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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
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PMID:Clinical pharmacokinetics of angiotensin II (AT1) receptor blockers in hypertension. 1085 85

The incidence of AF, the most common sustained arrhythmia in clinical practice, increases with age and coronary artery disease, hypertension and valvular heart disease are common underlying substrates; however, occasionally, AF may occur without any underlying heart disease. The most widely accepted theory of its mechanism is Moe's multiple wavelet hypothesis, although recent studies are helping to shed light on other mechanisms, including the focal origin of AF in some patients. Most patients experience palpitations, but fatigue, dyspnoea, and dizziness may also occur. Therapy includes prevention of thromboembolism, control of rate, and restoration and maintenance of sinus rhythm. The risks and benefits of each treatment modality need to be assessed according to each patient's circumstances. Unlike other arrhythmias, there is still no highly successful therapy for treating AF. However, significant advances are being made using non-pharmacological approaches to either prevent or cure this troublesome arrhythmia.
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PMID:Atrial fibrillation: epidemiology, mechanisms and management. 1089 90

The efficacy and safety of intravenous propafenone for conversion of recent-onset and chronic atrial fibrillation was assessed in 46 patients. 40 with atrial fibrillation associated with or without structural heart disease (mean age 63 +/- 14 years) and 6 patients with atrial fibrillation related to the Wolff-Parkinson-White syndrome (mean age 34.8 +/- 13 years). Propafenone treatment was administered at 2 mg/kg over 15 minutes under continuous electrocardiographic monitoring. In 28 of 32 (87.5%) patients with paroxysmal and/or recent-onset atrial fibrillation a stable sinus rhythm was restored within 1 hour after propafenone (mean 17 +/- 11 minutes) and in only 3 of 8 (37.5%) with chronic atrial fibrillation (p < 0.05). Conversion to sinus rhythm was obtained in 5 of 6 (83.3%) patients with atrial fibrillation related ventricular preexcitation, mean time 21 +/- 12 minutes. Propafenone had an additional effect reducing mean heart rate (141 +/- 21 to 102 +/- 15 beat per minute, p < 0.05) and the shortest preexcited R-R intervals was increased, mean 231.6 +/- 27.8 to 355 +/- 37.2 milliseconds (p < 0.001) in cases associated with ventricular preexcitation. Dizziness, hypotension and transient conduction disturbances occurred in only one patient with rheumatic valvular heart disease: EF 40%. Propafenone is an effective and safe antiarrhythmic drug for converting paroxysmal and/or recent-onset atrial fibrillation of various origins with a more limited efficacy in chronic atrial fibrillation.
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PMID:[Pharmacological cardioversion with intravenous propafenone in atrial fibrillation]. 1093 1

In every year since 1984, cardiovascular disease has claimed the lives of more females than males. More than 450,000 women succumb to heart disease annually, and 250,000 die of coronary artery disease. Despite the proportions, most women believe they will die of breast cancer. The perception that heart disease is a man's disease and that women are more likely to die of breast cancer is alarming. Although women develop heart disease about 10 years later than men, they are likely to fare worse after a heart attack. The poorer outcomes are due, in part, to the failure to identify heart attack symptoms. Approximately 35% of heart attacks in women are believed to go unnoticed or unreported. However, because of increased age, women are more likely to have co-morbid diseases such as diabetes and hypertension. In women, not only is "tightness" or discomfort in the chest a warning sign, but in addition, nausea and dizziness are common indicators of myocardial ischemia. Other symptoms include breathlessness, perspiration, a sensation of fluttering in the heart, and fullness in the chest. In comparison to men, women are less likely to undergo tertiary care interventions such as cardiac catheterization, angioplasty, thrombolytic therapy, and bypass surgery; to participate in cardiac rehabilitation; and to return to work full-time after myocardial infarction. In the past, most research about treatments for heart disease focused on men, and gender differences have been ignored. Recent studies are enrolling enough women to test if there are differences between men and women in outcomes. One of the major areas of research relates to estrogen and hormonal replacement therapy to reduce the relative risk of heart attack and stroke. The Women's Health Initiative is a major NIH-sponsored trial that addresses the issue of primary prevention of cardiac disease by hormonal replacement therapy. The results will be available in 2004. The Heart Estrogen/Progestin Replacement Study (HERS), disappointingly, did not show a significant reduction of coronary events in women taking hormonal replacement therapy, nor did the Estrogen Replacement and Atherosclerosis (ERA) trial of 309 postmenopausal women who underwent coronary angiography. New insight into the role of vitamins, phytoestrogens and other natural sources, and selective estrogen receptor modulators may provide other options for management. Until then, modification of risk factors and healthy life style choices are recommended for reducing the risk of cardiac disease. In fact, the key to a healthy heart in the year 2000 appears closely tied to life style choices. Prevention of disease is the key, and current recommendations are simply to stop smoking, or do not start; treat and control blood pressure >140/90 mm Hg; manage elevated lipids by diet, exercise, and cholesterol-lowering medications (if necessary); treat diabetes; lose weight so that BMI is <25; walk for 20-30 minutes at least three times a week; and take an aspirin tablet daily.
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PMID:Heart disease in women. 1114 May 44

Syncope is defined as a temporary interruption of cerebral perfusion with a sudden and transient loss of consciousness and spontaneous recovery. Approximately one third of the population experiences syncope at least once during a lifetime. Presyncopal signs and symptoms, including weakness, headache, blurred vision, diaphoresis, nausea, and vomiting are sometimes present for seconds or minutes prior to loss of consciousness. After syncope, the patients may present with persisting drowsiness, headache, dizziness, nausea, but not usually confusion. Causes of syncope have been categorized as cardiovascular, non-cardiovascular, and unexplained. Cardiovascular causes can be subdivided into structural heart disease, coronary heart disease, and arrhythmia. Non-cardiovascular causes include neurological, metabolic, psychiatric and other disorders.Orthostatic hypotension - one of the most frequent causes of syncope - has manifold etiologies comprising various neurological and internal diseases. Orthostatic hypotension usually can be attributed to an impairment of peripheral vasoconstriction or to a reduction of the intravascular volume. Signs and symptoms, including the above prodromi are often present just after rising from a supine or sitting position. Frequently, blood pressure decreases significantly without an increase in heart rate. Autonomic cardiovascular modulation is often reduced. Many of the patients with "unexplained" syncope experience neurally mediated (i. e. neurocardiogenic or vasovagal) syncope. In these patients, cardiovascular control may be stable for an extended period of time during orthostatic stress, then there is a sudden decrease in blood pressure and heart rate. Neurocardiogenic or neurally mediated syncope can be associated with painful or emotionally stressful situations such as anxiety or fear, with prolonged standing or specific trigger situations such as micturition, defecation, coughing or sneezing, visceral or carotid sinus stimulation, or with trigeminal or glossopharyngeal neuralgia. So far, the mechanisms of neurocardiogenic syncope are not completely understood. The passive 60 degrees to 70 degrees head-up tilt test is useful for the diagnosis of orthostatic and neurally mediated syncope. The sensitivity of the test can be improved by additional pharmacological provocation, e. g. by isoproterenol, or by increased orthostatic stress using lower body negative pressure stimulation. For the treatment of syncope one should first consider non-pharmacological options. Patients with orthostatic hypotension should avoid rapid changes of the body position from supine to standing, as well as high room temperature or other situations inducing peripheral vasodilatation. An increased intake of sodium and fluids, mild physical exercise or so-called postural counter-maneuvers can improve orthostatic tolerance. Among the drugs recommended for pharmacologic treatment are mineralocorticoids (e. g. fludrocortisone), vasoconstrictor agents (e. g. ephedrine, midodrine), adenosine receptor blockers (theophylline) and beta2-blockers (propanolol), anticholinergic agents, e. g. scopolamine or disopyramide, and negative cardiac inotropes, e. g. beta1-adrenergic blockers or disopyramide. Serotonin reuptake inhibitors (e. g. fluoxetine, sertraline), alpha2-adrenergic agonists (clonidine), central nervous system stimulants such as methylphenidate or phentermine are thought to be beneficial in specific cases. Cardiac pacemakers often seem to be recommended without adequate indication. The antidiuretic, V2-receptor specific, vasopressin analogue desmopressin increases the intravascular volume. Erythropoietin improves anemia and red blood cell decrease and augments blood pressure and cerebral oxygenation. In postprandial hypotension, octreotide, a somatostatin analogue, prostaglandin inhibitors such as indomethacin or ibuprofen, as well as metoclopramide or two cups of coffee per day might be beneficial.
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PMID:[Syncope - a systematic overview of classification, pathogenesis, diagnosis and management]. 1182 26

A prolonged Q-T interval is generally associated with increased risk of ventricular arrhythmias, like torsade de pointes, and death. It has recently become apparent that not only antiarrhythmic drugs such as sotalol and Kinidin, but also a variety of nonantiarrhythmic drugs, like certain antihistamines, antimicrobial drugs, psychiatric drugs, and cisapride, may induce prolongation of the Q-T interval and torsade de pointes. Special concern should be drawn to the co-administration of drugs that interfere with the metabolism and elimination of these drugs, such as ketoconazole. Patients with congenital long Q-T syndrome, patients with heart disease, with hypokalaemia or hypomagnesaemia, and women have an increased risk. Every sign on dizziness or syncope should be regarded as a warning sign of possible arrhythmia in patients treated with drugs that potentially prolong the Q-T interval. Measurement of the Q-T interval before and during treatment is generally recommended in high-risk patients.
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PMID:[Why is QT interval interesting?]. 1185 Nov 79

Many countries in Asia, Africa, Latin America, and the Caribbean offer substantial tax breaks to foreign corporations that set up shops in free-trade zones and waive environmental regulations and repress trade unions to further induce this practice. Workers in these shops--mainly women--perform repetitive machine-based motions, are exposed to toxic chemicals and unsafe equipment, and face dangerously high production quotas. Health problems caused by these working conditions include headache and dizziness, fatigue, anemia, forgetfulness, stomach pains, respiratory problems, hypertension, heart disease, and allergies. Water and air pollution and dumping of hazardous waste affect the health of entire communities. Since free-trade zones are a permanent feature of the global economy, organizing to protect workers and communities assumes critical importance. Groups such as the Border Committee of Women Workers in Mexico are providing workers with skills and support to make demands such as better treatment of pregnant workers. International labor, environmental, and public health advocates can support such efforts by providing assistance to worker-controlled organizations and pressuring governments to enforce laws intended to protect workers and their communities.
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PMID:Globalization causes a world of health problems. 1234 7

Cardiac arrhythmias are a well known cause of mortality for patients with heart disease. However, sinus tachycardia is a more unusual arrhythmia which can lead to serious heart damage or death. Even young patients with structurally normal hearts may become gravely ill. This case study outlines the condition of sinus tachycardia, and associated changes in heart function, altered cellular structure of the myocardium and compensatory mechanisms in the body. Treatment modalities, including electro-physiological studies and drug therapies to moderate the tachycardia and myocardial oxygen demand of the heart, are discussed. Fourteen year old 'Ben' was previously a well, active and outgoing youth who suddenly became critically ill. He endured weeks of hospitalisation, numerous serious complications including Torsade de pointes arrhythmia, Cheyne-Stokes respirations, nausea and dizziness during this acute phase. Despite challenges, Ben's severely compromised heart muscle recovered at a remarkable rate.
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PMID:Tachycardia's toll: tachycardia induced cardiomyopathy--a case study. 1259 74

External electrocardiographic loop recording permits extended cardiac rhythm monitoring and ECG storage before and after device activation. The purpose of the study was to assess the diagnostic yield of external loop recorders in patients with more than two syncopal events within the last 6 months and a negative tilt table test. Twenty-four consecutive patients (51 +/- 14 years, male n = 9) were enrolled with 3 +/- 4 recurrent syncopal events within the last 6 months and no overt structural heart disease. The loop recorder CardioCall continuously records a two-channel ECG via skin electrodes. When activated, up to 4.5 minutes of the ECG preceding activation is stored. The time between tilt table testing and monitoring was 5 +/- 4 weeks. The average monitoring period covered 50 +/- 22 days. Recording was either unsuccessful or terminated prematurely in 5 patients. The reasons were skin irritation secondary to the electrodes in two patients, cable damage in one patient, and two patients inadvertently erased the stored data when replacing the batteries. Fourteen patients activated the loop recorder at least once. Symptoms leading to device activation were syncope (n = 1), dizziness (n = 11), feeling unwell (n = 7), palpitations (n = 5), headaches (n = 1), and chest pain (n = 1). The loop recorder documented sinus tachycardia during the syncopal event. Sinus tachycardia was also observed in 7 other patients, and atrial flutter in two patients. Eight patients had recurrent syncope with two patients experiencing syncope prior to the monitoring period, one syncope occurred in a patient who inadvertently erased the stored data, one event coincided with sinus tachycardia, and 4 (17%) patients had syncope during 15 +/- 10 months after termination of loop monitoring. The external loop recorder was not very useful for arrhythmia detection in patients with syncopal events, no overt heart disease, and a negative tilt table test because the cardiac rhythm was stored in only 1 of 8 (13%) patients with recurrent syncope. Reasons for the low diagnostic yield of external loop recorders were infrequent syncopal events after the baseline evaluation, with rare events during the limited monitoring period in particular, and premature termination or unsuccessful recording in 21% of patients.
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PMID:Diagnostic yield of external electrocardiographic loop recorders in patients with recurrent syncope and negative tilt table test. 1293 Apr 97

The prevalence of AF is known to increase in the elderly. Some electrophysiological changes were reported in these patients, but the effects of age on AF inducibility and other electrophysiological signs associated with atrial vulnerability are unknown. The purpose of the study was to evaluate the effects of age on atrial vulnerability and AF induction. The study consisted of 734 patients (age 16-85 years, mean 61 +/- 15 years) without spontaneous AF who were admitted for electrophysiological study. Study was indicated for dizziness or ventricular tachyarrhythmia. Programmed atrial stimulation was systematically performed. One and two extrastimuli were delivered in sinus rhythm and atrial driven rhythms (600, 400 ms). Univariate and multivariate analysis of several clinical and electrophysiological data were performed. AF inducibility, defined as the induction of an AF lasting > 1 minute, was paradoxically and significantly decreased in elderly (> 70 years) patients compared to younger patients (< 70 years) (P < 0.01). AF inducibility was present in 40% of 62 patients < 40 years, 39% of 99 patients age 40-50 years, 37% of 130 patients age 50-60 years, 38% of 222 patients age 60-70 years, and only 28% of 221 patients > 70 years. There was no significant correlation with the sex, the presence of dizziness, the presence or not of an underlying heart disease, the left ventricular ejection fraction, and the presence of salvos of atrial premature beats on 24-hour Holter monitoring. There was a significant correlation with a longer atrial effective refractory period in the elderly (226 +/- 41 ms) than in younger patients (208 +/- 31 ms) (P < 0.001). Other electrophysiological parameters of atrial vulnerability did not change significantly. Increased atrial refractory period and age >70 years were independent factors of decreased AF inducibility. Programmed atrial stimulation should be interpreted cautiously before the age of 70 years. AF induction is facilitated by the presence of a short atrial refractory period in these patients. Surprisingly, AF inducibility decreases in patients > 70 years because their atrial refractory period increases. Therefore, increased AF prevalence in these patients should be explained by nonelectrophysiological causes.
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PMID:Influence of age on atrial fibrillation inducibility. 1500 50


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