Methodist DeBakey cardiovascular journal最新文献

The pulmonary veins normally drain into the left atrium, with the superior pulmonary veins typically situated anterior and inferior to the right pulmonary arteries. However, anomalies can happen. We encountered an exceedingly rare pulmonary vascular anomaly for a patient presenting with atypical chest pain, where the right superior pulmonary vein aberrantly ran posterior to the right pulmonary artery (RPA) and became compressed between the RPA and the right main bronchus. Coronary computed tomography angiography identified this specific pulmonary vein anomaly but revealed unremarkable coronary arteries.

Fat emboli may occur in patients after traumatic fractures or orthopedic procedures; however, their clinical detection is a very rare finding. Here, we describe a 77-year-old female who was admitted to the emergency department with a fracture of the right humerus. We diagnosed fat embolism after an ultrasound of the right subclavian vein. The embolism was detected by high-intensity transient signals present on the spectral Doppler. While these signals are well known for microembolization in transcranial Doppler, to our knowledge this is the first case report in the medical literature to observe and describe high-intensity transient signals seen in the upper extremities by spectral Doppler. Although it is unusual to detect a fat embolism in transit, we believe clinicians should be aware of this finding, particularly when evaluating high-risk patients.

Transthoracic echocardiography and cardiac magnetic resonance imaging revealed a well-defined globular mass attached to the anterolateral papillary muscle. The mass was hyperintense on T1 and T2 weighted images with suppression of signal on fat saturated and short tau inversion recovery (STIR) images. This imaging established the diagnosis of cardiac lipoma attached to the anterolateral papillary muscle, Papillary muscle is a very rare location of lipoma, which is rarely reported in the literature.

Despite significant advancements in managing acute ST-segment elevation myocardial infarctions, the prevalence of heart failure has not decreased. Emerging paradigms with a focus on reducing infarct size show promising evidence in the improvement of the incidence of heart failure after experiencing acute coronary syndromes. Limiting infarct size has been the focus of multiple clinical trials over the past decades and has led to left ventricular (LV) unloading as a potential mechanism. Contemporary use of microaxial flow devices for LV unloading has suggested improvement in mortality in acute myocardial infarction complicated by cardiogenic shock. This review focuses on clinical data demonstrating evidence of infarct size reduction and highlights ongoing clinical trials that provide a new therapeutic approach to the management of acute myocardial infarction.

The overarching goal of cardiogenic shock (CS) therapy is ensuring long-term survival. In recent years, increasing emphasis has been placed on analyzing mechanisms to improve outcomes in CS. This includes averting in-hospital mortality, modifying the disease process by promoting heart recovery while avoiding multiorgan failure, and circumventing complications related to both CS and treatment strategies deployed to treat CS. Heart replacement therapies represent a viable strategy for long-term survival but are restricted to a small, select percentage of patients. In this review we focus on pathophysiology of the shock state, with an emphasis on addressing reversible etiologies contributing to the decompensated state, optimizing physiological factors for recovery, and identifying therapeutic targets to promote recovery. We also review the known predictors of myocardial recovery, regardless of the etiology of CS. Lastly, we highlight the current gaps in knowledge in this field and support additional high-quality studies focusing on myocardial recovery in CS.

The 12th annual Utah Cardiac Recovery Symposium (U-CARS) in 2024 continued its mission to advance cardiac recovery by uniting experts across various fields. The symposium featured key presentations on cutting-edge topics such as CRISPR gene editing for heart failure, guideline-directed medical therapy for heart failure (HF) with improved/recovered ejection fraction (HFimpEF), the role of extracorporeal cardiopulmonary resuscitation (ECPR) in treating cardiac arrest, and others. Discussions explored genetic and metabolic contributions to HF, emphasized the importance of maintaining pharmacotherapy in HFimpEF to prevent relapse, and identified future research directions including refining ECPR protocols, optimizing patient selection, and leveraging genetic insights to enhance therapeutic strategies.

Chemotherapy has markedly improved cancer outcomes, yet cancer therapy-related cardiac dysfunction (CTRCD) poses a significant challenge, affecting around 10% of patients. CTRCD can be asymptomatic or present with heart failure symptoms. Multimodality imaging, particularly echocardiography, remains pivotal for monitoring cardiac function. Potential biomarkers for CTRCD assessment include troponin and B-type natriuretic peptide. Pharmacological interventions, such as dexrazoxane, angiotensin-converting enzyme inhibitors, and statins, play a crucial role in primary prevention and mitigating cardiotoxicity alongside cardiac rehabilitation programs. Thus, a comprehensive approach is essential for optimal cardiac recovery and improved patient outcomes.

Partial or complete imaging resolution of left ventricular (LV) systolic dysfunction in patients with heart failure with reduced ejection fraction (HFrEF) has gone by many names in the past few decades, including LV recovery, remission, reverse remodeling, and, most recently, improvement. This phenomenon has been described in a variety of clinical scenarios, including removal of an acute myocardial insult, unloading with durable LV assist devices, and treatment with various devices as well as pharmacotherapies, termed guideline-directed medical therapy (GDMT). Irrespective of definition, systolic improvement is associated with improved clinical outcomes compared to persistent systolic dysfunction. In the past few years, systolic improvement has been distinguished from HFrEF as a new clinical entity referred to as HF with improved EF (HFimpEF). Given the relative novelty of this condition, there is a paucity of data with regard to the clinical trajectory and management of this population. In this review, we describe the history of myocardial improvement terminology and explore notable findings that have led to the delineation of HFimpEF. Additionally, we highlight the importance of understanding LV trajectory and the potential opportunity for new GDMT management for clinicians when treating patients with HFimpEF.

Heart failure (HF) affects millions of individuals and causes hundreds of thousands of deaths each year in the United States. Despite the public health burden, medical and device therapies for HF significantly improve clinical outcomes and, in a subset of patients, can cause reversal of abnormalities in cardiac structure and function, termed "myocardial recovery." By identifying novel patterns in high-dimensional data, artificial intelligence (AI) and machine learning (ML) algorithms can enhance the identification of key predictors and molecular drivers of myocardial recovery. Emerging research in the area has begun to demonstrate exciting results that could advance the standard of care. Although major obstacles remain to translate this technology to clinical practice, AI and ML hold the potential to usher in a new era of purposeful myocardial recovery programs based on precision medicine. In this review, we discuss applications of ML to the prediction of myocardial recovery, potential roles of ML in elucidating the mechanistic basis underlying recovery, barriers to the implementation of ML in clinical practice, and areas for future research.

Heart failure with reduced left ventricular (LV) ejection fraction (HFrEF) is a morbid and life-threatening disease, arising secondary to abnormalities of cardiac structure and function that lead to adverse LV remodeling. Implementation of medical and device therapies results in significant improvements in patient outcomes that are associated with reverse LV remodeling and improved LV ejection fraction. This review provides an overview of the pathobiology of reverse LV remodeling in animal models and in HFrEF patients. We emphasize the differences between myocardial recovery and remission as well as the fragile nature of maintaining a state of myocardial remission.