Frontiers in cardiovascular medicine
-
Front Cardiovasc Med · Jan 2019
Central and Obstructive Apneas in Heart Failure With Reduced, Mid-Range and Preserved Ejection Fraction.
Background: Although central apneas (CA) and obstructive apneas (OA) are highly prevalent in heart failure (HF), a comparison of apnea prevalence, predictors and clinical correlates in the whole HF spectrum, including HF with reduced ejection fraction (HFrEF), mid-range EF (HFmrEF) and preserved EF (HFpEF) has never been carried out so far. Materials and methods: 700 HF patients were prospectively enrolled and then divided according to left ventricular EF (408 HFrEF, 117 HFmrEF, 175 HFpEF). All patients underwent a thorough evaluation including: 2D echocardiography; 24-h Holter-ECG monitoring; cardiopulmonary exercise testing; neuro-hormonal assessment and 24-h cardiorespiratory monitoring. ⋯ When compared to patients with NB, those with OA were older and more comorbid independently from background EF. Conclusions: Across the whole spectrum of HF, CA prevalence increases and OA decreases as left ventricular systolic dysfunction progresses. Different predictors and specific clinical characteristics might help to identify patients at risk of developing CA or OA in different HF phenotypes.
-
Front Cardiovasc Med · Jan 2019
A Protocol for Nurse-Practitioner Led Cardiovascular Follow-Up After Pregnancy Complications in a Socioeconomically Disadvantaged Population.
Background: Women who experience pregnancy complications have an increased risk of future cardiovascular disease when compared to their healthy counterparts. Despite recommendations, there is no standardized cardiovascular follow-up in the postpartum period for these women, and the Australian follow-up protocols that have been previously described are research-based. This study proposes a new model of care for a nurse practitioner-led postpartum intervention clinic for women who experience severe hypertensive disorders of pregnancy, gestational diabetes mellitus requiring medication, severe intrauterine growth restriction, idiopathic preterm delivery, or placental abruption, in a socioeconomically disadvantaged population. ⋯ All data is also collated into a registry, which aims to assess the efficacy of the intervention at improving modifiable cardiovascular risk factors and reducing cardiovascular risk. Discussion: There is limited information on the efficacy of postpartum intervention clinics in reducing cardiovascular risk in women who have experienced pregnancy complications. Analyses of the data collected in the registry will provide essential information about how best to reduce cardiovascular risk in women in socioeconomically disadvantaged and disease-burdened populations.
-
Front Cardiovasc Med · Jan 2019
Differences in microRNA-29 and Pro-fibrotic Gene Expression in Mouse and Human Hypertrophic Cardiomyopathy.
Background: Hypertrophic cardiomyopathy (HCM) is characterized by myocyte hypertrophy and fibrosis. Studies in two mouse models (R92W-TnT/R403Q-MyHC) at early HCM stage revealed upregulation of endothelin (ET1) signaling in both mutants, but TGFβ signaling only in TnT mutants. Dysregulation of miR-29 expression has been implicated in cardiac fibrosis. ⋯ Pathway analysis predicted upregulation of the anti-hypertrophic/anti-fibrotic liver X receptor/retinoid X receptor (LXR/RXR) pathway only in human myectomy tissue. Conclusions: Our in vitro studies suggest that activation of ET1 signaling in cardiac myocytes increases reactive oxygen species and stimulates TGFβ secretion, which downregulates miR-29a and increases collagen in fibroblasts, thus contributing to fibrosis. Our gene expression studies in mouse and human HCM reveal allele-specific differences in miR-29 family/profibrotic gene expression in mouse HCM, and activation of anti-hypertrophic/anti-fibrotic genes and pathways in human HCM.
-
Syncope is a common presentation to Emergency Departments (EDs). Estimates on the frequency of visits (0.6-1.7%) and subsequent rates of hospitalizations (12-85%) vary according to country. The initial ED evaluation for syncope consists of a detailed history, physical examination and 12-lead electrocardiogram (ECG). ⋯ Following risk stratification, decision for hospitalization should be based on the seriousness of the underlying cause for syncope or based on high-risk features, or the severity of co-morbidities. For those deemed intermediate risk, access to specialist assessment and related testing may occur in a syncope unit in the emergency department, as an outpatient, or in a less formal care pathway and is highly dependent on the local healthcare system. For syncope patients presenting to the ED, ~0.8% die and 10.3% suffer a non-fatal severe outcome within 30 days.
-
Front Cardiovasc Med · Jan 2018
Biventricular Increases in Mitochondrial Fission Mediator (MiD51) and Proglycolytic Pyruvate Kinase (PKM2) Isoform in Experimental Group 2 Pulmonary Hypertension-Novel Mitochondrial Abnormalities.
Introduction: Group 2 pulmonary hypertension (PH), defined as a mean pulmonary arterial pressure ≥25 mmHg with elevated pulmonary capillary wedge pressure >15 mmHg, has no approved therapy and patients often die from right ventricular failure (RVF). Alterations in mitochondrial metabolism, notably impaired glucose oxidation, and increased mitochondrial fission, contribute to right ventricle (RV) dysfunction in PH. We hypothesized that the impairment of RV and left ventricular (LV) function in group 2 PH results in part from a proglycolytic isoform switch from pyruvate kinase muscle (PKM) isoform 1 to 2 and from increased mitochondrial fission, due either to upregulation of expression of dynamin-related protein 1 (Drp1) or its binding partners, mitochondrial dynamics protein of 49 or 51 kDa (MiD49 or 51). ⋯ Conclusions: SAB caused group 2 PH. Impaired RV function and RV fibrosis were associated with increases in mitochondrial fission and expression of MiD51 and PKM2. While these changes would be expected to promote increased production of reactive oxygen species and a glycolytic shift in metabolism, further study is required to determine the functional consequences of these newly described mitochondrial abnormalities.