Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: UMLS:C0004153 (atherosclerosis)
77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Type 1 diabetes is associated with a substantially increased risk of cardiovascular disease that might not always be appreciated in view of the fairly young age of patients with this condition. In fact, in type 1 diabetes, the heart is subject to a variety of pathological insults, including accelerated atherosclerosis, cardiac autonomic neuropathy, and possibly intrinsic cardiomyopathy. Although the relation between hyperglycaemia and microvascular complications has been well established, a direct effect of hyperglycaemia on cardiovascular disease in type 1 diabetes has long been debated. More recently, several studies, most notably the Diabetes Control and Complications Trial/Epidemiology of Diabetes Interventions and Complications, have clarified this issue and provided conclusive evidence that hyperglycaemia is indeed a mediator of cardiovascular risk in type 1 diabetes and that intensive diabetes therapy can reduce cardiovascular disease outcomes. We review current concepts in type 1 diabetes and the heart, focusing on recent insights into the central role of hyperglycaemia.
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PMID:Type 1 diabetes, hyperglycaemia, and the heart. 1880 26

The aim of the work--the study of risk factors and detection of prevailing clinical form of diabetic foot infections (DFI) in dependence on type diabetes mellitus (DM). 157 patients with DM and DFI (25 type 1 DM cases and 132 type 2 DM cases) and 689 DM patients without DFI (282 type 1 DM cases and 407 type 2 DM cases) were examined. DFI cases differed from both type DM without DFI in greater number of complications. Associated with decompensated DM amputations and developing ulcerations were been mentioned in history in about a quarter of both type DM patients. DFI risk factors in type 1 DM appeared to be a combination of sensor and autonomic neuropathy (OR: 6.58; 95% CI: 2.74-14.9; a < 0.05), preprpoliferative retinopathy (RP) (OR: 4.62; 95% CI: 1.98-10.7; a < 0.05), in type 2 DM: macroangiopathy of lower extremities (OR: 4.59; 95% CI 2.98-7.1; a < 0.05), obesity (OR: 4.65; 95% CI 2.42-8.9; a < 0.05), concomitant exertional angina (OR 3.3; 95% CI 2.2-5.1; a < 0.05), a proteinuric stage of nephropathy (OR: 2.6; 95% CI: 1.74-3.9; a < 0.05), prominent sensor neuropathy (OR: 2.3; 95% CI 1.3-4.2; a < 0.05), preprpoliferative RP (OR: 2.1; 95% CI 1.41-3.13; a < 0.05). In type 1 DM and DFI neuropathic form of DFI prevailed (88%), in type 2 DM--neuroischemic form of DFI (66%). Ischemic form of DFI was determined in type 2 DM only (6%). In type 2 DM cases with DFI there was revealed a high rate of risk factors of atherosclerosis.
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PMID:[The risk factors and clinical forms of diabetic foot infections in dependence on the type of diabetes mellitus]. 1875 47

The metabolic syndrome of vascular risk is threatening large numbers of ever-younger people. To date, the syndrome has been chiefly viewed as a potential risk marker that confers a heightened probability of developing type 2 diabetes and occlusive atherothrombotic disease of large- and medium-sized arteries. Accumulating evidence suggests that the components of the metabolic syndrome may also adversely affect the microvasculature through several inter-related mechanisms. These include the following observations: classic risk factors for macrovascular disease such as high blood pressure and dyslipidaemia also accelerate microvascular complications of diabetes, lesser disturbances of glucose metabolism (i.e. impaired glucose tolerance) may be associated with some forms of microvascular dysfunction, non-glucose intermediary metabolites may promote renovascular hypertension thereby damaging the microvasculature, and insulin resistance appears to be directly associated with microvascular dysfunction. In turn, microvascular complications such as nephropathy and autonomic neuropathy may promote the development and progression of atherosclerosis. We argue that the vascular implications of the metabolic syndrome should be broadened to include the microvasculature. The hypothesis that vascular events can be prevented, or at least deferred, through earlier therapeutic intervention in pre-diabetic subjects with glucose intolerance is amenable to testing in clinical trials.
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PMID:Vascular disease in the metabolic syndrome: do we need to target the microcirculation to treat large vessel disease? 1957 72

To test the hypothesis that cardiovascular autonomic neuropathy (CAN) in Type 2 diabetes is a risk factor of coronary artery calcification (CAC), in this cross-sectional study, 118 patients (60 males, 58 females) with type 2 diabetes mellitus were randomly selected from the diabetes clinic of Kyungpook National University Hospital, Daegu, Korea, between January, 2008 and September, 2008. The subjects, whose mean age was 56.9+/-1.1 years, were tested for CAN by Ewing's method which employs five non-invasive tests of autonomic function. The coronary calcium score (CCS) was determined by Multi Detector-row Computed Tomography (MDCT). Statistical analysis was performed by using SPSS 13.0 (SPSS, Inc., Chicago,-Illinois). CAN was found in 31/118 (26.3%) patients. Compared to the patients without CAN, the patients with CAN were significantly older and had significantly higher triglyceride levels, blood pressure, pulse pressure, fasting c-peptide levels, CAN scores, and log-transformed coronary calcium scores [ln(CCS+1)]. The CAN scores correlated positively with ln(CCS+1) values (r = 0.214; P = 0.028). Multiple regression analysis using ln(CCS+1) as a dependent variable showed that CAN score (beta coefficient 0.623, 95% CI 0.059 approximately 1.188, P = 0.031) associated independently with ln(CCS+1). In conclusion, CAN was associated independently with CAC, which suggests that CAN is a risk factor of coronary atherosclerosis in patients with type 2 diabetes. This may help to explain the excess cardiovascular mortality seen in diabetic patients with CAN.
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PMID:Relationship between cardiovascular autonomic neuropathy and coronary artery calcification in patients with type 2 diabetes. 2018 62

The reduction of mortality from sudden cardiac arrest (SCA) in the setting of coronary heart disease (CHD) remains a major challenge, especially among patients with type 2 diabetes. Diabetes is associated with an increased risk of SCA, at least in part, from an increased presence and extent of coronary atherosclerosis (macrovascular disease). Diabetes also is associated with microvascular disease and autonomic neuropathy; and, these non-coronary atherosclerotic pathophysiologic processes also have the potential to increase the risk of SCA. In this report, we review the absolute and relative risk of SCA associated with diabetes. We summarize recent evidence that suggests that the increase in risk in patients with diabetes is not specific for SCA, as diabetes also is associated with a similar increase in risk for non-SCA CHD death and non-fatal myocardial infarction. These data are consistent with prior observations that coronary atherosclerosis is a major contributor to the increased SCA risk associated with diabetes. We also present previously published and unpublished data that demonstrates that both clinically-recognized microvascular and autonomic neuropathy also are associated with the risk of SCA among treated patients with diabetes, after taking into account prior clinically-recognized heart disease and other risk factors for SCA. We then discuss how these data might inform research and clinical efforts to prevent SCA. Although the prediction of SCA in this "high" risk population is likely to remain a challenge, as it is in other "high" risk clinical populations, we suggest that current recommendations for the prevention of SCA in the community, related to both lifestyle prescriptions and risk factor reduction, are likely to reduce mortality from SCA among patients with diabetes.
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PMID:Type 2 diabetes mellitus and the risk of sudden cardiac arrest in the community. 2019 71

Patients with diabetes mellitus are at higher risk of cardiac arrhythmias and sudden death. Although there are several animal and human studies on this topic, the pathophysiology of the increased electrical vulnerability in diabetes is complex and remain undefined. It is conceivable that an interplay of several concomitant factors may facilitate the occurrence of arrhythmias. Atherosclerosis as well as microvascular disease, which are increased in diabetic patients, may facilitate myocardial ischemia that predisposes to cardiac arrhythmias and sudden death. In addition, autonomic neuropathy and/or cardiac repolarization abnormalities such as prolonged QT interval and altered T-waves of the diabetic heart also increases electrical instability. Therefore, all these factors may simultaneously contribute to create an electrical instability leading to cardiac arrhythmias and sudden cardiac death. Recently, we have demonstrated that diabetes is the strongest predictor of atrial fibrillation (AF) progression and that diabetic patients frequently have asymptomatic episodes of AF with silent arrhythmia progression. Another recent study has reported that patients with type 2 diabetes and AF are at substantially higher risk of death of any cause compared with those without AF. These seminal studies emphasize that AF in diabetic patients should be regarded as a prognostic marker of adverse outcome and then a prompt aggressive management of all risk factors is required. In conclusion, diabetes mellitus significantly alters the cardiac electrophysiology throughout several complex mechanisms greatly contributing to create an electrical instability of the heart, which may lead to potentially life-threatening arrhythmias and sudden cardiac death.
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PMID:Cardiac electrophysiology in diabetes. 2044 Feb 55

We examined the relationship between the coefficient of variation in the R-R intervals (CVR-R) using electrocardiograms and the ultrasonic intima-media thickness (IMT) of the carotid artery, an atherosclerotic parameter, in type 2 diabetes mellitus (DM) patients with diabetic neuropathy (n=47, males/females: 29/18; mean age: 62 years). In this study, the CVR-R-related indexes, including CVR-R at rest (CVR-R(rest)), CVR-R with deep breaths (CVR-R(breath)) and their difference (CVR-R(breath) minus CVR-R(rest): CVR-R(dif)), were defined. Data such as body mass index, smoking habits, hemoglobin A1c, blood pressure, and serum low-density lipoprotein were collected. A significant inverse correlation was observed between max-IMT and CVR-R(dif) (beta=-0.34, p=0.042), but not CVR-R(rest) or CVR-R(breath), in multivariate analyses adjusted for all the data. Therefore, the CVR-R(dif) may serve as a clinical index for the diabetic autonomic neuropathy-atherosclerosis relation in type 2 DM patients.
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PMID:The correlation between CVR-R and carotid atherosclerosis in type 2 diabetes mellitus patients with diabetic neuropathy. 2068 28

Diabetic cardiomyopathy (DCM), although a distinct clinical entity, is also a part of the diabetic atherosclerosis process. It may be independent of the coexistence of ischemic heart disease, hypertension, or other macrovascular complications. Its pathological substrate is characterized by the presence of myocardial damage, reactive hypertrophy, and intermediary fibrosis, structural and functional changes of the small coronary vessels, disturbance of the management of the metabolic cardiovascular load, and cardiac autonomic neuropathy. These alterations make the diabetic heart susceptible to ischemia and less able to recover from an ischemic attack. Arterial hypertension frequently coexists with and exacerbates cardiac functioning, leading to the premature appearance of heart failure. Classical and newer echocardiographic methods are available for early diagnosis. Currently, there is no specific treatment for DCM; targeting its pathophysiological substrate by effective risk management protects the myocardium from further damage and has a recognized primary role in its prevention. Its pathophysiological substrate is also the objective for the new therapies and alternative remedies.
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PMID:Diabetic cardiomyopathy: from the pathophysiology of the cardiac myocytes to current diagnosis and management strategies. 2105 75

Diabetic heart disease is currently defined as left ventricular dysfunction that occurs independently of coronary artery disease and hypertension. Its underlying etiology is likely to be multifactorial, acting synergistically together to cause myocardial dysfunction. Multimodality cardiac imaging, such as echocardiography, nuclear, computed tomography, and magnetic resonance imaging, can provide invaluable insight into different aspects of the disease process, from imaging at the cellular level for altered myocardial metabolism to microvascular and endothelial dysfunction, autonomic neuropathy, coronary atherosclerosis, and finally, interstitial fibrosis with scar formation. Furthermore, cardiac imaging is pivotal in diagnosing diabetic heart disease. Thus, the aim of the present review is to illustrate the role of multimodality cardiac imaging in elucidating the underlying pathophysiologic mechanisms of diabetic heart disease.
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PMID:Multimodality imaging in diabetic heart disease. 2114 61

Hormones have influence on many tissues and organs including the cardiovascular system. This article analyzes fluctuations that happen in a child's cardiovascular system in selected endocrinopathies. We are pointing out the higher risk, in the course of diabetes, of development of arterial hypertension and atherosclerosis including participating mechanisms in their pathogenesis - disorders of the lipid metabolism, hiperinsulinaemia, insulin resistance or/and autonomic neuropathy. We are describing how the increased and reduced action of thyroid hormones on certain molecular pathways in the heart and vasculature causes relevant cardiovascular derangement. In the article, we are signaling also that the cardiovascular consequences of cortisol excess are elevation of blood pressure, obesity, hyperinsulinemia and/or dyslipidemia. This review analyzes the relationship of cortisol excess to these cardiovascular risk factors and to putative mechanisms for hypertension. In reference to clinical studies we are describing how the deficiency of the growth hormone is connected with a development of risk factors of cardiovascular diseases. In conclusion we underlined that early diagnosis and proper treatment of illnesses of the endocrine system can protect our pediatric patients from serious cardiac complications in later years.
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PMID:[Changes in the cardiovascular system in selected endocrinopathies in children]. 2148 56


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