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

The risk for systemic embolization was studied in 272 patients without mitral stenosis or prosthetic valves who were referred to the echocardiography laboratory with atrial fibrillation (AF). During a mean follow-up period of 33 months (range less than 1 to 83), 27 (10%) patients had a systemic embolic event, which was cerebral in 23 patients (85%) and peripheral in 4 (15%). In the analysis of individual variables, the risk of embolization was increased by female sex, underlying heart disease and left atrial size greater than or equal to 4.0 cm, but not by age, hypertension or type of AF (paroxysmal vs chronic). In multivariable analysis, left atrial size greater than or equal to 4.0 cm was the single strongest predictor of increased risk for embolization (p less than 0.001), but female sex (p = 0.014) and underlying heart disease (p = 0.027) also contributed. When each of these 3 factors was assigned 1 point in a risk score, embolic events were found to occur in none (0%) of 24 patients with a risk score of 0, in 2 (3%) of 83 patients with a risk score of 1, in 13 (11%) of 118 patients with a risk score of 2 and in 12 (26%) of 47 patients with a risk score of 3. The score allows patients with AF and without mitral stenosis to be stratified into high-, medium- and low-risk groups for systemic embolization. Such information could be useful in decision making for anticoagulation in patients with AF.
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PMID:Risk for systemic embolization of atrial fibrillation without mitral stenosis. 233 Aug 96

Sarcomere dynamics are related to the global left ventricular (LV) function in some representative pathological states, by using a theoretical model which combines sarcomere function, LV fibrous structure and geometry with the haemodynamic loading conditions. The analysis shows that pressure (concentric) hypertrophy due to hypertension or aortic stenosis is associated with an increase of the normal endocardial-to-epicardial gradient(s) of oxygen demand, which may be one of the causes for the development of endocardial fibrosis. The analysis also indicates that sarcomere shortening is relatively normal in compensated volume (eccentric) hypertrophy. Mitral stenosis demonstrates a case of decreased LV function, secondary to a chronic decrease in LV end diastolic volume, with sarcomeres that operate at their lowest length range. Conversely, the sarcomere function is depressed in cardiomyopathy; the heart's pumping function is maintained by appropriate adjustment mechanisms. However, the sarcomeres show minimal shortening and function at their highest length range with low (or zero) functional reserve. The study thus provides a quantitative tool that relates global LV function to local sarcomere dynamics in various pathological states.
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PMID:Mechanical pathophysiology of some heart diseases: a theoretical model study. 237 6

Unlike the left ventricle, the right ventricle is a thin-walled, low-pressure, volume-displacement pump that ensures adequacy of left ventricular filling and maintains a low pressure in the venous system. In healthy human subjects, there is no burden for right ventricular systolic emptying, because normal pulmonary vessels have a low impedance and show a passive recruitment when cardiac output increases. However, under a pathological condition like right-sided heart failure, the right ventricle may exert profound influences on the circulatory state. Right-sided heart failure most often results from primary or secondary pulmonary arterial hypertension. Pharmacologic vasodilation of the hypertensive pulmonary vascular bed is an ideal therapy for right-sided heart failure. The bipyridine derivative amrinone has positive inotropic and direct vasodilator properties, and therefore seems suitable for the therapy of right ventricular dysfunction accompanied by pulmonary arterial hypertension. In one study, 12 patients with right ventricular failure due to mitral valve stenosis were evaluated, and it was found that amrinone increased cardiac output by 25% and decreased pulmonary artery pressure by 30% to 50%. In a second study, the hemodynamic properties of amrinone versus sodium nitroprusside were compared in patients with aortic or mitral valve failure (n = 17), when both agents lowered systemic vascular resistance equally. Pulmonary vascular resistance decreased significantly (25%) only in the amrinone group.
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PMID:Effects of amrinone on the right side of the heart. 252 Oct 50

High-altitude pulmonary arterial hypertension affects people with a long-term residence at altitudes over 2500 m above the sea level and is characterized by elevated pulmonary artery pressure (over 35/15 mmHg). In order to assess the role of beta-adrenoreceptors in the development of high-altitude pulmonary arterial hypertension, we studied the beta-adrenoreceptor density on mononuclear leukocytes in Kirghiz male natives of Eastern Pamir (3600-4200 m above sea level) with the diagnosis of high-altitude pulmonary arterial hypertension, and in healthy men. It was shown that patients with signs of right ventricular hypertrophy (RVH) of the second and third grade have beta-adrenoreceptor density 4.5 times lower than control (2.27 +/- 0.22 vs. 9.85 +/- 1.28 fmol/10(6) cells). Values of Kd also proved to be lower, by 2.5 times (0.57 +/- 0.14 vs. 1.44 +/- 0.18 nM). Stimulation of adenylate cyclase by isoproterenol and other beta-agonists was lower in patients than in controls (+33% and +120%, respectively). These results demonstrate that the desensitization of beta-adrenoreceptors is present in patients with high-altitude pulmonary arterial hypertension associated with severe right ventricular hypertrophy. Patients with pulmonary arterial hypertension due to mitral stenosis do not have any signs of beta-adrenoreceptor desensitization associated with high plasma levels of catecholamines.
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PMID:Human adrenoceptor system response to the development of high altitude pulmonary arterial hypertension. 254 27

The echocardiographic study of 480 patients over 60 years (medium age: 75.4) revealed 37 (33 women) of them having mitral calcification (MC). The analysis of clinical and metabolic data of these 37 patients plus their electro, phono and echocardiographic assessment revealed: 1) MC was observed in 7.7% of this elderly population and its incidence tended to increase with age; 2) MC was more frequent and more pronounced in women; 3) cardiocirculatory abnormalities responsible for a high systolic pressure in the left ventricle, such as hypertension (64.9%) and aortic stenosis (10.8%) were the most commonly associated cardiac pathologies; 4) no history of illnesses usually aggressive to the mitral valve was detected; 5) plasma lipids and calcium were normal; 6) in 27.0% of patients with MC there was some degree of mitral stenosis and/or insufficiency and surgical correction has been considered in some cases; 7) changes in production and/or conduction properties were frequent, causing bradyarrhythmias, tachyarrhythmias and intraventricular block. Taking these points into consideration, a careful follow-up of confirmed cases is suggested, in order to detect and treat any complications without delay.
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PMID:[The importance of mitral calcification in the elderly]. 259 99

To evaluate the cardiac risk in patients undergoing noncardiac surgery, it has been identified by the multivariated analysis some major and independent correlates of fatal or life-threatening cardiac complications. The most important ones were the history of previous myocardial infarction in the preceding six months, clinical signs of congestive heart failure, third heart sound or jugular venous distention, and for some Authors instable angina class IV CCS. Other predictive factors of complications were premature ventricular and atrial contractions or ectopic rhythms within cardiac diseases, age over 70 years, intraperitoneal, intrathoracic, aortic or emergency operation, severe valvular aortic and mitral stenosis and poor general medical conditions. Stable angina, hypertension, hyperlipidemia and smoking habit were less important. The global evaluation of cardiac risk can be performed by multifactorial index subdividing the patients into four very different risk classes. This is obtained by scores assigned to each statistically significant factor.
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PMID:[Surgical cardiac risk in patients with heart diseases. I. Evaluation of the risk]. 260 75

Pulmonary hypertension in chronic mitral valve disease has been related most commonly to left ventricular dysfunction or mitral stenosis; its association with chronic, isolated mitral regurgitation and preserved left ventricular systolic function is unclear. In 41 catheterized patients with chronic mitral regurgitation (known history of mitral regurgitation for greater than 18 months) and preserved left ventricular systolic function (ejection fraction greater than 0.55), historic, electrocardiographic, echocardiographic and hemodynamic variables were analyzed. Ten patients (Group I) had normal pulmonary artery systolic pressure (less than 30 mm Hg), whereas 31 patients had pulmonary hypertension. Pulmonary artery systolic pressure was mildly increased (30 to 49 mm Hg) in 13 patients (Group II) and was greater than or equal to 50 mm Hg in 18 patients (Group III). Univariate analysis showed the more frequent occurrence of male gender and ruptured chordae tendineae in the groups with pulmonary hypertension. Mean pulmonary capillary wedge pressure, size of the V wave in pulmonary capillary wedge pressure and pulmonary arteriole resistance were higher, whereas cardiac index was lower in the hypertension groups. Multivariate stepwise analysis revealed higher mean pulmonary capillary wedge pressure and pulmonary arteriole resistance as the only variables independently differing among groups. In conclusion, pulmonary hypertension occurs frequently (76% of cases) in patients with chronic, isolated mitral regurgitation with preserved left ventricular systolic function. In these patients, a severe increase in pulmonary capillary wedge pressure is associated with elevation in pulmonary artery resistance, a finding similar to that in mitral stenosis.
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PMID:Isolated chronic mitral regurgitation with preserved systolic left ventricular function and severe pulmonary hypertension. 275 21

Mitral annulus calcification is a common finding in old people. In order to know the association of mitral annulus calcification with other pathologic conditions, 25 patients were studied by echocardiography, 20 females and 5 males. No significant differences _ere observed with respect to sex. The average age was 67 +/- 15 years. Mitral annulus calcification was associated with aortic sclerosis in 100% of the cases, to arterial hypertension in 19 (76%), to obstructive pulmonary disease in 8 (32%), to diabetes mellitus in 5 (20%), and to peripheral arterial insufficiency in 5 (20%). Mitral regurgitation was found in 14 cases, atrial fibrillation in 2 (8%). Complete A-V block was not observed, but there was enlargement of the left ventricle in 23 (92%) and of the left atrium in 17 (68%). The chest X-ray showed mitral annulus calcification in 5 (20%) with a sensitivity of 25% and a specificity of 100%. The M-mode echocardiogram showed LA-Ao ratio of 1.4 +/- 0.3, the mitral valve D-E excursion was reduced 11.9 +/- 3.1 mm. and also the E-F slope 28.6 mm/seg +/- 16.7 with appearance of mitral stenosis, but the two-dimensional study demonstrated that this was false. In all patients the left ventricle was dilated and fractional shortening was diminished. Echocardiography not only is a good diagnostic method for mitral annulus calcification, it also allow us to evaluate the hemodynamic consequences of this pathology which occurs in older patients and is often associated with other common illnesses of advanced age. In our study 56% of mitral annulus calcification cases were associated with mitral regurgitation.
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PMID:[Study of calcification of the mitral annulus. Importance of echocardiographic analysis]. 278 87

Cardiovascular manifestations develop in the majority of SLE patients at some time during the course of their illness, the most common being acute fibrinous pericarditis and pericardial effusion. Echocardiography has demonstrated an increased incidence of pericardial effusion, even in those who have minimal symptoms. Chronic adhesive pericarditis, pericardial tamponade, and constrictive pericarditis occur rarely. While myocarditis is commonly noted at autopsy, it is often silent clinically. Diagnosis during life can be confirmed only by endomyocardial biopsy. Electrocardiographic changes are often nonspecific. Endocarditis with superimposed nonbacterial verrucous vegetations (Libman-Sacks) is noted in more than 40% of hearts at autopsy, but is rarely diagnosed during life. Valve dysfunctions, such as aortic stenosis, aortic insufficiency, mitral stenosis, and mitral insufficiency, occasionally manifest during life and rarely may necessitate surgery. Atrial and ventricular arrhythmias, first degree AV block, and acquired CHB occur in association with pericarditis, myocarditis, vasculitis, and myocardial fibrosis, respectively. CCHB developing in newborns of mothers with SLE, particularly those who have an antibody to soluble tissue ribonuclear protein RO(SS-A), is increasingly being appreciated by both pediatric cardiologists and rheumatologists. Recently, severe coronary atherosclerosis resulting in angina pectoris and/or myocardial infarction in young adults has been noted, particularly in those who had developed risk factors such as hypertension and hyperlipidemia while receiving prolonged corticosteroid therapy. Rarely, coronary arteritis may produce similar symptoms. Congestive heart failure of either single or multiple etiologies carries an ominous prognosis. It remains a cause of high morbidity and mortality unless recognized early and treated properly. Extracardiac vascular manifestations of SLE include telangiectasia, vasculitis, livedo reticularis, Raynaud's phenomena, and thrombophlebitis, all of which may occur either alone or in different combinations. Evidence is now slowly accumulating that substantiates that immune complex deposition, complement activation and subsequent inflammatory reaction is responsible for the majority of the cardiovascular manifestations of SLE, for example, pericarditis, myocarditis, endocarditis, coronary arteritis, coronary atherosclerosis, and systemic and pulmonary vasculitis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiovascular manifestations of systemic lupus erythematosus: current perspective. 286 Jun 99

During a 12-year period, when more than 106,000 women were delivered, 28 women with peripartum heart failure of obscure etiology that initially was diagnosed as peripartum cardiomyopathy were studied. None had obvious underlying cardiac disease or iatrogenic fluid overload, and in all an assiduous search for underlying cardiovascular disease was launched. In 21 of these 28 women, heart failure was attributed to chronic underlying disease (chronic hypertension in 14, forme fruste mitral stenosis in four, and morbid obesity in one) or viral myocarditis. Importantly, these women also had multiple compounding cardiovascular factors--preeclampsia, cesarean section, anemia, and infection--which, when superimposed on those of pregnancy, acted in concert to cause heart failure. In seven women, the cause for cardiomegaly and global hypokinesis was not found, and peripartum cardiomyopathy was diagnosed. Compared with women with explicable causes of peripartum heart failure, these women did poorly: six had persistent cardiomegaly and heart failure, and four of these died within four months to eight years. From these observations, the authors conclude that idiopathic peripartum cardiomyopathy is uncommon, and that in most women with peripartum heart failure of obscure etiology, underlying chronic disease will be identified. Heart failure in these women ensues when the cardiovascular demands of normal pregnancy are amplified further by common pregnancy complications superimposed upon these underlying conditions that cause compensated ventricular hypertrophy.
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PMID:Peripartum heart failure: idiopathic cardiomyopathy or compounding cardiovascular events? 293 58


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