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Thyroid dysfunction is a common incidental finding among healthy individuals. It can affect various organs of the body, including the heart. Among many other heart complications, it can lead to pericardial effusion by causing increased permeability of albumin across the pericardial membrane that leads to exudative pericardial effusion. In hypothyroidism, the fluid collection process occurs over a period of months, giving enough time for the pericardial membrane to stretch and accommodate the fluid within itself without causing any symptoms. Eventually, the pericardial membrane stretches to its maximum capacity and has no room to accommodate any more fluid, resulting in cardiac tamponade in the patients. Patients with hypothyroidism-related cardiac tamponade usually remain asymptomatic or present with atypical symptoms such as bradycardia and a normal heart rate or high blood pressure, and the diagnosis comes into light only when patients present to the hospital with hemodynamic instability. In these cases, echocardiography successfully detects large pericardial effusion with collapsed cardiac chambers. To treat hypothyroidism-related cardiac tamponade, treating the underlying condition has been very successful in the majority of the asymptomatic patients, but pericardiocentesis is required in emergencies to relieve symptoms of patients presenting with hemodynamic instability. We believe hypothyroidism-related cardiac tamponade is a preventable condition if detected and treated in outpatient settings by family physicians. This will prevent occurrence of various complications arising from hypothyroidism, including pericardial effusion. This will lead to a better quality of life among patients with the added benefit of reduced health care burden due to reduced frequency of hospital admissions of acutely ill patients.

Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death worldwide. Many patients with acute exacerbations need intensive care. There are many cardiovascular risk factors and comorbid conditions linked with COPD. Troponin elevation is used for the diagnosis of myocardial infarction. However, it is commonly elevated in patients with COPD. This systematic review followed the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. PubMed and Scopus were searched for relevant articles. A total of 383 papers were identified. Out of the 383 papers, only 30 papers remained for final synthesis after removing duplicates, screening for relevant articles, and assessing eligibility criteria. After the quality appraisal, 11 papers were chosen for inclusion in this study. COPD is characterized by obstruction and inflammation of the airways. It is caused mainly by smoking, by causing harmful changes in the structure of the airways. It usually presents with dyspnea, cough, and/or production of sputum. Troponins are regulatory proteins found in the myocardium and skeletal muscles. The cause of its elevation in COPD and acute exacerbated chronic obstructive pulmonary disease (AECOPD) remains unclear. However, several reasons and factors have been suggested. The most intriguing fact is that high troponin in COPD, especially in exacerbations, has been linked in many articles to a higher risk of death. Furthermore, it could serve as a tool for better assessment and management of COPD patients. We found that troponin predicts death and poor outcomes in COPD and AECOPD. The exact mechanism of its elevations is not clear. We believe it can be a valuable tool for clinicians in better managing COPD and assessing the severity of the exacerbations.

Hematological malignancies often develop due to a vast spectrum of environmental and genetic etiologies. Chronic neutrophilic leukemia (CNL) can be described as a BCR-ABL1 (Philadelphia chromosome)-negative myeloproliferative neoplastic disease with various genetic mutations that may directly or indirectly play a role in its pathogenesis. A well-established mutation in CNL is the CSF3R (a cytokine receptor) which has been incorporated into the diagnostic criteria for the disease. However, evidence of other mutations such as SETBP1, ASXL1, and TET2 has also shed more light on the pathogenesis of this condition. Due to the unknown incidence and heterogeneous presentation of the disease, the diagnosis and management are often difficult and lack satisfactory data. The purpose of this review is to yield further insight into a disease that lacks awareness in the medical community. Using PubMed as a database, relevant studies and case reports were reviewed. The data compiled were used to acknowledge the disease in terms of etiology, clinical manifestation, molecular pathogenesis, and available treatment modalities. Though existing treatment modalities have been shown to induce clinical improvement, the outcomes are not reliable, and further research is required to reach a comprehensive “standard of care” for the disease.