Melatonin improves nitric oxide bioavailability in isoproterenol induced myocardial injury.

Isoproterenol administration is associated with cardiac inflammation and decreased NO availability. Melatonin has been reported to have cardioprotective effect. The aim of this study was to investigate the effect of melatonin on NO bioavailability and inflammation in myocardial injury induced by isoproterenol. Isoproterenol was administrated in male Wistar rats for 7 days to induce cardiac injury. The animals were divided into 3 groups: Control, Isoproterenol, Isoproterenol + Melatonin. Animals received melatonin for 7 days. Echocardiographic analysis was performed and the hearts were collected for molecular analysis. Animals that received isoproterenol demonstrated a reduction in left ventricle systolic and diastolic diameter, indicating the presence of concentric hypertrophy. Melatonin was able to attenuate this alteration. Melatonin also improved NO bioavailability and decreased NF-κß, TNFα and IL-1ß expression. In conclusion, melatonin exhibited a cardioprotective effect which was associated with improving NO bioavailability and decreasing the pro-inflammatory proteins.

The Pathogenesis of COVID-19 Myocardial Injury: An Immunohistochemical Study of Postmortem Biopsies.

Rationale: Myocardial injury associates significantly and independently with mortality in COVID-19 patients. However, the pathogenesis of myocardial injury in COVID-19 remains unclear, and cardiac involvement by SARS-CoV-2 presents a major challenge worldwide. Objective: This histological and immunohistochemical study sought to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 myocardial injury. Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19, and the myocardium samples were compared to a control group (n=11). Histological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against targets: caspase-1, caspase-9, gasdermin-d, ICAM-1, IL-1ß, IL-4, IL-6, CD163, TNF-α, TGF-ß, MMP-9, type 1 and type 3 collagen. The samples were also assessed for apoptotic cells by TUNEL. Histological analysis showed severe pericardiocyte interstitial edema and higher mast cells counts per high-power field in all COVID-19 myocardium samples. The IHC analysis showed increased expression of caspase-1, ICAM-1, IL-1ß, IL-6, MMP-9, TNF-α, and other markers in the hearts of COVID-19 patients. Expression of caspase-9 did not differ from the controls, while gasdermin-d expression was less. The TUNEL assay was positive in all the COVID-19 samples supporting endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 myocardial injury does not seem to relate to primary myocardiocyte involvement but to local inflammation with associated interstitial edema. We found heightened TGF-ß and interstitial collagen expression in COVID-affected hearts, a potential harbinger of chronic myocardial fibrosis. These results suggest a need for continued clinical surveillance of patients for myocardial dysfunction and arrythmias after recovery from the acute phase of COVID-19.

Resolvin D1 and E1 promote resolution of inflammation in rat cardiac fibroblast in vitro.

Cardiac fibroblasts (CFs) have a key role in the inflammatory response after cardiac injury and are necessary for wound healing. Resolvins are potent agonists that control the duration and magnitude of inflammation. They decrease mediators of pro-inflammatory expression, reduce neutrophil migration to inflammation sites, promote the removal of microbes and apoptotic cells, and reduce exudate. However, whether resolvins can prevent pro-inflammatory-dependent effects in CFs is unknown. Thus, the present work was addressed to study whether resolvin D1 and E1 (RvD1 and RvE1) can prevent pro-inflammatory effects on CFs after lipopolysaccharide (LPS) challenge. For this, CFs were stimulated with LPS, in the presence or absence of RvD1 or RvE1, to analyze its effects on intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion protein 1 (VCAM-1), monocyte adhesion and the cytokine levels of tumor necrosis factor alpha (TNF-α), interleukin-6(IL-6), interleukin-1beta (IL-1ß), monocyte chemoattractant protein-1 (MCP-1) and interleukin-10 (IL-10). Our results showed that CFs are expressing ALX/FPR2 and ChemR23, RvD1 and RvE1 receptors, respectively. RvD1 and RvE1 prevent the increase of ICAM-1 and VCAM-1 protein levels and the adhesion of spleen mononuclear cells to CFs induced by LPS. Finally, RvD1, but not RvE1, prevents the LPS-induced increase of IL-6, MCP-1, TNF-α, and IL-10. In conclusion, our findings provide evidence that in CFs, RvD1 and RvE1 might actively participate in the prevention of inflammatory response triggered by LPS.

Penetrating cardiac trauma: analysis of 240 cases from a hospital in Bogota, Colombia.

BACKGROUND: Trauma characteristics and its management is influenced by socioeconomic context. Cardiac trauma constitutes a challenge for surgeons, and outcomes depend on multiple factors including initial care, characteristics of the wounds, and surgical management. METHODS: This is a retrospective cross-sectional case series of patients with penetrating cardiac injuries (PCI) from January 1999 to October 2009 who underwent surgery in a trauma referral center in Bogotá, Colombia. Demographic variables, trauma characteristics, treatment, and outcomes were analyzed. RESULTS: The study included 240 cases: 96.2% males, mean age of 27.8 years. Overall mortality was 14.6%: 11.7% from stab wounds and 41.2% from gunshot wounds. Upon admission, 44% had a normal hemodynamic status and 67% had cardiac tamponade. About 32% had Grade II injuries and 29% Grade IV injuries. In 85% of the cases, there were ventricular compromise and 55% of patients had associated lesions. In 150 cases, a pericardial window was performed. Highest mortality occurred in wounds to the right atrium. In tamponade patients, mortality was 20% being higher for gunshot wounds (54.5%) than for stab wounds (18%) (p = 0.0120). CONCLUSIONS: The study evidenced predominance of stab wounds. Based on characteristics of the trauma, patients, and survival rate, there is most likely a high pre-hospitalization mortality rate. The difference in mortality due to stab wounds and those produced by gunshots was more related to technical difficulties of the surgical repair than with the type of injury established by the Injury Grading Scale. Mortality was higher in patients with cardiac tamponade. Surgical management was satisfactory using pericardial window as the diagnostic method and sternotomy as the surgical approach.

Oral glutamine reduces myocardial damage after coronary revascularization under cardiopulmonary bypass. A randomized clinical trial.

BACKGROUND: Glutamine is the most abundant free amino acid in the body. It modulates immune cell function and is an important energy substrate for cells in critically ill patients. Reduction of injury cardiac markers had been observed in patients receiving intravenous glutamine and in a pilot study with oral glutamine. The aim of this study was to analyze the effect of preoperative oral supplementation of glutamine on postoperative serum levels of cardiac injury markers. METHODS: A randomized clinical trial was performed in 28 Mexican patients with ischemic heart disease who underwent cardiopulmonary bypass with extracorporeal circulation. Patients were randomly assigned to receive oral glutamine (0.5 g/kg/day) or maltodextrin 3 days before surgery. Cardiac injury markers as troponin-I, creatine phosphokinase, and creatine phosphokinase-Mb were measured at 1, 12, and 24 hours postoperatively. RESULTS: At 12 and 24 hours serum markers levels were significantly lower in the glutamine group compared with controls (p = 0.01 and p = 0.001, respectively) (p = 0.004 and p < 0.001, respectively). Overall, complications were significantly lower in the glutamine group (p = 0.01, RR = 0.54, 95% CI 0.31-0.93). Mortality was observed with 2 cases of multiple organ failure in control group and 1 case of pulmonary embolism in glutamine group (p = 0.50). CONCLUSION: Preoperative oral glutamine standardized at a dose of 0.5 g/kg/day in our study group showed a significant reduction in postoperative myocardial damage. Lower cardiac injury markers levels, morbidity and mortality were observed in patients receiving glutamine.

Heart injury following intestinal ischemia reperfusion in rats is attenuated by association of ischemic preconditioning and adenosine.

PURPOSE: To investigate the effect of ischemic preconditioning (IPC) and adenosine as strategies to protect cardiac injury caused by intestinal IR in rats, based on increasing in adenosine bioavailability and improvement of cell energy state by IPC. METHODS: Male Wistar rats were submitted to 60 minutes of intestinal ischemia and 120 minutes of reperfusion. Intravenous injections of saline or Adenosine (AD) was administered five minutes before ischemia, five minutes before reperfusion and after 55 minutes reperfusion. Cardiac samples were obtained, fixed in formalin solution, embedded in paraffin, and sections of 5 µm were stained by hematoxylin-eosin. Histological analysis of myocardium was performed according occurrence of necrosis signs: piknosis, band contraction, eosinophilic cytoplasm, karyorrhexis and vacuolization (score - zero to 5). RESULTS: The groups submitted to ischemia alone (I=4.0), and reperfusion (IR=4.5) showed highest level of lesion compared to the others (I+IPC=3.3, IR+IPC=3.6, I+AD=3.0, IR+AD=3.8). The most interesting result was association of IPC and AD in IR model (IR+IPC+AD=1.2, p=0.002), showing preservation of the heart tissue, with fibers showing typical cross-striations and nuclei characteristics. Rare and small areas of tissue necrosis was observed and suggestion of capillaries congestion. CONCLUSION: Intestinal ischemia reperfusion promotes cardiac tissue injury. Ischemic preconditioning in association with adenosine is an efficient strategy to protect the heart against ischemia and reperfusion injury.

The calcium paradox - what should we have to fear?

The calcium paradox was first mentioned in 1966 by Zimmerman et al. Thereafter gained great interest from the scientific community due to the fact of the absence of calcium ions in heart muscle cells produce damage similar to ischemia-reperfusion. Although not all known mechanisms involved in cellular injury in the calcium paradox intercellular connection maintained only by nexus seems to have a key role in cellular fragmentation. The addition of small concentrations of calcium, calcium channel blockers, and hyponatraemia hypothermia are important to prevent any cellular damage during reperfusion solutions with physiological concentration of calcium.

Paradoxo do cálcio - o que temos a temer? / The calcium paradox - What should we have to fear?

O paradoxo do cálcio foi pela primeira vez citado em 1966 por Zimmerman et al. A partir daí, ganhou grande interesse por parte da comunidade científica internacional devido ao fato da ausência do íon cálcio produzir na célula muscular cardíaca dano semelhante à lesão de isquemia-reperfusão. Apesar de não serem conhecidos todos os mecanismos envolvidos no processo da lesão celular no paradoxo do cálcio, a conexão intercelular mantida somente pelo nexus parece ter papel chave na fragmentação celular. A adição de pequenas concentrações de cálcio, bloqueadores de canal de cálcio, hiponatremia ou hipotermia são importantes para evitar que haja lesão celular no momento da reperfusão com soluções com concentração fisiológica de cálcio.

The calcium paradox was first mentioned in 1966 by Zimmerman et al. Thereafter gained great interest from the scientific community due to the fact of the absence of calcium ions in heart muscle cells produce damage similar to ischemia-reperfusion. Although not all known mechanisms involved in cellular injury in the calcium paradox intercellular connection maintained only by nexus seems to have a key role in cellular fragmentation. The addition of small concentrations of calcium, calcium channel blockers, and hyponatraemia hypothermia are important to prevent any cellular damage during reperfusion solutions with physiological concentration of calcium.

Heart injury following intestinal ischemia reperfusion in rats is attenuated by association of ischemic preconditioning and adenosine

PURPOSE: To investigate the effect of ischemic preconditioning (IPC) and adenosine as strategies to protect cardiac injury caused by intestinal IR in rats, based on increasing in adenosine bioavailability and improvement of cell energy state by IPC. METHODS: Male Wistar rats were submitted to 60 minutes of intestinal ischemia and 120 minutes of reperfusion. Intravenous injections of saline or Adenosine (AD) was administered five minutes before ischemia, five minutes before reperfusion and after 55 minutes reperfusion. Cardiac samples were obtained, fixed in formalin solution, embedded in paraffin, and sections of 5 μm were stained by hematoxylin-eosin. Histological analysis of myocardium was performed according occurrence of necrosis signs: piknosis, band contraction, eosinophilic cytoplasm, karyorrhexis and vacuolization (score - zero to 5). RESULTS: The groups submitted to ischemia alone (I=4.0), and reperfusion (IR=4.5) showed highest level of lesion compared to the others (I+IPC=3.3, IR+IPC=3.6, I+AD=3.0, IR+AD=3.8). The most interesting result was association of IPC and AD in IR model (IR+IPC+AD=1.2, p=0.002), showing preservation of the heart tissue, with fibers showing typical cross-striations and nuclei characteristics. Rare and small areas of tissue necrosis was observed and suggestion of capillaries congestion. CONCLUSION: Intestinal ischemia reperfusion promotes cardiac tissue injury. Ischemic preconditioning in association with adenosine is an efficient strategy to protect the heart against ischemia and reperfusion injury. .

Polimorfismos del gen de apolipoproteína E y polimorfimo Pro12Ala del gen PPARy-2 en niños pre-puberes con factores de riesgo cardiometabólicos / Apolipoprotein E gene polymorphisms and Pro12Ala polymorfphism of PPARy-2 gene in children with risk factors to cardiometabolic disease

La resistencia a la insulina es muy frecuente en niños y adolescentes obesos, la cual conlleva a un significativo riesgo de desarrollar enfermedades cardiometabólicas causadas por la combinación de factores genéticos y factores asociados al estilo de vida. Evaluar la relación entre los polimorfismos del gen ApoE y el polimorfismo Pro12Ala del gen PPARγ2 en niños pre-púberes con factores de riesgo cardiometabólicos. Población y Métodos: Se evaluaron 141 niños (CANIA y Hospital “JM de los Ríos”), de los cuales 46 tienen obesidad, 33 hipercolesterolemia, 30 resistentes a la insulina (RI) y 32 controles. Se determinó colesterol total y fracciones, triglicéridos, glucosa, insulina e índice HOMA; se realizó extracción de ADN y análisis de los polimorfismos. La distribución de la frecuencia del alelo ε4 del gen de ApoE fue: 10,9% obesos, 7,6% hipercolesterolémicos, 18,3% RI y 4,6% controles. La frecuencia del polimorfismo Pro12Ala fue de 6,4% en la población estudiada. En los niños obesos e hipercolesterolémicos se observó aumento de colesterol total, LDL-c y triglicéridos asociados con la presencia del ε4; en el grupo con RI, se encontró que existen diferencias estadísticamente significativas entre el alelo ε4 con respecto al grupo control, lo que refiere que puede haber una relación clínica importante entre la presencia del alelo y el desarrollo de la enfermedad. No se encontró relación entre el polimorfismo Pro12Ala del gen PPARγ2 con factores de riesgo cardiometabólico. La presencia de varios polimorfismos en un mismo individuo podría estar asociada a factores de riesgo para enfermedad cardiometabólica

Insulin resistance (IR) is very frequent in children and adolescents obeses, which could contribute significantly in the development of cardiometabolic diseases, this could be associated to a combination of genetics factors and life’s style. Aim: To evaluate the relationship between ApoE gene polymorphisms and PPARγ2 gene Pro12Ala polymorphisms with risk factors to cardiometabolic disease in children. Population and Materials: 141 children (CANIA and Hospital “JM de los Ríos”), 46 with obesity, 33 with hypercholesterolemia, 30 with IR and 32 normal subjects. Total cholesterol and fractions, glucose, insulin and triglycerides were measured; also it was determinated the polymorphism genes on each patient. Results: The distribution of the frequency of the allele E4 of the ApoE gene were: 10, 9% obese, 7,6% hypercholesterolemia, 18,3% IR and 4,6% on normal subjects. The frequency of Pro12Ala polymorphism were up to 6,4% on the total subjects in the study. In the obese and hypercholesterolemic groups we found an increase of the total cholesterol, LDL-c and triglycerides, associated with the presence of allele ε4. In children with IR we got a significant difference of the presence of allele ε4 compared with the control group, which means that this allele could be related with the development of thedisease. It was not found a relation between the Pro12Ala of PPARγ2 gene and the development of obesity, hypercholesterolemia and insulin resistance in children. The presence of several polymorphisms in a same individual could be associated with risk factors to cardiometabolic disease

Hypoxia/reoxygenation-induced myocardial lesions in newborn piglets are related to interindividual variability and not to oxygen concentration.

OBJECTIVE: Evaluation of myocardial histological changes in an experimental animal model of neonatal hypoxia-reoxygenation. METHODS: Normocapnic hypoxia was induced in 40 male Landrace/Large White piglets. Reoxygenation was initiated when the animals developed bradycardia (HR <60 beats/min) or severe hypotension (MAP <15 mmHg). The animals were divided into four groups based on the oxygen (O(2)) concentration used for reoxygenation; groups 1, 2, 3, and 4 received 18%, 21%, 40%, and 100% O(2), respectively. The animals were further classified into five groups based on the time required for reoxygenation: A: fast recovery (<15 min); B: medium recovery (15-45 min); C: slow recovery (45-90 min); D: very slow recovery (>90 min), and E: nine deceased piglets. RESULTS: Histology revealed changes in all heart specimens. Interstitial edema, a wavy arrangement, hypereosinophilia and coagulative necrosis of cardiomyocytes were observed frequently. No differences in the incidence of changes were observed among groups 1-4, whereas marked differences regarding the frequency and the degree of changes were found among groups A-E. Coagulative necrosis was correlated with increased recovery time: this condition was detected post-asphyxia in 14%, 57%, and 100% of piglets with fast, medium, and slow or very slow recovery rates, respectively. CONCLUSIONS: The significant myocardial histological changes observed suggest that this experimental model might be a reliable model for investigating human neonatal cardiac hypoxia-related injury. No correlation was observed between the severity of histological changes and the fiO(2) used during reoxygenation. Severe myocardial changes correlated strictly with recovery time, suggesting an unreported individual susceptibility of myocardiocytes to hypoxia, possibly leading to death after the typical time-sequence of events.

Hypoxia/reoxygenation-induced myocardial lesions in newborn piglets are related to interindividual variability and not to oxygen concentration

OBJECTIVE: Evaluation of myocardial histological changes in an experimental animal model of neonatal hypoxiareoxygenation. METHODS: Normocapnic hypoxia was induced in 40 male Landrace/Large White piglets. Reoxygenation was initiated when the animals developed bradycardia (HR <60 beats/min) or severe hypotension (MAP <15 mmHg). The animals were divided into four groups based on the oxygen (O2) concentration used for reoxygenation; groups 1, 2, 3, and 4 received 18%, 21%, 40%, and 100% O2, respectively. The animals were further classified into five groups based on the time required for reoxygenation: A: fast recovery (<15 min); B: medium recovery (15-45 min); C: slow recovery (45-90 min); D: very slow recovery (>90 min), and E: nine deceased piglets. RESULTS: Histology revealed changes in all heart specimens. Interstitial edema, a wavy arrangement, hypereosinophilia and coagulative necrosis of cardiomyocytes were observed frequently. No differences in the incidence of changes were observed among groups 1-4, whereas marked differences regarding the frequency and the degree of changes were found among groups A-E. Coagulative necrosis was correlated with increased recovery time: this condition was detected post-asphyxia in 14%, 57%, and 100% of piglets with fast, medium, and slow or very slow recovery rates, respectively. CONCLUSIONS: The significant myocardial histological changes observed suggest that this experimental model might be a reliable model for investigating human neonatal cardiac hypoxia-related injury. No correlation was observed between the severity of histological changes and the fiO2 used during reoxygenation. Severe myocardial changes correlated strictly with recovery time, suggesting an unreported individual susceptibility of myocardiocytes to hypoxia, possibly leading to death after the typical time-sequence of events.

Ischemic myocardial injuries after cardiac malformation repair in infants may be associated with oxidative stress mechanisms.

BACKGROUND: Despite advances in pediatric cardiac surgery, perioperative myocardial injury can be the major determinant of postoperative dysfunction after cardiac surgery. This study investigated the pathology-related differences in 29 infants with congenital heart disease that led to death. The infants were treated at the University Hospital of Ribeirão Preto, Brazil. METHODS: The patients were divided into four groups: Group 1, 16 infants who underwent operations for congenital heart disease on cardiopulmonary bypass; Group 2, four infants who underwent off-cardiopulmonary bypass operations for congenital heart disease; Group 3, nine infants who died from congenital heart disease prior to surgical treatment; and Group 4 (control group), five infants with no congenital heart disease and who died from other causes. The myocardial injuries and oxidative stress mechanisms were assessed by histopathology and immunohistochemistry and were quantified by morphometrical analyses. RESULTS: Contraction band necrosis and dystrophic calcification were found primarily in infants of Group 1. Coagulation necrosis and healing were prominent in Group 2, while infants without repair (Group 3) showed mainly colliquative myocytolysis. Apoptotic cells were more prominent in the operative groups. The control group showed no significant myocardial lesions. Lipid peroxidation was the principal mechanism of oxidative stress accounting for the myocardial lesions. CONCLUSION: The diversity of the lesions observed in these hearts seemed to indicate a large spectrum of cell damage due to inadequate myocardial perfusion, especially when these infants underwent surgery. Oxidative mechanisms could be a common mediator in the pathogenesis of myocardial injuries, mediated by peroxidation of the membrane phospholipids and resulting in changes in the permeability of the cell membrane, cell death, and intracellular calcium overload. Furthermore, an immature and often hypertrophied myocardium may promote unfavorable conditions, leading to heart failure and a lethal outcome.

Aneurisma aorta torácica y falla cardíaca manejado con transplante cardíaco: descripción de un caso clínico / Aorta thoracic aneurysm and cardiac failure treated with cardiac transplant: description of a clinical case

Alrededeor de un 25% de aneurismas aórticos degenerativos afectan a la aorta torácica. En la mayoria de los casos afectan al arco y a la aorta desendente, a diferencia de los luéticosque tienen mayor frecuencia en aorta ascendente. A veces toda la aorta es estásica presentando multiples dilataciones que se extienden a aorta abdominal, dando lugar a aneurisma toracoabdominales. Existen factores predisponentes como la edad, hipertensión sistémica arterial (HTA), anomalias congénitas de la válvula aórtica, transtornos hereditarios del sistema conectivo, traumáticos y otros. Afecta a pacientes entre la quinta y la séptima décadas de la vida, siendo más frecuente en varones (3:1). En menores de 40 años la frecuencia es similar en ambos sexos, debido a la mayor frecuencia en mujeres durante el trecer trimestre del embarazo. La HTA es encontrada en el 80% de los casos, siendo el segundo factor predisponente en importancia.

Around 25% of degenerative aortic aneurysms affect the thoracic aorta. In the majority of cases they affect the arch and the descending aorta, unlike luetic aneurysms, which are more frequent in the ascending aorta. Sometime the entire aorta is in a state of stasis, presenting multiple dilatations that extend to the abdominal aorta giving rise to thoracoabdominal aneurysms. There are predispositional factors, among them systemic arterial hypertension (SAH), congenital anomalies of the aortic valve, hereditary connective system disorders and traumatisms. This condition affects patients in their 50s to 70s and is most frequent in males (3:1). In the under-40s, frequency is similar in both sexes, owing to the higher frequency among women during the third trimester of pregnancy. SAH is found in 80% of cases, being the second most important predispositional factor.

[Echocardiographic findings in children with "innocent" murmur]. / Achados ecocardiográficos em crianças com sopro "inocente".

OBJECTIVES: To access the frequency of abnormal echocardiographic findings in patients with diagnosis of innocent murmur. METHODS: A transversal study of 166 consecutive patients was carried out with diagnosis of innocent murmur evaluated in the pediatric cardiology outpatient clinic of "Instituto de Cardiologia/Fundação Universitária de Cardiologia", a tertiary reference center, between December 3, 2001 and December 2, 2002. History, clinical examination and echocardiogram were performed in all patients. Post-test probabilities of disease with positive and negative clinical examination were estimated, considering the echocardiogram as gold standard. RESULTS: Of the 166 patients evaluated, 11 showed some alteration in the echocardiogram: pulmonary stenosis (4), patent foramen ovale (2), atrial septal defect (1), bicuspid aortic valve (2), minimum aortic regurgitation (1) and ventricular septal defect (1). Negative post-test probability (probability of disease with diagnosis of innocent murmur) was of 6.6%. CONCLUSION: In a referral outpatient clinic the proportion of minor lesions is high in patients with diagnosis of innocent murmur. These injuries may not be related to the heart murmur, as in the patent foramen ovale and bicuspid aortic valve. However, they raise the question of the indication of echocardiogram taking into account the low risk of detected lesions and, on the other hand, the resolutive character of a daycare reference center.

Achados ecocardiográficos em crianças com sopro "inocente" / Echocardiographic findings in children with innocent murmur

OBJETIVOS: Avaliar a freqüência de alterações ecocardiográficas em pacientes com diagnóstico de sopro "inocente". Métodos. Estudo transversal de uma amostra de 166 pacientes com diagnóstico de sopro "inocente" avaliados no ambulatório de Cardiologia Pediátrica do Instituto de Cardiologia/Fundação Universitária de Cardiologia, um serviço terciário de referência, durante o período de 3/12/2001 a 2/12/2002. Todos os pacientes realizaram anamnese, exame físico, eletrocardiograma e ecocardiograma. Foram estimadas as probabilidades pós-teste de exame clínico considerando o ecocardiograma como padrão ouro. Resultados. Dos 166 pacientes estudados, 11 apresentaram alguma alteração ao ecocardiograma: estenose pulmonar leve (4), forame oval patente (2), aorta bicúspide (2), comunicação interatrial (1), insuficiência aórtica mínima (1), comunicação interventricular mínima (1). A probabilidade pós-teste negativo, ou seja, a probabilidade de lesão cardíaca com diagnóstico de sopro "inocente" foi de 6,6 por cento. Conclusão. Em ambulatório especializado, é alta a proporção de alterações ecocardiográficas em pacientes com diagnóstico de sopro "inocente". Estes achados podem não estar relacionados à presença de sopro, como o forame oval patente e a aorta bicúspide. No entanto, levantam a questão da indicação de ecocardiograma considerando, por um lado, o baixo risco das lesões detectadas e, por outro, o caráter resolutivo de um ambulatório de referência.

Atherosclerotic lesions, myocardial damage and lipidograms: a multiarterial study applying an atherometric system and canonical correlation.

472 autopsy subjects were examined with the following aims: to study the association pattern of atherosclerotic lesions between different arterial sectors, the impact of serum lipid disorders (total cholesterol, HDL-c, LDL-c, VLDL-c, and triglycerides were analyzed) and the association pattern between the atherosclerotic lesions in different arterial sectors and the degree of heart damage. For morphometric analysis of the vessels (aorta, circle of Willis, coronary, renal, iliac, and femoral arteris) the atherometric system was used. The most relevant results were as follows: the lipid disorders show their greatest impact in the heart, coronary and femoral arteries and abdominal aorta, whereas the strongest correlations between the atherosclerotic lesions in different arterial sectors were found in those with anatomical continuity.

Lesiones cardiacas asociadas a traumatismo craneotorácico / Cardiac lesions associated to craniothoracic trauma

Las lesiones cardiacas por traumatismo son poco frecuentes y se presentan con mayor frecuencia cuando éste es torácico-abdominal. En el Hospital General de Coyoacán Xoco del Departamento del Distrito Federal, se estudiaron 100 necropsias médico-legales, con características de traumatismos craneotorácicos. Se observaron 11 casos con lesiones cardiacas francas sin aparentes lesiones torácicas. Las lesiones cardiacas asociadas a traumatismo craneotorácico son poco frecuentes en las necropsias. Se obtuvieron datos generales de la averiguación previa de los casos estudiados: tipo de traumatismo, edad, sexo, tiempo de evoluación en los casos de internamiento y alcoholismo, entre otros. Se correlacionaron los hallazgos macroscópicos con el daño cardiaco observado. Se registraron ocho contusiones pericárdicas y tres endocárdicas, ocho endocarditis no bacterianas, cinco trombosis intramurales de la aurícula derecha y tres casos de trombosis de la coronaria derechas, de los cuales uno presentaba trombosis multiorgánica. Se discute el mecanismo de la lesión cerebral con la asociación a lesiones cardiacas sin daño torácico directo, con diferentes factores que pudieran participar en el mecanismo del daño