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)

The cause of recurrent resting angina one year after aorto-coronary bypass is presented. A 65 year old female with effort and resting angina with syncope had an isolated narrowing of the proximal portion of the left anterior descending artery on coronary angiography. Saphenous vein aorto-coronary bypass and cardiac plexectomy were performed on the 18 . 12 . 78, and an excellent result was obtained in the first postoperative year. Nocturnal angina with syncope recurred on the 31 . 12 . 79 and anterior subendo-cardial ischaemic changes were noted on the post critical electrocardiogramme. On control angiography 10 days later, the bypass graft was shown to be patent. A provocative test with methylergometrine showed spasm of the whole of the revascularised artery without any changes in the other vessels. Attacks of spontaneous angina with ST depression on Holter monitoring continued despite treatment with Nifedipine (6 capsules/day). The substitution of Diltiazem (3 capsules/day) prevented further recurrence with a follow-up of three months. The authors conclude that spontaneous angina after aorto-coronary bypass is not synonymous with graft dysfunction, and suggest that the effects of cardiac denervation in vasospastic angina, where Nifedipine and Diltiazem seem to have different modes of action, need further confirmation.
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PMID:[False failure of an aortocoronary bypass. Spasm of an artery revascularized by 2 saphenous vein graft]. 678 80

107 patients suffering from angina at rest associated with ST segment changes underwent coronary arteriography. 46 patients showed ST segment elevation during ischemic attacks (group I) while 61 patients exhibited ST segment depression during chest pain (group II). Non-significant coronary artery disease was more frequent in group I patients (group I 15%, group II 5%) as well as one vessel disease (group I 33%, group II 15%) while multivessel disease and left main involvement were more frequent in group II patients (group I 28%, group II 60%). Depression of left ventricular function was found in similar percentage of cases in both groups. During hospitalization all patients were treated with calcium antagonists (Nifedipine 10/20 mg every six hours) and/or nitrates (2% nitroglycerin ointment 2 inches every six/four hours) with one death (occurring after coronary arteriography) and eleven non-fatal myocardial infarctions. 50 patients underwent coronary bypass grafting with four perioperative deaths and six nonfatal myocardial infarctions. Most of the surgically treated patients were poorly responsive to medical treatment and had multivessel disease or left main involvement. Since these features are known to be related to a poor prognosis with medical treatment, surgical results in such patients seem satisfactory.
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PMID:[Angina at rest. Clinical, electrocardiographic and angiographic observations in 107 patients]. 678 46

The aim of this study was to assess the effects of the association of sublingual nifedipine and intravenous acebutolol on left ventricular inotropism. A series of 30 randomised patients underwent hemodynamic investigation repeated after a 30 minute interval comprising measurement of left ventricular (LVP) and aortic (AoP) pressures and ventriculography (Vo). Between the two Vo, Group I (N = 10) were given 20 mg sublingual nifedipine (N), Group II (N = 0) were given I mg/Kg acebutolol (A) intravenously in 5 minutes, and Group III (N = 10) the association of 20 mg sublingual N and I mg/Kg intravenous A. All patients had normal resting left ventricular function (ejection fraction greater than 0,55). In Group I, a significant improvement in left ventricular function with reduction of end diastolic pressure, increase ejection fraction, VCF and cardiac index was observed. THese changes were secondary to the reduction in aortic impedence with no effects on the contractile element (assessed by end systolic pressure/end systolic volume - ESP/ESV - ratio). In Group II, a significant reduction in these indices of left ventricular function was recorded secondary to a reduction in contractility. Group III had a special hemodynamic profile comprising: a reduction in afterload identical to that observed in Group I; a significantly greater reduction in the ESP/ESV ratio than in Group II; a greater reduction in the indices of left ventricular function (especially EF, VCF and CI) than in Group II, but the difference was not significant. The data obtained under the conditions of this acute hemodynamic investigation in patients with normal basal left ventricular function may be summarised thus: 1) Nifedipine alone has no detectable negative inotropic effects. 2) The association with acebutolol, nifedipine seems to potentiate myocardial depression (ESP/ESV). 3) This therapeutic association, the value of which has already been demonstrated in coronary insufficiency should be used carefully without precise knowledge of the left ventricular function.
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PMID:[Hemodynamic effects of the association of nifedipine and acebutolol]. 680 48

Nine patients with severe coronary artery disease and disabling angina receiving either regular metoprolol or oxprenolol, together with glyceryl trinitrate tablets as required for chest pain, were studied. Nifedipine 10 mg three times per day was compared to placebo in a double blind randomized control trial, using patient diary cards and exercise tests. The number of recorded episodes of angina during the placebo period of 15.0 +/- 2.1 (mean +/- s.e.m.) per patient per week was significantly reduced to 11.2 +/- 2.5 during the nifedipine period (P less than 0.05). Similarly, the recorded number of glyceryl trinitrate tablets consumed during the placebo period of 12.6 +/- 2.1 was significantly reduced to 9.1 +/- 2.0 tablets per patient per week during the nifedipine period (P less than 0.05). There was a statistically significant increase in both the duration of exercise to onset of chest pain (from 241 +/- 16.3 seconds on placebo to 306 +/- 38.4 seconds on nifedipine (P less than 0.05)) and the total work performed to the onset of chest pain during the nifedipine period compared to the control and placebo periods (P less than 0.05). There was a significant increase (P less than 0.05) in exercise time before the onset of appreciable ST depression (greater than 1 mm) on exercise testing during the nifedipine period (66.2 +/- 4.2 sec) compared to the control period (51.2 +/- 3.0 sec) and placebo periods (58.7 +/- 3.5 sec). Although nifedipine was generally well tolerated, one patient experienced a severe episode of angina whilst taking the drug, which required admission to hospital.
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PMID:The symptomatic and objective effects of nifedipine in combination with beta-blocker therapy in severe angina pectoris. 682 May 4

Experiments were performed on isolated rat aorta and superior mesenteric artery in order to study the action of nifedipine on norepinephrine and K-depolarization-evoked contractions and transmembrane calcium fluxes. Concentration-dependent contractions were obtained with norepinephrine in physiological solution and with Ca++ in K-depolarizing solution. Nifedipine caused a concentration-dependent depression of the maximum response. When aorta was depolarized by 40 mM KCI (instead of usual 100 mM KCI concentration), high concentrations of Ca++ evoked a relaxation that was also blocked by nifedipine. The action of nifedipine has been examined on Ca influx and efflux in arteries stimulated by norepinephrine and K-depolarization. Norepinephrine-evoked Ca influx, but not Ca efflux, was reduced by nifedipine. Concentration inhibitory curves for Ca influx and contraction could be superimposed. K-depolarization-dependent Ca entry and Ca efflux were blocked by nifedipine at concentrations lower than those required to antagonize norepinephrine actions. The results suggest that the action of nifedipine on artery contractility can be related to blockade of calcium entry through channels opened during depolarization or receptor-response coupling.
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PMID:Actions of nifedipine on calcium fluxes and contraction in isolated rat arteries. 682 65

The effect of intracoronary nifedipine on regional and global left ventricular performance, coronary vasomotility, and myocardial oxygen consumption is reported. Left ventricular pressures and volume indices of contractility and relaxation were simultaneously recorded in five patients without coronary artery disease. In these patients, nifedipine in the left main coronary artery not only delayed (+115 ms) anterior wall contraction but also slowed (3.5 vs 1.9 cm/s) and depressed it (-26%), resulting in a depression of global left ventricular ejection. This asynchrony and depression of regional contraction is considered to be responsible for the slowed isovolumic contraction and relaxation of the whole ventricle. In 10 other patients with coronary artery disease, coronary sinus blood flow and myocardial oxygen consumption were measured before and after intracoronary nifedipine. The observed decrease in myocardial oxygen consumption (-28%) depended primarily on a decrease in contractility and left ventricular performance. In a third study group of 12 patients with coronary artery disease, the effects of intracoronary nifedipine on the coronary vasomotility of 40 coronary segments (normal, prestenotic, stenotic, poststenotic) were quantitatively determined. Left ventricular haemodynamics and coronary sinus saturation were monitored while the cineangiograms were recorded before and after nifedipine. Nifedipine provoked vasodilatation of the normal (+10.3%), prestenotic, stenotic (+4 to 30%), and poststenotic (+16.4%) coronary segments, which persisted after the disappearance of its direct effects on the myocardium. This transient regional "cardioplegic" effect of nifedipine, associated with an increase in coronary blood flow, a reduction in myocardial oxygen consumption, and a vasodilatation of the epicardial vessels is likely to be beneficial during temporary coronary occlusion such as occurs in spasm or transluminal angioplasty.
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PMID:Influence of intracoronary nifedipine on left ventricular function, coronary vasomotility, and myocardial oxygen consumption. 683 31

Effects of calcium antagonists on the ST alternans and associated mechanical alternans during acute coronary occlusion were examined in anesthetized dogs. The heart rate was fixed by atrial pacing. The intravenous administration of 0.2 mg/kg verapamil attenuated the ST alternans as did 0.5 mg/kg diltiazem. Although these drugs significantly attenuated TQ depression during occlusion, the attenuation was observed after a longer period of occlusion and when the degree of TQ depression was comparable to that during the control occlusion. Nifedipine, 0.03 mg/kg, slightly attenuated the ST alternans, but 0.5 mg/kg dipyridamole had no effect. These results support the idea that slow inward currents are involved in the ST alternans. On the other hand, the mechanical alternans was attenuated in six of 11 dogs. It is probable that factors other than the electrical alternans may also contribute to the mechanical alternans.
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PMID:Effects of calcium antagonists on the electrical alternans of the ST segment and on associated mechanical alternans during acute coronary occlusion in dogs. 687 77

The action of four calcium antagonistic drugs, including verapamil, bepridil, nifedipine, and diltiazem, on calcium binding to cardiac sarcolemma from guniea pig was tested. It was found that verapamil (10(-6) to 10(-5) M) inhibited calcium binding to a great extent. Bepridil at the same concentrations was less potent than verapamil in the depression of calcium binding. Nifedipine and diltiazem did not affect sarcolemmal calcium binding. The differential action of the calcium antagonistic drugs was discussed.
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PMID:Differential actions of calcium antagonists on calcium binding to cardiac sarcolemma. 698 16

The clinical manifestations of symptomatic coronary arterial spasm were analyzed in 30 patients whose coronary arteriograms demonstrated no fixed severe obstructions. The study group consisted of 14 men and 16 women (average age, 47 years). Angina at rest was invariable and it was usually typical in quality, location, duration and response to nitroglycerin. Exertional angina occurred in 23 percent and syncope with angina in 33 percent. Spontaneous remission of angina for at least 1 month occurred in 57 percent of patients. Prinzmetal's variant angina occurred in 77 percent of patients and only S-T segment depression or T wave changes during angina occurred in 23 percent. Major arrhythmias during ischemia developed in 47 percent. Exericse tests were positive in 24 percent. Myocardial infarction, probably due to coronary spasm, occurred in 7 percent of patients. Isosorbide dinitrate and propranolol were effective therapy in only 39 percent and 6 percent of patients, respectively. Nifedipine, a calcium flux antagonist, was effective in 80 percent of patients. Patients with normal coronary arteriograms who have clinical features suggestive of coronary arterial spasm should be considered for further investigation, including long-term electrocardiographic monitoring and provocative testing for spasm.
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PMID:Syndrome of symptomatic coronary arterial spasm with nearly normal coronary arteriograms. 698 57

We studied the acute hemodynamic effects of nifedipine in 20 patients with angiographically proved coronary artery disease. Eight patients were studied during exercise-induced pain. There was an expected abnormal increase in pulmonary wedge pressure (28 +/- 8 mm Hg, mean +/- SD) accompanying chest pain (onset 179 seconds, duration 334 seconds) and ST-segment depression (2.2 +/- 0.9 mm) on the ECG. Pacing stress was used in six patients and increased left ventricular (LV) end-diastolic pressure (from 16 +/- 6 to 26 +/- 6 mm Hg), volumes (end-diastolic 63 +/- 20 to 81 +/- 22 ml/m2, end-systolic 26 +/- 15 to 47 +/- 16 ml/m2) and impaired ejection fraction (0.60 +/- 0.15 to 0.44 +/- 0.11) compared with control values. In both groups, nifedipine, 20 mg sublingually, significantly shortened duration of pain, reduced ST depression on the ECG (p less than 0.001) and reversed all hemodynamic abnormalities. In another group of six patients with recent (less than 4 months) acute myocardial infarction and moderately severe LV dysfunction at rest, nifedipine reduced LV end-diastolic pressure from 21 +/- 6 to 12 +/- 5 mm Hg and volumes (end-diastolic from 109 +/- 35 to 95 +/- 32 ml/m2, end-systolic from 41 +/- 15 to 31 +/- 7 ml/m2), while the ejection fraction improved significantly, from 0.43 +/- 0.08 to 0.58 +/- 0.11. Thus, the antianginal effect of nifedipine is associated with improved systolic emptying and reduced diastolic filling of the heart. Nifedipine appears to have no discernible adverse effects in patients with depressed LV function.
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PMID:Acute hemodynamic effects of nifedipine in patients with ischemic heart disease. 707 73


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