Methodist DeBakey cardiovascular journal最新文献

Chronic limb-threatening ischemia (CLTI) is a severe form of peripheral arterial disease that portends high morbidity and mortality. Patients may undergo various endovascular or open procedures with the goal of limb salvage. No-option CLTI patients represent a vulnerable population for whom conventional options have been exhausted, or anatomy precludes any attempts at revascularization, often resulting in amputation. Stem cell therapy is under investigation for these no-option CLTI patients. Regardless of revascularization technique, these patients are clinically challenging and require multidisciplinary efforts to achieve the best outcomes. Here we present a patient with unfavorable anatomy who underwent stem cell therapy injection for a nonhealing right first toe wound, and we include points to remember when considering stem cell treatment in patients with CLTI.

Takotsubo cardiomyopathy, also known as stress cardiomyopathy, is a reversible form of cardiomyopathy characterized by reduced ejection fraction with regional wall motion abnormalities, elevated cardiac enzyme levels, and signs of ischemia on electrocardiogram despite the absence of obstructive epicardial coronary artery disease. It is often preceded by intense emotional or physical illness stressors. This case describes a 65-year-old female patient who likely developed takotsubo cardiomyopathy precipitated by the stress of diverticulitis.

Heart failure (HF) remains a leading cause of death worldwide, with increasing prevalence and burden. Despite extensive research, a cure for HF remains elusive. Traditionally, the study of HF's pathogenesis and therapies has relied heavily on animal experimentation. However, these models have limitations in recapitulating the full spectrum of human HF, resulting in challenges for clinical translation. To address this translational gap, research employing human cells, especially cardiomyocytes derived from human-induced pluripotent stem cells (hiPSC-CMs), offers a promising solution. These cells facilitate the study of human genetic and molecular mechanisms driving cardiomyocyte dysfunction and pave the way for research tailored to individual patients. Further, engineered heart tissues combine hiPSC-CMs, other cell types, and scaffold-based approaches to improve cardiomyocyte maturation. Their tridimensional architecture, complemented with mechanical, chemical, and electrical cues, offers a more physiologically relevant environment. This review explores the advantages and limitations of conventional and innovative methods used to study HF pathogenesis, with a primary focus on ischemic HF due to its relative ease of modeling and clinical relevance. We emphasize the importance of a collaborative approach that integrates insights obtained in animal and hiPSC-CMs-based models, along with rigorous clinical research, to dissect the mechanistic underpinnings of human HF. Such an approach could improve our understanding of this disease and lead to more effective treatments.

John McCrae (1872-1918) was a Canadian physician, poet, and soldier who fought and died in the First World War. He penned perhaps his most memorable and lasting poem, "In Flanders Fields," shortly after the death of a comrade at the Second Battle of Ypres in 1915. The poem gained almost instant popularity, being used for recruiting efforts and victory bond sales throughout the remainder of the war, and solidified forever the symbol of the poppy as a memorial token for the service members who had perished. His death towards the end of the war, like that of so many others in the perilous years between 1914 and 1918, cut short the trajectory of what had already amounted to a brilliant career. As a close friend of such titans of medicine as William Osler and Harvey Cushing, as well as acquainted with the likes of Rudyard Kipling, it is not difficult to imagine the impact that his passing had upon the future of medicine and literature.

Cardiovascular diseases are the number one cause of death worldwide and in the United States (US). Cardiovascular diseases frequently progress to end-stage heart failure, and curative therapies are extremely limited. Intense interest has focused on deciphering the cascades and networks that govern cardiomyocyte proliferation and regeneration of the injured heart. For example, studies have shown that lower organisms such as the adult newt and adult zebrafish have the capacity to completely regenerate their injured heart with restoration of function. Similarly, the neonatal mouse and pig are also able to completely regenerate injured myocardium due to cardiomyocyte proliferation from preexisting cardiomyocytes. Using these animal models and transcriptome analyses, efforts have focused on the definition of factors and signaling pathways that can reactivate and induce cardiomyocyte proliferation in the adult mammalian injured heart. These studies and discoveries have the potential to define novel therapies to promote cardiomyocyte proliferation and repair of the injured, mammalian heart.

Peripheral arterial disease (PAD) represents a global health concern with a rising prevalence attributed to factors such as obesity, diabetes, aging, and smoking. Among patients with PAD, chronic limb-threatening ischemia (CLTI) is the most severe manifestation, associated with substantial morbidity and mortality. While revascularization remains the primary therapy for CLTI, not all patients are candidates for such interventions, highlighting the need for alternative approaches. Impaired angiogenesis, the growth of new blood vessels, is a central feature of PAD, and despite decades of research, effective clinical treatments remain elusive. Epigenetics, the study of heritable changes in gene expression, has gained prominence in understanding PAD pathogenesis. Here, we explore the role of epigenetic regulation in angiogenesis within the context of PAD, with a focus on long non-coding RNAs and fibroblast-endothelial cell transdifferentiation. Additionally, we discuss the interplay between metabolic control and epigenetic regulation, providing insights into potential novel therapeutic avenues for improving PAD treatments. This review aims to offer a concise update on the application of epigenetics in angiogenesis and PAD research, inspiring further investigations in this promising field.

Current therapies for heart failure aim to prevent the deleterious remodeling that occurs after MI injury, but currently no therapies are available to replace lost cardiomyocytes. Several organisms now being studied are capable of regenerating their myocardium by the proliferation of existing cardiomyocytes. In this review, we summarize the main metabolic pathways of the mammalian heart and how modulation of these metabolic pathways through genetic and pharmacological approaches influences cardiomyocyte proliferation and heart regeneration.

Rapid advancements in artificial intelligence (AI) have revolutionized numerous sectors, including medical research. Among the various AI tools, OpenAI's ChatGPT, a state-of-the-art language model, has demonstrated immense potential in aiding and enhancing research processes. This review explores the application of ChatGPT in medical hospital level research, focusing on its capabilities for academic writing assistance, data analytics, statistics handling, and code generation. Notably, it delves into the model's ability to streamline tasks, support decision making, and improve patient interaction. However, the article also underscores the importance of exercising caution while dealing with sensitive healthcare data and highlights the limitations of ChatGPT, such as its potential for erroneous outputs and biases. Furthermore, the review discusses the ethical considerations that arise with AI use in health care, including data privacy, AI interpretability, and the risk of AI-induced disparities. The article culminates by envisioning the future of AI in medical research, emphasizing the need for robust regulatory frameworks and guidelines that balance the potential of AI with ethical considerations. As AI continues to evolve, it holds promising potential to augment medical research in a manner that is ethical, equitable, and patient-centric.

Exercise has a profound effect on cardiovascular disease, particularly through vascular remodeling and regeneration. Peripheral artery disease (PAD) is one such cardiovascular condition that benefits from regular exercise or rehabilitative physical therapy in terms of slowing the progression of disease and delaying amputations. Various rodent pre-clinical studies using models of PAD and exercise have shed light on molecular pathways of vascular regeneration. Here, I review key exercise-activated signaling pathways (nuclear receptors, kinases, and hypoxia inducible factors) in the skeletal muscle that drive paracrine regenerative angiogenesis. The rationale for highlighting the skeletal muscle is that it is the largest organ recruited during exercise. During exercise, skeletal muscle releases several myokines, including angiogenic factors and cytokines that drive tissue vascular regeneration via activation of endothelial cells, as well as by recruiting immune and endothelial progenitor cells. Some of these core exercise-activated pathways can be extrapolated to vascular regeneration in other organs. I also highlight future areas of exercise research (including metabolomics, single cell transcriptomics, and extracellular vesicle biology) to advance our understanding of how exercise induces vascular regeneration at the molecular level, and propose the idea of "exercise-mimicking" therapeutics for vascular recovery.