Acute aortic syndrome: a new look at an old conundrum.

The term acute aortic syndrome (AAS), coined several years ago, is now widely recognised. In the light of new findings in aortic pathology and in an era when modern imaging techniques are widely available and interventional management of AAS is increasing, some morphological and diagnostic aspects of acute aortic pathology have been examined and the syndrome updated. This article provides a new, comprehensive overview of the pathology, diagnosis, evolution and management of patients with AAS. As acute aortic disease is the most common fatal condition in patients with chest pain, prompt recognition and treatment is of paramount importance.

Ezetimibe reduces plaque inflammation in a rabbit model of atherosclerosis and inhibits monocyte migration in addition to its lipid-lowering effect.

BACKGROUND AND PURPOSE: Ezetimibe, a selective inhibitor of intestinal cholesterol absorption, might also suppress inflammatory components of atherogenesis. We have studied the effects of ezetimibe on two characteristics of atherosclerotic plaques (infiltrate and fibrosis) and on expression of inflammatory genes in a rabbit model of accelerated atherosclerosis. EXPERIMENTAL APPROACH: Femoral atherosclerosis was induced by a combination of endothelial desiccation and atherogenic diet. Animals were randomized to ezetimibe (0.6 mg x kg(-1) x day(-1)), simvastatin (5 mg x kg(-1) x day(-1)), ezetimibe plus simvastatin or no treatment, still on atherogenic diet. A control group of rabbits received normolipidemic diet. KEY RESULTS: Rabbits fed the normolipidemic diet showed normal plasma lipid levels. Either the normolipidemic diet or drug treatment reduced the intima/media ratio (normolipidemic diet: 22%, ezetimibe: 13%, simvastatin: 27%, ezetimibe + simvastatin: 28%), compared with rabbits with atherosclerosis. Ezetimibe also decreased macrophage content and monocyte chemoattractant protein-1 expression in atherosclerotic lesions. Furthermore, ezetimibe reduced the increased activity of nuclear factor kappaB in peripheral blood leucocytes and plasma C-reactive protein levels in rabbits with atherosclerosis. In THP-1 cells, ezetimibe decreased monocyte chemoattractant protein-1-induced monocyte migration. Importantly, the combination of ezetimibe with simvastatin was associated with a more significant reduction in plaque monocyte/macrophage content and some proinflammatory markers than observed with each drug alone. CONCLUSIONS AND IMPLICATIONS: Ezetimibe had beneficial effects both on atherosclerosis progression and plaque stabilization and showed additional anti-atherogenic benefits when combined with simvastatin. Its effect on monocyte migration provides a potentially beneficial action, in addition to its effects on lipids.

Acute aortic syndrome: a new look at an old conundrum.

The term acute aortic syndrome (AAS), coined several years ago, is now widely recognised. In the light of new findings in aortic pathology and in an era when modern imaging techniques are widely available and interventional management of AAS is increasing, some morphological and diagnostic aspects of acute aortic pathology have been examined and the syndrome updated. This article provides a new, comprehensive overview of the pathology, diagnosis, evolution and management of patients with AAS. As acute aortic disease is the most common fatal condition in patients with chest pain, prompt recognition and treatment is of paramount importance.

Cardiac metastasis from uterine leiomyosarcoma.

Cardiac metastases are more frequent than primary heart neoplasias. Nearly any malignant tumour may metastasize to the heart, but the most common are carcinomas rather than sarcomas. We report the case of a patient who presented with heart metastasis 6 years after resection of an uterine leiomyosarcoma. The patient died thirty months after surgical resection without evidence of cardiac recurrence. Although cardiac metastases from uterine leiomyosarcoma are exceptional, they should be suspected in the presence of suggestive symptoms, since they can be associated with long survival after surgical treatment.

Aspectos morfológicos de la disección aórtica / Morphological aspects of aortic dissections

Introducción. La disección aórtica clásica forma parte del síndrome aórtico agudo. En esta revisión se exponen los aspectos anatómicos más relevantes de los pacientes con disección aórtica clásica. Desarrollo. Esta enfermedad se caracteriza desde el punto de vista morfológico por tres hechos importantes: la presencia de una puerta de entrada, una aorta con luz doble y un colgajo intimomedial que separa las dos luces. En muchos pacientes también se puede observar una puerta de reentrada y algunos puntos de comunicación entre las dos luces. Ponemos énfasis en el trayecto habitual que sigue la progresión del hematoma disecante y sus posibilidades evolutivas. Se señalan las marcas diacríticas que distinguen las luces verdadera y falsa y se enumeran la mayoría de las complicaciones que pueden tener lugar en estos pacientes, sobre todo, la rotura de la pared externa de la luz falsa, la regurgitación aórtica que acompaña a algunos pacientes con disección tipo A y la afectación de las ramas aórticas. Conclusión. El conocimiento de los distintos aspectos morfológicos y evolutivos de la disección aórtica ayuda a comprender y valorar mejor los resultados de la utilización de las técnicas no invasivas en estos pacientes, lo cual va a suponer una mejora tanto en el diagnóstico como en el tratamiento

Introduction. Classical aortic dissection is included as a part of acute aortic syndrome. In this review we describe the most significant anatomical aspects of patients with classical aortic dissection. Development. From the morphological point of view this disease is characterised by three important facts, namely, the presence of a port of entry, an aorta with double lumen and an intimal-medial flap that separates the two lumina. A port of re-entry and a number of points communicating the two lumina can also be observed in many patients. We focus on the trajectory usually followed by the progression of dissecting haematomas and the possible ways they can develop. The diacritic marks that distinguish true and false lumina are specified, and most of the complications that can occur in these patients are also listed, the most important being rupture of the external wall of the false lumen, the aortic regurgitation suffered by some patients with type A dissection, and involvement of the aortic branches. Conclusions. A more comprehensive knowledge of the different morphological and developmental aspects of aortic dissections can help to better understand and appraise the results of using non-invasive techniques in these patients, which will lead to improvements in both their diagnosis and their treatment

Thermomechanical behavior of human carotid arteries in the passive state.

Localized heating or cooling is expanding the clinical procedures used to treat cardiovascular diseases. Advantageous implementation and development of these methods are linked indissolubly to a deeper understanding of the arterial response to combined mechanical and thermal loads. Despite this, the basic thermomechanical behavior of human blood vessels still remains largely unknown, primarily due to the lack of appropriate experimental data. In this work, the influence of temperature on the passive behavior of human carotid arteries was studied in vitro by means of inflation tests. Eleven carotid segments were tested in the range 0-200 mmHg at four different temperatures of 17, 27, 37, and 42 degrees C. The results show that the combined change of temperature and stress has a dramatic effect on the dilatation coefficient of the arterial wall, which is shifted from negative to positive depending on the stress state, whereas the structural stiffness of the arterial wall does not change appreciably in the range of temperatures tested.

Effects of bosentan on neointimal response following coronary angioplasty.

BACKGROUND: Endothelins are important vasoconstrictors and cellular-growth promoters. ETA-specific antagonists have been shown to reduce neointimal response to injury in some experimental angioplasty models. However, there is little information on the effects of dual ETA/ETB receptor blockers, such as bosentan, on neointimal proliferation following experimental coronary angioplasty. MATERIALS AND METHODS: Coronary injury was achieved by directional atherectomy in the left anterior descending artery of 20 pigs. Animals were randomly assigned to receive a daily dose of oral bosentan (30 mg kg-1) (group I, n = 10) or no treatment (group II, n = 10). At 4 weeks, arteries were processed for histomorphometry and endothelin characterization. RESULTS: Vessel injury score was similar among the two groups. Overall, a linear correlation was found between injury and neointimal development (r = 0.57, P = 0.01). This correlation had a lower slope in group I compared with group II (P < 0.001), indicating a smaller amount of neointimal development for a similar degree of injury in bosentan-treated animals. Multivariate regression showed that neointimal response was reduced by oral treatment with bosentan (beta: -0.59 mm2, 95% CI: -1.11/-0.06 mm2). In addition, immunostaining revealed fewer positive endothelin areas in group I arteries. CONCLUSIONS: Oral treatment with bosentan reduces neointimal development following coronary angioplasty in this experimental model.

Fibrodisplasia del tronco tibioperoneo. A propósito de un caso / Arterial fibrodysplasia of tibioperoneal trunk. A case report

Se presenta el caso de un varón de 43 años con un cuadro de isquemia aguda producida por la trombosis de un aneurisma del tronco tibioperoneo secundario a una fibrodisplasia. Se realiza una revisión de la literatura, se discute la metodología diagnóstica y se revisan las diferentes opciones terapéuticas (AU)

[Effect of cAMP on the function of endothelial cells and fibromuscular proliferation after the injury of the carotid and coronary arteries in a porcine model]. / Efecto del AMPc sobre la función de las células endoteliales y la proliferación fibromuscular tras la lesión de las arterias carótida y coronaria en un modelo porcino.

INTRODUCTION AND OBJECTIVE: Reendothelization of damaged blood vessels protects against the vascular injury response. We evaluated in vivo whether a systemic increase in cAMP accelerates reendothelization and attenuates intimal hyperplasia in injured swine carotid and coronary arteries. METHODS: Both carotid arteries of 10 swines were subjected to balloon injury. Five animals had been treated with 2 ml (10 mg) of Forskolin, an activator of the adenylate cyclase, and another 5 with 2 ml of saline solution. These animals were sacrificed at day 8, and carotid artery reendothelization was evaluated. The descendent coronary (DC) artery of another 19 pigs was injured by atherotome. Nine animals had been treated with 2 ml of Forskolin, and another 10 with 2 ml of saline solution. These animals were sacrificed at day 28, with myointimal proliferation and arterial geometric remodelation being evaluated. Likewise, in these animals intracellular cAMP levels were measured at baseline and 28 and 60 minutes after saline solution or Forskolin administration and 90 min after arterial injury. RESULTS: Eight days after balloon injury, carotid artery reendothelization was greater in the Forskolin-treated group compared with the control group (p = 0.02), and the number of CD31 positive cells was statistically increased in the treated group (38 +/- 11 cells) versus controls (11 +/- 9 cells). Although the degree of vascular injury caused by atherotome was similar in all of the arteries in the control group, restenosis was only observed in 40% of these animals. Correlation analysis demonstrated that intracellular cAMP may condition arterial geometric remodeling and the diameter of the lumen after vascular injury. CONCLUSION: Our results suggest that cAMP may promote reendothelization and attenuate fibromuscular proliferation.

Atorvastatin prevents glomerulosclerosis and renal endothelial dysfunction in hypercholesterolaemic rabbits.

BACKGROUND: Numerous studies have shown that elevated plasma cholesterol can exacerbate renal disease. However, the effect of lipids on renal structure and vascular function in normal kidneys is less well established. Therefore, the aim of this study was to evaluate the impact of hypercholesterolaemia on glomerular structure and vascular reactivity of segmental arteries in rabbits. In addition, we also studied whether or not atorvastatin can prevent these structural and vascular alterations in hypercholesterolaemic rabbits. METHODS: Male New Zealand rabbits were fed either a normal rabbit chow or a diet containing 1% cholesterol and treated or not with atorvastatin (1 mg/kg/day) for 12 weeks. Dose-response curves to acetylcholine (10(-9)-10(-4) mol/l) and sodium nitroprusside (10(-9)-10(-4) mol/l) were studied in segmental arteries in the presence or absence of the thromboxane A2/PGH2 receptor antagonist ifetroban (10(-5) mol/l). Glomerular size and structure were also evaluated. RESULTS: Compared with control animals, hypercholesterolaemic rabbits presented glomerular hypertrophy and several types of injuries (capillary collapse, hyalinosis and alterations of Bowman's capsule), suggesting diffuse glomerulosclerosis. Segmental arteries also showed relaxing responses to acetylcholine and sodium nitroprusside which were lower than and similar to, respectively, those of control animals. The presence of ifetroban improved the acetylcholine response only in hypercholesterolaemic rabbits. Atorvastatin treatment prevented vascular and most glomerular changes associated with hypercholesterolaemia even in the presence of very high cholesterol levels. CONCLUSIONS: Atorvastatin exerts a protective effect on renal damage associated with hypercholesterolaemia even in the presence of deleterious levels of plasma cholesterol.

Atherosclerotic aortic rupture: documentation by transesophageal echocardiography.

We report a case of a 77-year-old woman who had a rupture of the descending thoracic aorta as a complication of an atherosclerotic aortic plaque. Transesophageal echocardiography enabled the diagnosis of aortic rupture and was very useful in the patient's surgical management.

[Aspiration of large intracoronary thrombus after apparently successful angioplasty. Therapeutic implications]. / Aspiración de gran trombo intracoronario tras angioplastia aparentemente con éxito. Implicaciones terapéuticas.

We present a case in which, after performing an optimal angioplasty after an acute myocardial infarction with intracoronary thrombus, normal coronary flow was not achieved. After aspirating through the guiding catheter we obtained a large thrombus that the histopathologic study confirmed as a recent thrombus and, subsequently, normal flow was reestablished. The procedure was completed with a successful intracoronary stent implantation, with an uneventful clinical course. The therapeutic and diagnostic implications of this case are discussed.

The protective role of atorvastatin on function, structure and ultrastructure in the aorta of dyslipidemic rabbits.

Responses to both an endothelium-dependent (acetylcholine 10(-9)-10(-5) mol/l) and an endothelium-independent vasodilator (sodium nitroprusside 10(-10)-10(-6) mol/l) were studied in aortic rings from rabbits fed or not with a diet containing 0.5% cholesterol plus 14% coconut oil for 14 weeks and treated or not with atorvastatin (2.5 mg/kg/day). Morphometric and ultrastructure analyses were also performed. Rabbits fed the dyslipidemic diet presented higher plasma cholesterol and triglyceride concentrations than controls (P < 0.05). This was associated with intima-media thickening and, consequently, aortic stenosis (29 +/- 3%) since vessel cross-sectional area did not change. Endothelial cells presented numerous alterations in dyslipidemic rabbits. Atorvastatin treatment only reduced plasma levels in dyslipidemic rabbits (P < 0.05), which were nevertheless higher than those of controls. In addition, it prevented the reduction in acetylcholine relaxation in hypercholesterolemic animals. Atorvastatin administration also enhanced the response to acetylcholine in rabbits fed a control diet. Likewise, atorvastatin treatment reduced lesion area and consequently increased aortic lumen in dyslipidemic rabbits but did not modify media thickening. It also prevented the majority of the ultrastructural changes observed in endothelial cells. In conclusion, chronic atorvastatin treatment exerts a protective role in vascular function, structure and ultrastructure even in the presence of high cholesterol and triglyceride plasma levels.

Effect of atorvastatin on endothelium-dependent constrictor factors in dyslipidemic rabbits.

Relaxations to acetylcholine and contractions to acetylcholine in the presence of the nitric oxide (NO) synthesis inhibitor (L-N(G)-nitroarginine methyl ester, L-NAME) were studied in aortic rings from rabbits fed either a control or a diet containing 0.5% cholesterol+14% coconut oil for 14 weeks and treated or not with atorvastatin (2.5 mg kg(-1) day(-1)). Rings were incubated with the endothelin (ET(A)) receptor antagonist BQ123, and/or the thromboxane A(2) (TXA(2))/prostaglandin H(2) (PGH(2)) receptor antagonist ifetroban. In rabbits, high cholesterol and triglyceride plasma levels were associated with intimal thickening and blunted acetylcholine-relaxation as compared with controls. By contrast, acetylcholine+L-NAME response was higher. Incubation with either ifetroban or BQ123 increased acetylcholine-relaxation in both diet groups and it reduced the constrictor response only in dyslipidemic rabbits. Removal of endothelium reduced acetylcholine+L-NAME contraction in dyslipidemic rabbits, although increased it in control animals. Atorvastatin treatment reduced plasma lipid levels and lesion size in dyslipidemic animals. Likewise, it prevented acetylcholine-relaxation reduction. In addition, atorvastatin reduced constrictor response in dyslipidemic rabbits but only in rings with endothelium. Incubation with either ifetroban or BQ123 did not further modify these responses in atorvastatin-treated animals in any group. These data suggest that ET and TXA(2) availabilities seem to participate in the endothelial dysfunction associated with dyslipidemia. Atorvastatin treatment reduces intimal thickening and improves endothelial dysfunction in rabbits. This effect seems to be a consequence of its ability to act on ET and TXA(2) systems.

[The cost effectiveness of echography biopsy]. / Rentabilidad de la ecopsia.

Ecopsy is a postmortem technique which, by means of echography-guided puncture and/or aspiration obtains material for histological analysis. This study compared cost and time employed in 100 ecopsies and 100 classic necropsies and confirmed that cost of materials in ecopsy is 65% lower than that in necropsy. Physicians, necropsy technicians, laboratory technicians and secretary team personnel spent 33%, 54%, 19% and 32% less time than in necropsy. The clinical report of ecopsy was finished within nine days even with the brain study included.

Disruption of cadherin-related junctions triggers autocrine expression of vascular endothelial growth factor in bovine aortic endothelial cells : effects on cell proliferation and death resistance.

The mechanisms involved in the blockade of proliferation in confluent endothelial cells are insufficiently understood. In this regard, the continuity of intercellular junctions appears to be critical to the regulation of endothelial monolayer cell growth. The present study examined the hypothesis that the disruption of the intercellular adherens junctions will trigger both endothelial cell proliferation and autocrine production of growth factors. With this purpose, we assessed the changes in growth, death resistance, and expression of vascular endothelial growth factor (VEGF) under conditions of disruption of the intercellular junctions between endothelial cells. Disruption of cell junctions was produced by means of a specific anti-vascular endothelial cadherin monoclonal antibody, EGTA, or cytochalasin D. Our results disclosed that these maneuvers induce an increase in VEGF mRNA production, with transcription of the 121-, 165-, and 189-amino acid isoforms of VEGF. Further evidence of the relationship between endothelial cells monolayer continuity and VEGF protein expression was obtained by the demonstration of an increase in VEGF protein, as determined by Western blot, induced by the aforementioned maneuvers, as well as by immunocytochemical detection of increased VEGF staining in the areas surrounding a mechanical endothelial injury and in endothelial cells at subconfluence. In functional terms, the autocrine expression of VEGF was associated with growth-promoting and cytoprotective effects, as assessed by [(3)H]thymidine uptake, (51)Cr release, and flow cytometry. In conclusion, our results reveal that disruption of homophilic interendothelial junctions induces VEGF expression. Under these conditions, autocrine VEGF appears to have a relevant role in death inhibition and proliferation of endothelial cells.

AT(1) receptor antagonism reduces endothelial dysfunction and intimal thickening in atherosclerotic rabbits.

The effects of angiotensin (AT)(1) receptor antagonists on functional and morphological alterations associated with atherosclerosis are not well known. The current study was performed to examine the long-term effects of valsartan (3 or 10 mg/kg per day for 10 weeks) on endothelial function and structural changes in aorta from rabbits fed with either a control diet or a cholesterol-enriched diet. Rabbits fed with the cholesterol-rich diet showed higher (P<0.05) plasma levels of cholesterol than did controls. Treatment with valsartan (3 or 10 mg/kg per day) did not alter plasma cholesterol levels or systolic arterial pressure in any group. Contractions induced by angiotensin II were comparable in both control and hypercholesterolemic rabbits and were markedly reduced by treatment with valsartan. Relaxations induced by acetylcholine were lower in hypercholesterolemic rabbits than in controls. Treatment with valsartan (3 or 10 mg/kg per day) enhanced (P<0.05) this response in hypercholesterolemic rabbits but not in controls. Lumen and media cross-sectional areas were comparable in control and hypercholesterolemic rabbits. Vessel area was higher (P<0.05) in hypercholesterolemic rabbits than in controls. Intimal lesion was 29.5+/-6% in cholesterol-fed rabbits and nonexistent in control rabbits. Treatments with 3 and 10 mg/kg per day valsartan reduced (P<0.05) intimal lesion to 2.4+/-0.7% and 2.7+/-0.9%, respectively, and increased lumen area in hypercholesterolemic rabbits. No changes in either vessel or media cross-sectional areas were observed in these animals. In summary, angiotensin II, through AT(1) receptors, appears to play a key role in the development of the vascular functional and structural changes associated with hypercholesterolemia. AT(1) receptor antagonists, besides their antihypertensive effects, could be an important therapeutic tool to reduce the development of atherosclerosis.

Clinical, anatomic, and echocardiographic characteristics of aneurysms of the mitral valve.

This study describes the clinical, anatomic, echocardiographic, and Doppler features of 13 patients with mitral valve aneurysms. Eleven patients had definitive criteria for infective endocarditis. Transesophageal echocardiography was superior to conventional echocardiography in detecting and assessing aneurysms. Patients with heart failure required surgery. Echocardiographic detection of this lesion should not be, by itself, an immediate surgical indication.