Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dialysis patients constitute a high-risk subset of patients for developing cardiovascular disease, which accounts for nearly 50% of deaths. After stratification for age, race and gender, cardiovascular mortality is 10-20 times higher in dialysis patients than in the general population. Cardiovascular disease in this population cannot be fully explained by the high prevalence of classical cardiovascular risk factors (age, hypertension, diabetes, hyperlipidemia, smoking, etc.). Thus, the involvement of "new" cardiovascular risk factors (hyperhomocysteinemia, hyperfibrinogenemia, high lipoprotein (a) levels, oxidative stress, inflammation, etc.), and uremia-related factors (anemia, impaired calcium-phosphorus metabolism, hyperparathyroidism, accumulation of endogenous inhibitors of nitric oxide synthesis, etc.) has been also invoked to play a role in the increased cardiovascular risk in these patients. Endothelial dysfunction is the initial event in the development of atherosclerosis. Uremic patients exhibit an endothelial dysfunction, even before starting dialysis, which persists o is even aggravated under dialysis treatment. Uremic patients must be considered at high risk of developing cardiovascular disease. Thus cardiovascular risk factors in these patients should be managed early, aggressive and multifactorially in order to reduce their high cardiovascular morbidity and mortality.
 ...
PMID:[Cardiovascular risk in patients with chronic renal failure. Patients in renal replacement therapy]. 1198 73

The established risk factors for atherosclerosis such as hypertension, smoking, diabetes mellitus, hyperlipidemia, and hyperhomocysteinemia do not explain clinical and epidemiological features of coronary heart disease (CHD). The role of infectious disease as a CHD risk factor may partly explain these features. Chronic infection with various microorganisms, particularly, Chlamydia pneumoniae, Cytomegalovirus (CMV) and Helicobacter pylori may play a role in etiological factors, linking inflammation and atherogenesis. Results from epidemiological studies, pathology of atherosclerotic plaques, animal studies, molecular biology and clinical antibiotic trials indicated a positive association between C. pneumoniae infection and CHD. Chronic infection might also influence preexisting plaque by enhancing T cell activation, which participate in destabilization of intimal cap. However, the exact nature of pathophysiological link between the organisms and CHD remains to be elucidated. Future antibiotic interventional studies may help to further clarify the role of chronic infection and inflammation in CHD.
 ...
PMID:Chronic infections and atherosclerosis. 1200 6

We present a young male patient referred to our hospital with leg ulcers on both legs that were more than 3 years refractory to standard treatment with compression therapy. By thrombophilia screening factor V Leiden mutation, hyperhomocysteinemia and evidence for impaired fibrinolysis were found. Treatment with folic acid in combination with long-term oral anticoagulant therapy was added to non-elastic compression therapy. The leg ulcers showed slow improvement and complete healing within 3 years. During a 6-year follow-up period neither new thrombo-embolic events occurred nor recurrence of ulcerations. This case suggests a potential synergistic pathogenic role of factor V Leiden, hyperhomocysteinemia and impaired fibrinolysis in the development of postthrombotic syndrome and his sequelae. We postulate that increased formation of thrombi in the microcirculation of the skin in combination with ambulatory venous hypertension due to recurrent deep venous thrombosis might explain our observation.
 ...
PMID:Recurrent leg ulcers in a young man with hyperhomocysteinemia, factor V Leiden and impaired fibrinolysis. 1201

Retinal vein occlusion (RVO) is a relatively common disease that is often associated with a variety of systemic disorders including arterial hypertension, diabetes mellitus, dyslipidemia, and systemic vasculitis. There are various types of RVO, categorized on the basis of the site of occlusion and on the type of consequent vascular damage. Central retinal vein occlusion (CRVO) is the most frequently occurring and clinically relevant type of RVO. In addition to the well-known classical risk factors, new hemostasis-related ones have been investigated in patients affected by CRVO. The data concerning a number of parameters remain contradictory; yet, high levels of type 1 plasminogen activator inhibitor (PAI-1) and hyperhomocysteinemia appear to play a significant role in the pathogenesis of this disease. Although based on a limited number of studies, this new knowledge could eventually provide important indications regarding prognosis and therapeutic strategies.
 ...
PMID:Cardiovascular and thrombophilic risk factors for central retinal vein occlusion. 1202 Jun 23

Overt hypothyroidism may result in accelerated atherosclerosis and coronary heart disease (CHD) presumably because of the associated hypertension, hypercholesterolemia, and hyperhomocysteinemia. As many as 10%-15% of older women have subclinical hypothyroidism (SH) and thyroid autoimmunity. Whether SH is associated with risk for CHD is controversial. We examined 57 women with SH and 34 healthy controls. SH was defined as an elevated thyrotropin (TSH) (>4.5 mU/L) and normal free thyroxine (FT(4)) level (8.7-22.6 nmol/L). None of the patients had been previously treated with thyroxine. In all participants we determined blood pressure, body mass index (BMI), and fasting TSH, FT(4), antibodies to thyroid peroxidase and thyroglobulin, total cholesterol (TC), high-density lipoprotein cholesterol (HDL-C), low-density lipoprotein cholesterol (LDL-C), triglycerides, folic acid, vitamin B(12), creatinine, and total plasma homocysteine levels. The SH and control groups did not differ in their total homocysteine values. Mean diastolic blood pressure was increased in SH patients versus controls (82 vs. 75 mm Hg; p < 0.01). Mean values of TC, HDL-C, LDL-C, triglycerides, TC/HDL-C, and LDL-C/HDL-C were not different in patients with SH compared with controls. Individual analysis revealed that the percentage of patients with SH having hypertension (20%), hypertriglyceridemia (26.9%), elevated TC/HDL-C (11.5%), and LDL-C/HDL-C (4%) ratios were higher than the percentages in controls. Hyperhomocysteinemia (> or = 10.98 micromol/L) was observed in 29.4% of SH and was not significantly different from the percentage in controls (21.4%). No significant correlation between TSH and biochemical parameters was detected. We conclude that subclinical hypothyroidism in middle-aged women is associated with hypertension, hypertriglyceridemia, and elevated TC/HDL-C ratio. This may increase the risk of accelerated atherosclerosis and premature coronary artery disease in some patients.
 ...
PMID:Risk factors for cardiovascular disease in women with subclinical hypothyroidism. 1209 4

Often ignored, neurocognitive dysfunction in chronic heart failure represents a daunting morbidity progressing to loss of self-reliance. Although the precise mechanisms arbitrating the development of this disorder remain elusive, microembolization and cerebral hypoperfusion are implicated. Other causes of cognitive decline may include prior cardiac surgery, chronic hypertension, sleep disordered breathing, hyperhomocysteinemia, dementia of aging, and more traditional causes such as Alzheimer's disease. The discovery of neurocognitive defects in heart failure must prompt a well-constructed diagnostic evaluation to search for the underlying causes since this process may be at least partially reversible in many cases.
 ...
PMID:Difficult cases in heart failure: the challenge of neurocognitive dysfunction in severe heart failure. 1214 48

Two siblings, a boy age 12 and his sister age 4 years, presented with proteinuria and hematuria, hypertension, and chronic hemolytic anemia. At age 13 years, the boy developed an episode of severe hypertensive encephalopathy and transient renal failure. Both children are attending normal school, have no neurologic symptoms, and only minimal pigmentary retinal abnormalities. Renal biopsy showed a chronic thrombotic microangiopathic nephropathy. Both patients had hyperhomocysteinemia and mild methylmalonic aciduria. Fibroblasts showed decreased cobalamin uptake, reduced methyl- and adenosyl-cobalamin formation, and deficient incorporation of formate and propionate, compatible with the Cbl-C complementation group, but milder than that found in cells from most patients. Both patients and their father carry a balanced reciprocal translocation. Parenteral hydroxycobalamin treatment reduced the homocysteine levels, and methylmalonic acid disappeared. Increasing the dosage of hydroxycobalamin from 1 to 2.5, then 5 mg daily together with betaine, further reduced homocysteine levels (boy from 118 to 23 microM and girl from 59 to 14 microM). With this treatment, hemolysis has stopped, hematuria has disappeared, proteinuria has almost normalized, and creatinine clearance has been stable. Investigations for chronic thrombotic microangiopathy should include testing for this unusual but treatable disorder, regardless of age of presentation.
 ...
PMID:Cobalamin disorder Cbl-C presenting with late-onset thrombotic microangiopathy. 1221 Mar 50

We studied vascular responses in spontaneously hypertensive rats (SHR) of both genders after methionine (Met) loading to test whether or not there were gender differences. SHRs were divided into 5 groups: male control (MSHR), female control (FSHR), methionine-loaded (+Met) males (MSHR[+Met]) and females (FSHR[+Met]), and male SHR with both 17beta-estradiol (E2) and Met administration (MSHR[+E2+Met]). Treated groups received Met (1g/kg body weight per day) in water for 6 weeks. Systolic blood pressure (SBP) was monitored weekly. Aortic contractile (phenylephrine-induced) and relaxant (acetylcholine-induced as endothelium-dependent relaxation, or EDR) responses as well as endothelial suppression (with nitric oxide synthase inhibitor) were evaluated at the end of experiments. Serum homocysteine (Hcy) level was also determined. Met overloading caused a nearly 3-fold increase in serum Hcy in each gender (moderate hyperhomocysteinemia, or HHcy). As age increased, SBP increased in all groups; FSHR(+Met) had the least elevation and significantly less increase of SBP than FSHR at the end of 6 weeks. There was also a significant increase of EDR in FSHR(+Met) compared with both FSHR and MSHR(+Met). FSHR(+Met) had the highest level of endothelium suppression. Furthermore, EDR in MSHR(+E2+Met) was significantly higher than that in MSHR(+Met). Direct Hcy feeding appeared to reduce the development of hypertension in female SHR in 3 weeks. Hence, SBP development was partially alleviated, whereas EDR and endothelium suppression were enhanced in female SHR with HHcy. E2 could mimic the gender-dependent effect of HHcy on EDR enhancement in MSHR; moreover, reduction of SBP development occurred in Hcy-fed FSHR.
Hypertension 2002 Sep
PMID:Vascular responses in male and female hypertensive rats with hyperhomocysteinemia. 1221 74

Hyperhomocysteinemia is associated with arterial hypertension and endothelial dysfunction in healthy humans. Placebo-controlled vitamin intervention studies cannot distinguish intrinsic actions of homocysteine (tHcy) and folate concentrations on the endothelium. The present two-period crossover study investigates the effects of tHcy lowering through oral folic acid on antioxidant status and resistance vessel reactivity in patients with established coronary artery disease (CAD). We investigated 27 male patients with angiographically documented multivessel CAD aged 50 (range 46-56) years. Resistance vessel reactivity was assessed by measurement of postischemic reactive hyperemia (RH) in the forearm using venous occlusion plethysmography at baseline, after 6 weeks of treatment with 5 mg of oral folic acid, and after a washout period of another 6 weeks. Plasma folate increased 3.49-fold with a mean tHcy reduction of 21.3%. Peak reactivity of resistance vessels improved significantly (18.97-23.60 ml/min(-1) per 100 ml; P = 0.01) with unchanged total antioxidant status (TAS; 0.912-0.944 microM; P = 0.4). This effect was limited to subjects (n = 14) with a tHcy reduction >2 microM (median reduction, 14.4-9.6 microM, P < 0.001). In the 13 subjects with a below-median reduction, tHcy remained unaltered (9.7-9.6 microM, P = 0.88) and TAS increased significantly (0.923-1.055 microM, P = 0.006), whereas RH peak flow was not affected (20.22-22.99 ml/min(-1) per 100 ml, P = 0.28). Homocysteine lowering >2 microM through folic acid supplementation improves resistance vessel reactivity in patients with CAD. Our data support the hypothesis that homocysteine lowering may have intrinsic vasoprotective effects largely independent of folate.
 ...
PMID:Effects of folate treatment and homocysteine lowering on resistance vessel reactivity in atherosclerotic subjects. 1223 46

Hyperhomocysteinemia (Hhe), linked to cardiovascular disease by epidemiological studies, may be an important factor in adverse cardiac remodeling in hypertension. Specifically, convergence of myocardial and vascular alterations promoted by Hhe and hypertension may exacerbate cardiac remodeling and myocardial dysfunction. We studied male spontaneously hypertensive rats fed one of three diets: control, intermediate Hhe inducing, or severe Hhe inducing. After 10 wk of dietary intervention, cardiac function was assessed in vitro, and cardiac and coronary arteriolar remodeling were monitored by histomorphometric, immunohistochemical, and biochemical techniques. Results showed that Hhe induced diastolic dysfunction, as characterized by the diastolic pressure-volume curve, without significant changes in baseline systolic function. Perivascular collagen levels were increased by Hhe, and there was an increase in left ventricular hydroxyproline levels. Myocyte size was not affected. Coronary arteriolar wall thickness increased with Hhe due to smooth muscle hyperplasia. Mast cells increased in parallel with Hhe and collagen accumulation. In summary, 10 wk of Hhe caused coronary arteriolar remodeling, myocardial collagen deposition, and diastolic dysfunction in hypertensive rats.
 ...
PMID:Hyperhomocysteinemia leads to adverse cardiac remodeling in hypertensive rats. 1238 35


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>