Methodist DeBakey cardiovascular journal最新文献

{"title":"Cinematic Rendering of a Fenestrated Patent Foramen Ovale Within a Left-Sided Atrial Septal Pouch.","authors":"Amy Avakian, Muhammad Umair","doi":"10.14797/mdcvj.1869","DOIUrl":"10.14797/mdcvj.1869","url":null,"abstract":"<p><p>Photorealistic cinematic rendering disclosed a fenestrated patent foramen ovale embedded within the otherwise fused inferior wall of a left-sided septal pouch. The fenestrations were not resolvable on conventional axial, multiplanar, or oblique long-axis reformats because of partial volume averaging across the thin septum primum. This case illustrates a diagnostic ceiling of cross-sectional reformatting and a complementary anatomic role for cinematic rendering in thin-tissue interatrial septal pathology.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"106-109"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009034","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Maya Medicine: An Analysis of the Maya Concept of the Cardiovascular System.","authors":"Juan J Olivero, Garabed Eknoyan","doi":"10.14797/mdcvj.1844","DOIUrl":"10.14797/mdcvj.1844","url":null,"abstract":"<p><p>Among pre-Columbian cultures, the Maya (ca. 2000 BCE-1697 CE) are widely considered to have built one of the most culturally advanced societies in the Americas. Their legacy features advanced hieroglyphic writing, monumental architecture, the invention of zero, and a highly precise calendar used to record elite history and regulate agriculture. Practiced by shamans as part of their religious duties, Maya medicine was a rich oral tradition passed down through generations. It was a holistic discipline that blended religious, magical, and psychic elements with limited scientific knowledge. Rather than being strictly theoretical, it was a practical framework made up of symptom lists, incantations, rituals, and therapeutic recipes. Disease was attributed to evil spirits or divine punishment, and treatment consisted mostly of plant-based remedies. Their knowledge of anatomy was scant, and their concept of physiology was a vague homeostasis of cold and hot. Pulse-taking was used to assess imbalances, and bleeding was used to restore health. Ritual human sacrifice and cardiac extraction helped formulate their concept of the cardiovascular system. The heart was considered the site of vital power where circulating blood was vitalized. Blood was considered a life force that enlivened individuals and made them strong. The heart was also linked to moods and emotions.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"119-125"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588212/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009100","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Setting Sail.","authors":"Philip Alexander","doi":"10.14797/mdcvj.1946","DOIUrl":"https://doi.org/10.14797/mdcvj.1946","url":null,"abstract":"<p><p>These contrasting images are presented by Philip Alexander, MD, a native Texan, retired physician, and accomplished musician and artist. After 41 years as an internal medicine physician, Dr. Phil retired from his practice in College Station in 2016. A lifelong musician and former music professor, he often performs as an oboe soloist for the Brazos Valley Symphony Orchestra. He began exploring visual art in 1980, evolving from pencil sketches-including an official White House portrait of President Ronald Reagan-to the computer-generated drawings featured in this journal. His images, which first appeared in this journal in the spring of 2012, are his own original creations. If you would like to see your art published in the <i>Methodist DeBakey Cardiovascular Journal</i>, submit your creation online at journal.houstonmethodist.org as a \"Humanities\" entry.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"130-132"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588211/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009143","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hypertrophic Cardiomyopathy is a Disease of Sarcomere Proteins.","authors":"A J Marian","doi":"10.14797/mdcvj.1900","DOIUrl":"10.14797/mdcvj.1900","url":null,"abstract":"<p><p>Hypertrophic cardiomyopathy (HCM) is a primary disease of cardiac myocytes caused by mutations in genes encoding sarcomere proteins. The ensuing phenotype, however, is multicellular, induced by biological and functional changes in myocytes and non-myocyte cardiac cells, particularly fibroblasts. The molecular genetic basis of HCM has been partially elucidated, and over three dozen genes are implicated as causes of HCM. <i>MYBPC3</i>, which encodes myosin binding protein C3, is the most common causal gene, followed by <i>MYH7</i>, which encodes the β-myosin heavy chain (β-MYH or MYH7) protein. Approximately 35% to 40% of HCM cases are caused by mutations in the <i>MYBPC3</i> and <i>MYH7</i> genes. Mutations in genes encoding the thin filament, Z disk, and other sarcomere-associated proteins cause about 10% to 15% of HCM cases. Overall, the genetic discoveries identify HCM as a disease of sarcomere proteins. Nevertheless, the causal genes for a significant fraction of patients with clinically diagnosed HCM remain unknown. This, in part, may reflect the oligogenic nature of HCM in a subset of cases, phenocopy conditions, including overdiagnosis of HCM, and the current approach to genetic screening. Advances in the molecular genetic basis of HCM have ushered in the applications of genetic discoveries to care for patients with HCM, including genetic testing and the development of specific therapies that target the underpinning mechanism of HCM. Identification of additional causal genes and the development of new therapies, including genetic interventions to target and correct the causal mutation, are expected to further impact the clinical management of patients with HCM.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"51-67"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588226/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009129","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dr. George P. Noon's Influence on Our Practice of Medicine.","authors":"James B Young, Arvind Bhimaraj","doi":"10.14797/mdcvj.1945","DOIUrl":"10.14797/mdcvj.1945","url":null,"abstract":"<p><p>Two physicians describe the impact Dr. George P. Noon had on his partners, trainees, referring colleagues, administrators, and Methodist Hospital overall. They share the many ways he influenced their careers at different points in the evolution of cardiovascular medical and surgical patient care. This essay accompanies the In Memoriam that also appears in this issue of the journal.1.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"115-118"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588224/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008972","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetic Dilated Cardiomyopathy: A Review.","authors":"Madelyn Boslough, Matthew R G Taylor, Luisa Mestroni, Raffaela Lombardi","doi":"10.14797/mdcvj.1849","DOIUrl":"10.14797/mdcvj.1849","url":null,"abstract":"<p><p>Dilated cardiomyopathy (DCM) is a leading cause of nonischemic heart failure. Genetic causes are identifiable in 25% to 30% of patients. This review describes the pathophysiology underlying genetic DCM, the genes most strongly associated with DCM, and both standard and novel therapies for treating genetic DCM.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"68-77"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588208/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Shot Heard Round the World: A Reflection on Emerson's \"Concord Hymn\" and the United States Semiquincentennial.","authors":"James B Young, Justin C Cordova","doi":"10.14797/mdcvj.1874","DOIUrl":"https://doi.org/10.14797/mdcvj.1874","url":null,"abstract":"<p><p>During the 250th anniversary year of the United States of America, paeans, songs, poems, speeches, and monuments abound. Since its founding, countless efforts have been made to celebrate the country's annual accomplishments, including ever grander holiday fetes on the fourth of July. By all accounts, 2026 has been a yearlong chant of \"U-S-A!\" despite major contemporary challenges, including a war and global economic uncertainty. In retrospect, similar conditions were present during the 1775 to 1783 United States Revolutionary War with 13 British colonies in North America-a terrifying event that resulted in much destruction, suffering, and countless deaths. It also led to the propagation of a genre of revolutionary \"war poetry,\" sparked by the pathos of military conflict that developed over millennia. Ralph Waldo Emerson (1803-1882) was a quintessential American author and Transcendentalist whose literary efforts attempted to surpass ordinary experience, often through a theological or spiritual bent. His \"Concord Hymn,\" written in 1837, was commissioned to eulogize the historic 1775 opening engagement of the Revolutionary War and was later sung at the dedication of its battle monument. Perhaps the poem is best remembered for the closing lines of its first stanza, \"Here once the embattled farmers stood/And fired the shot heard round the world.\"</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"126-129"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588227/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009191","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cholesterol: Facts and Opinions by a Non-lipid Cardiologist.","authors":"Robert Roberts","doi":"10.14797/mdcvj.1826","DOIUrl":"10.14797/mdcvj.1826","url":null,"abstract":"<p><p>Plasma low-density lipoprotein cholesterol (LDL-C) is the main cause of coronary artery disease (CAD). All cells synthesize their own cholesterol when needed to form membranes for the cell wall and other cellular structures, including the synthesis of vitamin D. Cholesterol in excess of the cell's needs is dumped into the bloodstream to be metabolized by the liver and secreted into the intestine. Of the circulating cholesterol, 80% is derived from this excessive endogenous cholesterol, with only a small proportion from diet. Thus, it is not surprising that lowering plasma LDL-C to levels as low as 5 to 10 mg/dL is associated with further reduction in cardiac events and no apparent increase in adverse events. Individuals at increased risk for CAD should embrace a more favorable lifestyle and simultaneously be started on a lipid-lowering agent, which initially should be a statin. Taken by hundreds of millions of patients for over three decades, statins are highly efficacious and safe and are said to be safer than aspirin. Although the plasma LDL-C level for optimal efficacy and safety has yet to be determined, the future goal is likely to be around 40 mg/dL, a level observed in infants.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"22-27"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588225/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149008969","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Is the Commitment to LDL-C Eternal?","authors":"Allan D Sniderman","doi":"10.14797/mdcvj.1845","DOIUrl":"10.14797/mdcvj.1845","url":null,"abstract":"<p><p>Low-density lipoprotein cholesterol (LDL-C) has been the cornerstone of cardiovascular risk assessment and therapy since 1988. Every guideline group and consensus report has repeated and reinforced this commitment. Yet in 2019, the European Society of Cardiology/European Atherosclerosis Society Lipid Guidelines declared that (1) apolipoprotein B (apoB) was a more accurate marker of cardiovascular risk than LDL-C or non-high-density lipoprotein cholesterol (HDL-C); (2) that apoB was a more accurate marker of the adequacy of therapy to lower cardiovascular risk than LDL-C or non-HDL-C; (3) that apoB was essential to diagnose disorders such as type III hyperlipoproteinemia and familial combined hyperlipidemia; and (4) that apoB could be measured more accurately, particularly at low concentrations, than LDL-C or non-HDL-C. Yet LDL-C remained the dominant metric for clinical care in their recommendations, and in the 7 years since, there has been minimal organized teaching about apoB in either Europe or the United States. In 2026, the American College of Cardiology/American Heart Association/Multisociety dyslipidemia guideline followed virtually the same course. Based on the evidence, apoB was ranked above both LDL-C and HDL-C for assessment of risk and the effectiveness of therapy. However, the actual recommendations ranked apoB below both and, as written, make it unlikely that apoB will be commonly used in clinical care for either purpose. How can this be, and what can we learn? LDL-C transformed cardiovascular care, and the effort to teach patients and doctors about LDL-C is unprecedented. How much of the resistance to apoB is the concern that it is too late to change? How many who write the guidelines have routinely used apoB in their clinical care? I believe that an unreasonable commitment to continuity of message and too closed a process of deliberation and review have produced this unprecedented contradiction between the guideline recommendations and the evidence. This article outlines the critical need to re-evaluate the framework and procedural standards governing our current guidelines.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"15-21"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588204/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting Lipoprotein(a): A New Era in Cardiovascular Disease Prevention.","authors":"Yakubu Bene-Alhasan, Vijay Nambi, Layla A Abushamat, Christie M Ballantyne","doi":"10.14797/mdcvj.1836","DOIUrl":"10.14797/mdcvj.1836","url":null,"abstract":"<p><p>Lipoprotein(a), or Lp(a), is a genetically determined low-density lipoprotein-like particle that is elevated in approximately one in five individuals worldwide and represents an independent causal risk factor for atherosclerotic cardiovascular disease and calcific aortic stenosis. Elevated Lp(a) levels contribute significantly to residual cardiovascular risk despite optimal management of traditional risk factors. The pathogenicity of Lp(a) derives from its unique structure and enrichment with oxidized phospholipids, conferring proinflammatory, prothrombotic, and proatherogenic properties. Current guidelines recommend at least one-time universal screening, with elevated levels informing personalized decisions regarding lipid-lowering therapy intensification. Novel unapproved therapies, including an antisense oligonucleotide (pelacarsen), small interfering RNAs (olpasiran, lepodisiran), and an oral small molecule (muvalaplin), have demonstrated Lp(a) reductions of up to 99% and are being tested in ongoing phase 3 cardiovascular outcomes trials to determine whether pharmacologic Lp(a) lowering translates into reduced cardiovascular events. We discuss current knowledge on genetics, biology, epidemiology, and measurement of Lp(a), examine its causal association with cardiovascular disease, and discuss emerging therapeutic strategies that may usher in a new era of cardiovascular disease prevention.</p>","PeriodicalId":39207,"journal":{"name":"Methodist DeBakey cardiovascular journal","volume":"22 4","pages":"28-39"},"PeriodicalIF":0.0,"publicationDate":"2026-09-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13588214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149009128","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}