ABSTRACT
Obstructive sleep apnea (OSA) is an increasingly relevant cause of cardiovascular morbidity worldwide. Although the association between OSA and the cardiovascular system is well-known, the extent of its effects is still a topic of interest, including pathophysiologic mechanisms, cardiovascular sequelae, and OSA therapies and their effects. Commonly described mechanisms of cardiovascular etiologies revolve around sympathetic activation, inflammation, and intermittent hypoxia resulting from OSA. Ultimately, these effects lead to manifestations in the cardiovascular system, such as arrhythmias, hypertension, and heart failure, among others. The resulting sequelae of OSA may also have differential effects based on gender and age; several studies suggest female gender to have more susceptibility to cardiovascular mortality, as well as an increase in age. Furthermore, several therapies for OSA, both established and emerging, show a reduction in cardiovascular morbidity and may even reduce cardiovascular burden. Namely, the establishment of CPAP has led to improvement in hypertension and cardiac function in patients with heart failure and even reduced the progression of early stages of atherosclerosis. Effective management of OSA decreases abnormal neural sympathetic activity, which results in better rhythm control and blood pressure control, both in waking and sleep cycles. With newer therapies for OSA, its effects on the cardiovascular system may be significantly reduced or even reversed after long-term management. The vast extent of OSA on the cardiovascular system, as well as current and future therapeutic strategies, will be described in detail in this review.
ABSTRACT
Inferior vena cava (IVC) filters and endovascular devices are used to mitigate the risk of pulmonary embolism in patients presenting with lower extremity venous thromboembolism in whom long-term anticoagulation is not a good option. However, the efficacy and beneï¬t of these devices remain uncertain, and controversies exist. This review focuses on the current use of IVC ï¬lters and other endovascular therapies in clinical practice. The indications, risks, and beneï¬ts are discussed based on current data. Further research and randomized controlled trials are needed to characterize the patient population that would beneï¬t most from these interventional therapies.
ABSTRACT
Surgical myectomy with concomitant valvular repair has been demonstrated to be safe in the treatment of hypertrophic obstructive cardiomyopathy (HOCM). It is unclear which risk factors predispose patients to develop complete heart block (CHB). We present a unique case of a 66-year-old female with rheumatic heart disease and HOCM admitted for aortic valve (AV) repair and septal myectomy, complicated by a presentation of complete heart block. The histology slide showed fibrosis of the septum, suggesting atrioventricular conduction disease from rheumatic fever, which likely contributed to her presentation. This case highlights the importance of elucidating the etiology of HOCM before undergoing cardiac surgery to guide postsurgical management and improve clinical outcomes.
ABSTRACT
Spontaneous coronary artery dissection (SCAD) is a rare cause of acute coronary syndrome in young patients. Supportive care is recommended for most uncomplicated cases. However, it is unclear if revascularization plays a role in treating SCAD, particularly in the setting of cardiogenic shock. We present a case of a 40-year-old female with no past medical history admitted for SCAD that was complicated by the Society for Cardiovascular Angiography & Interventions (SCAI) stage D cardiogenic shock. She was successfully managed with a percutaneous left ventricular assist device without revascularization. Repeat angiogram showed healed left anterior descending (LAD) SCAD with recovery of left ventricular (LV) systolic function. This case highlights the importance of supportive care in the treatment of SCAD, as revascularization by percutaneous coronary intervention (PCI) and coronary artery bypass graft surgery (CABG) can pose a significant perioperative risk in this patient population.
ABSTRACT
Pericarditis is the inflammation of the pericardial layers. Myopericarditis is diagnosed when this inflammation involves the myocardium, which is marked by elevated serum cardiac enzymes. With these two pathologies sharing overlaps in etiology, we present a case of a young patient with a recent history of COVID-19 infection who presented with pleuritic and positional chest pain with troponin I elevation and serial ECG changes attributed to myopericarditis as a post-viral sequela of severe acute respiratory syndrome coronavirus 2 (SARSCoV2) infection. This case demonstrates the importance of identifying and managing the potential cardiac complications in coronavirus disease 2019 (COVID-19) patients, regardless of age or symptom onset.
ABSTRACT
Hypothyroidism is known to cause bradycardia, but there are no direct comparisons of the level of thyroid-stimulating hormone (TSH) to heart rate (HR) to assist in therapeutic hormonal management. This case presents a patient who developed symptomatic junctional bradycardia and underwent serial TSH testing to attempt to improve her HR while minimizing systemic toxicity from levothyroxine. The patient had a history of paroxysmal atrial fibrillation on beta-blocker therapy and hypothyroidism and developed symptomatic junctional bradycardia following a lapse in her thyroid supplementation. Upon initiation of hormonal replacement therapy, serial TSH levels were assessed as she continued to have episodic bradycardia with severe hypertension. Given the lack of evidence correlating TSH levels to HR, this case report calls for further studies to be conducted to create reliable guidelines in therapeutic management to prevent bradycardia events while minimizing systemic levothyroxine toxicity.
ABSTRACT
West Nile Virus (WNV) myocarditis is nearly fatal, according to the current medical literature. We report a previously healthy 37-year-old Caucasian male who presented to our facility with two days of progressive lower extremity weakness, fever, edema, and shortness of breath found to have left ventricular global hypokinesis with an ejection fraction of less than 25%, consistent with acute viral myocarditis. He also has concomitant WNV meningoencephalitis due to his altered mentation. He was found to have a positive serum WNV IgM suggestive of a diagnosis of WNV myocarditis. He was intubated and was placed on vasoactive pressors for supportive care due to evidence of mixed cardiogenic and septic shock. After two weeks of hemodynamic support, we discovered a near-complete cardiac recovery, as shown on a repeat transthoracic echocardiography (TTE) and a normalized mean arterial blood pressure. This is a unique case report because near fatality is often associated with WNV myocarditis secondary to tachyarrhythmia, and there are currently no documented cases that are suggestive of cardiac recovery from the current literature.
ABSTRACT
Breakdown of the blood-central nervous system barrier (BCNSB) is a hallmark of many neuroinflammatory disorders, such as multiple sclerosis (MS). Using a mouse model of MS, experimental autoimmune encephalomyelitis (EAE), we show that endothelial-to-mesenchymal transition (EndoMT) occurs in the CNS before the onset of clinical symptoms and plays a major role in the breakdown of BCNSB function. EndoMT can be induced by an IL-1ß-stimulated signaling pathway in which activation of the small GTPase ADP ribosylation factor 6 (ARF6) leads to crosstalk with the activin receptor-like kinase (ALK)-SMAD1/5 pathway. Inhibiting the activation of ARF6 both prevents and reverses EndoMT, stabilizes BCNSB function, reduces demyelination, and attenuates symptoms even after the establishment of severe EAE, without immunocompromising the host. Pan-inhibition of ALKs also reduces disease severity in the EAE model. Therefore, multiple components of the IL-1ß-ARF6-ALK-SMAD1/5 pathway could be targeted for the treatment of a variety of neuroinflammatory disorders.
Subject(s)
Encephalomyelitis, Autoimmune, Experimental , Monomeric GTP-Binding Proteins , Multiple Sclerosis , Activin Receptors/metabolism , Animals , Central Nervous System/metabolism , Mice , Mice, Inbred C57BL , Monomeric GTP-Binding Proteins/metabolism , Neuroinflammatory Diseases , Receptor Protein-Tyrosine Kinases/metabolism , Signal TransductionABSTRACT
Calcified amorphous tumor (CAT) of the heart is a rare nonneoplastic tumor. A 71-year-old woman presented with a mobile mass within the left ventricular outflow tract during her elective transthoracic echocardiogram. The patient exhibited no symptoms, and intraoperative findings showed the mass originating from the anterior leaflet of the mitral valve. Transthoracic and transesophageal echo failed to diagnose and localize the origin of the tumor. The tumor origin is unclear, but CAT of the mitral valve may be associated with mitral annular calcification. Surgical excision of the mass definitively diagnoses the tumor and reduces the risk of embolization.