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)

Thirty patients with variant angina pectoris (VAP) were analyzed for electrocardiographic features during episodes of VAP. Twenty-nine of these patients had cardiac catheterization, and an autopsy study was performed in one. The patients showed predominantly concave upright T-waves during pain. An increase of R wave amplitude (expressed as delta R) of more than 10% was seen in 17/30 patients (57%). The primary ST-T changes produced by the VAP episodes were conspicuous in two patients with pre-existent complete left and right bundle branch block. Serious dysrhythmias, including ventricular fibrillation (VF), ventricular tachycardia (VT), ventricular premature beats (VPBs) (more than five/min, multifocal and R on T phenomenon), and 2 degrees atrioventricular block were found in thirteen patients (43%). The development of dysrhythmias was related to the duration of VAP episodes. The average time to onset of dysrhythmias was 3.54 min. The dysrhythmias were not contingent upon pre-existing coronary artery anatomy (defined by Friesinger's coronary score), left ventricular ejection fraction or left ventricular segmental abnormalities. The location of the ST-segment elevation and the presence of dysrhythmias during the episodes of VAP (A-V blocks, ventricular tachycardia and fibrillation) were not predictive factors of the coronary anatomy. Eight patients (27%) developed myocardial infarction (MI). Five of them had nontransmural MIs and three developed transmural MIs. The development of MI was not related to the severity of the VAP attacks (appreciated by the magnitude of ST-segment elevation and R wave changes) but showed a relation to the development of an unstable pattern which preceded the infarction. Sixteen patients underwent exercise testing. In eight of them, the coronary arteriograms were normal (Group I); in the remaining eight, significant proximal coronary artery obstructive disease was found (Group II). Group I patients displayed a normal ST-segment response and functional aerobic capacity (FAI = 4.4 +/- 14) as well as normal heart rate (HR) and double product (SBP X HR) responses (HR = 154 +/- 21; SBP X 21; SBP X HR = 290 +/- 71). During exercise, a normal delta R was observed. With one exception, Group II patients showed an abnormal ST-segment response with an overall low exercise capacity (FAI = 57 +/- 17) and decreased hemodynamic response (HR = 27; SBP X HR = 130 +/- 40). FAI, HR, SBP X HR Group I vs. Group II = P less than .005/less than .02/less than .005. The abnormal ST-segment response included elevation in four patients and depression in three. During exercise, Group I with ST-elevation displayed a normal (negative) delta R response; while Group II with ST-depression displayed an abnormal delta R response (positive or no change). There was no difference in the coronary score between Group II patients with ST-segment elevation or depression.
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PMID:Prinzmetal's variant angina: electrocardiographic and angiographic correlations. 714 73

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

A 60-year-old man had recurrent episodes of spontaneously occurring pain in the chest which were associated with ST-segment elevation consistent with Prinzmetal's angina. The simultaneous elevation of the S-T segment in anterior and inferior electrocardiographic leads with initial ST-segment depression followed by elevation in high lateral leads suggested that heightened vascular reactivity in variant angina may involve multiple coronary vessels during the same episode of vasospasm.
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PMID:Prinzmetal's angina. Aternating ST-segment deviation in anterior and inferior electrocardiographic leads during the same episode of pain. 736 92

Holter system electrocardiograms were recorded for 617 patients who were treated at the Department of Cardiology, Tokai University Hospital. In cases of arrhythmia, ventricular premature contraction (VPC) was the most predominant, in 291 cases (69%) out of 423 with arrhythmia, followed by 59 (14%) with supraventricular premature contraction (SVPC), 23 (5.4%) with paroxysmal atrial tachycardia, 17 (4%) with second degree A-V block and 10 (2.3%) with transient atrial fibrillation (AF). In addition, nine (2.1%) cases of ventricular tachycardia (VT), one (0.2%) of transient ventricular fibrillation (VF) and one (0.2%) of third degree A-V block were found in particularly severe arrhythmia cases. Six out of nine cases of VT were cases of acute myocardial infarction (AMI) and all died suddenly while in the hospital or after discharge. Mild or moderate changes in ST-T were often observed even in normal subjects. Of the 617 cases, only 18 (2.9%) showed a significant elevation or depression of ST. Among these, three definitely had variant angina pectoris (Prinzmetal type). The above results indicate Holter EKGs are very useful for the diagnosis of arrhythmia and can also be used as a means of evaluating the prognosis in some cases, but there still are some problems in connection with its use for the diagnosis of ischemic heart disease except for the diagnosis of variant angina pectoris.
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PMID:Holter system electrocardiographic studies on 617 cases. 738 65

1. The preventive effects of monatepil, a new calcium antagonist with alpha 1-adrenoceptor blocking activity, on ischaemic electrocardiographic changes in rat models of vasospastic angina were evaluated and compared with those of the existing calcium antagonists (diltiazem, verapamil, nicardipine and nifedipine). 2. In order to assess the contribution of the alpha 1-adrenoceptor blocking action of monatepil to its anti-vasospastic action, the anti-ST depression effect of prazosin, an alpha 1-adrenoceptor blocker, was also examined. 3. Monatepil given orally (3-30 mg/kg) inhibited vasopressin (0.2 IU/kg, i.v.)-induced ST depression which is considered to indicate ischaemic electrocardiographic changes in a vasospastic angina. This effect of monatepil was more potent and long-lasting than that of diltiazem, and was similar to that of verapamil and nicardipine. At a dose of 30 mg/kg, monatepil produced a significant inhibition, even at 7 h after administration. 4. Monatepil given intravenously (0.3 mg/kg) exerted a significant inhibitory effect on methacholine (16 micrograms/kg, intracoronary arterial administration; i.c.a.)-induced ST elevation which seems to be caused by coronary vasospasm. This effect was more potent or equipotent to those of the existing calcium antagonists. 5. These results indicate that monatepil produces the preventive effect on the drug-induced ischaemic electrocardiographic changes in rats and suggest that monatepil may have potential for the treatment of vasospastic angina.
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PMID:Preventive effect of a new calcium antagonist, monatepil, on drug-induced ischaemic electrocardiographic changes in rats. 830 12

Vasospastic angina was demonstrated clinically and angiographically in a 54-year-old patient with systemic triglyceride storage disease and cardiomyopathy. He and his younger sister had been diagnosed in 1985 as having systemic triglyceride storage with Jordans' anomaly. In 1993, he began complaining of rest and effort chest pain in the morning, which was accompanied by ST depression by ECG. Sublingual nitroglycerine was effective for treating this pain. Intracoronary injection of acetylcholine induced severe coronary vasoconstriction in the left anterior descending artery. Left ventricular contraction was diffusely impaired. Deposits of numerous triglyceride droplets and a decrease in the density of myofibrils in cardiocytes were found in the specimens obtained by endomyocardial biopsy. The impaired left ventricular contraction may have been due to the changes in myocardial cells. His sister complained of a similar chest pain that was completely controlled by calcium channel antagonis. Thus, our cases demonstrated vasospastic angina associated with cardiomyopathy secondary to systemic triglyceride storage disease with Jordans' anomaly, though the causal relationship between these conditions remains unclear.
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PMID:Vasospastic angina in patients with systemic triglyceride storage disease with Jordans' anomaly and cardiomyopathy. 868 55

The relationship between autonomic nervous system activity (ANA) and coronary vasoreactivity during transient myocardial ischemia was determined in patients with vasospastic angina (VA). ANA was measured by power spectral analysis of heart rate variability and humoral factors following intravenous infusion of insulin in 24 patients with VA and 6 control patients. Nine (38%) of the VA patients had significant ST segment depression (STD), and 4 of these patients had symptomatic STD. The frequency of anginal episodes in the 9 patients with VA and STD was significantly greater than that in the 15 VA patients without STD (3.4 +/- 3.1 vs 0.5 +/- 0.8 episodes/week, p < 0.05). The increase in the LF/HF ratio 30 min after insulin injection in patients with STD was significantly greater than that in patients without STD (34 +/- 31% vs 4 +/- 34%, p < 0.05). All of the patients with VA and STD had significant coronary vasospasm in response to the infusion of < or = 20 micrograms of acetylcholine, higher levels of nocturnal parasympathetic activity, and greater norepinephrine production in response to insulin stimulation than the VA patients without STD. These findings suggest that increased vagal tone and hyperreactivity to adrenergic stimulation may trigger vasospasm in patients with VA.
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PMID:Coronary hyperreactivity to adrenergic stimulation and increased nocturnal vagal tone trigger coronary vasospasm. 980 51

A 26-year-old female with idiopathic moyamoya disease developed chest pain with concomitant ST depression on electrocardiography. Coronary angiography detected no stenotic lesions in the epicardial coronary arteries. The clinical diagnosis was vasospastic angina pectoris. She was medicated with calcium antagonists, which reduced the frequency of chest pain episodes. Angina pectoris is a rare occurrence in young patients with moyamoya disease. Coronary artery disease and moyamoya disease may have common etiological factors.
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PMID:Moyamoya disease and coronary artery disease--case report. 1121 39

Although beta-blockers can not be used for the treatment of vasospastic angina, the effect of beta-blockers with vasorelaxant property on coronary vasospasm remains uncertain. In this study, we evaluated the effect of betaxolol, a new beta-blocker with calcium antagonistic property, as an additional therapy on vasospastic angina (VSA) with anginal attacks on effort. We enrolled 12 patients with VSA and anginal attacks with ST segment depression during exercise stress test. All patients received 1.25-5 mg of betaxolol for 3 months. Treadmill exercise stress test and adenosine triphosphate stress thallium-201 myocardial scintigraphy were performed before and 3 months after the onset of the betaxolol treatment. The other drugs including calcium antagonists, nitrates and nicorandil were continued. No patients experienced the exacerbation of angina during the betaxolol treatment. Exercise time to chest pain (317.5+/-72.1-454.2+/-75.5 s, P<0.01) and maximal ST segment depression (1.67+/-0.67-1.16+/-0.46 mm, P<0.01) obtained by exercise stress test, the defect score (8.6+/-2.7-5.3+/-2.1, P<0.01), the extent score (14.8+/-5.8-8.8+/-4.6%, P<0.01), the severity score (17.5+/-7.3-11.3+/-5.2, P<0.01) and washout rate (31.4+/-5.6-37.6+/-5.0%, P<0.01) obtained by the scintigraphy were improved by betaxolol. Our results suggest that betaxolol increases regional myocardial blood flow and improves exercise capacity in patients with VSA. Betaxolol may become a drug for a new potential therapy for VSA.
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PMID:Beneficial effects of betaxolol, a selective antagonist of beta-1 adrenoceptors, on exercise-induced myocardial ischemia in patients with coronary vasospasm. 1455 35

Coronary collateral circulation usually develops as a consequence of recurrent ischemia associated with severe stenosis. In exceptional cases, it can develop with moderate coronary lesions if there is severe recurrent vasospasm. In this situation, the presenting clinical features of vasospastic angina (i.e., effort angina with ST-segment depression) can be identical to those of a severe permanent lesion. We present a patient who exhibited effort angina and ST-segment depression on treadmill testing. Angiography showed severe right coronary artery stenosis and the development of coronary collateral circulation from the other main artery. After repeated intracoronary bolus injection of nitroglycerin, only a moderate stenosis was still apparent and the collateral circulation had disappeared.
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PMID:[Moderate coronary lesion with severe vasospasm and the development of collateral circulation in a patient with effort angina and ST-segment depression]. 1605 35


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