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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors present a group of 143 hypertonic patients divided into three subgroups by the stage of hypertension (WHO). The objective was to detect an association between the incidence of cardiac dysrhythmias and the stage of hypertension and left ventricular (LV) morphological and functional parameters resp. which were assessed by echocardiography (ECHOCR). The authors investigated the systolic pressure (BPs) and diastolic pressure (BPd) on admission and the following ECHOCR parameters: weight of the left ventricle, tension of the LV wall during end systole, maximum tension of the LV wall, fractionated shortening of the Lv wall and the relative width of the LV wall. Comparison of clinical and ECHOCR parameters in groups revealed significantly lower values of BPs on admission in patients in the first stage of hypertension (p less than 0.01), the tension of the LV wall during end systole was in the third stage of hypertension significantly higher (p less than 0.01). In patients in the first stage there was a positive correlation between systolic pressure on admission and the fractional shortening of the LV (r = 0.568, p less than 0.025) and between diastolic pressure and the maximum tension of the LV wall (r = 0.572, p less than 0.025). They did not reveal an association between different stages of hypertension and the incidence of dysrhythmias. The group of patients with chronic atrial fibrillation had significantly larger dimensions of the left atrium, as compared with other groups of dysrhythmias. The authors were unable to reveal an association between the assessed morphological and functional parameters of the LV in different stages of hypertension and the incidence of dysrhythmias.
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PMID:[Echocardiographic indicators in various stages of hypertension and their relation to the incidence of dysrhythmia]. 152 59

Thrombus formation in the left atrium and left ventricle is primarily due to stasis of blood which causes activation of the coagulation system. Migration of thrombotic material into the circulation depends on the dynamic forces of the circulation. Atrial fibrillation is the commonest underlying cardiac disorder predisposing to thromboembolism. Rheumatic mitral stenosis, left atrial enlargement, prior myocardial infarction, hypertension, and echocardiographic left ventricular hypertrophy are risk factors for thromboembolic stroke in elderly patients with chronic atrial fibrillation. Non-valvular atrial fibrillation accounts for 45% of cardiac sources of thromboembolic stroke and includes patients with ischemic heart disease, hypertension, thyrotoxic heart disease, hypertrophic cardiomyopathy, chronic sinoatrial disorder, and idiopathic atrial fibrillation. 15% of cardiac sources of thromboembolic stroke are associated with acute myocardial infarction, 10% with left ventricular aneurysm and mural thrombi remote from an acute myocardial infarction, 10% with rheumatic valvular heart disease, and 10% with prosthetic cardiac valves. Mitral valve prolapse, mitral annular calcium, nonischemic cardiomyopathies, infective endocarditis, nonbacterial thrombotic endocarditis, left atrial myxoma, paradoxical embolism associated with congenital heart disease, calcific aortic stenosis, and complex atherosclerotic plaque within the proximal aorta also contribute to thromboembolism.
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PMID:Etiology and pathogenesis of thromboembolism. 176 43

The cerebral CT-scan results of 72 patients with chronic atrial fibrillation (AF) were compared to those of an age- and sex-matched control group, affected by muscle-tensive headache. None of the patients in the study had any neurologic symptoms. All were normal on neurologic examination. Mean age was 68 years in both groups. Patients with atrial fibrillation had a higher prevalence of hypertension, diabetes and hyperlipidemia, although the differences were not significant. Thirty-two patients (44.4%) with AF showed hypodense lesions on cerebral CT-scan, suggestive of small infarcts, whereas this finding was present only in eight control subjects (11.1%) (p less than 0.05). These results confirm in part the observations reported in literature and suggest a more thorough examination of the problem regarding the prophylaxis of thrombo-embolic risk in patients affected by chronic AF.
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PMID:Silent cerebral ischemia in patients with chronic atrial fibrillation--a case-control study. 236 81

I review the present understanding of thromboembolic complications and their prevention in patients with nonrheumatic atrial fibrillation. Chronic atrial fibrillation carries an annual 3-6% risk of thromboembolic complications, which is 5-7 times greater than that of controls with sinus rhythm. Paroxysmal atrial fibrillation is associated with a lower risk of thromboembolic complications than chronic atrial fibrillation. Heart failure and systemic hypertension seem to be significant clinical risk factors for stroke in patients with atrial fibrillation, but disagreement persists, and, with few exceptions, subgroups at particular risk have not been convincingly identified. The risk of stroke in persons with thyrotoxic atrial fibrillation seems to be lower than believed previously. Clinical studies have shown that left atrial dilatation is a consequence of the duration of atrial fibrillation rather than a cause, but the relation of left atrial enlargement to stroke is uncertain. Cerebral blood flow may be reduced during atrial fibrillation but seems to increase after cardioversion to sinus rhythm. A high prevalence of silent cerebral infarction has been detected in patients with chronic atrial fibrillation, but there seems to be a low risk of silent cerebral infarction in persons with paroxysmal atrial fibrillation. The one prospective study published to date on stroke prevention in patients with nonrheumatic chronic atrial fibrillation showed that anticoagulation with warfarin significantly reduced the incidence of thromboembolic complications.
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PMID:Thromboembolic complications in atrial fibrillation. 240 47

The major antihypertensive mechanism of calcium antagonists is by decreasing the systemic vascular resistance, modified by the counter-regulatory responses of the baroreflexes and the renin-angiotensin-aldosterone system. In severe hypertension, the concept that calcium overload of the vascular myocyte could precipitate or aggravate peripheral vasoconstriction provides a logical basis for the use of these agents as first choice therapy; nifedipine, especially, has been well tested. As monotherapy for mild to moderate hypertension each of the three first-generation agents compares well with beta-blockers. Calcium antagonists may have a special role in the therapy of certain patient groups (elderly, black) or in those subjects whose life style involves intense physical or mental exertion (hemodynamics better maintained than with beta-blockade) or in patients with early end-organ damage such as left ventricular hypertrophy or renal insufficiency. However, the goal blood pressure may not be reached during monotherapy so that drug combinations may be required. Further indications for these compounds are as follows. Verapamil and diltiazem are frequently used in supraventricular tachycardias including acute and chronic atrial fibrillation. In the arrhythmias of the Wolff-Parkinson-White syndrome, there is the potential danger of provocation of anterograde conduction. Further indications for calcium antagonists, still under evaluation, include congestive heart failure (controversial), hypertrophic cardiomyopathy (verapamil), primary pulmonary hypertension (high doses required), Raynaud's phenomenon (nifedipine and diltiazem effective), peripheral vascular disease (proof not yet documented), cerebral insufficiency and subarachnoid hemorrhage (nimodipine promising), migraine, exertional bronchospasm, renal disease, atherosclerosis (experimental), and primary aldosteronism (nifedipine inhibits aldosterone release). Second-generation agents include dihydropyridines, such as nitrendipine, nicardipine, felodipine, amlodipine, nisoldipine, nimodipine, and isradipine. From these will be selected agents that are longer acting and provide higher vascular selectivity. New preparations of existing agents include slow-release formulations of nifedipine, verapamil, and diltiazem. Minor side effects include those caused by vasodilation (flushing and headaches), constipation (verapamil), and ankle edema. Serious side effects are rare and result from improper use of these agents, as when intravenous verapamil is given to patients with sinus or atrioventricular nodal depression from drugs or disease, or nifedipine to patients with aortic stenosis. The potential of a marked negative inotropic effect is usually offset by afterload reduction, especially in the case of nifedipine. Yet caution is required when calcium antagonists, especially verapamil, are given to patients with myocardial failure unless caused by hypertensive heart disease. Drug interactions of calcium antagonists occur with other cardiovascular agents such as alpha-adrenergic blockers, beta-adrenergic blockers, digoxin, quinidine, and disopyramide.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Calcium channel antagonists. Part III: Use and comparative efficacy in hypertension and supraventricular arrhythmias. Minor indications. 315 29

In a randomly selected population of 9067 individuals, 32-64 years of age in 1967-1970, 25 (0.28%) had chronic atrial fibrillation (CAF). Eight had lone atrial fibrillation. In 1984 the cases were compared with an age- and sex-matched control group of 50 and found to have more cerebrovascular accidents (6 versus 2; P less than 0.05), congestive heart failure (9 versus 1; P less than 0.001), and valvular rheumatic heart disease (3 versus 0) or history consistent with rheumatic fever (6 versus 0; P less than 0.01). The mortality in the CAF group was 60% higher due to an excess in cardiovascular (relative risk 6.1; P less than 0.05) and cerebrovascular (relative risk 12.2; P less than 0.05) causes. The prevalence or incidence of ischaemic or hypertensive heart disease or the presence of coronary risk factors did not significantly differ in the two groups. By M-mode echocardiography the left atrial size, left ventricular enddiastolic dimension and left ventricular mass were increased in the CAF patients, while the systolic left ventricular shortening was significantly less. Thus, the prevalence of CAF is low in a randomly selected population 32-64 years of age and CAF is not strongly associated with ischaemic heart disease or hypertension. The CAF patients have an increased risk of dying prematurely particularly from cerebrovascular causes, even in the absence of valve disease.
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PMID:Chronic atrial fibrillation--epidemiologic features and 14 year follow-up: a case control study. 349 34

Chronic atrial fibrillation without valvular disease has been associated with increased stroke incidence. The impact of atrial fibrillation on the risk of stroke with increasing age was examined in 5184 men and women in the Framingham Heart Study. After 30 years of follow-up, chronic atrial fibrillation appeared in 303 persons. Age-specific incidence rates steadily increased from 0.2 per 1000 for ages 30 to 39 years to 39.0 per 1000 for ages 80 to 89 years. The proportion of strokes associated with this arrhythmia was 14.7%, 68 of the total 462 initial strokes, increasing steadily with age from 6.7% for ages 50 to 59 years to 36.2% for ages 80 to 89 years. In contrast to the impact of cardiac failure, coronary heart disease, and hypertension, which declined with age, atrial fibrillation was a significant contributor to stroke at all ages.
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PMID:Atrial fibrillation: a major contributor to stroke in the elderly. The Framingham Study. 363 64

This literature review was conducted to determine: (a) the rate of bleeding (major, minor and fatal) during long term oral anticoagulant therapy (greater than 4 weeks) in various disorders (ischaemic cerebrovascular disease, prosthetic cardiac valves, chronic atrial fibrillation, ischaemic heart disease and venous thrombosis); and (b) the clinical and laboratory risk factors which predispose such patients to bleeding. Using strictly defined methodological criteria, 167 studies were evaluated and classified into 1 of 5 categories based on the strength of the study design, with level I (randomised trials) representing studies which provided the most reliable information and level V (cases series) the least reliable. The risk of bleeding was substantial, and was most marked in patients with ischaemic cerebrovascular disease (29%), ischaemic heart disease (19%) and venous thromboembolism (23%). Major bleeding in venous thrombosis and cerebrovascular disease was frequently associated with an underlying risk factor. In venous thromboembolism these coexisting conditions (cancer, recent surgery and paraplegia) were also predisposing factors for thrombosis. In cerebrovascular disease major bleeding was almost always intracerebral, possibly because of associated hypertension or the cerebrovascular disease per se. We were unable to determine whether bleeding events were concentrated soon after commencing anticoagulant therapy. Haemorrhagic episodes frequently occurred when the prothrombin time (or thrombotest) was within the targeted therapeutic range, but the relationship between bleeding and the level of anticoagulant therapy was properly evaluated in only 1 study (in venous thrombosis) which demonstrated that the risk of bleeding was reduced by using a less intense anticoagulant regimen. In conclusion, the risk of bleeding during oral anticoagulant therapy is substantial. Our analysis was limited by the lack of concise reporting of clinical and laboratory information and we would suggest that future clinical studies report these in greater detail.
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PMID:Risk of haemorrhage associated with long term anticoagulant therapy. 390 38

Digoxin remains a very useful agent for chronic atrial fibrillation or for the ectopic beats associated with heart failure. But when rapid control of the ventricular rate is required to arrhythmias such as atrial fibrillation, atrial flutter, or paroxysmal atrial tachycardia, a slow infusion of verapamil is the agent of choice. In general, verapamil may be added to digoxin or given intravenously while a digoxin effect is awaited, unless there is digitalis toxicity. In digitalis toxicity, lignocaine remains the agent of choice for ventricular arrhythmias, and is given in the same doses as for acute myocardial infarction; phenytoin is used for digitalis-arrhythmias with A-V block. Verapamil may be infused very cautiously for digitalis-induced supraventricular tachyarrhythmias. The use of oral agents such as quinidine, disopyramide and mexilitene for chronic prophylaxis of ventricular ectopic beats is of doubtful effectiveness, unless the ectopic activity is symptomatic. Serious ventricular arrhythmias may be induced by quinidine and disopyramide. Beta-blockade is especially useful for ectopic beats associated with anxiety, or when arrhythmias are associated with angina of effort or hypertension. As always, major contraindications to the use of beta-blockade include cardiomegaly, heart failure or asthma.
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PMID:Anti-arrhythmic agents in ischemic heart disease: supraventricular arrhythmias, digitalis toxicity and chronic stable ventricular ectopic beats. 708 6

To evaluate the response of patients with chronic atrial fibrillation (AF) to exercise and to demonstrate if prognosis could be predicted, 200 male patients (64 +/- 1 years) with AF were identified retrospectively who underwent resting echocardiography and symptom-limited treadmill testing. They were classified by underlying disease into three subgroups: hypertension or no underlying disease (LONE; n = 102), ischemic heart disease (IHD; n = 45) and history of congestive heart failure or valvular disease (CHF-VD; n = 53). Maximal exercise capacities for LONE, IHD and CHF-VD were (mean +/- 1 SEM) 8.0 +/- 0.3, 6.4 +/- 0.4 and 6.0 +/- 0.3 metabolic equivalents, respectively (p < 0.01), and resting left ventricular ejection fractions were 61.7 +/- 1.6, 60.1 +/- 2.2 and 49.5 +/- 1.9%, respectively (p < 0.01). Stepwise multiple regression analysis demonstrated that, except for group classification (R2 = 0.13, p < 0.01), no clinical, exercise or morphologic variables could predict exercise capacity. After a mean 39.1-month follow-up (range 1-78), 17 of the 200 had died from cardiovascular causes. The rate of cardiac death using Kaplan-Meier survival analysis was significantly greater in CHF-VD patients (p < 0.01). However, Cox hazard function and Kaplan-Meier survival analysis demonstrated that neither echocardiographic measurements of cardiac size or function at rest, nor exercise or clinical variables were significant predictors of outcome. AF patients with a history of CHF and/or VD demonstrated a reduced exercise tolerance ad a worse prognosis than those without morphologic heart disease or those with IHD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise capacity and prognosis in patients with chronic atrial fibrillation. 772 99


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