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)

Asymptomatic episodes of ST segment and/or T wave changes are often reported during Holter monitoring in patients with angina pectoris. However, the interpretation of such changes is debated relative to silent myocardial ischemia. We studied 11 patients admitted to the CCU because of frequent episodes of unstable anginal attacks who had undergone repeated periods of Holter monitoring, characterized by predominantly occurring asymptomatic episodes of ST segment and/or T wave changes associated with less frequent typical anginal attacks. In a total of 89 days of Holter monitoring, the patients evidenced 520 episodes of transient ECG changes including 180 of ST elevation, 73 of ST depression, and 267 of T wave alterations. Only 12% of episodes were symptomatic. Coronary injection during asymptomatic ST-T changes was performed in eight patients. In six it was possible to document spontaneous coronary spasm. In seven patients ergonovine administration induced anginal pain, ST-T changes, and coronary spasm. In all patients the anginal attacks completely disappeared with medical treatment and the asymptomatic episodes were abolished in six and reduced in four. Our findings support the hypothesis that in certain selected unstable anginal patients, transient asymptomatic ECG changes are caused by acute myocardial ischemia.
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PMID:Vasospastic ischemic mechanism of frequent asymptomatic transient ST-T changes during continuous electrocardiographic monitoring in selected unstable angina patients. 705 33

The present case is a 49-year-old female who began to feel a chest pain during exercise 2 years ago. Recently, the chest pain occurred during light exercise as well as at rest. The electrocardiogram during the attack showed remarkable ischemic ST segment depression. No abnormality was found in the coronary cineangiography. She was diagnosed as Syndrome X. However, coronary cineangiography during an attack on another day showed a severe spasm in the left main trunk. Thus, a spasm must be considered as one of the causes of "Syndrome X".
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PMID:Angiographic evidence of left main trunk spasm as a possible cause of syndrome X. 709 99

Twelve patients with documented coronary arteriosclerosis and severe stable angina pectoris were treated with the beta blocker pindolol, 5 mg four times a day, utilizing a double-blind crossover protocol. Following 4 weeks of baseline observation with no active treatment, pindolol and placebo were given for 4 weeks each. End points evaluated were episodes of angina pectoris/week, number of nitroglycerin tablets used per week, time on treadmill test until onset of angina pectoris, double product of heart rate and blood pressure at onset of angina pectoris, and amount of ST depression during the treadmill exercise test. Episodes of angina pectoris and nitroglycerin consumption were reduced by 18% on placebo and 32% on pindolol (not significant). All of the improvement occurred in the third and fourth weeks of pindolol treatment. Less difference between pindolol and placebo was noted when the placebo period came after the pindolol period, suggesting a carry-over effect of pindolol. With pindolol, treatment exercise tolerance was increased 13% (33 seconds) over baseline levels but only 2% over the levels achieved with placebo treatment (not significant). ST depression with exercise was 6% less when patients were on pindolol than when they were on placebo (not significant). There was a marked decrease in myocardial oxygen demand as measured by the double product of blood pressure and pulse during exercise (23% reduction when on pindolol and no change when on placebo, p less than 0.01). This study shows that there was an important placebo effect when treatment of angina pectoris was evaluated and that pindolol significantly reduced myocardial oxygen demand but evidence of ischemia was not significantly reduced. Possible mechanisms to explain the disparity between reduction in estimated myocardial oxygen demand (double product) and objective improvement in ischemia include coronary spasm and altered regional flow resulting from beta blockade. Alternative explanations may be the relatively small fixed dose of pindolol and the small number of patients studied.
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PMID:Randomized double-blind study of pindolol in patients with stable angina pectoris. 710 37

Thromboxane A2 (TxA2), released by aggregating platelets, has been proposed as a potential mediator of coronary vasospasm. We studied six patients with variant angina, a clinical syndrome due to coronary vasospasm, and one patient with frequent recurrent episodes of transient ST-segment depression at rest in whom the spasm was demonstrated angiographically. All patients underwent continuous ECG monitoring for 2 days before and 2 days after a single, low, i.v. dose of aspirin (2 mg/kg), which reduced TxB2 (the stable metabolite of TxA2) to less than 3% of the control values. There were 129 transient ischemic episodes during control and 146 after aspirin, when platelet TxB2 was reduced to negligible levels. The duration, severity and incidence of symptomatic episodes were not significantly affected by TxA2 blockade. We conclude that platelet TxA2 is probably not responsible for the initiation of coronary vasospasm.
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PMID:Failure of thromboxane A2 blockade to prevent attacks of vasospastic angina. 711 86

Introduction of L-timolol maleate into the clinics for glaucoma treatment has been a great success as it produces relatively few side effects, such as miosis, ciliary spasm and headache, which are associated with the use of pilocarpine. Recent reports indicated, however, that L-timolol produces asthmatic attacks, cardiovascular suppression and central depression. D-Timolol was found to be as effective as L-timolol in lowering the intraocular pressure and aqueous humor production. However it was much less potent than L-timolol in inhibiting cardiac contractility and heart rate stimulated by isoproterenol and was less active in blocking beta-adrenergic receptors in tracheal muscle. It is suggested that the D-isomer of timolol could be used to treat glaucoma instead of L-isomer without producing untoward side effects in cardiovascular and bronchial tissues.
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PMID:Effects of D-timolol on intraocular pressure, heart rate, cardiac contractility, and tracheal muscle function. 718 3

Studied were the total water extracts (infusions) of wild sunflower (Doronicum hungaricum Rchb), and separately of alcohol and water extracts. It was found that the pharmacologic and toxicologic effects were governed by the water-soluble flactions. At oral administration to albino mice the total water extract corresponding to 10 g of the dried plant per kg b. w. no toxic phenomena were observed. At subcutaneous injection of the water extract of 10 g of the dried plant per kg b. w. and venous injection of 3.5 g of the dried plant per kg b. w. of albino mice as well as venous injection of the water extract corresponding to 2.5 g of the dried plant per kg b. w. of cats with narcosis there was enhancement of breathing followed by depression of this process along with a drop of the systemic blood pressure down do the zero line, and exitus. A negative intropic effect was produced on an isolated frog heart by a water extract corresponding to 1 g of the dried plant/100 cm3-500 cm3, and a moderate spasm--on an isolated rabbit intestine by an extract 1/100 cm3-500 cm3. The venous injection of the extract to cats with narcosis at 0.05 to 1.0 g of the dried plant per kg b. w. caused depression. All these effects were blocked after atropine treatment. In an experiment with 3 cows with the use of 50 g of finely ground dried plant mass inthe daily ration per cow for 10 days a moderate enhancement of milk secretion was produced. It is believed that the phenomena observed are due to M cholinemimetic action.
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PMID:[Pharmacological and toxicological studies on wild sunflower Doronicum hungaricum Rchb]. 720 Dec 4

The effects of aspirin (4.0 g/day) given orally to eight patients with variant angina were observed. An exercise stress test performed in the morning was positive in two of seven patients during placebo administration, whereas a test performed in the afternoon at the same exercise work load resulted in negative findings. During aspirin administration, the afternoon exercise test repeatedly provoked anginal attacks associated with electrocardiographic changes (S-T segment elevation in five and S-T depression in two). Rate-pressure product at the end of the exercise test during aspirin administration was significantly lower than that during placebo administration (p less than 0.01). During aspirin administration, the frequency of angina increased markedly, and the attacks occurred not only during the night or early morning but also in the daytime in six of the eight patients. Our observations suggest that aspirin, in this large dose, reduces the capacity for exercise and provokes exercise-induced coronary arterial spasm in patients with variant angina.
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PMID:Exercise-induced angina provoked by aspirin administration in patients with variant angina. 723 94

Two patients complained of chest pain while at rest and during physical activities. However there seemed to be no direct relation between exertional angina and an increasing level of work performed, indicating that these patients had a variable threshold of angina during exercise. In one patient spontaneous chest pain was associated with transient S-T segment changes in precordial leads, and during coronary arteriography the administration of ergonovine induced spasm of the left anterior descending coronary artery. The other patient showed S-T segment elevation in inferior leads during an ergonovine-induced anginal attack and coronary arteriography revealed a spontaneous spasm of the right coronary artery. In both patients repeated exercise tests yielded different results, because the chest pain and S-T segment depression occurred at different work loads with large differences in heart rate-systolic blood pressure product. It is concluded that a variable threshold of angina during exercise is a clinical manifestation in some patients with vasospastic angina and is probably due to the difference in coronary arterial tone at the onset of exercise.
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PMID:Variable threshold of angina during exercise: a clinical manifestation of some patients with vasospastic angina. 724 42

The unique association of both exercise-induced coronary arterial spasm and S-T segment depression with normal findings on selective coronary arteriography is described. The patient had a prior history of typical effort angina that had recently progressed to angina at rest. Despite the change in anginal pattern, the electrocardiogram disclosed S-T segment depression that was consistent with subendocardial ischemia, during both exercise testing and spontaneous chest pain. Exercise thallium-201 scintigraphy demonstrated the presence of large perfusion defects of the anterior and septal walls of the left ventricle. Coronary arteriographic findings, in the absence of symptoms, were entirely normal. Severe localized, reversible coronary spasm of the proximal left anterior descending coronary artery was subsequently demonstrated during spontaneous angina, isometric arm exercise and after the administration of ergonovine maleate. After treatment with isosorbide dinitrate and nifedipine, the patient had no further chest pain or electrocardiographic changes, and a repeated thallium-201 stress test revealed normal findings and greatly improved exercise tolerance.
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PMID:Exercise-induced coronary spasm with S-T segment depression and normal coronary arteriography. 724 43

This report describes a case of a patient with a history of classical angina of effort which developed into an unstable progressive syndrome. A 42-year-old-woman was admitted to the hospital because of resting angina pectoris. Examination revealed signs of septal subepicardial ischemia in the resting electrocardiogram and a positive ergometric test with marked depression of the S-T segment. Hemodynamic studies showed in the ventriculogram a clearly defined area of hypokinesis on the anterolateral segment of the ventricle and the coronariography revealed normal vessels. During exercise the patient developed anginal pain and an elevation of the S-T segment in a lead II electrocardiogram. During the pain episode, selective left and right coronariographies showed the presence of a severe spasm in the first portion of the anterior descending branch. In the course of one of the injections the patient developed ventricular fibrillation, this was reverted with a 400 watts/sec shock. The patient was discharged from the hospital a few days after and has been successfully treated with nitrates and calcium blocking agents. This case represents the first time that a coronary spasm in normal vessels has been adequately documented by us.
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PMID:[Exercise-induced coronary artery spasm. Angiographic demonstration and results of medical treatment]. 732 47


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