Chronic cough is a distressing and prevalent symptom in interstitial lung disease (ILD), significantly impairing quality of life (QoL) and contributing to disease progression, particularly in idiopathic pulmonary fibrosis (IPF). It is associated with physical discomfort, psychological distress, and social isolation and is often refractory to conventional therapies. The pathophysiology of cough in ILD is complex and multifactorial, involving neural hypersensitivity, structural lung changes, inflammatory processes, and comorbid conditions such as gastroesophageal reflux disease (GERD). Evaluating cough in ILD relies on subjective and objective tools to measure its severity, frequency, and impact on daily life, although standardization of these measures remains challenging. Management strategies span pharmacological interventions, including neuromodulators such as opiates, antifibrotic agents, pharmacologic and surgical GERD treatments, and non-pharmacological approaches like behavioral therapies, cough suppression techniques, and pulmonary rehabilitation and physiotherapy. Emerging treatments, such as P2X3 receptor antagonists and airway hydration therapies, offer promising avenues but require further investigation through robust clinical trials. This review aims to demonstrate the importance of addressing cough in ILD as a significant symptom and present objective and subjective methods of quantifying coughs, while providing insights into effective and emerging therapeutic options. By highlighting these potential therapies, we hope to guide healthcare practitioners in considering them through a thorough evaluation of benefits and risks on a case-by-case basis, with relevance both in the U.S. and internationally.

Aim: Deep brain stimulation (DBS) involves implanting electrodes in specific brain areas. High-frequency Stimulation (HFS) and low-frequency Stimulation (LFS) target motor and non-motor symptoms differently. DBS is crucial in Parkinson's disease treatment for managing medication-resistant symptoms and improving quality of life. This review aims to evaluate the differential impact of high-frequency and low-frequency deep brain stimulation (DBS) on motor symptoms in Parkinson's disease (PD) patients. This systematic review adheres to PRISMA guidelines and focuses on clinical studies involving human subjects. Methods: Systematic search in electronic databases (PubMed, Google Scholar, Science Direct, Cochrane Collaboration Database of Randomized Trials) was performed to identify randomized controlled trials (RCTs) up to 13th July 2024. Results: Among 126 pooled patients from 8 RCTs, it was found that LFS significantly improved gait stability, swallowing, and verbal fluency with minimal adverse effects. Conversely, HFS was effective in reducing rigidity and tremor but was associated with potential side effects such as gait and speech impairment. Conclusion: The review highlights the nuanced effects of STN-DBS frequencies in Parkinson's treatment, suggesting high-frequency improves rigidity and tremor but may cause side effects, while low-frequency enhances gait stability and speech, necessitating further research for optimized, patient-specific therapies.

Nonischemic dilated cardiomyopathy (DCM) is a complex cardiovascular condition often characterized by genetic pathogenesis. Comprehensive genetic testing has become a crucial aspect of DCM diagnosis and management, offering insights into prognosis and the identification of at-risk individuals. This case series and mini literature review examines the diagnostic and therapeutic dimensions of DCM, emphasizing the role of genetic evaluation. We delve into distinct genetic pathways associated with DCM and their pathogenetic mechanisms, emphasizing the evolving significance of genetic markers, particularly in cases where arrhythmia risk is heightened. The historical reliance on cardiac morphology to subtype cardiomyopathies is being complemented by the identification of genetic variants, further refining DCM subtypes, and aiding in clinical management.The giant sarcomere protein, titin, is a pivotal determinant of cardiomyocyte stiffness and plays a crucial role in cardiac strain sensing. Titin's extensive size and complexity make it susceptible to dysregulation, which has far-reaching consequences in cardiac disorders. This case series with a literature review explores the molecular mechanisms governing titin-based forces in both health and disease. It highlights the influence of isoform diversity and post-translational modifications on myocardial stiffness and contractility. In the context of cardiac diseases, we discuss how titin properties are altered, focusing on changes in titin stiffness and protein quality control. Notably, we address the pathomechanisms associated with truncation in the titin gene (TTN) in human cardiomyopathy, shedding light on potential therapeutic approaches for conditions such as HFpEF and TTN-truncation cardiomyopathy.This comprehensive understanding of DCM and Titin’s role in cardiac physiology and pathology provides a solid foundation for addressing cases like that of our patients, who were presented with features of heart failure and arrhythmias. Despite immediate and extensive resuscitative measures, the patient's protracted response to the treatment raised questions about the potential underlying genetic factors contributing to their clinical presentation. These cases underscore the importance of genetic evaluation in unraveling the complexity of cardiomyopathies, ultimately enhancing our ability to manage and treat such challenging cases.

Introduction and importance: Congenital bicuspid aortic valve (BAV) is a common cardiac malformation predisposing individuals to aortic stenosis, regurgitation, and aortopathy. This risk persists even after aortic valve replacement (AVR). Case presentation: We report a case of a male in his 60s with a history of BAV who underwent bioprosthetic aortic valve replacement (BVR) and ascending aorta/root repair in 2014. The patient was noncompliant with follow-up and presented nine years later with severe bioprosthetic aortic stenosis and an 8.0 cm ascending aortic aneurysm with no symptoms. Emergent redo BVR and aneurysm repair were successful. Clinical discussion: It should be emphasized that successful outcomes for BAV patients require a lifelong commitment to surveillance, even after surgical intervention. Noncompliance can lead to life-threatening consequences like bioprosthetic valve deterioration or progressive aortic dilation. Conclusion: This case highlights the importance of early BAV diagnosis for ongoing monitoring, accessible follow-up care after complex cardiac procedures, and addressing patient barriers to treatment adherence.

Aortic transection, a near-complete tear through the layers of the aorta, is a critical condition often resulting from trauma such as motor vehicle collisions. The urgency of managing aortic transection underscores the critical need for effective interventions. We report the case of a male in his early 50’s with no significant medical history who presented to the emergency department following a motor vehicle collision, sustaining multiple injuries including a descending thoracic aortic transection. Rapid diagnostic assessment confirmed the severity of the injury, necessitating immediate intervention. Endovascular aortic repair (EVAR) was successfully employed, highlighting its efficacy in managing acute aortic injuries. The patient responded well to treatment, underscoring the importance of timely intervention in improving patient outcomes. This case emphasizes the critical role of rapid diagnostic assessment and endovascular intervention in managing life-threatening thoracic aortic injuries, particularly in the acute setting.