Lipoprotein(a) Predicts Vascular Disease Risk 09/03/25
Welcome to Cardiology Today â Recorded September 03, 2025. This episode summarizes 5 key cardiology studies on topics like comorbidities and cardiomyocytes. Key takeaway: Lipoprotein(a) Predicts Vascular Disease Risk.
Article Links:
Article 1: Experiences of Stalking and Obtaining a Restraining Order Are Associated With Onset of Cardiovascular Events in Women: A Prospective Analysis in the Nurses’ Health Study II. (Circulation)
Article 2: Evaluation of Lipoprotein(a) as a Prognostic Marker of Extracoronary Atherosclerotic Vascular Disease Progression. (Circulation)
Article 3: PIEZO1 Overexpression in Hereditary Hemorrhagic Telangiectasia Arteriovenous Malformations. (Circulation)
Article 4: Cellular Reprogramming by PHF7 Enhances Cardiac Function Following Myocardial Infarction. (Circulation)
Article 5: Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment. (European heart journal)
Full episode page: https://podcast.explainheart.com/podcast/lipoproteina-predicts-vascular-disease-risk-09-03-25/
đ Featured Articles
Article 1: Experiences of Stalking and Obtaining a Restraining Order Are Associated With Onset of Cardiovascular Events in Women: A Prospective Analysis in the Nurses’ Health Study II.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40785542
Summary: This prospective study within the Nurses’ Health Study II found that women who experienced stalking, particularly those who obtained restraining orders, had a significantly higher risk of developing cardiovascular events. The increased risk highlights the long-term cardiovascular consequences of interpersonal violence and the potential need for targeted screening and intervention in women with a history of stalking. These findings underscore the importance of addressing violence as a cardiovascular risk factor.
Article 2: Evaluation of Lipoprotein(a) as a Prognostic Marker of Extracoronary Atherosclerotic Vascular Disease Progression.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40718930
Summary: This study evaluated lipoprotein a as a marker for extracoronary atherosclerotic vascular disease progression. Results indicated that elevated lipoprotein a levels are associated with a higher risk of developing extracoronary atherosclerotic vascular disease and related complications, suggesting it may serve as a useful prognostic biomarker. These results reinforce the need for considering lipoprotein a levels in risk assessment for atherosclerotic vascular disease.
Article 3: PIEZO1 Overexpression in Hereditary Hemorrhagic Telangiectasia Arteriovenous Malformations.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40665909
Summary: This research investigated the role of PIEZO1 in hereditary hemorrhagic telangiectasia arteriovenous malformations. The study found that PIEZO1 is overexpressed in arteriovenous malformations associated with hereditary hemorrhagic telangiectasia, particularly those caused by activin receptor-like kinase 1 mutations. This suggests a potential therapeutic target for managing arteriovenous malformations in hereditary hemorrhagic telangiectasia.
Article 4: Cellular Reprogramming by PHF7 Enhances Cardiac Function Following Myocardial Infarction.
Journal: Circulation
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40631661
Summary: This study identified PHF7 as a potent epigenetic factor that enhances the direct reprogramming of fibroblasts into cardiomyocytes in vitro. In a model of myocardial infarction, PHF7-mediated reprogramming improved cardiac function. These findings suggest PHF7 could be a key factor in developing cell-based therapies for ischemic heart disease.
Article 5: Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment.
Journal: European heart journal
PubMed Link: https://pubmed.ncbi.nlm.nih.gov/40892534
Summary: This review article discusses the mechanisms and treatment of left ventricular hypertrophy and myocardial fibrosis in Heart Failure with Preserved Ejection Fraction. It highlights the role of comorbidities like hypertension, obesity, and diabetes in promoting adverse cardiac remodeling and fibrosis. The review emphasizes the need for targeted therapies addressing these underlying comorbidities to improve outcomes in Heart Failure with Preserved Ejection Fraction.
đ Transcript
Today’s date is September 03, 2025. Welcome to Cardiology Today. Here are the latest research findings.
Article number one. Experiences of Stalking and Obtaining a Restraining Order Are Associated With Onset of Cardiovascular Events in Women: A Prospective Analysis in the Nurses’ Health Study II. This prospective study within the Nurses’ Health Study II found that women who experienced stalking, particularly those who obtained restraining orders, had a significantly higher risk of developing cardiovascular events. The increased risk highlights the long-term cardiovascular consequences of interpersonal violence and the potential need for targeted screening and intervention in women with a history of stalking. These findings underscore the importance of addressing violence as a cardiovascular risk factor.
Article number two. Evaluation of Lipoprotein(a) as a Prognostic Marker of Extracoronary Atherosclerotic Vascular Disease Progression. This study evaluated lipoprotein a as a marker for extracoronary atherosclerotic vascular disease progression. Results indicated that elevated lipoprotein a levels are associated with a higher risk of developing extracoronary atherosclerotic vascular disease and related complications, suggesting it may serve as a useful prognostic biomarker. These results reinforce the need for considering lipoprotein a levels in risk assessment for atherosclerotic vascular disease.
Article number three. PIEZO1 Overexpression in Hereditary Hemorrhagic Telangiectasia Arteriovenous Malformations. This research investigated the role of PIEZO1 in hereditary hemorrhagic telangiectasia arteriovenous malformations. The study found that PIEZO1 is overexpressed in arteriovenous malformations associated with hereditary hemorrhagic telangiectasia, particularly those caused by activin receptor-like kinase 1 mutations. This suggests a potential therapeutic target for managing arteriovenous malformations in hereditary hemorrhagic telangiectasia.
Article number four. Cellular Reprogramming by PHF7 Enhances Cardiac Function Following Myocardial Infarction. This study identified PHF7 as a potent epigenetic factor that enhances the direct reprogramming of fibroblasts into cardiomyocytes in vitro. In a model of myocardial infarction, PHF7-mediated reprogramming improved cardiac function. These findings suggest PHF7 could be a key factor in developing cell-based therapies for ischemic heart disease.
Article number five. Left ventricular hypertrophy and myocardial fibrosis in heart failure with preserved ejection fraction: mechanisms and treatment. This review article discusses the mechanisms and treatment of left ventricular hypertrophy and myocardial fibrosis in Heart Failure with Preserved Ejection Fraction. It highlights the role of comorbidities like hypertension, obesity, and diabetes in promoting adverse cardiac remodeling and fibrosis. The review emphasizes the need for targeted therapies addressing these underlying comorbidities to improve outcomes in Heart Failure with Preserved Ejection Fraction.
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đ Keywords
comorbidities, cardiomyocytes, cardiac remodeling, interpersonal violence, cellular reprogramming, cardiovascular events, hereditary hemorrhagic telangiectasia, Heart Failure with Preserved Ejection Fraction, left ventricular hypertrophy, extracoronary disease, restraining order, stalking, myocardial infarction, prognosis, myocardial fibrosis, PHF7, PIEZO1, vascular endothelial growth factor receptor 2, atherosclerotic vascular disease, women’s health, biomarker, lipoprotein(a), arteriovenous malformations, activin receptor-like kinase 1, fibroblasts.
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Concise summaries of cardiovascular research for professionals.
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