively). The contrast transit time method demonstrated reliable intra- (p \u3c 0.0001) and inter-observer correlation (p \u3c 0.001). Conclusions We describe a novel method for the quantification of CO and estimation of PVR using contrast echocardiography transit time. This technique adds to the methodologies used for noninvasive hemodynamic assessment, but requires further validation to determine overall applicability

Application of Novel Genomic Markers to Identify New Pathways in Left Ventricular Remodeling

BACKGROUND: Left ventricular assist devices (LVAD) are increasingly utilized as destination therapy for patients with advanced congestive heart failure (CHF). LVAD has been shown to reverse left ventricular (LV) remodeling by unloading the left ventricle. Transcriptional profiling of the LV tissue before and after LVAD therapy has been utilized to examine the impact of LV unloading on pathways involved in LV remodeling. In this study, we used deep sequencing of the LV tissue to study the interplay of different species of transcripts in LV remodeling. METHODS: LV samples were acquired under informed consent from patients with ischemic cardiomyopathy (ICMP) undergoing surgical placement of LVADs (PRE-LVAD). After a variable period of time, a second LV sample was acquired (POST-LVD) from the same patients, during heart transplantation. Both the PRE- and POST-LVAD samples were preserved in an RNA preservative solution and RNA was isolated by homogenization and Trizol extraction. Total nucleic acids were DNAse treated, and depleted of ribosomal RNA prior to true single molecule sequencing (tSMS) on the SeqLL RNAseq platform. Raw reads were aligned to the human genome, and then counted per transcript to render reads (R) per thousand bases of exon (K) per million (M) total informative reads (RPKM), and then compared within subjects to identify transcripts affected by the LVAD support. RESULTS: Analysis of differentially expressed genes (DEGs) identified 175 coding and 28 non-coding transcripts that were significantly affected by the mechanical unloading during LVAD support. A dominant group of transcripts (\u3e20) were either close, or identical matches to transcripts previously identified as sequestered in stress granules (SGs). The integrated stress response (ISR) involves sequestration of low priority, translationally paused transcripts into SGs, which are self-assembling structures nucleated by a family of amyloid/prion-like proteins, such as TIA1 and G3BP1/2. LVAD support was associated with movement in well-known SG transcripts such as CEP63, CIRBP, EIF3K, TANK, TCEA3, and TPM1, in what appears to be an overall shift in the translational machinery towards transcripts essential to cardiomyocyte survival. CONCLUSIONS: The myocardial transcriptome is dynamically regulated in advanced CHF and following LVAD support. The expression profiles of coding and noncoding RNAs altered in response to LVAD support can be used to understand the pathways involved in LV remodeling. In this study, normalization of transcripts involved in stress granule formation in LV tissue suggests an important role for these pathways in reversal of LV remodeling, and provides a blueprint for druggable targets

Mechanisms of action of mesenchymal stem cells in cardiac repair: Potential influences on the cardiac stem cell niche

Clinical and basic studies of cell-based myocardial therapy have proceeded at a rapid pace. Cell therapy could lead to successful cardiac regeneration or repair by any of three general mechanisms: differentiation of the administered cells into all of the cellular constituents of the heart; release of factors capable of paracrine signaling from the administered cells; and fusion of the administered cells with the existing constituents of the heart. Here, we argue that a fourth general mechanism could be operative: stimulation of endogenous repair by injected cells, which and might cause the regeneration of stem cell niches. In a porcine model of myocardial infarction, allogeneic mesenchymal stem cells stimulated substantial improvement in the ejection fraction, reduction of infarct size, and the growth of a rim of new cardiac tissue in the region in which the mesenchymal stem cells were injected. These effects occurred in the absence of definitive cardiac myocyte differentiation. After myocardial infarction, porcine hearts exhibit evidence of cardiac myocytes that have entered the cell cycle, neovascularization, and reduced levels of apoptosis. These data, in addition to new insights regarding the presence of endogenous cardiac stem cells, strongly support the concept that the heart could contain stem cell niches. Effective cell therapy could lead to restoration of these niches through multifaceted cell-cell interactions

Hematuria: An algorithmic approach to finding the cause

Many conditions can cause hematuria, but the differential diagnosis can be simplified with a systematic approach. We discuss the common causes of hematuria and how to evaluate it