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Background: Cardiac lesions are responsible for approximately 60-70% of sudden deaths. Histopathological examination of heart on autopsy plays an essential role in determining the cause of death. Hence, the present study was undertaken to study the histopathological spectrum of uncommon lesions in the heart and blood vessels that arise from heart, which either proved to be a primary or contributory to the cause of deaths in clinical autopsies. Method: This prospective study was conducted in the Department of Pathology of a Tertiary care hospital over a period of one year from Jan 2020 to Dec 2020. During the study period, a total of 19 cases with uncommon lesions in heart and aorta were studied. The available clinical data had been collected from hospital records in these clinical autopsy cases. Cases of myocardial infarction were excluded. Results: Out of 19 cases, 11 cases were found in the age group of 15-40 years and 8 cases were of 40-50 years. Among 19 cases, 9 (47.4%) were inflammatory lesions, 4 (21.1%) cases of degenerative changes like fatty infiltration of heart, 2 cases of neoplastic etiology and one case each of aneurysm of sinus of Valsalva, mural thrombi in heart, myocardial hypertrophy and one case of aortic dissection. Conclusion: In the present study, inflammatory lesions (myocarditis and tuberculous myocarditis) was the commonest histopathologic finding followed by fatty infiltration of the heart. Other lesions like aortic dissection and aneurysm of sinus of Valsalva were the uncommon lesions seen in our study. Thus, histopathology in autopsy plays a vital role in the study of some of the rare cardiac lesions contributing to the knowledge of pathology. [ABSTRACT FROM AUTHOR]

Summary: Background: The phenotypical profile of cardiovascular malformations in patients with congenital rubella syndrome (CRS) is varied. We aimed to describe the profile of cardiac defects among CRS patients detected in the sentinel CRS surveillance in India during 2016–22. Methods: Sentinel sites enrolled infants with suspected CRS based on presence of cardiac defects, hearing impairment, eye signs, or maternal history of febrile rash illness. Suspected CRS cases underwent detailed systemic examination, including echocardiography and serological investigation for rubella. Cardiac defects were categorized as ‘Simple’ or ‘Complex’ as per the National Heart, Lung, and Blood Institute classification. We compared the distribution of cardiac defects among laboratory confirmed CRS cases and seronegative discarded cases. Findings: Of the 4578 suspected CRS cases enrolled by 14 sites, 558 (12.2%) were laboratory confirmed. 419 (75.1%) laboratory confirmed cases had structural heart defects (simple defects: n = 273, 65.2%, complex defects: n = 144, 34.4%), with ventricular septal defect (42.7%), atrial septal defect (39.4%), patent ductus arteriosus (36.5%), and tetralogy of Fallot as the commonest defects (4.5%). Laboratory confirmed CRS cases had higher odds of left to right shunt lesions (OR = 1.58, 95% CI: 1.15–2.17). This was mainly on account of a significant association of PDA with CRS (OR = 1.77, 95% CI: 1.42–2.21). Mortality was higher among CRS patients with complex heart defects (HR = 2.04, 95% CI: 1.26–3.30). Interpretation: Three-fourths of the laboratory confirmed CRS cases had structural heart defects. CRS patients with complex cardiac defects had higher mortality. Detecting CRS infection early and providing timely intervention for cardiovascular defects is critical for the management of CRS patients. Funding: Ministry of Health and Family Welfare, Govt of India, through Gavi, the Vaccine Alliance.

ABSTRACT: Chronic kidney disease (CKD) is characterized by irreversible morphostructural lesions that can progressively evolve to chronic renal insufficiency and kidney failure. It is known that the heart and kidneys are closely related, and that communication between these organs occurs through a variety of pathways; subtle physiological changes in one of them are compensated by the other. Histopathological cardiac evaluation through routine staining presents a limitation to identify specific or discreet lesions in the cardiomyocytes. This study aimed to evaluate serum troponin levels in cats with CKD, associated with clinical and pathological findings, as well as to correlate the morphostructural cardiac lesions to determine their distribution through macroscopic and histological assessments and anti-cardiac troponin C (cTnC) immunohistochemistry (IHC). To this end, 20 cats (18 diagnosed with CKD and two controls) were selected. Anti-human cTnC IHC was conducted after necropsy and separation in eight regions of each collected heart. Heart fragments from two cats without CKD were used as controls. The anti-human cTnC antibody is useful in detecting cardiac lesions and has shown decreased expression in cardiomyocytes of cats with CKD. Serum troponin was above the reference values in 11/18 (61.11%) animals and decreased expression for the cTnC antibody was observed in individual cardiomyocytes in 9/18 (50%) animals. It was verified that the number of regions with decreased expression for the cTnC antibody in cardiomyocytes is significantly correlated with serum troponin. The anti-human cTnC antibody has been found effective in detecting cardiac lesions and has shown decreased expression in the cardiomyocytes of cats with CKD. Correlation was observed between increased serum cTnI and loss of immunoreactivity at anti-cTnC antibody IHC in cats with CKD, which proves damage to cardiomyocytes secondary to kidney disease.

Purpose: to evaluate the importance of increasing cardioenzymes in the diagnosis of infectious heart lesions.Object and methods: Under observation were 71 children aged 3 to 17 years (average age – 6.6 ± 0.4 years) who received treatment at the clinic of Pediatric Research and Clinical Center for Infectious Diseases. All children in the acute period of illness and 49 patients with follow-up history were identified with levels of creatine phosphokinase (CPK), MВ fractions of creatine phosphokinase (CPK-MВ), lactate dehydrogenase (LDH), C-reactive protein (CRP), aspartate aminotransferase (AST). Follow-up observation and examination of patients was performed after 1 month and after 1 year. All children were examined for a wide range of pathogens of acute respiratory viral infections, active herpes virus infections (EBV, CMV, HHV-6 type), B19 parvovirus, Chlamydophila pneumoniae, Mycoplasma pneumonia, enteroviruses and bacterial respiratory pathogens. All examined patients underwent electrocardiography and echocardiography.The results of the study. In the examined patients with an increased level of “cardioenzymes” (CPK-MВ, LDH, AST) against the background of acute respiratory infection (ARI), a wide range of diseases was established with damage to both the upper respiratory tract and lower (bronchitis, bronchiolitis, pneumonia), and also other infectious nosologies, including respiratory syndrome (infectious mononucleosis, enterovirus and parvovirus infection). The etiological structure was dominated by a group of herpesvirus (53%) and bacterial infections (25%), as well as their combinations. An analysis of the dynamics of the main biochemical and hematological parameters characterizing the severity of the systemic inflammation syndrome (leukocytes, SRE, CRP, CPK), as well as reflecting myocardial injuries and used in cardiology practice (CPK- MВ, LDH, AST), revealed a long-term (within 1 year observations) the preservation of a moderately elevated level of CPK-MВ, unlike other indicators that returned to normal within 1 month. An increase in CPK-MВ was recorded in 79% of patients with drip infections, while the average level of CPK-MВ in the total sample exceeded the normal values by 1.8-2.4 times.Conclusion. It was found that elevated levels of CPK-MВ and LDH can be used as criteria for the formation of dynamic observation groups and early rehabilitation.

Background: To evaluate the efficacy and safety of ascending aortoiliac bypass surgery for one-stage repair of adult coarctation of the aorta (CoA) and concomitant cardiac disease. Methods: From March 2012 to October 2018, 51 consecutive CoA patients were treated with ascending aorta to bilateral iliac artery bypass concomitant with and cardiac surgerical procedures performed for a variety of reasons. A Y-shaped graft was used for the bypass procedure. We evaluated early outcomes, including postoperative death, systolic blood pressure and differences between upper and lower limb blood pressure. Results: The average age was 41 years and 64.7% of patients were men. Simultaneous cardiac procedures included aortic valve replacement, ventricular septal defect repair, Bentall procedures and Wheat procedures. No deaths occurred in the early postoperative period. Three patients had delayed healing at the site of the abdominal lower quadrant incisions. The average systolic pressure in the upper limb and the average difference between the upper- and lower-limb blood pressure decreased significantly after surgery (162.7 ± 13.4 mmHg vs 128.4 ± 6.7 mmHg, P =.000; 69.6 ± 15.6 mmHg vs 8.7 ± 7.6 mmHg, P =.000, respectively); The systolic blood pressure in the lower limb increased after bypass surgery (93.1 ± 6.2 mmHg vs 119.6 ± 7.7 mmHg, P =.000). The follow-up rate was 100%, with an average follow-up time of 61 months. Six patients (11.8%) had graft stenosis or occlusion. Three patients (5.9%) underwent endovascular embolectomy. Conclusions: In our small series, ascending aortoiliac bypass for one-stage repair of CoA with concomitant cardiac lesions appears safe and efficacious in effectively reduceing differences between upper and lower limb systolic blood pressure. Further study with larger sample size and longer follow-up is needed. [ABSTRACT FROM AUTHOR]

ABSTRACT The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus.

Background and objectives: Cardiovascular malformations are the commonest form of congenital defects and could result in significant morbidity. Antenatal and early postnatal detection is still unreliable, especially in developing countries and low-income communities. The aim of the study was to assess the value of early pulse oximetry in the detection of cardiac lesions among asymptomatic term newborns with subnormal oxygen saturation. Patients and methods: A cross-sectional study was conducted at the well-baby nursery of a community hospital, between March and August 2013. A total of 120 asymptomatic, apparently healthy term newborns who had persistent postductal SpO2

Although many clinical trials have demonstrated its efficacy during active compression-decompression cardiopulmonary resuscitation (ACD-CPR), the Ambu® CardioPump seems likely to cause severe and sometimes lethal injuries. In this paper, we report two cases observed at the Institute of Legal Medicine of Nancy, France. A 67-year-old man collapsed in the street, in the presence of witnesses, and without any sign of trauma. The autopsy revealed a flail chest, a wound of the left ventricle, a rupture of the right ventricle, and a wrenching of the inferior vena cava. A 71-year-old woman was found in her apartment during an accidental fire. The autopsy revealed a sternal fracture, many rib fractures, and a perforation of the superior vena cava, the pericardium, and the heart. Despite articles focusing on complications of the use of the CardioPump in the late 1990s, this technique is still used in practice. These two cases emphasize that iatrogenic injuries must be taken into account in the CardioPump benefit/risk balance and the relevance of its daily use. [ABSTRACT FROM AUTHOR]

Background The etiology of infective endocarditis (IE) is changing. More aggressive forms with multiple IE cardiac lesions have become more frequent. This study sought to explore the relationship between contemporary causative microorganisms and IE cardiac lesions and to analyze the impact of multiple lesions on treatment choice. Methods In 246 patients hospitalized for IE between 2008 and 2015, cardiac lesions caused by IE were analyzed by echocardiography, classified according to the 2015 European Society of Cardiology guidelines and correlated with microbiological data. We defined a new parameter, the Echo IE Sum, to summarize all IE cardiac lesions in a single patient, enabling comprehensive comparisons between different etiologies and treatment strategies. Results Staphylococcus aureus was associated with the development of large vegetation (OR 2.442; 95% CI 1.220–4.889; p = 0.012), non-HACEK bacteria with large vegetation (OR 13.662; 95% CI 2.801–66.639; p = 0.001), perivalvular abscess or perivalvular pseudoaneurysm (OR 5.283; 95% CI 1.069–26.096; p = 0.041), and coagulase-negative staphylococci (CoNS) with leaflet abscess or aneurysm (OR 3.451; 95% CI 1.285–9.266, p = 0.014), and perivalvular abscess or perivalvular pseudoaneurysm (OR 4.290; 95% CI 1.583–11.627; p = 0.004). The Echo IE Sum significantly differed between different etiologies ( p < 0.001), with the highest value in non-HACEK and the lowest in streptococcal endocarditis. Patients operated for IE had a significantly higher Echo IE Sum vs those who were medically treated ( p < 0.001). Conclusion None of the IE cardiac lesions is microorganism-specific. However, more severe lesions were caused by S. aureus , CoNS, and non-HACEK bacteria. The highest propensity to develop multiple lesions was shown by the non-HACEK group. Higher Echo IE Sum in patients sent to surgery emphasized the importance of multiple IE cardiac lesions on treatment choice and potential usage of Echo IE Sum in patient management. [ABSTRACT FROM AUTHOR]

The present study was performed to evaluate the clinical symptoms and cardiovascular complications in patients with typical and atypical Kawasaki disease (KD). This retrospective study was conducted on the medical records of 176 patients with KD for three years. The study population was divided into two groups of typical and atypical based on the KD clinical criteria. The two groups were compared in terms of demographic data, clinical symptoms, cardiac lesions, and laboratory markers. Based on the diagnostic criteria, 105 (60%) and 71 (40%) patients were diagnosed with typical and atypical KD, respectively. The mean age of the typical patients (38.16 months) was higher than that of the atypical group (24.03 months) at the time of diagnosis (p < 0.05). The results revealed no significant difference between the two groups regarding the seasonal distribution of KD onset (p = 0.422). However, the most common season for the diagnosis of the disease was spring, followed by winter. There was no significant difference between the two groups in terms of fever duration (p = 0.39). Furthermore, vomiting was more common in the atypical patients than in the typical group (p = 0.017). In terms of the cardiac lesions, ectasia (p = 0.005) and lack of tapering of the distal coronary vessels (p = 0.015) were more frequently detected in the atypical group than in the typical group. Considering the laboratory findings, thrombocytosis (p = 0.010) and anemia (p = 0.048) were more common in the atypical group, compared to those in the typical group. On the other hand, the typical group had a higher serum alanine aminotransferase level (adjusted for age) (p = 0.012) and Hyponatremia (serum sodium concentration ≤130 mmol/L) (p = 0.034). Based on the findings of the current study, the fever duration from onset to diagnosis was slightly more in atypical KD patients than in the typical group, but not statistically significant, possibly due to more timely diagnosis of atypical KD. There was no difference in coronary aneurysm between the two groups at the time of diagnosis. The atypical group had a higher frequency of coronary ectasia and lack of tapering, indicating cardiac involvement. Consequently, these conditions should be given more attention in the atypical patients. Furthermore, the higher frequency of anemia and thrombocytosis in the atypical patients can be useful for diagnosis of this kind of KD.

Background: The phenotypical profile of cardiovascular malformations in patients with congenital rubella syndrome (CRS) is varied. We aimed to describe the profile of cardiac defects among CRS patients detected in the sentinel CRS surveillance in India during 2016-22., Methods: Sentinel sites enrolled infants with suspected CRS based on presence of cardiac defects, hearing impairment, eye signs, or maternal history of febrile rash illness. Suspected CRS cases underwent detailed systemic examination, including echocardiography and serological investigation for rubella. Cardiac defects were categorized as 'Simple' or 'Complex' as per the National Heart, Lung, and Blood Institute classification. We compared the distribution of cardiac defects among laboratory confirmed CRS cases and seronegative discarded cases., Findings: Of the 4578 suspected CRS cases enrolled by 14 sites, 558 (12.2%) were laboratory confirmed. 419 (75.1%) laboratory confirmed cases had structural heart defects (simple defects: n = 273, 65.2%, complex defects: n = 144, 34.4%), with ventricular septal defect (42.7%), atrial septal defect (39.4%), patent ductus arteriosus (36.5%), and tetralogy of Fallot as the commonest defects (4.5%). Laboratory confirmed CRS cases had higher odds of left to right shunt lesions (OR = 1.58, 95% CI: 1.15-2.17). This was mainly on account of a significant association of PDA with CRS (OR = 1.77, 95% CI: 1.42-2.21). Mortality was higher among CRS patients with complex heart defects (HR = 2.04, 95% CI: 1.26-3.30)., Interpretation: Three-fourths of the laboratory confirmed CRS cases had structural heart defects. CRS patients with complex cardiac defects had higher mortality. Detecting CRS infection early and providing timely intervention for cardiovascular defects is critical for the management of CRS patients., Funding: Ministry of Health and Family Welfare, Govt of India, through Gavi, the Vaccine Alliance., Competing Interests: None declared., (© 2023 The Author(s).)

Trypanosoma cruzi is a hemoflagelate parasite associated with heart dysfunctions causing serious problems in Central and South America. Beagle dogs develop the symptoms of Chagas disease in humans, and could be an important experimental model for better understanding the immunopathogenic mechanisms involved in the chagasic infection. In the present study we investigated the relation among biological factors inherent to the parasite (trypomastigote polymorphism and in vitro infectivity) and immunoglobulin production, inflammation, and fibrosis in the heart of Beagle dogs infected with either T. cruzi Y or Berenice-78 strains. In vitro infectivity of Vero cells as well as the extension of cardiac lesions in infected Beagle was higher for Y strain when compared to Berenice-78 strain. These data suggested that in vitro infectivity assays may correlate with pathogenicity in vivo. In fact, animals infected with Y strain, which shows prevalence of slender forms and high infectivity in vitro, presented cardiomegaly, inflammation, and fibrosis in heart area. Concerning the immunoglobulin production, no statistically significant difference was observed for IgA, IgM or IgG levels among T. cruzi infected animals. However, IgA together IgM levels have shown to be a good marker for the acute phase of Chagas disease.

Background Transient tachypnea of the newborn (TTN) is considered a benign disorder. Given its self-limiting nature, few studies have looked for associated pathology. This study explores the association of TTN with structural cardiac lesions. Methods Over a six-month period, all inborn term and late preterm neonates with TTN (without predisposing factors) underwent 2D echocardiography within the first ten days of life, after tachypnea had subsided. Equal number of neonates born during the same period, matched for birth weight, gestational age, sex, and mode of delivery but without tachypnea, also underwent echocardiography before ten days of life. The cardiologist performing the echocardiography was blinded to the presence or absence of tachypnea. Results Thirty-six neonates with tachypnea and equal number of controls underwent echocardiography. Due to matching, there was no significant difference in birth weight, gestational age, sex, or mode of delivery between the two groups. Mean age at echocardiography also did not significantly differ. Neonates with TTN had significantly more structural cardiac lesions than those without (16 [44.44%] vs 5 [13.39%]; p < 0.009). Conclusion Significantly more neonates with TTN have associated structural cardiac lesions. All neonates with TTN should be screened for underlying structural cardiac lesions. [ABSTRACT FROM AUTHOR]

The aim of this study was to evaluate the profile of the enzymes creatine kinase (CK), creatine kinase MB (CK-MB) and lactate dehydrogenase (LDH) in Wistar rats infected with 250 (GI, n = 24) or 1000 (GII, n = 24) Toxocara canis eggs. Animals were evaluated on days 7, 15, 30, 60, 120 and 180 post-infection (DPI). Only the GI rats showed an increase in CK and CK-MB, at 15 and 30 DPI, respectively. Anti-Toxocara spp. antibodies were detected by ELISA in infected animals. Despite of the presence of eosinophilic infiltrate in the heart of three infected animals, none larva was recovered from the organ neither by acid digestion nor by Baermann procedure. Eosinophilia was observed in both groups but there was no significant difference in the eosinophil counts between GI and GII (p = 0.2239). It is possible to consider that cardiac lesion is an eventual finding in murine model for toxocariasis.O objetivo do presente estudo foi avaliar o perfil das enzimas creatinoquinase (CK), creatinoquinase-MB (CK-MB) e lactato desidrogenase (LDH) em ratos Wistar infectados com 250 (GI, n = 24) ou 1000 (GII, n = 24) ovos de Toxocara canis. Os animais foram avaliados nos dias 7, 15, 30, 60, 120 e 180 pós-infecção (DPI). Observou-se que apenas os animais do GI apresentaram aumento da atividade de CK e CK-MB aos 15 e 30 DPI, respectivamente. Anticorpos anti-T. canis foram detectados por ELISA nos animais infectados. Apesar da presença de infiltrado eosinofílico em três animais infectados, nenhuma larva foi recuperada do coração pela digestão ácida ou pela técnica de Baermann. Eosinofilia foi observada em todos os momentos em GI e GII, sem diferença significativa entre os grupos (p = 0,2239). Pode-se considerar que as lesões cardíacas foram um achado eventual no modelo murino para toxocaríase.

INTRODUCTION: Cardiovascular disease is the leading cause of morbidity and mortality in patients on maintenance hemodialysis. We investigated the pattern and correlates of cardiac lesions in a group of Cameroonians on chronic hemodialysis.METHODS: This was a cross-sectional study conducted at the Yaoundé General Hospital's hemodialysis unit, involving 45 patients (29 men, 64%) on maintenance hemodialysis for at least three months using a native arterio-venous fistula. Cardiovascular risk factors, biological, electrocardiographic and echocardiographic data were collected. RESULTS: Hypertension (29%), chronic glomerulonephritis (24%) and diabetes mellitus (24%) were the main etiological factors of chronic kidney disease. Blood pressure was controlled in 14 (31%) patients. Nineteen (42%) patients had anemia and 5 (14%) had a calcium-phosphorus product >55 mg2/dl2. All patients had at least one cardiovascular risk factors with hypertension (95%), anemia (42%) and high calcium-phosphorus product (42%) being the most frequent. Thirty-eight (84%) patients had at least one cardiac lesion and 11 (29%) had three or more lesions. The cardiac lesions were left ventricular hypertrophy (60%), valvular calcifications (38%), heart failure (36%), conduction disorders (33%), pericardial effusion (13%), valvular diseases (11%) and ischemic heart diseases (2%). Left ventricular hypertrophy was significantly associated with a longer duration on dialysis and low hemoglobin level (both p=0.047) while cardiac failure and valvular calcifications were associated with advanced age and high interdialytic weight gain (both p=0.05). CONCLUSION: Cardiac lesions and cardiovascular risk factors are frequent in these patients receiving sub-optimal dose maintenance hemodialysis despite their younger age, suggesting an increased susceptibility to cardiovascular complications.

Introduction: Cardiovascular disease is the leading cause of morbidity and mortality in patients on maintenance hemodialysis. We investigated the pattern and correlates of cardiac lesions in a group of Cameroonians on chronic hemodialysis. Methods: This was a cross-sectional study conducted at the Yaoundé General Hospital's hemodialysis unit, involving 45 patients (29 men, 64%) on maintenance hemodialysis for at least three months using a native arterio-venous fistula. Cardiovascular risk factors, biological, electrocardiographic and echocardiographic data were collected. Results: Hypertension (29%), chronic glomerulonephritis (24%) and diabetes mellitus (24%) were the main etiological factors of chronic kidney disease. Blood pressure was controlled in 14 (31%) patients. Nineteen (42%) patients had anemia and 5 (14%) had a calcium-phosphorus product >55 mg²/dl². All patients had at least one cardiovascular risk factors with hypertension (95%), anemia (42%) and highcalcium-phosphorus product (42%) being the most frequent. Thirty-eight (84%) patients had at least one cardiac lesion and 11 (29%) had three or more lesions. The cardiac lesions were left ventricular hypertrophy (60%), valvular calcifications (38%), heart failure (36%), conduction disorders (33%), pericardial effusion (13%), valvular diseases (11%) and ischemic heart diseases (2%). Left ventricular hypertrophy was significantly associated with a longer duration on dialysis and low hemoglobin level (both p<0.047) while cardiac failure and valvular calcifications were associated with advanced age and high interdialytic weight gain (both p <0.05). Conclusion: Cardiac lesions and cardiovascular risk factors are frequent in these patients receiving sub-optimal dose maintenance hemodialysis despite their younger age, suggesting an increased susceptibility to cardiovascular complications. [ABSTRACT FROM AUTHOR]

Abstract: Serum levels of cardiac troponins serve as biomarkers of myocardial injury. However, troponins are released into the serum only after damage to cardiac tissue has occurred. Here, we report development of a mouse model of doxorubicin (DOX)-induced chronic cardiotoxicity to aid in the identification of predictive biomarkers of early events of cardiac tissue injury. Male B6C3F1 mice were administered intravenous DOX at 3mg/kg body weight, or an equivalent volume of saline, once a week for 4, 6, 8, 10, 12, and 14weeks, resulting in cumulative DOX doses of 12, 18, 24, 30, 36, and 42mg/kg, respectively. Mice were sacrificed a week following the last dose. A significant reduction in body weight gain was observed in mice following exposure to a weekly DOX dose for 1week and longer compared to saline-treated controls. DOX treatment also resulted in declines in red blood cell count, hemoglobin level, and hematocrit compared to saline-treated controls after the 2nd weekly dose until the 8th and 9th doses, followed by a modest recovery. All DOX-treated mice had significant elevations in cardiac troponin T concentrations in plasma compared to saline-treated controls, indicating cardiac tissue injury. Also, a dose-related increase in the severity of cardiac lesions was seen in mice exposed to 24mg/kg DOX and higher cumulative doses. Mice treated with cumulative DOX doses of 30mg/kg and higher showed a significant decline in heart rate, suggesting drug-induced cardiac dysfunction. Altogether, these findings demonstrate the development of DOX-induced chronic cardiotoxicity in B6C3F1 mice. [Copyright &y& Elsevier]

Neuroleptics are a suspected cause of sudden death in psychiatric patients, especially in those with pre-existing cardiac lesions. As these lesions were previously shown to be associated with selenium (Se) deficiency, the aim of the present study was to evidence the possible protective effect of Se supplementation against cardiac lesions induced by the combination of the neuroleptic drugs levomepromazine and risperidone in the rabbit. Two groups of 6 rabbits were treated with 3 mg/kg of levomepromazine daily intramuscularly combined with 1 mg/kg of risperidone intramuscularly every other week for 3 consecutive months, and one group additionally received a solution of sodium selenite (2 μg/kg/day) intramuscularly during the whole treatment period. Furthermore, one group of six untreated animals was given the Se supplementation and another group of six control animals received saline daily. Blood samples were drawn before and at the end of the treatment period for the measurement of serum Se levels. At the end of the study, all animals were sacrificed and their hearts were removed for the measurement of tissue Se concentrations. In addition, the hearts were prepared for histopathological examination. A variety of cardiac lesions was found in the neuroleptics-treated animals without supplementation and to a lesser extent in the control and Se-supplemented untreated animals. Importantly, only rare cardiac lesions were observed in neuroleptics-Se-treated animals. The most striking differences in Se concentrations were noted in the myocardium: as compared to controls, there was a 43% reduction in neuroleptics-treated, but non-Se-supplemented animals (p < .01), at the end of the treatment period, whereas only a 14% reduction (p < .05) was noted in the neuroleptics-Se-treated animals. These results confirm that neuroleptics induce cardiac lesions associated with Se deficiency. Selenium supplementation markedly decreased the incidence and severity of neuroleptics-induced cardiac lesions and these findings may serve as a basis for further evaluation of the protective role of Se supplementation in neuroleptics-treated patients. However, Se supplementation in normal animals without Se deficiency was also shown to be cardiotoxic. [ABSTRACT FROM AUTHOR]

Abstract: Chagas disease is characterized by cardiac lesions and a high level of PGE2. Our objective was to investigate the role of PGE2 in cardiac lesions. BALB/c mice were infected with Trypanosoma cruzi (1×103 trypomastigote forms) and were treated daily with PBS, meloxicam (0.5mg/kg) or etoricoxib (0.6mg/kg). The animals were sacrificed on the 21st day of infection and we collected the cardiac tissue and spleen cells for tissue culture. We observed that treatment with COX-2 inhibitors was able to decrease synthesis of PGE2 by spleen cells. This reduction was accompanied by reduction of the inflammatory infiltrate, parasite nets, cardiac fibrosis and fewer COX-2 positive cells in cardiac tissue obtained from these animals. In conclusion, treatment with COX-2 inhibitors, and consequent inhibition of PGE2 synthesis, was able to reduce the cardiac damage observed during the acute phase of experimental Chagas disease, thus demonstrating the involvement of this mediator in the cardiac lesion. [Copyright &y& Elsevier]

Eighteen male Wistar rats aged six weeks were divided equally into Methamphetamine (MA), Placebo and Control group. MA group were injected with 50mg/kg body weight of Methamphetamine hydrochloride (MAHCl) in normal saline, Placebo group were injected with normal saline only, while Control group not injected with anything. Five MA group rats died within four hours of injection and their hearts collected on the same day. Another MA group rat was sacrificed two days after injection. Placebo and control group were sacrificed at similar intervals. Collected hearts were studied for cardiac lesions under light microscopy using special staining and immunohistochemistry. Microscopic examination of the myocardium of the rats that died on the first day of injection showed loss of nuclei in some myocytes, indicating cell death. Some areas in the sub-endocardium region showed internalization and enlargement of myocyte nuclei, consistent with regeneration of cells. There were very few foci of necrosis observed in these samples. The heart samples from the single rat that survived injection for two days showed foci of infiltration of macrophage-like cells that were later revealed to be regenerating myocytes. There were also spindle-like fibroblasts, macrophages and a few leucocytes found within these foci. The overall appearance of the myocardium did not indicate any inflammatory response, and the expected signs of necrosis were not observed. These results suggest a need to re-evaluate the toxic and lethal dosages of MA for use in animals testing. Cause of death was suspected to be due to failure of other major organs from acute administration of MA. Death occurred within a time period where significant changes due to necrosis may not be evident in the myocardium. Further investigations of other organs are necessary to help detect death due to acute dosage of MA. [ABSTRACT FROM AUTHOR]

Abstract: A 43-year-old woman was found dead in a car in the supine position. She had been suffering from depression for 2 years and hesitation wounds on the left forearm and wrist were observed. On microscopic examination, pulmonary congestion and edema were observed with heart failure cells in many alveoli, thereby suggesting not only acute but also chronic heart failure. Drug screening in the blood by gas chromatography–mass spectrometry (GC–MS) revealed the presence of amoxapine and levomepromazine, and their concentrations in tissues were determined by GC–MS with three-step solvent extraction followed by acetylation. The concentration of amoxapine in the blood and liver was 0.86–1.77 and 18.76μg/ml, respectively; the levels were much higher than the therapeutic level but did not reach the lethal level. The concentrations of levomepromazine in tissues were within the therapeutic level. Based on the pathological and toxicological findings, the cause of death was determined to be amoxapine poisoning on the basis of chronic heart failure due to the chronic use of psychotropic drugs. [Copyright &y& Elsevier]

Although cardiac tumors are rare, they nevertheless represent an important subgroup, the diagnosis of which is challenging for the primary care physician. Symptoms are not characteristic and serious complications including stroke, myocardial infarction and even sudden death from arrhythmia may be the first signs of tumor. The most common primary cardiac neoplasm is the benign myxoma and the most frequent primary malignant lesion is sarcoma. Cardiac metastases from distant primary carcinomas are now frequently encountered. Echocardiography until the past decade was the only consistently reliable and available non-invasive diagnostic tool. New non-invasive CT and MRI exams are changing the diagnostic approach. Echocardiography and angiocardiography with or without coronary arteriography remain routine methods for evaluating cardiac neoplasms. However, CT provides additional diagnostic information and is regarded as essential for adequate staging and treatment planning, particularly when surgical resection is being considered. This chapter reviews the wide spectrum of intracardiac thrombi and tumors including their incidence and imaging characteristics with particular reference to the CT findings and differential diagnosis. [ABSTRACT FROM AUTHOR]

Purpose: Cardiac involvement is not well defined in myeloproliferative disorders (MPD). The purpose of this study was to evaluate the cardiac involvement by transthoracic echocardiography in MPD. Materials and methods: The study groups were 36 patients (mean age: 58±15 years, 20 female and 16 male) with MPD and 30 age-matched healthy controls. MPD group included 15 essential thrombocythemia (ET), eight chronic phase chronic myelogenous leukemia (CML), seven idiopathic myelofibrosis (MF) and six polcythemia vera patients. Results: Valvular regurgitations were present in 14 patients (39%) and eight controls (27%), (P>0.05). Mitral regurgitation (MR) was more prominent in CML compared to controls (P=0.044). The rates of annular calcifications, valvular thickening, and vegetation like lesions were not different between MPD and control groups. Pulmonary hypertension (PHT) was present in six (17%) patients, but none of the controls (P=0.021). The rates of PHT in CML and MF were significantly higher than controls (P<0.05). The rate of PHT was not different in-between MPD patients with and without thromboembolic events, however, in MPD cases with thromboembolic events PHT was more common compared to controls (P=0.037). Conclusion: This study showed that valvular lesions were not more prevalent in MPD. PHT was the most prominent cardiac pathology in MPD (especially in CML, MF and thromboembolic events subgroups) compared to controls. Further evaluation of the cardiac changes in MPD subgroups with extended studies including trans-oesophageal echocardiography and longer follow-up periods would be appropriate. [Copyright &y& Elsevier]

Considerable information has been gained over the last few decades on several disease processes afflicting free-ranging cetaceans from a pathologist's point of view. Nonetheless, there is still a dearth of studies on the hearts of these species. For this reason, we aimed to improve our understanding of cardiac histological lesions occurring in free-ranging stranded cetaceans and, more specifically, in deep-diving Cuvier's beaked whales. The primary cardiac lesions that have been described include vascular changes, such as congestion, edema, hemorrhage, leukocytosis, and intravascular coagulation; acute degenerative changes, which consist of contraction band necrosis, wavy fibers, cytoplasmic hypereosinophilia, and perinuclear vacuolization; infiltration of inflammatory cells; and finally, the presence and/or deposition of different substances, such as interstitial myoglobin globules, lipofuscin pigment, polysaccharide complexes, and intra- and/or extravascular gas emboli and vessel dilation. This study advances our current knowledge about the histopathological findings in the cardiac muscle of cetaceans, and more specifically, of Cuvier's beaked whales.

The rapid emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has created a global health emergency. While most human disease is mild to moderate, some infections lead to a severe disease characterized by acute respiratory distress, hypoxia, anosmia, ageusia, and, in some instances, neurological involvement. Small-animal models reproducing severe disease, including neurological sequela, are needed to characterize the pathophysiological mechanism(s) of disease and to identify medical countermeasures. Transgenic mice expressing the human angiotensin-converting enzyme 2 (hACE2) viral receptor under the control of the K18 promoter develop severe and lethal respiratory disease subsequent to SARS-CoV-2 intranasal challenge when high viral doses are used. Here, we report on SARS-CoV-2 infection of hamsters engineered to express the hACE2 receptor under the control of the K18 promoter. K18-hACE2 hamsters infected with a relatively low dose of 100 or 1,000 PFU of SARS-CoV-2 developed a severe and lethal disease, with most animals succumbing by day 5 postinfection. Hamsters developed severe lesions and inflammation within the upper and lower respiratory system, including infection of the nasal cavities causing marked destruction of the olfactory epithelium as well as severe bronchopneumonia that extended deep into the alveoli. Additionally, SARS-CoV-2 infection spread to the central nervous system (CNS), including the brain stem and spinal cord. Wild-type (WT) hamsters naturally support SARS-CoV-2 infection, with the primary lesions present in the respiratory tract and nasal cavity. Overall, infection in the K18-hACE2 hamsters is more extensive than that in WT hamsters, with more CNS involvement and a lethal outcome. These findings demonstrate the K18-hACE2 hamster model will be valuable for studying SARS-CoV-2. IMPORTANCE The rapid emergence of SARS-CoV-2 has created a global health emergency. While most human SARS-CoV-2 disease is mild, some people develop severe, life-threatening disease. Small-animal models mimicking the severe aspects of human disease are needed to more clearly understand the pathophysiological processes driving this progression. Here, we studied SARS-CoV-2 infection in hamsters engineered to express the human angiotensin-converting enzyme 2 viral receptor under the control of the K18 promoter. SARS-CoV-2 produces a severe and lethal infection in transgenic hamsters that mirrors the most severe aspects of COVID-19 in humans, including respiratory and neurological injury. In contrast to other animal systems, hamsters manifest disease with levels of input virus more consistent with natural human infection. This system will be useful for the study of SARS-CoV-2 disease and the development of drugs targeting this virus.

A 41-year-old Japanese female developed polyarthritis with fusiform deformity. Diagnosis of rheumatoid arthritis was made and anti-inflammatory drugs were prescribed. Later thrombophlebitis in legs and cardiac lesions developed. The clinical course and treatment of this patient are briefly discussed. [ABSTRACT FROM AUTHOR]

Patients with neurofibromatosis have a higher incidence of anatomic cardiac abnormalities. However, there is little data regarding incidence of arrhythmias in this population. It is known that these patients have a higher mortality than the normal population, and it is possible that some deaths may be due to preventable causes such as cardiac arrhythmias. We report a patient with neurofibromatosis who was treated for a refractory seizure disorder for 8 years. However, video/EEG monitoring demonstrated that the patient had recurrent syncopal seizures secondary to sinus node dysfunction. Complete resolution of symptoms occurred after a permanent pacemaker implantation. We believe this is the first reported case of sinus node dysfunction associated with neurofibromatosis.Copyright © 2001 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Electrical injury may lead to damage to the conducting tissue, myocardial changes and even sudden cardiac death. Victims of low-voltage electrocution may have no electric marks, burns or other signs typical of electrical injuries. In these cases, the absence of other specific findings could make the identification of the cause of death very difficult. A broad spectrum of cardiac changes in cases of electrocution has been described in the literature, including the break-up of myocardial fibres, cardiomyolysis, haemorrhagic areas, the separation of myofibres and alternating hypercontracted-hyperdistended myocytes. All the described alterations, however, cannot be exclusively attributed to electrocution, since no specific morphological cardiac findings have so far been identified in electrocution. However, a few histological patterns recur, and their knowledge may be important for the forensic pathologist. This literature review describes the main pathological patterns observed in cases of fatal electrocution based on a literature search carried out up to September 2019 in the databases PubMed and Scopus. The search criteria included the keywords for cardiac lesions and electrocution. On the grounds of the literature data, a list of major and minor diagnostic markers for the passage of the electrical current through the heart tissue was created.

The objective of the present study was to evaluate the clinical signs, electrocardiographic signs and evolution of histopathological lesions in the heart of sheep experimentally infected by Trypanosoma vivax during the acute and chronic phases of infection as well as to investigate the presence of parasitic DNA in the heart using polymerase chain reaction (PCR). Twenty-two male sheep were divided into the following four groups: G1, which consisted of six sheep infected by T. vivax that were evaluated until 20 days post-infection (dpi; acute phase); G2, which consisted of six sheep infected by T. vivax that were evaluated until 90 dpi (chronic phase); and G3 and G4 groups, which each consisted of five uninfected sheep. At the end of the experimental period, electrocardiographic evaluations and necroscopic examinations were performed. Fragments of the heart were collected and stained by Hematoxylin-Eosin and Masson's trichrome, and the fragments were also evaluated by PCR for T. vivax. G2 animals presented clinical signs suggestive of heart failure and electrocardiogram alterations characterized by prolonged P, T and QRS complex durations as well as by a cardiac electrical axis shift to the left and increased heart rate. In these animals, mononuclear multifocal myocarditis and interstitial fibrosis were also observed. PCR revealed positivity for T. vivax in two G1 animals and in all G2 animals. Thus, these findings suggested that T. vivax is responsible for the occurrence of cardiac lesions, which are related to heart failure, electrocardiographic alterations and mortality of the infected animals. Image 1 • It was possible to identify Trypanosoma vivax in the cardiac sheep tissue. • The T. vivax should be considered responsible for the occurrence of cardiac lesions. • Lesions are related to signs of heart failure. • Are still related to electrocardiographic changes and mortality of infected animals. [ABSTRACT FROM AUTHOR]

The present study was performed to evaluate the clinical symptoms and cardiovascular complications in patients with typical and atypical Kawasaki disease (KD). This retrospective study was conducted on the medical records of 176 patients with KD for three years. The study population was divided into two groups of typical and atypical based on the KD clinical criteria. The two groups were compared in terms of demographic data, clinical symptoms, cardiac lesions, and laboratory markers. Based on the diagnostic criteria, 105 (60%) and 71 (40%) patients were diagnosed with typical and atypical KD, respectively. The mean age of the typical patients (38.16 months) was higher than that of the atypical group (24.03 months) at the time of diagnosis (p < 0.05). The results revealed no significant difference between the two groups regarding the seasonal distribution of KD onset (p = 0.422). However, the most common season for the diagnosis of the disease was spring, followed by winter. There was no significant difference between the two groups in terms of fever duration (p = 0.39). Furthermore, vomiting was more common in the atypical patients than in the typical group (p = 0.017). In terms of the cardiac lesions, ectasia (p = 0.005) and lack of tapering of the distal coronary vessels (p = 0.015) were more frequently detected in the atypical group than in the typical group. Considering the laboratory findings, thrombocytosis (p = 0.010) and anemia (p = 0.048) were more common in the atypical group, compared to those in the typical group. On the other hand, the typical group had a higher serum alanine aminotransferase level (adjusted for age) (p = 0.012) and Hyponatremia (serum sodium concentration ≤130 mmol/L) (p = 0.034). Based on the findings of the current study, the fever duration from onset to diagnosis was slightly more in atypical KD patients than in the typical group, but not statistically significant, possibly due to more timely diagnosis of atypical KD. There was no difference in coronary aneurysm between the two groups at the time of diagnosis. The atypical group had a higher frequency of coronary ectasia and lack of tapering, indicating cardiac involvement. Consequently, these conditions should be given more attention in the atypical patients. Furthermore, the higher frequency of anemia and thrombocytosis in the atypical patients can be useful for diagnosis of this kind of KD. [ABSTRACT FROM AUTHOR]

Eighteen male Wistar rats aged six weeks were divided equally into Methamphetamine (MA), Placebo and Control group. MA group were injected with 50mg/kg body weight of Methamphetamine hydrochloride (MAHCl) in normal saline, Placebo group were injected with normal saline only, while Control group not injected with anything. Five MA group rats died within four hours of injection and their hearts collected on the same day. Another MA group rat was sacrificed two days after injection. Placebo and control group were sacrificed at similar intervals. Collected hearts were studied for cardiac lesions under light microscopy using special staining and immunohistochemistry. Microscopic examination of the myocardium of the rats that died on the first day of injection showed loss of nuclei in some myocytes, indicating cell death. Some areas in the sub-endocardium region showed internalization and enlargement of myocyte nuclei, consistent with regeneration of cells. There were very few foci of necrosis observed in these samples. The heart samples from the single rat that survived injection for two days showed foci of infiltration of macrophage-like cells that were later revealed to be regenerating myocytes. There were also spindle-like fibroblasts, macrophages and a few leucocytes found within these foci. The overall appearance of the myocardium did not indicate any inflammatory response, and the expected signs of necrosis were not observed. These results suggest a need to re-evaluate the toxic and lethal dosages of MA for use in animals testing. Cause of death was suspected to be due to failure of other major organs from acute administration of MA. Death occurred within a time period where significant changes due to necrosis may not be evident in the myocardium. Further investigations of other organs are necessary to help detect death due to acute dosage of MA.