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Explore the source record for details and available documents.
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Although macroangiopathies such as peripheral vascular disease (PVD), cerebral vascular disease (CVD), and coronary heart disease (CHD) can often be observed in patients with diabetes mellitus, they are not specific for diabetes mellitus. Moreover, it is unclear whether their progressive mechanism is different. In the present study, we compared the risk factors among the diabetic macrovascular complications. Univariate analyses showed that in all patients, age at examination, duration of diabetes, thrombin-antithrombin III complex (TAT) level, fibrinogen level, lipoprotein (a) (Lp(a)) level, total cholesterol (T-Chol) level, and existence of microagiopathy were risk factors for PVD. Age, duration of diabetes, insulin level, TAT level, fibrinogen level, HDL cholesterol (HDL-Chol) level, hypertension, and nephropathy were risk factors for CVD. Only fibrinogen level was a risk factor for CHD. Moreover, Lp(a) level was a risk factor for PVD and CVD in male patients, but not in females. On the other hand, insulin level was a risk factor for CVD in female patients, but not in males. Multivariate analyses showed that TAT level, T-Chol level, and neuropathy were independent variables for PVD and that age, TAT level, and HDL-Chol level were independent variables for CVD. On the other hand, only fibrinogen level was the independent variable for CHD in males. Our results suggest that the progressive mechanism of PVD and CVD might be different from that of CHD and might differ according to gender in Japanese diabetic patients.
Cell surface adhesion molecule expression is likely to be important in inflammation, atherosclerosis and cancer, and soluble forms of many of these molecules are present in plasma. We measured levels of the soluble form of platelet endothelial cell adhesion molecule-1 (sPECAM) by ELISA in the serum of 77 patients with frank atherosclerosis, 69 patients with inflammatory connective tissue disease, and 39 patients with cancer. Each group of patients was controlled by an equal number of age- and sex-matched healthy subjects. There was no difference between sPECAM in patients with atherosclerosis and their matched controls or between patients with connective tissue disease and their controls. However, sPECAM levels were lower (16.6 +/- 5.0 ng/ml, mean +/- SD) in patients with cancer than in their controls (21.1 +/- 4.4 ng/ml, P < 0.001). No differences were found in sPECAM levels between the major subgroups of each type of disease, or as a result of factors such as age, sex or smoking in the controls. In contrast to levels of many other soluble adhesion molecules, levels of sPECAM are not altered in inflammatory or atherosclerotic vascular disease and therefore appear to have little relevance in these conditions. However, there may be significant differences in sPECAM levels in patients with low levels in cancer. Additional investigations are therefore justified.
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Vascular nitric oxide (NO) is involved in many physiologic and pathophysiologic processes throughout the body. Many vascular diseases have a reduction in the activity of endothelium-derived NO as an important component involved in the initiation and/or progression of the disease. It is now known that there are multiple mechanisms for this reduction in NO activity with one or more mechanisms operating depending on the specific condition or stage of a disease. In other instances, the therapy for certain diseases is responsible for the reduction in NO activity and contributes to the acceleration of vascular disease. This review details the known mechanisms of dysfunction of the NO pathway leading to vascular diseases, which provides the rationale for why certain therapies can improve while other therapies adversely affect vascular health.
Vascular disease underlies many of the complications of diabetes and includes coronary, cerebral, renal, peripheral and retinal vascular abnormalities. Magnesium (Mg) and potassium (K) deficiencies occur frequently in diabetic patients. Because of the vasoconstrictive effects of hypomagnesemia and hypokalemia and the adverse effects of Mg and K deficiency on carbohydrate metabolism we hypothesize that routine Mg and K supplementation of all hypomagnesemic diabetics will ameliorate or prevent the ravages of diabetic vascular disease.
Vascular disease is the most common cause of death in the industrialized world. Although significant progress has been made in treating these disorders, more therapeutic agents must be developed that effectively prevent, arrest, or reverse this disease. Recent insights into the pathogenesis of vascular disease have opened up a new frontier of molecular therapies that target molecules as diverse as adhesion molecules and transcription factors. The biological rationale for these new therapies and their prospects for success are discussed.
Vascular disease in the pediatric population is a poorly understood process which is often underestimated in its incidence. The common beginnings of such ubiquitous diseases as atherosclerosis manifest themselves at a cellular level shortly after birth. Other common systemic disorders, including congestive heart failure and sepsis, are also intricately associated with dysfunctional vasculature. Progress in the understanding of normal and pathophysiologic processes within the vascular system begins with the "control center"--the endothelial cell. The purpose of this review is to consolidate a body of knowledge on the processes that occur at the cellular level within the blood vessel wall, and to simplify the understanding of how imbalances in these physiologic parameters result in vascular disease.
More than 30 years have passed since the first human heart transplantation was performed. Since then, short-term survival after heart transplantation has been markedly improved, but this development has not been paralleled with a similar improvement in long-term survival. One of the major reasons for this is the subsequent development of heart allograft vascular disease, an obliterative disease in the coronary arteries of the transplanted heart. The dubious effect of re-vascularization in this disease, the less favorable outcome after repeat heart transplantation, and the low donor supply have called for intensified research for new and efficient prophylactic therapies against heart allograft vascular disease. This research has lead to improved knowledge about diagnosis, etiology, pathogenesis, prophylaxis, and treatment possibilities. The most important among these seem to be: (i) the introduction of intravascular ultrasound for early detection of the disease; (ii) evidence to suggest that hyperlipidemia, insufficient immunosuppressive therapy, human leukocyte antigen (HLA)-mismatch, and infection with cytomegalovirus (CMV) all may promote allografts vascular disease; and (iii) the introduction of at least two promising prophylactic therapies in humans namely 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors and calcium entry blockers, and others potentially promising e.g. angiotensin-converting enzyme-inhibitors, angiopeptin, mycophenolate mofetil and rapamycin. This review summarizes present knowledge on the possibilities of inhibiting or treating heart allograft vascular disease incorporating evidence from both human and experimental studies.
Physical inactivity is a risk factor for cardiovascular disease. Regular aerobic and resistance training increases exercise capacity and plays a role both in the primary and secondary prevention of cardiovascular disease. Patients with coronary artery disease, peripheral vascular disease, or diabetes mellitus must be considered individually when prescribing exercise because their clinical status can vary greatly. In addition, a majority of these patients have multiple comorbid disorders such as renal, neurologic, and retinal disease that may affect their ability to exercise safely. Therefore, a preparticipation medical evaluation is required. An exercise prescription should be tailored to each person's unique set of circumstances and reflect an effort to maximize the anticipated benefits while minimizing the risks.
This review examines the pathology, clinical effects and physiological disturbances produced by vascular disease and autonomic neuropathy in the lower limb in diabetic subjects. Atherosclerosis is a major factor in causing foot lesions in diabetics. The distribution of the disease frequently makes vascular reconstructive surgery difficult or impossible but an aggressive approach to reconstruction is justified because the results of major amputations are bad. Arterial calcification probably has no significant effect on the blood supply to the foot. There is some evidence that disease of arteries in the foot may be associated with the development of ulcers or gangrene. Disease of the arterioles and capillaries is frequent, but there is little evidence that this microangiopathy causes lesions. Autonomic neuropathy affecting the limb is also common, and although there are several mechanisms by which this might predispose to ulcers or gangrene, there is little evidence of such a direct relationship. In a patient presenting with ulceration or gangrene of the foot it is often impossible to determine the relative roles of vascular disease, affecting large or small vessels, and neuropathy, either somatic or autonomic, in the development of the lesion. Further progress depends on the development of more direct methods for assessing microvascular and autonomic nervous function.
Vascular problems involving the brachiocephalic vessels may occur from atherosclerosis, trauma, vasculitis, infection, and procedures for congenital heart disease. A wide variety of symptoms and signs may result from such disorders. This study is a report of five unusual manifestations of brachiocephalic vascular diseases. Diagnosis, management, and previous surgical experience is discussed relating to each case illustrating the complexity and variability of brachiocephalic vascular pathology.
Vascular endothelial cells, critically situated at the blood-tissue interface, exert important effects on vascular tone and permeability, regulate the coagulation and fibrinolytic systems, mediate translocation of inflammatory cells to the tissue compartment, and modulate proliferation of vascular smooth muscle cells. As the physiology of the endothelium has been defined, defects in endothelial function have been identified in association with human disease, and a syndrome of dysfunctional endothelium has been described. Although it remains debatable whether a coherent syndrome of endothelial dysfunction exists, disordered endothelial biology appears to contribute to the pathophysiology of human vascular disease. Identification of specific molecular mechanisms offers potential targets for novel therapeutic interventions, including genetic modification of endothelial cells in vivo.