Pericardial diseases in patients with hypothyroidism

Heart ◽  
2019 ◽  
Vol 105 (13) ◽  
pp. 1027-1033 ◽  
Author(s):  
Johnny Chahine ◽  
Chandra K Ala ◽  
James L Gentry ◽  
Kevin M Pantalone ◽  
Allan L Klein

Hypothyroidism is a well-known cause of pericardial effusion (with an incidence of 3%–37%) and can cause cardiac tamponade in severe cases. In this review, we present the current knowledge on the epidemiology of hypothyroid-induced pericardial diseases, the mechanism through which low thyroid hormone levels affect the pericardium, the associated clinical manifestations, diagnostic tests and management options. Hypothyroidism causes pericardial effusion through increased permeability of the epicardial vessels and decreased lymphatic drainage of albumin, resulting in accumulation of fluid in the pericardial space. Interestingly, autoimmunity does not seem to play a major role in the pathophysiology, and a majority of effusions are asymptomatic due to slow fluid accumulation. The diagnosis is generally made when the pericardial disease is associated with an elevated thyroid-stimulating hormone level, and other secondary causes are excluded. Management consists of thyroid replacement therapy, along with pericardial drainage in case of tamponade.In conclusion, hypothyroidism-induced pericardial diseases are underdiagnosed. Initiating treatment early in the disease process and preventing complications relies on early diagnosis through systematic screening per guidelines.

2016 ◽  
Author(s):  
Terrence D. Welch ◽  
Kyle W Klarich ◽  
Jae K. Oh

The pericardium consists of a fibrous sac and a serous membrane. Because of its simple structure, the clinical syndromes involving the pericardium are relatively few but vary substantially in severity. Cardiac tumors may be either primary or secondary and either benign or malignant, with attachment sites throughout the endocardium. Cardiovascular trauma should be suspected in all patients with chest injuries or severe generalized trauma. Cardiovascular injury may be either blunt or penetrating. This review covers pericardial disease, cardiac tumors, and cardiovascular trauma. Figures show an electrocardiogram in acute pericarditis; acute pericarditis with delayed gadolinium enhancement of the pericardium shown with cardiac magnetic resonance imaging; underlying cause of pericardial effusion requiring pericardiocentesis; pericardial pressure-volume curves; large pericardial effusion with swinging motion of the heart resulting in electrical alternans; typical pulsed-wave Doppler pattern of tamponade; underlying causes of constrictive pericarditis in patients undergoing pericardiectomy; pericardial calcification seen on a chest radiograph; thickened pericardium; typical pulsed-wave Doppler pattern of constrictive pericarditis; typical mitral annular tissue velocities in constrictive pericarditis; a diagnostic algorithm for the echocardiographic diagnosis of constrictive pericarditis; simultaneous right ventricular and left ventricular pressure tracings in restrictive cardiomyopathy; computed tomographic scan showing inflammatory constrictive pericarditis; systolic and diastolic transesophageal echocardiographic images of a large left atrial myxoma attached to the atrial septum; a decision tree of management options for patients with suspected papillary; transesophageal echocardiographic examples of aortic valve, mitral valve, left ventricular outflow tract, and tricuspid valve papillary fibroelastomas; and transesophageal short-axis view of the descending thoracic aorta in a hypotensive patient after a motor vehicle accident. The table lists tamponade versus constriction versus restrictive cardiomyopathy. This review contains 18 highly rendered figures, 1 table, and 77 references.


2019 ◽  
Vol 47 (5) ◽  
pp. 2262-2268
Author(s):  
Caie Li ◽  
Qiming Zhao ◽  
Xiangyang Wu ◽  
Jing Yu

Tuberculosis is still the leading cause of pericardial disease in developing nations. A definite diagnosis of tuberculosis is usually relatively difficult, especially when its manifestations are not typical. We report a 19-year-old man who presented with chest obstruction, shortness of breath, edema of the lower extremities, and mild fever for 14 days. The manifestations of tuberculosis pneumonia were not typical, except for a small high-density shadow in the left upper lung field near the pleura, with a small amount of pleural effusion on chest computed tomography. The tuberculin skin test, acid-fast stain of sputum and pericardial effusion, and bacterial culture showed negative results. Echocardiography showed three free-floating irregular masses in a large amount of pericardial effusion. The masses and exudates were removed by pericardiectomy. The masses were composed of hyperplastic granulation tissue and dead tissue without a normal architecture, mixed with numerous caseous substances, which confirmed the diagnosis of tuberculous pericarditis. This is a unique report of a patient who presented with tuberculous pericarditis with multiple solid masses in a large amount of pericardial effusion, without typical clinical manifestations of tuberculosis.


Author(s):  
Bernard Paelinck ◽  
Aleksandar Lazarević ◽  
Pedro Gutierrez Fajardo

Echocardiography is the cornerstone for the diagnosis of pericardial disease. It is a portable technique allowing morphological and functional multimodality (M-mode, two-dimensional, Doppler, and tissue Doppler) imaging of pericardial disease. In addition, echocardiography is essential for differential diagnosis (pericardial effusion vs pleural effusion, constrictive pericarditis vs restrictive cardiomyopathy) and allows bedside guiding of pericardiocentesis. This chapter describes normal pericardial anatomy and reviews echocardiographic features of different pericardial diseases and their pathophysiology, including pericarditis, pericardial effusion, constrictive pericarditis, pericardial cyst, and congenital absence of pericardium.


Aetiology 460Syndromes of pericardial disease 461Acute pericarditis without effusion 461Pericardial effusion with or without tamponade 462Constrictive pericarditis 464Effusive-constrictive pericarditis 465Calcific pericarditis without constriction 465Viral pericarditis 466Tuberculous pericarditis 468Uraemic pericarditis 469Neoplastic pericardial disease 470Myxoedematous effusion ...


ESC CardioMed ◽  
2018 ◽  
pp. 1561-1563
Author(s):  
Michael Arad ◽  
Yehuda Adler

Pericardial diseases manifest as a part of a systemic condition or in isolation. The clinical presentation is driven by inflammation (i.e. pericarditis), excess fluid accumulation (pericardial effusion), or pericardial stiffening (constriction). Corresponding symptoms and signs may include pain, stigmata of systemic inflammation, atrial arrhythmia, haemodynamic compromise, or chronic heart failure. Pericardial tumours and space-occupying lesions are uncommon and may be incidentally detected or present as one of the above-mentioned forms of pericardial disease. Aetiological work-up is usually unnecessary in acute pericarditis but is indicated in the incessant/chronic form and to exclude bacterial infection. Pericardial effusions need to be investigated when large and promptly evacuated when associated with haemodynamic compromise. The hallmark of constrictive physiology is ventricular interdependence. It is important to distinguish transient constriction and to treat inflammation according to aetiology prior to making a decision on surgical relief by pericardiectomy.


2018 ◽  
Author(s):  
David W. Schoenfeld

Diseases of the pericardium represent a wide range of clinical syndromes that vary substantially in severity, from a benign pericardial effusion to fatal constrictive pericarditis or hemopericardium. Acute pericarditis is the most common pericardial disease, with viral and idiopathic as the most frequent etiologies. Typically, acute pericarditis can be managed as an outpatient with dual-agent therapy consisting of aspirin or nonsteroidal anti-inflammatory drug plus colchicine and rarely requires admission. Pericardial effusions are fluid collections in the pericardial cavity. They are a common incidental finding, can be associated with other systemic disease, and at their extreme, cause life-threatening cardiac tamponade. Cardiac tamponade exists on a spectrum with patients who are quasi stable to those where cardiovascular collapse and death are imminent. Cardiac tamponade may be temporized with fluid boluses, but treatment is through pericardiocentesis and occasional surgical intervention. Constrictive pericarditis is progressive process with poor prognosis in which the pericardium becomes rigid and causes diastolic dysfunction, leading to heart failure. Once the diagnosis is made, definitive management is surgical but carries a high operative risk. This review contains 7 highly rendered figures, 5 videos, 3 tables, and 42 references. Key Words: cardiac tamponade, constrictive pericarditis, effusive-constrictive pericarditis, pericardial effusion, pericarditis, pericardiocentesis


2011 ◽  
Vol 12 (2) ◽  
pp. 25-26 ◽  
Author(s):  
Umar Abubakar ◽  
P O Adeoye ◽  
O A Adebo ◽  
V O Adegboye ◽  
E B Kesieme ◽  
...  

Rationale. Pericarditis has been reported as the most common cardiac complication of HIV disease, followed by pericardial effusion. Methods. A retrospective review was conducted of all 68 patients treated for pericardial diseases between August 2003 and July 2008 at University College Hospital, Ibadan, Nigeria. HIV-positive patients (N=42) were compared with those who were HIV negative (N=26). Results. More male than female patients presented with pericardial disease, and the HIV-positive patients were younger than those who were HIV negative. Pericardial effusion was the commonest mode of presentation, accounting for 20 HIV-positive patients (47.7%) and 13 HIV-negative patients (50%). Pericardiostomy was the commonest surgical intervention performed in HIV-positive patients (N=15), while the majority of HIV-negative patients had pericardiocentesis. Conclusion. Pericardial effusion was the commonest cardiac presentation in HIV-positive patients in our setting. We recommend that patients with pericardial effusion be investigated for HIV infection.


ESC CardioMed ◽  
2018 ◽  
pp. 1561-1563
Author(s):  
Michael Arad ◽  
Yehuda Adler

Pericardial diseases manifest as a part of a systemic condition or in isolation. The clinical presentation is driven by inflammation (i.e. pericarditis), excess fluid accumulation (pericardial effusion), or pericardial stiffening (constriction). Corresponding symptoms and signs may include pain, stigmata of systemic inflammation, atrial arrhythmia, haemodynamic compromise, or chronic heart failure. Pericardial tumours and space-occupying lesions are uncommon and may be incidentally detected or present as one of the above-mentioned forms of pericardial disease. Aetiological work-up is usually unnecessary in acute pericarditis but is indicated in the incessant/chronic form and to exclude bacterial infection. Pericardial effusions need to be investigated when large and promptly evacuated when associated with haemodynamic compromise. The hallmark of constrictive physiology is ventricular interdependence. It is important to distinguish transient constriction and to treat inflammation according to aetiology prior to making a decision on surgical relief by pericardiectomy.


Author(s):  
David Adlam

The pericardium forms a continuous sac around the heart, analogous to the pleura surrounding the lungs, and the peritoneum surrounding the abdominal viscera. Between the parietal and visceral layers of the serous pericardium is the pericardial space, which normally contains a small volume of pericardial fluid. The clinical spectrum of pericardial diseases can be divided into: pericarditis, caused by acute inflammation; pericardial effusion, or fluid accumulation in the pericardial space, leading to tamponade; and constrictive pericarditis, caused by chronic infiltration or inflammation leading to pericardial constriction.


Toxins ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 78
Author(s):  
Lachlan A. Bourke ◽  
Christina N. Zdenek ◽  
Edgar Neri-Castro ◽  
Melisa Bénard-Valle ◽  
Alejandro Alagón ◽  
...  

The toxin composition of snake venoms and, thus, their functional activity, can vary between and within species. Intraspecific venom variation across a species’ geographic range is a major concern for antivenom treatment of envenomations, particularly for countries like French Guiana that lack a locally produced antivenom. Bothrops asper and Bothrops atrox are the most medically significant species of snakes in Latin America, both producing a variety of clinical manifestations, including systemic bleeding. These pathophysiological actions are due to the activation by the venom of the blood clotting factors Factor X and prothrombin, thereby causing severe consumptive coagulopathy. Both species are extremely wide-ranging, and previous studies have shown their venoms to exhibit regional venom variation. In this study, we investigate the differential coagulotoxic effects on human plasma of six venoms (four B. asper and two B. atrox samples) from different geographic locations, spanning from Mexico to Peru. We assessed how the venom variation of these venom samples affects neutralisation by five regionally available antivenoms: Antivipmyn, Antivipmyn-Tri, PoliVal-ICP, Bothrofav, and Soro Antibotrópico (SAB). The results revealed both inter- and intraspecific variations in the clotting activity of the venoms. These variations in turn resulted in significant variation in antivenom efficacy against the coagulotoxic effects of these venoms. Due to variations in the venoms used in the antivenom production process, antivenoms differed in their species-specific or geographical neutralisation capacity. Some antivenoms (PoliVal-ICP, Bothrofav, and SAB) showed species-specific patterns of neutralisation, while another antivenom (Antivipmyn) showed geographic-specific patterns of neutralisation. This study adds to current knowledge of Bothrops venoms and also illustrates the importance of considering evolutionary biology when developing antivenoms. Therefore, these results have tangible, real-world implications by aiding evidence-based design of antivenoms for treatment of the envenomed patient. We stress that these in vitro studies must be backed by future in vivo studies and clinical trials before therapeutic guidelines are issued regarding specific antivenom use in a clinical setting.


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