UMLS:C0012833 - FACTA Search

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

Query: UMLS:C0012833 (dizziness)
9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

34 patients have been controlled after beta-blocking therapy, for a mean period of 5 years. Symptoms and evolution: syncope disappeared, angoy passed from 47% to 23%, dyspnea from 65% to 47%, dizziness from 70% to 54%, weakness from 30% to 37%. A systolic murmur was present in 75% of the cases. Two patients died by heart failure. Phonocardiogram: the systolic murmur was unchanged, like the carotid pulse. Paradoxical splitting of the 2 degrees sound was more frequent, atrial sound unimodified, isometric contraction shortened (60%) and the Q-1 degree sound interval prolonged (90%). Electrocardiogram: 1 degree A/V block appeared in 24% of the cases, complete A/V block in 9%, atrial fibrillation in 3%. Left atrial enlargement was more frequent; left ventricular hypertrophy unchanged. Heart catheterization (10 cases, after a mean period of 5.5 years): left ventricular pressure gradient passed from 80% to 90%; a low cardiac index from 20% to 30%; telediastolic pressure of left ventricle was unmmodified in 10% of cases, more elevated in 50%, less elevated in 40%. Chest X ray: cardiac size was unchanged in 65% of cases, enlarged in 32%; smaller in 3%. In conclusion, symptoms improved in most of the patients; no case of sudden death was observed. Some data however show that the evolution of the myocardiopathy goes on to congestive heart failure and arise doubts on the real usefullness of beta-blocking drugs in the disease.
...
PMID:[beta-Blocking therapy in obstructive hypertrophic cardiomyopathy. Long term results (author's transl)]. 610 83

There were 84 confirmed cases of congestive (or dilated) cardiomyopathy (CCM or DCM), 57 of hypertrophic nonobstructive cardiomyopathy (HNCM) and 52 of hypertrophic obstructive cardiomyopathy (HOCM) collected from 15 cardiology divisions of university or national hospitals in Japan. Out of the 193 patients with cardiomyopathy, 145 (75%) were male and 48 (25%) female (M/F ratio = 3:1). The mean age of the patients was 34.1 years. Patients with HNCM or HOCM were usually asymptomatic, but palpitation was the most common symptom, followed in frequency by chest oppression, dyspnoea, chest pain, arrhythmia and syncope in HNCM, and by dyspnoea, chest oppression, chest pain, dizziness and syncope in HOCM. ST-T abnormalities were most frequently observed, 90.3% in HNCM and 86.3% in HOCM. Left ventricular hypertrophy was observed in 76.4% of HNCM and in 79.1% of HOCM. Abnormal Q waves were observed equally in HNCM (32.4%) and in HOCM (35.3%). A fourth sound was more common (69.2% in HNCM; 75.8% in HOCM) than a third sound (39.7% in HNCM; 36.5 in HOCM). The heart size on conventional radiography was within normal limits or slightly enlarged; the mean cardiothoracic ratio was 0.52 in HNCM and 0.54 in HOCM. A cumulative survival rate in 149 patients with hypertrophic cardiomyopathy demonstrated that the 10-year survival rate after the time when the diagnosis was made was 34.2% for CCM, 81.7% for HNCM and 84.4% for HOCM. Autopsy studies in 11 patients with hypertrophic cardiomyopathy revealed that marked fibre disarray of the heart could be detected by the endomyocardial biopsy of the right ventricular septum in 40% at most of the patients with hypertrophic cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Hypertrophic obstructive and non-obstructive cardiomyopathy in Japan. Diagnosis of the disease with special reference to endomyocardial catheter biopsy. 668 27

Losartan potassium is the first of a new class of orally active antihypertensive drugs which antagonise the action of angiotensin (AT) II at the AT1 receptor subtype. Losartan potassium is converted by the liver to the active metabolite E-3174, which is a more potent antagonist at the AT1 receptor. E-3174 is responsible for most of the pharmacological effects of losartan potassium, and its long half-life contributes to the extended duration of action of the drug. Losartan potassium is effective as a once-daily antihypertensive agent. In mild to moderate hypertension, losartan potassium has similar efficacy to enalapril, atenolol and felodipine extended release. When losartan potassium is combined with hydrochlorothiazide there is a further reduction in blood pressure. Losartan potassium is well tolerated in mild, moderate and severe essential hypertension, with dizziness being reported as the only drug-related adverse effect. The overall rate of patient withdrawal from therapy due to adverse experiences with losartan potassium is lower (2.3%) than that of placebo (3.7%). First-dose hypotension is uncommon, perhaps due to the slower onset of action of the drug, and cough does not appear to be a significant problem. A number of areas concerning the safety and efficacy of losartan potassium remain to be clarified. In particular, long term tolerability studies are needed; cough only became apparent as an adverse effect of ACE inhibitors after 3 to 4 years of use. Postmarketing surveillance has shown that angioedema, a rare but life-threatening adverse effect of ACE inhibitors, also occurs with losartan potassium. Further data are needed on the use of losartan potassium in patients with renal impairment before accepting the recommendation that dosage adjustment is not necessary. The pharmacokinetics and pharmacodynamics of losartan potassium in patients with hepatic disease also require further investigation. Losartan potassium increases uric acid secretion and lowers plasma uric acid levels, which may be of benefit when losartan potassium is combined with a thiazide diuretic, but which may otherwise lead to uric acid stone formation and possibly to nephropathy. Simple control of blood pressure is no longer an adequate goal in the management of hypertension. Any new antihypertensive agent should also reduce cardiovascular events, prevent or cause regression of end-organ damage such as left ventricular hypertrophy, atherosclerosis and renal failure, and should not impair quality of life. Such data on losartan potassium are not currently available. Losartan potassium is likely to be used in patients who are intolerant of ACE inhibitors, but its future in the management of hypertension will depend on long term tolerability studies and data on its effects beyond simple blood pressure control.
...
PMID:A risk-benefit assessment of losartan potassium in the treatment of hypertension. 901 Jun 43

Angiotensin II receptor blockers (ARBs) represent a new class of effective and well tolerated orally active antihypertensive agents. Recent clinical trials have shown the added benefits of ARBs in hypertensive patients (reduction in left ventricular hypertrophy, improvement in diastolic function, decrease in ventricular arrhythmias, reduction in microalbuminuria, and improvement in renal function), and cardioprotective effect in patients with heart failure. Several large long-term studies are in progress to assess the beneficial effects of ARBs on cardiac hypertrophy, renal function, and cardiovascular and cerebrovascular morbidity and mortality in hypertensive patients with or without diabetes mellitus, and the value of these drugs in patients with heart disease and diabetic nephropathy. The ARBs specifically block the interaction of angiotensin II at the AT1 receptor, thereby relaxing smooth muscle, increasing salt and water excretion, reducing plasma volume, and decreasing cellular hypertrophy. These agents exert their blood pressure-lowering effect mainly by reducing peripheral vascular resistance usually without a rise in heart rate. Most of the commercially available ARBs control blood pressure for 24 h after once daily dosing. Sustained efficacy of blood pressure control, without any evidence of tachyphylaxis, has been demonstrated after long-term administration (3 years) of some of the ARBs. The efficacy of ARBs is similar to that of thiazide diuretics, beta-blockers, angiotensin-converting enzyme inhibitors or calcium channel blockers in patients with similar degree of hypertension. Higher daily doses, dietary salt restriction, and concomitant diuretic or ACE inhibitor administration amplify the antihypertensive effect of ARBs. The ARBs have a low incidence of adverse effects (headache, upper respiratory infection, back pain, muscle cramps, fatigue and dizziness), even in the elderly patients. After the approval of losartan, five other ARBs (candesartan cilexetil, eprosartan, irbesartan, telmisartan, and valsartan) and three combinations with hydrochlorothiazide (irbesartan, losartan and valsartan) have been approved as antihypertensive agents, and some 28 compounds are in various stages of development. The ARBs are non-peptide compounds with varied structures; some (candesartan, losartan, irbesartan, and valsartan) have a common tetrazolo-biphenyl structure. Except for irbesartan, all active ARBs have a carboxylic acid group. Candesartan cilexetil is a prodrug, while losartan has a metabolite (EXP3174) which is more active than the parent drug. No other metabolites of ARBs contribute significantly to the antihypertensive effect. The variation in the molecular structure of the ARBs results in differences in the binding affinity to the receptor and pharmacokinetic profiles. The differences observed in lipid solubility, absorption/distribution, plasma protein binding, bioavailability, biotransformation, plasma half-life, and systemic elimination influence the time of onset, duration of action, and efficacy of the ARBs. On the basis of the daily mg dose, the antihypertensive potency of the ARBs follows the sequence: candesartan cilexetil > telmisartan approximately = losartan > irbesartan approximately = valsartan > eprosartan. After oral administration, the ARBs are rapidly absorbed (time for peak plasma levels = 0.5-4 h) but they have a wide range of bioavailability (from a low of 13% for eprosartan to a high of 60-80% for irbesartan); food does not influence the bioavailability, except for valsartan (a reduction of 40-50%) and eprosartan (increase). A limited dose-peak plasma levels/areas under the plasma level-time curve proportionality is observed for some of the ARBs. Most of these drugs have high plasma protein binding (95-100%); irbesartan has the lowest binding among the group (90%). The steady-state volumes of distribution vary from a low of 9 L (candesartan) to a high of 500 L (telmisartan). (ABSTRACT TRUNCATE
...
PMID:Clinical pharmacokinetics of angiotensin II (AT1) receptor blockers in hypertension. 1085 85

Aortic valve stenosis is the most frequent reason for prosthetic valve replacement in adults. Its incidence increases with age. Development of the most frequent form, degenerative-calcific aortic stenosis, is related to atherosclerotic risk factors. The narrowing of the aortic valve orifice leads to creation of a systolic pressure drop, the gradient, between left ventricle and ascending aorta. The pressure overload from aortic stenosis causes concentric left ventricular hypertrophy and later heart failure. Typical symptoms of severe aortic stenosis include dyspnea, angina, and dizziness or syncope. On auscultation, a loud systolic murmur over the base of the heart is apparent, which is transmitted to the carotids. The ECG often shows left ventricular hypertrophy. The most important diagnostic technique is echocardiography, which allows to measure the gradient and to calculate the orifice area, which determine the degree of severity. The development of symptoms or impaired left ventricular function in severe aortic stenosis should prompt surgical treatment by valve replacement. Truly asymptomatic patients with preserved left ventricular function should be followed conservatively.
...
PMID:[Aortic valve stenosis]. 1545 62

Cardiovascular manifestation of diabetes has remarkable therapeutic and prognostic implications. Diabetic cardiomyopathy is a distinct heart muscle disease in patients with well-controlled diabetes mellitus that cannot be ascribed to coronary artery disease, hypertension or any other known cardiac disease. It is characterized by left ventricular diastolic dysfunction that can be detected in 52-60% of well-controlled type II diabetic subjects using contemporary Doppler techniques. Pathophysiologically, hyperglycaemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function and induce myocardial inflammation. Insulin resistance with hyperinsulinaemia and decreased insulin sensitivity are responsible for left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy are dispnoea, arrhythmias, atypical chest pain or dizziness. The treatment of diabetic cardiomopathy should be initiated as early as diastolic dysfunction is identified. Various therapeutic options include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), use of ACE inhibitors, beta blockers and calcium channel blockers. Daily physical activity and reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio, and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles. Metformin and thiazolidinendiones are used to treat insulin resistance, but have different mechanisms of action. Metformin reduces free fatty amino acids effluvium from fat cells, thereby suppressing hepatic glucose production and indirectly improving peripheral insulin sensitivity and the endothelial function. In contrast, thiazolidinediones improve peripheral insulin sensitivity by reducing circulating free fatty amino acids, but also increasing production of adiponectin, which improves insulin sensitivity. Beta-adrenoceptor blocking agents are effective in preventing or reversing myocardial dilatation and remodelling, while ACE inhibitors facilitate blood flow through microcirculation in coronary vascular bed, fat and skeletal muscle, as well as improve insulin action at the cellular level.
...
PMID:[Diabetic cardiomyopathy: old disease or new entity?]. 1808 46

Pulmonary hypertension is a disorder characterized by an increase in mean pulmonary arterial pressure (mPAP > 25 mmHg), which is responsible for the transport of blood from the heart to the lungs. Increased pressure leads to decreased flow of blood through the lungs and decreased oxygen deliverance throughout the body. The disorder causes right ventricular hypertrophy and can quickly lead to death, especially with the severe forms of pulmonary hypertension. Symptoms include fatigue, shortness of breath, dizziness and peripheral edema in the lower extremities. Symptoms are usually delayed in appearance and progress slowly, which leads to a late diagnosis and often a poor prognosis. Despite large advances in the last 10 years, there is still about a 15% annual mortality for diagnosed patients. Despite the number of medications available, there are still no cures for this fatal disease. Current therapies include endothelin receptor antagonists, prostacyclin agonists and cGMP-specific 3',5'-cyclic phosphodiesterase (PDE5) inhibitors or combinations. Recent strategies have shown promise in animal models to prevent the onset of pulmonary hypertension when it is induced. However, few of them show a sustained benefit in clinical trials. Strategies for the cure of this debilitating disease should be the focus of future research.
...
PMID:Current and future treatment of pulmonary hypertension. 2238 53

Diabetic cardiomyopathy is a controversial clinical entity that in its initial state is usually characterized by left ventricular diastolic dysfunction in patients with diabetes mellitus that cannot be explained by coronary artery disease, hypertension, or any other known cardiac disease. It was reported in up to 52-60% of well-controlled type-II diabetic subjects, but more recent studies, using standardized tissue Doppler criteria and more strict patient selection, revealed a much lower prevalence. The pathological substrate is myocardial damage, left ventricular hypertrophy, interstitial fibrosis, structural and functional changes of the small coronary vessels, metabolic disturbance, and autonomic cardiac neuropathy. Hyperglycemia causes myocardial necrosis and fibrosis, as well as the increase of myocardial free radicals and oxidants, which decrease nitric oxide levels, worsen the endothelial function, and induce myocardial inflammation. Insulin resistance with hyperinsulinemia and decreased insulin sensitivity may also contribute to the left ventricular hypertrophy. Clinical manifestations of diabetic cardiomyopathy may include dyspnea, arrhythmias, atypical chest pain, and dizziness. Currently, there is no specific treatment of diabetic cardiomyopathy that targets its pathophysiological substrate, but various therapeutic options are discussed that include improving diabetic control with both diet and drugs (metformin and thiazolidinediones), the use of ACE inhibitors, beta blockers, and calcium channel blockers. Daily physical activity and a reduction in body mass index may improve glucose homeostasis by reducing the glucose/insulin ratio and the increase of both insulin sensitivity and glucose oxidation by the skeletal and cardiac muscles.
...
PMID:Diabetic cardiomyopathy: ongoing controversies in 2012. 2322 71

Glycogen storage diseases (GSDs) comprise a large, heterogeneous group of disorders characterized by abnormal glycogen deposition. Multiple cases in the literature have demonstrated an association between GSD type I and pulmonary arterial hypertension (PAH). We now also report on two patients with GSD type III and PAH, a novel association. The first patient was a 16-year-old girl of Nicaraguan descent with a history of hepatomegaly and growth retardation. Molecular testing identified a homozygous 17delAG mutation in AGL consistent with GSD type IIIb. At the age of 16, she was found to have PAH and was started on medical therapy. Two years later, she developed acute chest pain and died shortly thereafter. The second patient is a 13-year-old girl of Colombian descent homozygous for the c.3911dupA mutation consistent with GSD IIIa. An echocardiogram at age 2 showed left ventricular hypertrophy, which resolved following the institution of a high protein, moderate carbohydrate diet during the day and continuous gastric-tube feeding overnight. At the age of 12, she was found to have pulmonary hypertension. She was started on sildenafil, and her clinical status has shown marked improvement including normalization of her elevated transaminases. PAH may be a rare association in patients with GSD IIIa and IIIb and should be evaluated with screening echocardiograms for cardiac hypertrophy or if they present with symptoms of right-sided heart failure such as shortness of breath, chest pain, cyanosis, fatigue, dizziness, syncope, or edema. Early diagnosis of PAH is important as increasingly effective treatments are now available.
...
PMID:Two Cases of Pulmonary Hypertension Associated with Type III Glycogen Storage Disease. 2343 Aug 32

A 77-year-old Portuguese woman reported gradual worsening of burning and numbness in the feet and hands, fatigue, anorexia, weight loss, diarrhoea and decreased visual acuity. She had a medical history of atrial fibrillation and recent episodes of dizziness and blood pressure fluctuations. There was no relevant family history. The diagnostic workup documented a severe axonal sensorimotor peripheral neuropathy, a monoclonal IgG kappa protein on serum, a severe left ventricular hypertrophy on the echocardiogram and probable vitreous deposits of amyloid on ophthalmologic examination. Pain and dysautonomia with an axonal neuropathy and multisystemic involvement raised the possibility of amyloidosis. The presence of a detectable monoclonal protein, older age at disease onset and absence of family history of disease usually suggest immunoglobulin light-chain amyloidosis. However, in this case, both the genetic testing and the biopsy of the salivary glands confirmed transthyretin amyloidosis. In those patients with a monoclonal protein, particularly in sporadic and late-onset cases, the diagnosis of transthyretin amyloidosis can be challenging, mimicking immunoglobulin light-chain amyloidosis.
...
PMID:A sporadic case of late-onset familial amyloid polyneuropathy with a monoclonal gammopathy. 2605 37

<< Previous 1 2 3 Next >>