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)

Alkalosis was used for stress testing for coronary artery spasm in 70 patients (average age: 56 years) with resting angina. A rapid intravenous infusion of an alkaline buffer (THAM) immediately followed by 5 minutes' maximal ventilation increased the arterial pH to 7.67 +/- 0.5. Anginal pain and ECG changes were observed in 24 Patients, with ST elevation in 10 cases and ST depression in 14 cases. The ischaemic changes occurred during hyperventilation in 16 cases and in the 3 minutes following the test in 8 cases. The heart rate increased from 66 +/- II to 71 +/- 14 bpm (p less than 0,01) but systolic blood pressure fell from 139 +/- 12 to 130 +/- 12 mm Hg during hyperventilation; there was no significant change in the rate-pressure product (1130 +/- 1750 to 8990 +/- 2690). In all cases, the angina and ischaemic changes regressed after intravenous Trinitrin. Coronary angiography was performed in 56 patients: in the 24 patients with positive responses (Group I) and in 30 of the 46 patients with negative responses (Group II). Significant coronary artery narrowing (greater than 70%) was observed in 21 patients of Group I: in the 3 patients without coronary lesions an intravenous injection of 0.4 mg methylergometrine provoked coronary spasm. In Group II, significant narrowing was demonstrated in 18 patients: in the 12 other patients, coronary spasm could not be induced by methylergometrine. Therefore, in the absence of organic coronary lesions, an excellent correlation has been shown between the alkalosis and methylergometrine tests. This stress test was repeated in 16 of the 24 patients in Group I one hour after administration of 20 mg of Nifedepine: the test was negative in all cases. We conclude that the alkalosis test could be useful in the coronary care unit as a stress test for coronary spasm to determine the antianginal treatment of choice and to evaluate its efficacity.
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PMID:[Clinical application of the alkalosis induction test for coronary artery spasm]. 680 Mar 22

Twelve patients 8 females and 4 males, whose ages varied from 33 to 60 years (median 50.6 years), were seen at the Hospital for Cardiology and Neurology of the Mexican Institute for Social Security. All were diagnosed as having angor pectoris, through the clinical history and physical exam. Three patients had stable angor and in nine it was of an unstable type. The resting ECG showed signs of subepicardial ischemia in five cases. In eight the stress ECG according to the Bruce technic showed depression of the ST segment over 1 mm. In one patient atrial stimulation was performed with a pacemaker and ischemic changes of the ST segment were normal in all cases; in two however, coronary spasm that reversed with nitroglycerin appeared. The left ventriculogram was normal in all but one that revealed diaphragmatic hypokinesia associated with right coronary spasm. All patients were followed from two to fifty six months (median 19.4), and only in one case the angor pectoris remained unchanged. In all others it decreased or disappeared. During this time there were no deaths, myocardial infarctions or severe arrhythmias.
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PMID:[Angina pectoris with normal coronary arteries]. 680 91

Reported is a case of baclofen overdose in a 23-year-old woman. The patient manifested typical symptoms of baclofen overdose, including hypotonia, respiratory depression, and seizures. She was treated successfully with positive pressure ventilation, sedation, and intravenous antibiotics, and was discharged from the hospital on the 14th day following admission with no residual neurological signs, to be followed up in medical and psychiatric outpatient clinics. As baclofen becomes increasingly popular in the treatment of muscle spasm in certain neurological disorders, its availability for misuse increases.
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PMID:Baclofen overdose. 682 97

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

Exercise tests were performed in 14 patients with untreated variant angina with frequent spontaneous attacks and in 15 patients after treatment abolished the attacks. (1) Anginal attacks associated with ST elevation were induced by exercise in 79% of untreated patients. By contrast, ST elevation was not observed in treated patients and ST depression was induced in 53% of the cases. (2) Exercise-induced ST elevation in untreated patients was shown in the same leads as the spontaneous attacks. (3) Exercise-induced ST elevation appeared initially during the recovery phase after exercise in 36% of untreated patients. Exercise-induced ST depression appeared during or immediately after exercise. (4) The reproducibility of exercise-induced ST elevation was low with repeated tests at different stages, but exercise-induced ST depression was consistently observed. (5) The exercise-induced ST depression and lack of ST changes in treated patients were highly suggestive of the presence and absence of organic coronary artery disease, respectively. However, the exercise-induced ST elevation in untreated patients did not differentiate between the presence or absence of organic stenosis of the coronary arteries. The results of exercise tests vary with the stage of variant angina. It is suggested that a coronary arterial spasm is a trigger mechanism for exercise-induced angina in cases of variant angina with frequent spontaneous attacks.
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PMID:Exercise test in variant form of angina pectoris. Comparison of the results with spontaneous attacks. 685 52

79 ECGs, recorded during angina pectoris, from 52 patients were studied to determine the relations of arrhythmias and ST-segment changes and to evaluate the relationship between the prevalence of arrhythmias, the severity of coronary artery disease and left ventricular function. Arrhythmias were found in 22% of the ECGs (VPCs in 9, VT in 4, SVPCs in 3, sinus bradycardia in 1). Angina pectoris attacks accompanied by ST-segment elevation, ST-segment depression or unchanged ST-segment showed disturbances of rhythm in 47%, 24% and 0%. If coronary spasm without significant coronary stenoses was the cause for myocardial ischemia, arrhythmias appeared with 75% more often than in myocardial ischemia caused by organic stenoses (19%). Patients with disturbances of rhythm during spontaneous angina pectoris do not have anymore deterioration in left ventricular function than patients without arrhythmias.
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PMID:[Arrhythmia in unstable angina pectoris]. 686 19

Variant angina with ST elevation indicates transmural myocardial ischaemia and is due to spasm of a large epicardial coronary artery. Spasm occurs in arteries with varying degrees of fixed obstruction, giving rise to different clinical profiles of variant angina. However, coronary angiography is required to differentiate between those with minor coronary disease, and those with significant (greater than 70%) obstruction. In patients with minor coronary disease or normal arteries, beta-blockers are contraindicated, and treatment with calcium antagonist vasodilators should be commenced after documentation of spontaneous or ergonovine induced spasm. Patients with significant fixed coronary obstructions require bypass grafting if technically feasible. The role of coronary spasm is not confined to variant angina, as it causes angina at rest with ST depression, and may also cause myocardial infarction and sudden death.
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PMID:Coronary artery spasm. 692 80

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

The prevalence rate of exercise- S-T segment elevation of 0.1 mV or greater in symptomatic patients is 3.0 to 6.5 percent in most studies. S-T segment elevation is associated with a more severe degree of myocardial ischemia than depression and frequently implies a high grade coronary stenosis in the vessel that supplies the site of ischemia. Leads V4 to V6 and bipolar lead CM5 have been found to be relatively insensitive in detecting exercise-induced S-T segment elevation. The pathogenesis of S-T segment elevation is different in three clinical patient subsets reviewed. In patients afer infarction, the largest of the three subgroups, exercise-induced S-T segment elevation usually appears in leads with Q waves, is more common after anterior myocardial infarction and implies underlying akinetic of dyskinetic wall motion. Of patients with variant angina, 10 to 30 percent have during exercise S-T segment elevation that is most likely provoked by coronary arterial spasm. The natural history of variant angina is cyclic, and clinical observations and laboratory findings are dependent on particular phases in the disease process and treatment. Finally, 0.2 to 1.7 percent of symptomatic patients without infarction or variant angina have exercise-induced S-T segment elevation. Although most of the latter have fixed high grade coronary arterial stenoses at angiography, the exact pathogenetic mechanism of S-T segment shift in this patient group is not yet fully understood.
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PMID:S-T segment elevation and coronary spasm in response to exercise. 701 17

Local experimental subarachnoid hemorrhage (SAH) was produced over the cerebral cortex in 15 cats. The cellular response was monitored using ion-specific electrodes for extracellular potassium (K+) and calcium (Ca++) activity, DC cortical potential, and electrocorticogram. The response was characterized by a profound cellular depolarization and extracellular calcium (Ca++) depletion which accompanied extracellular potassium (K+) accumulation. The prehemorrhage baseline calcium levels measured 1.14 +/- 0.11 mM, and were lowered to 0.4 to 0.7 mM/liter in different experiments. The K+ accumulation reached levels between 16 and 31 mM from a baseline of 3.17 +/- 0.52 mM and were cleared to normal or nearly normal within 5 minutes. The Ca++ levels also returned to normal within 5 minutes, but remained depressed for the duration of the experiment in two animals. These results confirm that blood extravasated into the subarachnoid space had a direct effect on parenchymal elements. The combination of transient K+ elevations and calcium depression may play an important role in the development of vascular spasm by inducing or facilitating a contraction in the muscular layer in the wall of major intracranial vessels.
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PMID:Effect of subarachnoid hemorrhage on the extracellular microenvironment. 705 30


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