Malaria and Vascular Endothelium / A Malária e o Endotélio Vascular

Involvement of the cardiovascular system in patients with infectious and parasitic diseases can result from both intrinsic mechanisms of the disease and drug intervention. Malaria is an example, considering that the endothelial injury by Plasmodium-infected erythrocytes can cause circulatory disorders. This is a literature review aimed at discussing the relationship between malaria and endothelial impairment, especially its effects on the cardiovascular system. We discuss the implications of endothelial aggression and the interdisciplinarity that should guide the malaria patient care, whose acute infection can contribute to precipitate or aggravate a preexisting heart disease.

O acometimento do sistema cardiovascular em pacientes com doenças infecciosas e parasitárias pode ocorrer tanto por mecanismos intrínsecos à doença como em decorrência de intervenção medicamentosa. A malária é uma dessas doenças, tendo em vista que a agressão endotelial generalizada que se observa na infecção por Plasmodium pode causar distúrbios circulatórios. O objetivo deste artigo é discutir a relação entre malária e o comprometimento endotelial, em especial suas consequências sobre o sistema cardiovascular, a partir de uma revisão da literatura. Discutem-se as repercussões da agressão endotelial, bem como a interdisciplinaridade que deve nortear a atenção ao paciente malárico cuja infecção aguda pode contribuir para precipitar ou agravar doença cardíaca preexistente.

Manifestaciones cardiovasculares de la toxocariasis humana / Cardiovascular manifestations of human toxocariasis

La toxocariasis es una infección parasitaria producida por un helminto que en el ser humano no alcanza su estadio adulto. El hombre es para sus especies, Toxocara canis y Toxocara cati, un hospedador paraténico. Dicha infección puede producir el síndrome de larva migrans visceral, el síndrome de larva migrans ocular y la toxocariasis inaparente. En el síndrome de larva migrans visceral el compromiso de órganos puede incluir hígado, pulmón, piel, sistema nervioso, musculoesquelético, riñón y corazón. Sobre este último, cada vez se reconoce más la importancia que pueden tener las manifestaciones cardiovasculares de la toxocariasis y la relevancia clínica de considerarlas. En el presente artículo, haciendo una búsqueda sistemática de información, se revisan los principales aspectos clinicopatológicos de las manifestaciones cardiovasculares de la toxocariasis incluyendo su fisiopatología, hallazgos de laboratorio, diagnóstico y opciones terapéuticas, con el objeto de llamar la atención acerca de la importancia de esta zoonosis y su relevancia para la medicina cardiovascular en adultos y en niños.

Toxocariasis is a parasitic infection produced by helminths that cannot reach their adult stage in humans. For their etiological species (Toxocara canis and Toxocara cati), man is a paratenic host. Infection by such helminths can produce a variety of clinical manifestations, such as: visceral larvae migrans syndrome, ocular larvae migrans syndrome and covert toxoca-riasis. In the visceral larvae migrans syndrome, the organs that are mainly involved include liver, lungs, skin, nervous system, muscles, kidneys and the heart. Regarding the latter, the importance of cardiovascular manifestations in toxocariasis, as well as its clinical relevance, has increasingly begun to be recognized. The current article is based on a systematic information search, focused mainly on the clinical and pathological aspects of cardiovascular manifestations in toxocariasis, including its pathophysiology, laboratory findings, diagnosis and therapeutical options, with the objective of highlighting its importance as a zoonosis and its relevance to the fields of cardiovascular medicine in adults and children.

[Features hemodynamics and its relationship with some clinical manifestations in women with connective tissue dysplasia].

AIM: To elucidate genetically determined character of cardiovascular pathology with realization of its clinical manifestations at systemic, organ and tissue levels in patients with connective tissue dysplasia (CTD) at obstetric-gynecological setting. MATERIALS AND METHODS: This study involved 614 women with classified and non-classified forms of CTD including 268 primigravidas, mean age 24.8 ± 3.46 yr (group 1) and 346 gynecological patients with genital prolapse, mean age 44.5 ± 10 yr (group 2). Each group was divided into subgroups 1A and 2A with predominant clinical manifestations on the part of the stromal-muscular component and 1B and 2B with the predominance of the vascular component. The methods used included laboratory analysis, ECG, ultrasound, echocardiographic , X-ray, combined urodynamic studies, MGT and laser flowmetry. RESULTS: Prolapse of mitral valve (PMV) was diagnosed in 100 and 88.3% of the patients in groups 1 and 2 respectively with regurgitation in 1-2 valves in 140 (52.1%) and 143 (47.7%) ones, primary varicosis in 41 (15.2%) and 136 (39.5%), mixomatous degeneration in 65 (24.3%) and 107 (30.9%), predisposition to tissue hemorrhage in 37 (13.8%) and 64 (18.5%), vegetovascular dystonia in 50 and 60%. Patients of subgroup 1A with joint hypermobility and PMV exhibited a higher degree of uterine maturity (4.6 ± 1.75 scores). Rapid labor correlated with apical forms of genital prolapse (subgroups 1A, 2A); in the latter subgroup, they occurred in 83% ofthe patients, grade III rectocele occurred in 62.5%, protrusion and relaxation of pelvic floor in 50%. Pathology of the anorectal segment of pelvic diaphragm was diagnosed in more than 50% of the parous and nulliparous women (subgroups 1A and 2A). End diastolic volume was 102.7 ± 31.08 and 65.7 ± 59.48 ml in subgroups 2A and 2B respectively in association with a decrease of left ventricle mass to 135.6 ± 36.6 and 168.5 ± 86.97 g Hyperemic bloodflow prevailed in subgroup 1A while microcirculation index increased to 6.6 ± 1.84, perfusion coefficient to 2.2 ± 0.91, variation coefficient to 28.9 ± 5.46, relative HF amplitude to 21.9 ± 5.1 (control: 18.3 ± 1.29). CONCLUSION: CTD is always realized at the level of cardiovascular system. Its form and the type of dysregulation of suprasegmental CNS regions are genetically determined and inter-related In combination with minor cardiac abnormalities, they determine the type of hemodynamics including microcirculation and the degree of dysmorphism in the form of disorders in pelvic organs and structures including changes in the stromal-vascular histion level. The type of hemodynamics (microcirculation) determines dysregulatory processes in cells and intercellular matrix with the development of pathomorphological changes in the form of rheologic disturbances, vasculitis, thickening and loosening of basal membrane, smooth cell dystrophy, swelling of collagen fibers, loss of their elasticity, and reduction of the collagenous network.

Studies on cardiovascular fluke (Digenea: Spirorchiidae) infections in sea turtles from the Great Barrier Reef, Queensland, Australia.

Twenty-seven sea turtles (23 Chelonia mydas and four Eretmochelys imbricata) from northeast Queensland were found to be infected with cardiovascular flukes and/or their eggs. Five had originated from turtle farms in the Torres Strait, five from an oceanarium on Magnetic Island (146 degrees 56'E, 19 degrees S) and the remainder from coral reefs in the Torres Strait or near Townsville. The incidence of flukes and/or eggs in the groups was 4.8 per cent (5 of 104), 33.3 per cent (5 of 15) and 72.2 per cent (17 of 22), respectively. Affected animals ranged in size from 18 to 108 cm (curved carapace length) and weighed between 0.5 and 77 kg. The average number of flukes per host was 47. Flukes were recovered from the three chambers of the heart and major vessels (right aortic arch and brachiocephalic artery), where they were attached to the walls or free in the lumen. They were subsequently identified as Haplotrema spp. and/or Learedius spp. In 59.2 per cent (16 of 27) of turtles, flukes were not found, although their eggs were detected microscopically. Gross pathological changes associated with the presence of flukes included thickening and hardening of arterial walls (four turtles), thrombus formation (three), chronic pneumonia (two) and an excess of pericardial or peritoneal fluid (four). Microscopically, the essential changes was that of chronic inflammation, as evidenced by the proliferation of epithelial cells, reticulo-endothelial cells and fibroblasts in areas accessible to flukes and/or eggs. Multiple diffuse egg granulomas were a prominent feature of most organs, the spleen and lungs being predilection sites. Proliferative changes had occurred in the endocardium and in the endothelium of vessels supplying the spleen, stomach, intestine and pancreas (18 turtles). The walls of major arteries, lungs, liver, brain, crop and stomach were also acutely inflamed (eight turtles). Haemorrhage was recorded in the lungs and/or brain of eight turtles with heavy fluke infestations. Other vascular changes, viz. congestion, oedema and hypertrophy of arterial/arteriolar walls, resulted from the inhibition of blood flow by parasitic emboli.