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. Cardiovascular disease is a leading cause of morbidity and mortality with heart failure constituting a large portion of this spectrum. Heart failure patients have 90-day readmission rates of nearly 41% associated with a high expense. Numerous strategies to reduce readmissions have been attempted with the CardioMEMS pulmonary artery pressure monitoring system as one of the more successful ones. As this device becomes used more frequently, it is important to recognize procedural complications. We present of a rare complication where a patient underwent successful device placement and was subsequently found to have dampened waveforms which were due to device migration. . A 79-year-old male underwent successful CardioMEMS placement due to recurrent heart failure hospitalizations. 6 months later, the transmitted waveforms appeared dampened, and repeat angiography revealed a device that had migrated. Rather than abandoning the device, it was recalibrated and continued to transmit data and helped manage the patient's heart failure. . CardioMEMS is a cost-effective tool to help reduce heart failure hospitalizations. Device migration is a rare complication and can lead to inaccurate data. However, as seen in this case, the device can be successfully recalibrated and can continue to be utilized to help reduce heart failure admissions.
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http://dx.doi.org/10.1155/2020/3856940 | DOI Listing |
J Palliat Care
September 2025
Department of Healthcare Administration and Policy, School of Public Health, University of Nevada, Las Vegas, NV, USA.
ObjectivesRecently, atrial fibrillation (AF) has contributed to an increase in cardiovascular deaths in the U.S. Palliative care (PC) and atrial ablation (AA) procedure can elevate quality of life of high-risk AF patients, who are associated with multiple comorbidities.
View Article and Find Full Text PDFPLoS One
September 2025
Biobank of Jiangsu Cancer Hospital, Jiangsu Institute of Cancer Research & The Affiliated Cancer Hospital of Nanjing Medical University, Nanjing, Jiangsu, PR China.
Heart failure (HF) and lung cancer (LC) often coexist, yet their shared molecular mechanisms are unclear. We analyzed transcriptome data from the NCBI Gene Expression Omnibus (GEO) database (GSE141910, GSE57338) to identify 346 HF‑related differentially expressed genes (DEGs), then combined weighted gene co-expression network analysis (WGCNA) pinpointed 70 hub candidates. Further screening of these 70 hub candidates in TCGA lung cancer cohorts via LASSO, Random Forest, and multivariate Cox regression suggested CYP4B1 as the only independent prognostic marker.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiology, Fuzhou University Affiliated Provincial Hospital, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Introduction: Kidney stone disease is associated with numerous cardiovascular risk factors. However, the findings across studies are non-uniformly consistent, and the control of confounding variables remains suboptimal. This study aimed to investigate the association between kidney stone and cardiovascular disease.
View Article and Find Full Text PDFAm J Physiol Heart Circ Physiol
September 2025
Division of Pediatric Critical Care, Department of Pediatrics, University of California, San Francisco, USA.
Right ventricular (RV) failure is the primary cause of death among patients with pulmonary arterial hypertension (PAH). Patients with congenital heart disease-associated PAH (CHD-PAH) demonstrate improved outcomes compared to patients with other forms of PAH, which is related to the maintenance of an adaptively hypertrophied RV. In an ovine model of CHD-PAH, we aimed to elucidate the cellular, microvascular, and transcriptional adaptations to congenital pressure overload that support RV function.
View Article and Find Full Text PDFJCI Insight
September 2025
Department of Pharmacology, University of Michigan, Ann Arbor, United States of America.
Cardiac hypertrophy is a common adaptation to cardiovascular stress and often a prelude to heart failure. We examined how S-palmitoylation of the small GTPase, Ras-related C3 botulinum toxin substrate 1 (Rac1), impacts cardiomyocyte stress signaling. Mutation of the cysteine-178 palmitoylation site impaired activation of Rac1 when overexpressed in cardiomyocytes.
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