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Intraatrial reentrant tachycardia, or atrial flutter, is a common postoperative problem after Fontan repair, which involves an atriopulmonary connection. A modification of Fontan repair, total cavopulmonary connection, minimizes the portion of the right atrium exposed to stretch and hypertension; however, atrial flutter continues to occur after this procedure. We postulated that the intraatrial lateral tunnel suture line of total cavopulmonary connection, in the absence of physiologic alterations such as atrial hypertension or stretch, provides the necessary electrophysiologic substrate for atrial flutter. The purpose of this study was to produce a canine model of total cavopulmonary connection (1) to establish that the intraatrial suture line alone is sufficient to permit sustained atrial flutter and (2) to characterize the pathways of resulting reentrant arrhythmias. After induction of general anesthesia, 25 to 30 kg dogs (n = 17) underwent median sternotomy, cradling of the pericardium, and placement of a pacing electrode on the right atrial appendage. Normothermic cardiopulmonary bypass was initiated. The total cavopulmonary connection suture line was placed through a standard right atriotomy,simulating construcion of the lateral tunnel. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were placed through bilateral ventriculotomies. By means of atrial burst pacing and programmed extrastimulation, induction of atrial flutter was attempted. If atrial flutter could not be induced, isoproterenol was infused and the stimulation protocol was repeated. After induction of atrial flutter, mapping of the activation sequence was performed. Before suture line placement, no dog had inducible atrial flutter. After placement of the suture line, sustained atrial flutter was reproducibly induced in every dog, although isoproterenol was required for this in three (17.6%). The mean flutter cycle length was 177 +/- 30 msec. In each case, the atrial flutter circuit was limited to the right atrium, with the left atrium being passively activated. The atrial flutter circuit was dependent on a corridor of myocardium that resulted from conduction block on the free wall, created by the lateral margin of the total cavopulmonary connection. In no case was the atriotomy integral to the atrial flutter circuit. This study establishes that the total cavopulmonary connection baffle suture line alone, without alteration in circulatory physiology, creates a sufficient anatomic substrate for atrial flutter in a short-term canine model. Delineation of the anatomic boundaries of the reentrant circuit raises the possibility of targeting areas within the circuit that could be modified, potentially reducing the incidence of postoperative atrial flutter after total cavopulmonary connection.
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PMID:Atrial flutter after lateral tunnel construction in the modified Fontan operation: a canine model. 860 65

Atrial fibrillation is a frequent arrhythmia which has a high prevalence after 65 years of age, thus the typical patient's age is about 75. There are two atrial fibrillation predictors: traditional factors of cardiovascular risk (age, male sex, high blood pressure, diabetes), and structural heart disorders (heart failure, valvular heart disease). All preventive measures to reduce atrial fibrillation incidence, must be directed towards these factors. Additionally, left atrial size, ejection fraction and ventricular hypertrophy are echocardiographic predictors. Atrial fibrillation doubles the mortality rate and is related to an annual stroke rate of 4.5%. The stroke risk factors are: age, hypertension, diabetes, previous stroke, congestive heart failure, coronary heart disease, mitral stenosis, prosthetic heart valves and thyrotoxicosis. Left atrial size and ventricular disfunction are echocardiographic stroke risk factors. Each patient's risk can be stratified on the basis of these factors. All of this information is essential to handle the arrhythmia appropriately; this arrhythmia may be more important than has been thought. Atrial flutter is not very frequent and so it is less studied; however it is an arrhythmia with a similar clinical context to atrial fibrillation, although, probably, with a smaller embolic risk.
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PMID:[Epidemiology, risk factors, and pathogeny of atrial fibrillation and atrial flutter]. 875 90

To evaluate the significance of P-wave duration and morphology for the development of post-operative atrial fibrillation/flutter, we investigated 189 consecutive patients scheduled for elective coronary artery bypass surgery. The longest pre-operative total P-wave duration was measured from the standard electrocardiogram at a paper speed of 50 mm.s-1 (mean of two independent observers). By the signal averaging technique we determined the pre-operative total P-wave duration, and root-mean square voltage of the last 10, 20, and 30 ms of the filtered (40-250 Hz) P-wave from a vector composite of three orthogonal leads at noise level 0.2 microV. Forty-two (22%) of the patients developed atrial fibrillation/flutter. Older age (mean +/- SD) 62 +/- 8 vs 56 +/- 8 years (P < 0.000), increasing body weight 83 +/- 11 vs 79 +/- 12 kg (P = 0.05), treatment for hypertension 26 vs 13% (P = 0.04), and a longer P-wave duration in the standard electrocardiogram 129 +/- 12 vs 124 +/- 12 ms (P = 0.01) were associated with development of atrial fibrillation/flutter documented by a 12-lead electrocardiogram. Logistic regression analysis identified independent predictors, estimated adjusted relative risk (95% confidence interval) of atrial fibrillation/flutter: with age > 60 years, the relative risk was 4.46 (2.05-9.73), and body weight > 80 kg, the relative risk was 3.81 (1.71-8.46). Thus, P-wave duration and morphology did not provide significant information on the risk of atrial fibrillation/flutter when controlling for the effects of increasing age and body weight.
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PMID:Re-evaluation of the role of P-wave duration and morphology as predictors of atrial fibrillation and flutter after coronary artery bypass surgery. 880 25

Direct current electric shocks have been used to terminate atrial arrhythmias (cardioversion) in humans since the 1960s. The likelihood of successful cardioversion and maintenance of sinus rhythm is increased if the left atrium is not markedly enlarged and fibrotic, if there is no marked left atrial hypertension (e.g., mitral stenosis), and if the arrhythmia is not long-standing. To minimize the risk of thromboembolic phenomena, therapeutic anticoagulation should be established for at least 3 weeks before and for 4 weeks after cardioversion; coumadin is usually used for this purpose. A more recent approach uses transesophageal echocardiography to demonstrate the absence of thrombi in the left atrium and left atrial appendage. If no thrombi are evident, 48 hours of heparin anticoagulation may be adequate prior to cardioversion. Anticoagulation is still required after cardioversion. Quinidine and digitalis, singly or in combination, are frequently used to achieve and maintain sinus rhythm in association with cardioversion. For the procedure itself, traditional hand-held paddle electrodes or self-adhesive electrode pads may be used; the apex-anterior and anterior-posterior positions are equally effective. Gel couplants and firm pressure should always be used with hand-held paddles to reduce transthoracic impedance and maximize current flow. Electrodes should be widely separated to avoid shunting of current along the chest wall between electrodes. Generally, electrodes should be large in size; small "pediatric" electrodes should only be used in infants < 1 year of age (< 10 kg). Shocks should always be synchronized to the R wave to avoid the vulnerable period and the inadvertent induction of ventricular fibrillation. Initial shocks for atrial fibrillation should begin at 100 J; atrial flutter generally requires a smaller shock (initial shocks at 50 J). Effective anesthesia, not merely sedation, is required to achieve amnesia and avoid pain. Exciting new developments in defibrillation and cardioversion have occurred. It is now understood that excessive energy and current may induce cardiac damage, and recent studies suggest such damage may be mediated in part by free radicals. New shock waveforms, such as biphasic and multiphasic waveforms from multiple encircling electrodes, may be superior to the standard damped sinusoidal waveform.
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PMID:Transthoracic cardioversion of atrial fibrillation and flutter: standard techniques and new advances. 890 72

In order to terminate atrial flutter (AF) overdrive transesophageal left atrial pacing (TELAP) was performed in 760 patients with paroxysmal AF. There were 315 women and 415 men (mean age 59 years). In 260 patients, TELAP was used in an outpatient setting. Approximately half of the patients (51%) had coronary artery disease and/or arterial hypertension, and 23% of the patients had no structural heart disease. The duration of AF ranged between 1 hour and 1 month. TELAP was performed in 312 patients without any antiarrhythmic drug (AAD) administration (group I) and in 448 patients after administration of AAD (procainamide and/or amiodarone) in conventional doses (group II). TELAP resulted in immediate return of sinus rhythm in 85 patients (27%) of group I and in 222 patients (50%) of group II (P < 0.001). TELAP converted AF to atrial fibrillation (AFIB) in 185 of group I and in 214 (48%) of the group II patients (P < 0.01). In addition, within 1-2 days after TELAP AFIB converted to sinus rhythm spontaneously or after AAD in 87 patients of group I (28%) and in 84 (19%) of the group II patients (P < 0.01). In general sinus rhythm was restored in 172 (55%) of the group I and in 306 (68%) of the group II patients (P < 0.005). AF was converted to AFIB in 98 (31%) of the group I and in 130 (29%) of the patients in group II patients (NS). TELAP was ineffective in 42 (13.5%) of the group I and in 12 (3%) of the group II patients (P < 0.001). TELAP was an effective noninvasive method for the treatment of recent onset AF. Our experience showed that after TELAP, sinus rhythm was restored in most of the patients with paroxysmal AF within 1-2 days. In some patients TELAP converted AF to AFIB, making it easier to control the heart rate with AAD. Treatment with AAD before TELAP increased its effectiveness.
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PMID:Combined transesophageal left atrial pacing and antiarrhythmic therapy in the treatment of atrial flutter. 894 75

Anticoagulant therapy is not conventionally used in the treatment of patients with atrial flutter. This recommendation has been based on sparse clinical experience, and recent preliminary reports suggest a significant risk of thromboembolism for these patients. A retrospective study was undertaken to assess the frequency of thromboembolic events as well as potential risk factors for these events in a cohort of patients with atrial flutter referred for radiofrequency ablation treatment. Eighty-six consecutive patients with a primary diagnosis of atrial flutter were evaluated. A history of embolic events was noted in 12 of 86 patients (14%) with atrial flutter, with an annual risk of approximately 3%. There were no differences in the prevalence of coronary artery disease, cardiomyopathy, valvular disease, or atrial fibrillation between the 2 groups of patients having an embolic event and those of patients without embolic events. Left ventricular function and left atrial size were also similar between the 2 groups. The only significant risk factor was hypertension (p < 0.05). However, in a regression model with other clinical variables (i.e., age, gender, left atrial size, presence or absence of any cardiac disease, length of time in flutter, left ventricular function, type of flutter, flutter cycle length, type of secondary arrhythmias) no significant predictors were found. Patients with transient ischemic attacks or pulmonary emboli were then excluded from the analysis in order to compare the thromboembolic risk in the present study to that reported in major atrial fibrillation trials. The overall risk becomes 7% (6 of 86), which over a mean follow-up period of 4.5 years yields an annual risk of approximately 1.6%. Although this risk is only 1/3 of that for patients with atrial fibrillation, this risk is higher than previously recognized for patients with chronic atrial flutter. Anticoagulant therapy should be seriously considered for these patients.
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PMID:Risk of thromboembolism in chronic atrial flutter. 911 61

Sotalol's usefulness in treatment of atrial fibrillation and atrial flutter is unproven. This study evaluated (1) the efficacy of sotalol in preventing recurrences of paroxysmal atrial fibrillation or atrial flutter and controlling ventricular rate (in chronic atrial fibrillation or relapse of paroxysmal atrial arrhythmias), (2) the safety of sotalol, and (3) predictors of sotalol efficacy. Thirty-three patients, 28 with paroxysmal and five with chronic atrial fibrillation or atrial flutter, received an average dose of 265 +/- 119 mg of oral sotalol per day. During a 10 +/- 12 month follow-up, recurrence rate for paroxysmal arrhythmia was 64%, with a 50% recurrence at 4.6 months. For patients with chronic atrial fibrillation, ventricular rates were well controlled with sotalol administration (136 +/- 33 beats/min versus 88 +/- 23 beats/min; p = 0.04). No patient with chronic atrial fibrillation converted to sinus rhythm during the study. Side effects necessitated sotalol discontinuation in three patients. By multivariate analysis, younger age, higher ejection fraction, and absence of hypertension independently predicted sotalol efficacy.
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PMID:Efficacy and safety of sotalol in patients with refractory atrial fibrillation or flutter. 931 91

Atrial flutter (AFL) is a common problem in children who have undergone a Fontan operation for single ventricle physiology. Although this has been attributed to the atrial stretch inherent in the earlier forms of this operation, AFL has persisted in spite of a modification that minimizes atrial distension. Therefore, it was hypothesized that AFL following the modified Fontan procedure may result from anatomic barriers related to suture lines rather than from atrial stretch or hypertension. In a series of experiments performed in dogs under general anesthesia, the modified Fontan repair was simulated by placing only the suture line of the intra-atrial repair. No baffle was placed, thus avoiding any hemodynamic alterations. After closure of the atriotomy, 253 point unipolar atrial endocardial form-fitting electrodes were inserted through the mitral and tricuspid valves via bilateral ventriculotomies. Induction of AFL was attempted with atrial burst pacing and programmed extrastimulation, and activation sequence maps of subsequent reentry were generated from the endocardial electrodes. Atrial flutter was induced in all of 17 dogs, with a median cycle length of 177 +/- 31 ms. Activation sequence maps demonstrated conduction block along the crista terminalis corresponding to the free wall portion of the suture line. This created an isthmus between the suture line and tricuspid annulus, which appeared critical for sustaining AFL, although the circuit used both the septal and free wall surfaces of the right atrium. In seven dogs, a cryolesion was placed from the tricuspid annulus to the free wall segment of the suture line, terminating the AFL, in all seven. When the free wall segment of the suture line was moved 5 mm medial to the crista terminalis, AFL was induced in four of five dogs, but only in the presence of isoproterenol and at a shorter cycle length (136 +/- 8 ms, P < .001). Atrial flutter was not inducible, even with the addition of isoproterenol, in any of five dogs in which the suture line was placed 10 mm anterior to the crista terminalis and incorporated into closure of the atriotomy. This acute canine model of the modified Fontan operation demonstrates that conduction block from the free wall portion of the suture line creates an isthmus of tissue between the suture line and the tricuspid annulus. This is a sufficient substrate to produce AFL; no hemodynamic alteration is required. Injury to the crista terminalis is a significant risk factor in this model, which suggests that a modification of the suture line might reduce the incidence of AFL in patients following this operation.
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PMID:A canine model of atrial flutter following the intra-atrial lateral tunnel Fontan operation. 953 85

Based on multiple studies, clear, guided anticoagulation therapy is recommended for patients with atrial fibrillation. The value of anticoagulation therapy in patients with atrial flutter, however, is less well established. Little is known about the incidence of thromboembolism in patients with atrial flutter. We evaluated the risk of thromboembolism in 191 consecutive unselected patients referred for treatment of atrial flutter. A history of embolic events was noted in 11 patients. Acute embolism (<48 hours) occurred in 4 patients (3 after direct current cardioversion, 1 after catheter ablation). During follow-up of 26+/-18 months, 9 patients experienced thromboembolic events. During the follow-up, the overall embolic event rate (including acute embolism and thromboembolic events during follow-up) was 7 % in this patient population. Risk indicators for an embolic event in an univariate analysis were organic heart disease (p = 0.037), depressed left ventricular function (p = 0.02), history of systemic hypertension (p = 0.004), and diabetes mellitus (p = 0.0038). Using multivariate analysis, a history of hypertension was the only independent predictor for elevated embolic risk in this patient population (odds ratio = 6.5; 95% confidence intervals 1.5 to 45). Thus, the thromboembolic risk is higher than previously recognized for patients with atrial flutter. Anticoagulation therapy may decrease this risk.
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PMID:Risk of thromboembolic events in patients with atrial flutter. 1007 8

National and international societies have issued guidelines on the management of heart failure: The European Society of Cardiology, WHO, ACC/AHA Task Force Report, US Department of Health and Human Services, German Society of Cardiology. The therapeutic approaches to heart failure have undergone considerable changes during the last few years. The guidelines have to be updated almost yearly due to new results from prospective randomized studies. Although an agreement could be reached with respect to general measures and drug treatment, no agreement on mechanical devices, pacemakers and surgical interventions has been reached. The basis for medical treatment of chronic heart failure depends on diuretics, digitalis, ACE inhibitors, and beta-blockers. Calcium antagonists and other positive inotropic drugs, other than digitalis, should be avoided as far as possible. Thiazides, loop diuretics and aldosterone antagonists are needed for acute and chronic treatment of heart failure, alone or in combination (diuretic resistant heart failure!). Digitalis glycosides are needed in patients with atrial fibrillation with a fast ventricular rate or atrial flutter and in patients with systolic dysfunction, large hearts and symptomatic failure class NYHA III and IV. However, digitalis does not convert atrial fibrillation to sinus rhythm. Today there is no question that ACE inhibitors improve the prognosis of all patients with heart failure in all stages, if ejection fraction is reduced. Therefore, most patients after myocardial infarction or after having experienced pump failure due to myocarditis or cardiomyopathy are treated with ACE inhibitors and diuretics. The beneficial effects of ACE inhibitors seem to be most pronounced the worse the situation is. Relative risk reductions (mortality!) between 10% and 40% have been published depending on the severity of symptomatic left ventricular dysfunction. Those patients with high absolute risk have more to gain than those with low risk for any given "risk reduction", of course. Recent studies also indicate that most high risk cardiac patients profit from ACE inhibitors even if pump function is normal (i.e., patients with coronary heart disease, diabetes mellitus, cerebral vascular disease, hypertension) (15). AT1 antagonists can substitute for ACE inhibitors, if the latter are not tolerated due to cough. Up to now, beta-blocking agents apart from diuretics seem to be the best investigated drugs in heart failure. Large controlled studies with bisoprolol, carvedilol and metoprolol in addition to diuretics, digitalis and ACE inhibitors convincingly yielded positive results in chronic left ventricular failure patients. Reduction of mortality by 35% and even of sudden cardiac deaths by 40% have been proven beyond doubt. Thus, heart failure patients today should also receive beta-blocking agents in all stages of the disease. In the era of controlled prospective studies (evidence-based medicine), physicians are well advised to use only drugs that have been proven beneficial in large controlled studies.
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PMID:The management of heart failure--an overview. 1119 49

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