Cardiac neoplasms are rare and the vast majority are metastatic in origin. Symptoms of cardiac neoplasms (primary or metastatic) usually appear late in the course of the disease and are often ignored because of the more severe effects of the primary malignant disorder or its therapy. Consequently, cardiac neoplasms, especially metastatic ones, are often not discovered until autopsy.
To assess the incidence of cardiac neoplasms at autopsy and to determine the sites of origins of metastatic cardiac neoplasms.
The pathology records from consecutive autopsies performed at the University Health Network, Toronto, Ontario, from January 1973 to May 2004 were reviewed. They showed 266 cases of neoplasms involving the heart among 11,432 consecutive autopsies. These cases were then categorized based on their system of origin and further subclassified into specific primary site categories. As well, the type of cardiac tissue affected was noted in 193 cases (72.6%).
The 266 autopsy cases involving cardiac neoplasms represented 2.33% of the total number of autopsies. Among the 266 cases, two neoplasms were primaries, while 264 were metastatic in origin. Metastatic cardiac neoplasms most frequently metastasized from the respiratory system, followed (in order of decreasing frequency) by the hematopoietic, gastrointestinal, breast and genitourinary systems. A minority of metastatic cardiac neoplasms were found to have spread from other systems. Cardiac neoplasms most frequently involved the pericardium, followed (in order of decreasing frequency) by the myocardium, epicardium and endocardium.
There were 132 times more metastatic cardiac neoplasms than primary cardiac neoplasms found in the present study. The most common sites of metastatic origin were the lungs, bone marrow (leukemia/multiple myeloma), breasts and lymph nodes (lymphoma). Leukemias were more prevalent in the present study than in previous studies. The pericardium was the tissue that was most frequently affected by metastatic cardiac neoplasms.
Comment In: Can J Cardiol. 2006 Jan;22(1):8016511961
Inflammatory diseases of the aorta include routine atherosclerosis, aortitis, periaortitis, and atherosclerosis with excessive inflammatory responses, such as inflammatory atherosclerotic aneurysms. The nomenclature and histologic features of these disorders are reviewed and discussed. In addition, diagnostic criteria are provided to distinguish between these disorders in surgical pathology specimens. An initial classification scheme is provided for aortitis and periaortitis based on the pattern of the inflammatory infiltrate: granulomatous/giant cell pattern, lymphoplasmacytic pattern, mixed inflammatory pattern, and the suppurative pattern. These inflammatory patterns are discussed in relation to specific systemic diseases including giant cell arteritis, Takayasu arteritis, granulomatosis with polyangiitis (Wegener's), rheumatoid arthritis, sarcoidosis, ankylosing spondylitis, Cogan syndrome, Behçet's disease, relapsing polychondritis, syphilitic aortitis, and bacterial and fungal infections.
Consensus statement on surgical pathology of the aorta from the Society for Cardiovascular Pathology and the Association For European Cardiovascular Pathology: II. Noninflammatory degenerative diseases - nomenclature and diagnostic criteria.
Surgical aortic specimens are usually examined in Pathology Departments as a result of treatment of aneurysms or dissections. A number of diseases, genetic syndromes (Marfan syndrome, Loeys-Dietz syndrome, etc.), and vasculopathic aging processes involved in vascular injury can cause both distinct and nonspecific histopathologic changes with degeneration of the media as a common denominator. Terminology for these changes has varied over time leading to confusion and inconsistencies. This consensus document has established a revised, unified nomenclature for the variety of noninflammatory degenerative aortic histopathologies seen in such specimens. Older terms such as cystic medial necrosis and medionecrosis are replaced by more technically accurate terms such as mucoid extracellular matrix accumulation (MEMA), elastic fiber fragmentation and/or loss, and smooth muscle cell nuclei loss. A straightforward system of grading is presented to gauge the extent of medial degeneration and synoptic reporting tables are provided. Herein we present a standardized nomenclature that is accessible to general pathologists and useful for future publications describing these entities.
Mitral valve disease (MVD) is a significant clinical problem that is becoming more common in the 21st century. The pathogenesis of MVD seems to be changing and is not well understood.
The present study details the morphological findings in 192 native mitral valves excised over a one-year period at the Toronto General Hospital, Toronto, Ontario. The mean patient age was 59.7+/-12.3 years at operation.
There were 106 men (55.2%) and 86 women (44.8%) in the present study. The most frequent changes in the surgically excised valvular leaflets were fibrosis (78.6%) and thickening (66.2%). Fusion (32.3%) and calcification (25.2%) were common changes at the commissures. Chordae tendineae most often showed evidence of thickening (47.9%) and fibrosis (37.0%). In total, 110 valves showed mitral incompetence (57.3%), 72 showed mitral stenosis (37.5%), and 10 showed a combination of stenosis and incompetence (5.2%).
In the present series, MVD was most frequently caused by postinflammatory (rheumatic) valve disease (RVD) (35.9%), followed by myxomatous degeneration (33.3%). Patients with RVD were usually female (66.7%), while those with myxomatous degeneration were more likely to be male (76.6%). RVD remains a significant problem even though the incidence of acute rheumatic fever with cardiac involvement has declined in Canada. This most likely reflects the current sociodemographic composition of the referral population.
Cites: Am Fam Physician. 2000 Jun 1;61(11):3343-50, 3353-410865929
The St. Jude Medical Silzone (Silzone) mechanical heart valve was voluntarily recalled (January 2000) due to an unusually high incidence of paravalvular leaks. We present the first series of human morphological data on the failure of these valves.
Nineteen Silzone valves were evaluated from the 176 Silzone valves implanted in 147 patients at our institution between 1997 and 1999. Explanted prostheses were fixed in 10% formalin, photographed, and X-rayed. Histological sections were collected from the sewing cuff, accompanying tissues, and thrombus. For comparison, six age-matched SJM-standard valves were similarly analyzed.
Nineteen Silzone valves from 16 patients (10 male, six female, 52.0 +/- 15.2 years) were examined. Significantly more mitral (15/95) prostheses were removed than aortic (4/81) despite the nearly equal number implanted (p = 0.027). Fifteen of the Silzone valves (13/16 patients) were explanted in the early postoperative period (within six months of implantation), although collection continued for eight years after our institution stopped implanting them. The common indications for surgical explantation were paravalvular leak (8/12) and clinically suspected infective endocarditis (IE) (four patients, five valves). IE was not confirmed by histology or culture in any valve. The sewing cuffs of many Silzone valves showed large regions of pannus, granulation tissue, and purulent exudate. Polymorphonuclear leukocytes were more common in the sewing cuff of Silzone valves; however, the cellular infiltrate was superficial when compared to SJM-standard valves.
This is the largest morphologically analyzed series of Silzone explants. It demonstrates a consistent pattern of atypical tissue incorporation into the silver-coated sewing ring particularly in the mitral position. Clinical and morphologic features of IE (sterile) are seen in the early postimplant period. Prosthesis-related problems were almost wholly seen at the mitral site, in our group. Our current data indicate that although early failure due to dehiscence and paravalvular leak is a problem, Silzone valves that "survive" past six months will likely function as well as the SJM-standard prosthesis.
The severe acute respiratory syndrome (SARS) pandemic in Toronto resulted in a large number of autopsies on its victims. We describe the pulmonary pathology of patients who died in the 2003 Toronto outbreak. Autopsy material from the lungs of 20 patients who died between March and July 2003 were characterized by histology, molecular biology, and immunohistochemistry for cytokeratins, thyroid transcription factor-1, CD68, Epstein-Barr virus, cytomegalovirus, and human herpes simplex viruses. Matched controls were obtained from patients who died of other causes over the same interval. The mean duration of illness was 27 days (range 5-108 days). Post-mortem lung tissues from 19 of 20 patients with probable SARS were positive for SARS-associated coronavirus by RT-PCR. Histologically, all patients showed varying degrees of exudative and proliferative phase acute lung injury, evidenced in conventional and immunohistochemical stains by edema, inflammatory infiltrate, pneumocyte hyperplasia, fibrinous exudates, and organization. Eight of 20 patients showed predominantly a diffuse alveolar damage pattern of acute lung injury, six showed predominantly an acute fibrinous and organizing pneumonia pattern, and the remainder showed an admixture of the two patterns. Squamous metaplasia and scattered multinucleate giant cells were present in most cases. Vascular fibrin thrombi were a common finding and were often associated with pulmonary infarcts. Special stains demonstrated vascular endothelial damage of both small- and mid-sized pulmonary vessels. Two cases were complicated by invasive fungal disease consistent with Aspergillosis, and another by coinfection with cytomegalovirus. Our findings indicate that the lungs of patients who die of SARS are almost always positive for the SARS-associated coronavirus by RT-PCR, and may show features of both diffuse alveolar damage and acute fibrinous and organizing pneumonia patterns of acute injury. Cases of SARS may be complicated by coexistent infections and therapy-related lung injury.
Severe acute respiratory syndrome (SARS) is a transmissible febrile respiratory illness caused by a recently discovered coronavirus. Various patterns of disease progression may be observed that have different implications for the prognosis in those affected by SARS. The appearance of the lungs on chest radiographs of patients with this condition may be normal or may include focal airspace opacity or multifocal or diffuse opacities. Thoracic computed tomography (CT) is more sensitive in depicting SARS than is conventional chest radiography, and CT images obtained in patients with normal chest radiographs may show extensive disease and airspace consolidation. However, because the radiologic appearance of SARS is not distinct from that of other diseases that cause lower respiratory tract infection, early identification of SARS will depend in part on the prompt recognition of clusters of cases of febrile respiratory tract illness. To aid in the differential diagnosis and management of SARS, radiologists must be familiar with the typical clinical and histopathologic findings, as well as the radiologic features of the disease.
Efforts to contain severe acute respiratory syndrome (SARS) have been limited by the lack of a standardized, sensitive, and specific test for SARS-associated coronavirus (CoV). We used a standardized reverse transcription-polymerase chain reaction assay to detect SARS-CoV in lung samples obtained from well-characterized patients who died of SARS and from those who died of other reasons. SARS-CoV was detected in all 22 postmortem lung tissues (to 10(9) viral copies/g) from 11 patients with probable SARS but was not detected in any of the 23 lung control samples (sample analysis was blinded). The sensitivity and specificity (95% confidence interval) were 100% (84.6% to 100%) and 100% (85.1% to 100%), respectively. Viral loads were significantly associated with a shorter course of illness but not with the use of ribavirin or steroids. CoV was consistently identified in the lungs of all patients who died of SARS but not in control patients, supporting a primary role for CoV in deaths.
Cites: MMWR Morb Mortal Wkly Rep. 2003 Mar 28;52(12):241-6, 24812680518
To provide an overview of the severe acute respiratory syndrome (SARS) outbreak in Toronto, Ontario, which experienced the largest outbreak outside Asia, and to review what has been learned during the past year.
MEDLINE search of all studies related to SARS, including review of the Centers for Disease Control and Prevention, World Health Organization (WHO), and Health Canada Web sites.
During the SARS outbreak in Toronto, 438 people had been diagnosed as having suspected or probable SARS and 44 people died. Elderly people and those with comorbid illnesses were at greatest risk of complications or death. Transmission was via direct contact with respiratory secretions. The use of gloves, gowns, N95 masks, and eye protection was effective in preventing transmission. No transmission occurred before symptom onset or after recovery. Serologic tests suggest that antibodies may not appear until 28 days after illness onset. Molecular tests give their greatest yield during the second week of illness. The value of ribavirin treatment remains questionable. The combination of interferon plus corticosteroids appears to be better than corticosteroids alone. Postmortem examination revealed pulmonary edema and evidence of diffuse alveolar damage. Very few morphological changes were noted in other organs despite the presence of viral RNA as detected by polymerase chain reaction.
On July 5, 2003, the WHO declared that the SARS outbreak was over. Since then, new cases of SARS have been reported in Asia. With global travel, the disease can rapidly spread throughout the world. Therefore, we must remain vigilant to prevent another pandemic.