Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monophotonic absorption densitometry of the forearm is an exact method for the evaluation of the bone mineralisation, provided the positioning of the forearm is strictly controlled. It is also able to demonstrate progressive enlargement of the bones with age, up until the ages of about 60 to 70 years. The measurements should be performed in two sites: diaphyseal (cortical bone) and epiphyseal (cortical and trabecular bone). The curves obtained from 1,011 controls are in agreement with the current state of knowledge concerning the variations in bone mass during life in both sexes. In women, the number of pregnancies has no influence on the mineralisation index (MI). The values obtained in 156 osteoporotic patients and in 53 subjects with idiopathic hypercalciuria were appreciably lower than those obtained in age-matched controls. In individual subjects, this method appears to be much more discrimination than the measurement of the trabecular bone volume (TBV) for the diagnosis of osteoporosis and no statistically significant correlation was observed between the MI and the TBV. In male controls, there was a depression of the mean curves around the age of 45 years in all four sites of measurement. This depression was also observed in male subjects with hypercalciuria. They correspond to the generations born between 1930 and 1940. The responsibility of a relative nutritional deficiency affecting growing boys during the 1939-45 war is proposed.
Rev Rhum Mal Osteoartic 1985 Dec
PMID:[Bone densitometry by monochromatic photon absorption. Study of a normal population and values obtained in various pathological conditions]. 409 71

Left ventricular function was studied in 15 patients both before and after intravenous administration of Practolol (an agent blocking selectively the heart beta-adrenergic receptors (beta 1)), while the heart rate was constant by right atrial pacing. The negative inotropic effect linked to the negative chronotropic effect of the beta-adrenergic blockage, represented approximately one quarter of the overall depression of the contractility. Right atrial pacing determined a decrease of the left ventricular end-diastolic pressure and an increase of the pacing rate by 20% above the spontaneous heart rate, after administration of 30 mg of Practolol, brought the contractility back to its control level.
Arch Mal Coeur Vaiss 1974 Oct
PMID:[Effects of selective beta adrenergic block on myocardial contractility. Relative role of negative inotropic and chronotropic effects]. 421 30

Molsidomine, a new venous vasodilator, was studied in 40 cases of stable angina by ergometric stress testing. 1. In 10 patients, one hour after 2 mg molsidomine sublingually, the work inducing a 1 mm ST depression (WST 1) increased by 94% (p less than 0,05), the total work by 52% (p less than 0,005) and the maximum ST depression (ST max) fell by 45% (p less than 0,01). Resting heart rate was unchanged. There was a mild fall in systemic blood pressure. 2. Molsidomine had a significant synergic effect in 3 groups of 10 patients on betablocker therapy but with ischaemic changes on exercise: a) Molsidomine 1 mg sublingually increased WST 1 by 36% (p less than 0,05); at a 2 mg dosage, by 55% (p less than 0,001). ST max decreased from 2,4 +/- 0,4 mm to 1,3 +/- 0,3 (p less than 0,005) and 1,2 +/- 0,33 (p less than 0,001) respectively. The maximal effect was obtained with 1 mg in 5 out of 10 patients. b) One and three hours after 2 mg Molsidomine sublingually or orally: WST 1 increased from 97% to 110% (p less than 0,005): ST max decreased in similar proportions (p less than 0,005). c) 2 mg Molsidomine and 230 mg isosorbide dinitrate orally were compared after two hours: WST 1 increased by 130% after Molsidomine (p less than 0,005) and by 112% after isosorbide (p less than 0,005). ST max decreased in similar proportions (p less than 0,005). The blood pressure fell less with molsidomine. Molsidomine appeared to be better tolerated than isosorbide. (5 cases of mild headache in 40 patients compared to 4 cases out of 10 patients). The results of a preliminary clinical trial are reported. The association of molsidomine (2 mg per os three times daily) reduced the number of anginal attacks by over 50% in 16 out of 17 patients inadequately controlled by betablockade alone. 3 patients complained of headache at the onset of therapy. The efficacity was comparable and the tolerance better than in 28 patients with isosorbide dinitrate and betablockade, and in 10 patients with nifedipine and betablockade. In conclusion, molsidomine is a venous vasodilator with useful pharmacokinetic properties. It seems to be effective and well tolerated in the treatment of angina whether used alone or in association with betablockers.
Arch Mal Coeur Vaiss 1981 Apr
PMID:[Ergometric study of a new vasodilator agent in angina: molsidomine. Value of combination with beta-blockaders]. 611 71

Beta-blocking agents may induce vascular syndromes related to environmental temperature, accentuation of arterial diseases, gangrene of the extremities. Incidence and severity are variable with beta-blocking agent's properties: cardioselectivity, intrinsic sympathomimetic activity, cardiac depression, and with the patient's disease. The risk of complication is greater with hypertension disease because of the reduction of arterial compliance and quantitative and qualitative alterations of adrenergic receptors.
J Mal Vasc 1984
PMID:[Peripheral vascular complications of beta-blocking agents]. 614 17

Mitral valve prolapse ( MVP ) , responsible for most of the symptoms which had previously been interpreted as being due to neurocirculatory disorders or cardiac neurosis , is being recognised more often and has an incidence of about 6-8 % in an unselected population . Although this condition was considered for a long time to be a benign auscultatory abnormality , it may be the cause of serious cardiac complication . Arrhythmias predominate with an incidence of 60 to 80 % on continuous electrocardiography . In a series of 245 patients with mitral valve prolapse confirmed on echocardiography , 52 patients chosen at random were studied to determine the incidence pf ST changes , disturbances of heart rate , QT interval , changes of QRS , arrhythmias with resting , exercise and continuous ECG over 24 hours ( HMS = Holter Monitoring System ) . Abnormalities of ventricular repolarisation , especially flattening of the T wave and , less commonly , St depression were observed in about one third of the patients . These changes were more common in the inferior but were also found in the left precordial leads . 73 % of the 52 patients had a heart rate of 75/mn and their QT intervals showed the following changes : 30.7 % Had a duration greater than the 120 th percentile ; 19.2 % had a duration greater than the upper limit of normal . The other 50 % had a QT interval of around the 100 th percentile . None had a duration of less than the 90 th percentile . In 22.5 % patients , QRS changes due to conduction defects were recorded ( 15 % right bundle branch block - RBBB - , 7.5 % incomplete RBBB ) . HMS is the method of choice for detection of arrhythmias . Resting ECG only showed premature ventricular contractions ( PVCs ) in 12.5 % , compared to 32.5 % on exercise ECG and 62.5 % on HMS . 50 % PVCs were monomorphic , 5 % polymorphic , 7.5 % in salvos and 7.4 % supraventricular in origin . The circadian variation of PVC was striking with a high incidence during periods of activity . There was no statistical correlation between the incidence of PVCs , age , sex , type of MVP and the symptoms and auscultatory findings . The theories on the pathogenesis of the arrhythmias are divided between that based on an underlying cardiomyopathy ( confirmed by the presence of degenerated myocytes on electron microscopy ) and the mechanical hypothesis ( chordae tendinae irritating the endocardium or traction on the papillary muscle with resulting ischaemia ) which provide a better explanation of the clear predominance of monomorphic PVCs . The treatment of Barlow's syndrome is discussed . In our opininon , therapy is only required for ventricular arrhythmias detected by a sufficiently sensitive method such as HMS . Most authors use beta blockers , eventually in association with quinidine Therapeutic successes have also been observed with mexiletine , amiodarone , aprindine and less commonly with disopyramide .
Arch Mal Coeur Vaiss 1980 Sep
PMID:[Electrocardiographical changes and rhythm disorders in Barlow's syndrome]. 615 62

The predictive value of exercise stress testing was assessed by correlating the results with coronary angiography in a group of 100 patients 50 with inferior and 50 with anterior wall infarction. The following observations were made: --The exercise ECG was positive in 57 p. 100 of cases, more commonly in the inferior infarction group (74 p. 100), ST depression representing over 3/4 of the responses to exercise. On the other hand, the test was only positive in 40 p. 100 of anterior wall infarctions, ST depression again being the most commonly recorded response (65 p. 100). --The overall incidence of post-infarction angina was 45 p. 100; it was more common after inferior (70 p. 100) than anterior infarction (22 p. 100). --Multivessel disease was also more severe in the inferior infarction group (86 p. 100) than in anterior infarction (46 p. 100). However, ventricular aneurysms were twice as common in the anterior infarction group. --Exercise testing detected 80 p. 100 of cases with multivessel disease, especially when the LAD artery was involved, in the inferior infarction group. In the anterior infarction group, almost 50 p. 100 of patients with multivessel disease were not diagnosed. Despite an overall sensitivity of 73 p. 100 the predictive value of exercise stress testing was excellent (84 p. 100). In conclusion, in the presence of persisting angina after myocardial infarction coronary angiography should be performed to determine the severity of the multivessel disease. Exercise stress testing is a useful but imperfect method of detecting this high risk group. Its predictive value is however better in inferior (94 p. 100) than in anterior wall infarction (65 p. 100). Persisting angina was found to be a parameter of very high specificity (100 p. 100) for the presence of multivessel disease.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Predictive value of the exercise test after primary infarction]. 640 28

A subgroup of 22 patients with Prinzmetal angina and a good clinical response to treatment with calcium inhibitors was studied to determine whether the ergonovine provocation test could help decide when to stop treatment. Before treatment, all patients had ST elevation during the ergonovine test which was performed in the coronary care unit. After 9,4 +/- 4,7 months' treatment, all 22 patients were asymptomatic. Their treatment was discontinued and the ergonovine test repeated. Twelve of the 22 patients had no anginal pain or ST segment changes during the test. Without therapy, none of these 12 patients have experienced recurrence of angina during a follow up period of 4,2 +/- 2,9 months. Angina with ST elevation occurred in 7 patients during the ergonovine test, as observed during their initial provocation tests. In 3 other patients, ergonovine induced ST depression in the leads in which ST elevation had been recorded during their initial tests. Treatment was restarted in these 10 patients with positive tests. There were no complications. Spontaneous remissions of symptoms and negative ergonovine tests may be observed in some patients with Prinzmetal angina. Without treatment this group of patients may remain asymptomatic for several months.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Must the medical treatment of vasospastic angina be continued indefinitely?]. 640 39

Sixty patients without organic heart disease presenting with chest pain suggestive of angina pectoris and angiographically normal coronary arteries underwent clinical, hemodynamic and metabolic investigation. The study of myocardial lactate metabolism during atrial pacing (168 +/- 14 bpm) allowed identification of two groups: --40 patients with a normal coefficient of lactate extraction (K greater than or equal to 9 per cent); --20 patients with a pathologically low coefficient of lactate extraction (K less than 9 per cent) reflecting myocardial ischemia. In the first group, chest pain was often atypical (75 per cent of cases). Hemodynamic investigation showed minor abnormalities of the left ventricle in 48 per cent of cases. The diagnosis of angina was rejected in these patients. In the second group, the majority of patients developed chest pain (85 per cent of cases) at the maximal heart rate with significant ST depression (80 per cent of cases). The chest pain was typical of angina pectoris in 50 per cent of cases. Hemodynamic and angiographic investigation of the left ventricle was completely normal in nearly all cases. Only these patients with clinical, electrocardiographic and metabolic signs of myocardial ischemia can be considered as having angina with normal coronary arteries. Although studies of myocardial lactate metabolism and other signs of myocardial ischemia distinguish clearly between these two groups of patients, the coronary hemodynamics were similar. Resting coronary flow, its increase for the same myocardial oxygen demands and coronary resistances were comparable in both groups, and not significantly different from the values obtained in a control group of patients without coronary artery disease or chest pain. These results confirm that about 30 per cent of patients investigated for chest pain suggestive of angina pectoris who have angiographically normal coronary arteries, develop signs of myocardial ischemia during atrial pacing. The physiopathological explanation remains unclear as coronary hemodynamics have been found to be normal.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Angina pectoris with normal coronary arteries: clinical, hemodynamic and metabolic study]. 640 43

Effort angina is the result of acute myocardial ischemia on exercise due to an imbalance between myocardial oxygen demand and supply. During exercise, ischemia is provoked by an increase in myocardial oxygen needs (tachycardia, increased blood pressure, etc.) which cannot be met by increased coronary blood flow. The commonest cause of insufficient flow is coronary atherosclerosis. Coronary spasm does, however, play a role, whether it occurs during exercise on normal or atheromatous coronary vessels. Classical anti-anginal therapy is directed towards a reduction in the intense adrenergic activity associated with exercise, and to the limitation of myocardial oxygen consumption. Calcium inhibitors which cause peripheral vasodilation, decrease ventricular wall tension and coronary resistance, are usually reserved for unstable or resistant angina. We studied 10 patients with stable effort angina for over 2 years with significant (greater than 70 per cent) atheromatous lesions on coronary angiography unsuitable for surgical treatment. The patients underwent a randomised double blind trial to compare the effects of propranolol, diltiazem and placebo. Exercise ECG was performed after a treatment period of one week, 3 hours after drug administration. The results showed a significant improvement of work capacity with propranolol and diltiazem as compared to placebo. Propranolol (160 mg/day) was more effective than diltiazem (180 mg/day) in 6 patients. In 4 cases, the improvement with diltiazem and propranolol was the same. The association of the two drugs in one open study in 5 patients was even more effective in 3 patients. The small number of patients studied makes it impossible to draw any firm conclusions. Although calcium inhibitors are the treatment of choice in coronary spasm and betablockers in effort angina, diltiazem exerts an anti-anginal effect by reduction of myocardial oxygen consumption without depression of myocardial contractility, as other workers have shown.
Arch Mal Coeur Vaiss 1983 Feb
PMID:[Are calcium inhibitors useful in the treatment of effort angina pectoris]. 640 53

This study comprised 165 cases of coronary artery spasm (147 men and 18 women) with an average age of 49,2 years (range 27 to 73 years). Smoking was a particularly significant risk factor. Symptoms were usually of recent onset (80%) and dominated by attacks of angina pectoris either at rest alone or associated with angina of effort. 14% of cases of spasm were observed during acute myocardial infarction. Some cases presented with syncope due to cardiac arrhytmias. The basal electrocardiogramme was normal in 53% of cases. Exercise stress testing may be normal (30/65 cases) or positive (ST depression recorded in 26/65 cases). In 5 cases, ST elevation was observed. Left ventricular function was usually normal: 115 patients (70%) had organic atherosclerotic lesions, with 1, 2 and 3 vessel disease in 40%, 18% and 22% respectively. Spasm was spontaneous in 24,2% of cases but most commonly provoked by ergometrine. Criteria of spasm only applied to focal spasm and exclused catheter--induced spasm. The most common site of spasm was the right coronary artery (50,3% of cases), followed by the left anterior descending (31% of cases) and left circumflex (10,3% of cases). The outcome of these 165 cases depended on the therapeutic options (surgical treatment in 48 cases). The medium term results were generally good with a low mortality rate and follow up showed that the calcium antagonists provided effective prophylaxis against recurrence of spasm.
Arch Mal Coeur Vaiss 1983 Jun
PMID:[Coronary artery spasm. Apropos of 165 cases]. 641 13


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