Cardiomyopathy Associated with Anti-SARS-CoV-2 Vaccination: What Do We Know?

The SARS-CoV-2 pandemic has mobilized many efforts worldwide to curb its impact on morbidity and mortality. Vaccination of the general population has resulted in the administration of more than 6,700,000,000 doses by the end of October 2021, which is the most effective method to prevent hospitalization and death. Among the adverse effects described, myocarditis and pericarditis are low-frequency events (less than 10 per 100,000 people), mainly observed with messenger RNA vaccines. The mechanisms responsible for these effects have not been specified, considering an exacerbated and uncontrolled immune response and an autoimmune response against specific cardiomyocyte proteins. This greater immunogenicity and reactogenicity is clinically manifested in a differential manner in pediatric patients, adults, and the elderly, determining specific characteristics of its presentation for each age group. It generally develops as a condition of mild to moderate severity, whose symptoms and imaging findings are self-limited, resolving favorably in days to weeks and, exceptionally, reporting deaths associated with this complication. The short- and medium-term prognosis is favorable, highlighting the lack of data on long-term evolution, which should be determined in longer follow-ups.

Hypertrophic cardiomyopathy masked by pericarditis

Hypertrophic cardiomyopathy used to be regarded as a rare untreatable cause of sudden death in young male athletes. This report is the case of a middle-aged female patient with hereditary hypertrophic cardiomyopathy masked by superimposed pericarditis and revealed by autopsy. This case report illustrates how co-morbidity can hide a crucial diagnosis. This case report also illustrates the value of autopsy disclosing a familial disease that is increasingly recognized and dramatically more treatable than a few decades ago. Sudden death due to hypertrophic cardiomyopathy has become preventable, if the diagnosis is made soon enough. The lessons for patient care from this case include the importance of not missing the diagnosis of hypertrophic cardiomyopathy in female patients.

"Bread and butter" fibrinous pericarditis

Pericarditis is the inflammatory process involving the pericardium as a result of a systemic disease or a primary pericardium disorder.1 The actual incidence of pericarditis is difficult to ascertain,2 most probably because of under-reported or misdiagnosed cases. In the 19th century, Sir William Osler stated that pericarditis was one of the most serious diseases overlooked by practitioners.3 Even so, the rate of hospitalization by this diagnosis is estimated in 3.32 cases per 100,000 person-years, which corresponds to 0.2% of all causes of hospitalization in cardiology centers,4 with an incidence of 1.06% found in autopsy case series.5 Didactically, pericarditis can be morphologically classified in five types: (i) fibrinous; (ii) serous; (iii) purulent; (iv) hemorrhagic; or (v) caseous.6 The image presented herein refers to a typical fibrinous pericarditis, also known as "bread and butter" pericarditis.7 In such an entity, the pericardium, which is regularly smooth and bright, becomes opaque and granular, and macroscopically resembles two pieces of buttered bread pressed together then pulled apart. The histology shows the deposition of fibrin and leukocytic exudate involving the pericardial leaflets.8 Antonio Benivieni (1443-1502), a Florentine physician and a contemporary of Leonardo da Vinci, was assigned the first description of fibrinous pericarditis. However, René Laennec (1781-1826), also known for creating the stethoscope, was the first to register the analogy of this type of pericarditis with "buttered bread"9 in his book, A Treatise on the Diseases of the Chest and on Mediate Auscultation.10 The image presented in Figure 1 was obtained during the autopsy of a 25-year-old man who presented a 5-day history of high-grade fever, odynophagia, chest pain, and bloody sputum. He was hospitalized presenting marked leukocytosis with blasts in the peripheral blood smear and died 14 days later due to multiple organ failure. The autopsy revealed fibrinous pericarditis with a brighter yellow exudate than usual (probably due to hyperbilirubinemia, with direct and indirect bilirubin levels of 4.61 mg/dL and 2.07 mg/dL, respectively), lungs with "beefy red consolidation" due to alveolar edema, hemorrhage, hyaline membrane, and diffuse neutrophilic infiltrate. The patient's bone marrow was hypercellular at the expense of immature myeloid cells with areas of necrosis. The immunohistochemical study evidenced diffuse positivity for myeloperoxidase; CD117-positivity for 30% of the viable cells; CD34-positivity for 1% of the viable cells; and negativity for the terminal deoxynucleotidyl transferase­all of which were consistent with the diagnosis of M3 acute myeloid leukemia (French-American-British classification).11 Acute myocardial infarction, trauma/surgery, infection, uremia, systemic diseases, and neoplasia are among the most common causes of fibrinous pericarditis. Among the neoplasia, lung and breast malignancies stand out, followed by lymphomas and leukemia,12 although pericardial infiltration by nonlymphocytic leukemia is rarer.13 In a large case series of 420 postmortem examinations of the heart in acute leukemia,14 only 20 patients had symptoms of heart disease in life, and 9 of them had pericarditis at autopsy. In only 2 of the 9 patients, the pericarditis was the result of leukemic cell infiltrates into the pericardium; in 4 patients it was hemorrhagic; and in 2 it was pyogenic. Only 1 case remained with uncertain etiology, being fibrinous and unassociated with pericardial leukemic infiltrates, hemorrhages, or organisms, which also occurred in our case. The histopathologic study of the pericardium failed to reveal neoplastic cells, microorganisms, and viral inclusion; therefore, the precise etiology of the pericardial disease was not disclosed.

Pericardite bacteriana com subsequente desenvolvimento de endocardite mural por levedura do complexo Candida parapsilosis / Bacterial pericarditis with subsequent development of mural endocarditis caused by Candida parapsilosis complex yeast

A infecção primária do pericárdio e do endocárdio é rara. Este estudo descreve a evolução de uma criança com cardite reumática aguda, complicada com pericardite infecciosa bacteriana, secundária a abscessos de pele e endocardite fúngica. O tempo prolongado de internação, o uso de cateter venoso central e a antibioticoterapia de amplo espectro foram os fatores que provavelmente favoreceram a colonização, a candidíase invasiva e o desenvolvimento da endocardite por levedura do complexo Candida parapsilosis.(AU)

The primary infection of pericardium and endocardium rarely occurs. This study reports the evolution of a child with acute rheumatic carditis with subsequent pericardial bacterial infection, due to cutaneous abscess and fungal endocarditis. Probably, the long hospital stay, the usage of central venous catheter and the broad-spectrum antibiotics enhanced the colonization, the invasive candidiasis induction and the development of fungal endocarditis by Candida parapsilosis complex yeast.(AU)

Epicardial lesions in Chagas' heart disease reflect an inflammatory process.

OBJECTIVE: Furnish a more detailed anatomicopathological description of the epicardial lesions in chronic chagasic cardiopathy, evaluate their incidence and discuss their probable pathogenesis METHODS: We examined the hearts of 39 chronic chagasic cardiopathy patients who underwent autopsies and submitted to histological analysis the epicardial lesions. RESULTS: Milk spots, characterized by well defined white areas in the epicardium were found in 80% of the cases, mainly on the anterior face of the right ventricle. Histological analysis revealed abrupt fibrous thickening of the epicardium, with no elastic fibers, inflammation or blood vessels. Chagasic rosary, characterized by small round whitish granules deposited sequentially along the coronary vessels were present in 23% of the hearts. They presented the same histological structure as the milk spots, but interestingly were only found immediately above the coronary artery branches. Villous plaque was found on the apex or anterior face of 21% of the hearts. It is characterized by an exophytic aspect, probably due to previous localized pericardial adhesion. Microscopic analysis revealed foci of inflammatory infiltrate and vascular proliferation, typical of epicarditis still under organization. In addition to the lesions described above, the vast majority of cases presented sparse mononuclear inflammatory cells with occasional foci. CONCLUSION: We concluded that epicardial lesions related to chronic chagasic heart disease are probably a result of epicardial reactions to chronic inflammatory process.

Lesões epicárdicas na cardiopatia chagásica são reflexo de processo inflamatório / Epicardial lesions in Chagas' heart disease reflect an inflammatory process

OBJETIVO: Fornecer descrição anatomopatológica detalhada das lesões epicárdicas na cardiopatia chagásica crônica, avaliar sua incidência e discutir sua provável patogênese. MÉTODOS: Foram examinados os corações de 39 pacientes portadores de cardiopatia chagásica crônica submetidos a necropsia, com exame histológico das lesões epicárdicas. RESULTADOS: Manchas lácteas, caracterizadas por áreas bem definidas de cor branca do epicárdio, foram observadas em 80 por cento dos casos, predominantemente na face anterior do ventrículo direito. Histologicamente, foi observado abrupto espessamento fibroso do epicárdio, não havendo fibras elásticas, processo inflamatório ou vasos sangüíneos. Rosário chagásico, caracterizado por pequenos grânulos esbranquiçados, arredondados, seqüencialmente dispostos ao longo dos vasos coronarianos, esteve presente em 23 por cento dos corações. Apresentavam a mesma estrutura histológica que as manchas lácteas, mas de forma intrigante ocorriam apenas imediatamente acima de ramos arteriais coronarianos. Placa vilosa esteve presente na ponta ou na face anterior de 21 por cento dos corações, caracterizando-se pelo aspecto exofítico, provavelmente em decorrência da adesão pericárdica prévia localizada. A microscopia, foram observados focos de infiltrado inflamatório e proliferação vascular, típicos de epicardite em organização. Além das lesões descritas, havia células inflamatórias mononucleares esparsas, com agrupamentos focais, no epicárdio de praticamente todos os casos. CONCLUSÃO: Concluímos que as lesões epicárdicas da cardiopatia chagásica crônica são provavelmente conseqüentes à reação do epicárdio ao processo inflamatório crônico.

OBJECTIVE: Furnish a more detailed anatomicopathological description of the epicardial lesions in chronic chagasic cardiopathy, evaluate their incidence and discuss their probable pathogenesis METHODS: We examined the hearts of 39 chronic chagasic cardiopathy patients who underwent autopsies and submitted to histological analysis the epicardial lesions. RESULTS: Milk spots, characterized by well defined white areas in the epicardium were found in 80 percent of the cases, mainly on the anterior face of the right ventricle. Histological analysis revealed abrupt fibrous thickening of the epicardium, with no elastic fibers, inflammation or blood vessels. Chagasic rosary, characterized by small round whitish granules deposited sequentially along the coronary vessels were present in 23 percent of the hearts. They presented the same histological structure as the milk spots, but interestingly were only found immediately above the coronary artery branches. Villous plaque was found on the apex or anterior face of 21 percent of the hearts. It is characterized by an exophytic aspect, probably due to previous localized pericardial adhesion. Microscopic analysis revealed foci of inflammatory infiltrate and vascular proliferation, typical of epicarditis still under organization. In addition to the lesions described above, the vast majority of cases presented sparse mononuclear inflammatory cells with occasional foci. CONCLUSION: We concluded that epicardial lesions related to chronic chagasic heart disease are probably a result of epicardial reactions to chronic inflammatory process.

Pericardite aguda pós-influenza ou pós-vacina antiinfluenza: atualização / Acute pericarditis following Influenza infection or vaccine: update

As pericardites com etiologias idiopática e viral se confundem. Nem sempre existem achados clínicos que distinguem uma da outra, e é provável que muitos casos de pericardite idiopática sejam causados por infecções virais não reconhecidas. A influenza, virose que acomete principalmente o trato respiratório, pode também desencadear complicações cardíacas, como miocardites e pericardites. Por sua potencialidade mórbida, tem sido, nos últimos anos, alvo de campanhas nacionais de imunização por vacina. A pericardite pós-influenza e a pericardite pósvacina antiinfluenza são doenças cada vez mais enfrentadas pelo médico. O presente trabalho objetiva revisar a literatura mundial, fazendo uma atualização do tema delimitado

Cholesterol pericarditis. A specific but rare cause of pericardial disease.

During a diagnostic investigation in a 40-year-old male with pericardial effusion associated with hypothyroidism, cholesterol pericarditis was detected. We report a brief review on the etiopathogeny, clinical findings, and therapeutical possibilities of this entity.