Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
 21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ten patients 28-54 years old with recurrent attacks of variant angina (chest pain associated with transient ST-segment elevation) culminating in acute myocardial infarction were studied. Systemic blood pressure and heart rate remained unchanged or decreased during chest pain. Diagnosis of myocardial infarction was made on the basis of pathognomonic enzyme changes and T-wave inversions persisting for several weeks (seven patients) or development of Q waves (three patients). Complications were similar to the ones previously observed in conventional myocardial infarction. None of these patients died. Past history was characterized by absence of effort angina. Exercise stress testing after infarction was normal, and coronary arteriography revealed a spectrum of pathology, ranging from normal arteriograms to three-vessel disease. Intraaortic balloon pumping was ineffective in two patients, but subsequent coronary bypass surgery shortly after myocardial infarction was not followed by further attacks of chest pain. Follow-up of these patients revealed a benign course. Alcohol drinking and cigarette smoking appeared to be very prevalent in this group.
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PMID:The syndrome of variant angina culminating in acute myocardial infarction. 75 98

We evaluated the effect of ethanol on exercise performance until angina in 12 patients in a double-blind, randomized study. The mean resting heart rate times systolic blood pressure was not changed after Fresca but was increased after 2 ounces of ethanol (P less than 0.001) and after 5 ounces of ethanol (P less than 0.01). Compared to the control periods, the mean exercise time until angina was not different after Fresca but was decreased after 2 ounces of ethanol (P less than 0.001) and after 5 ounces of ethanol (P less than 0.001). Compared to the control periods, the mean maximal ischemic ST-segment depression after angina was not changed after Fresca but was increased after 2 ounces of ethanol (P less than 0.01) and after 5 ounces of ethanol (P less than 0.001). Drinking 5 ounces or 2 ounces of ethanol decreases exercise duration until angina and increases ischemic ST-segment depression after angina.
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PMID:Effect of ethanol on angina pectoris. 77 61

As part of a cardiovascular survey study on the relationships between physical fitness and coronary heart disease, 5249 Copenhagen males aged between 40 and 59 were interviewed to identify a history of gout. Subjects who had experienced attacks of painful swelling, with abrupt onset and remission in one to two weeks, diagnosed and treated as gout by their own physician, were regarded as having experienced gout. In an initial cross-sectional examination, 86 men fulfilled the criteria. At a one year follow-up examination it was discovered that 56 men had had gout during the year of observation. Among these 18 were new cases. At the end of the study a total of 104 men had experienced gout and these were compared, with respect to the continuously distributed variables, those 104 gout subjects were compared to 208 computer selected age-matched controls drawn at random from the entire sample. The gout cases were found to have higher relative weights, higher diastolic blood pressure and lower levels of physical fitness estimated by use of a bicycle ergometer test. Angina pectoris occurred more frequently among the gout cases than among controls. No significant differences in the occurrence of myocardial infarction, intermittent claudication or renal stones were found. The habits of smoking and coffee consumption were equal in gout cases and controls. Alcohol consumption and consumption of drugs were higher in gout cases than controls. Gout was the most frequent in the lowest social classes.
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PMID:Occurrence of gout in Copenhagen males aged 40-59. 95 64

A 64-year-old man had episodes of angina pectoris several hours after ingestion of alcohol. Otherwise, anginal attacks never occurred. He was diagnosed as having variant angina based on the typical ST elevation in leads II, III and aVF during the anginal attacks. We performed an alcohol challenge test on his 4th admission day. He was given 540 ml of "sake" at 6:00 p.m. and anginal attacks with ST elevations occurred 9.5 hours after its ingestion. The peak value of plasma ethanol was 136 mg/dl at 9:00 p.m. and it returned to 0 when angina occurred. By alcohol ingestion, urinary excretion of Mg increased in association with a slight decrease in serum Mg. The ratio of serum Ca to Mg was increased from 4.0 at the control state before taking alcohol to 4.5 at the occurrence of anginal attack. Mg content in red blood cells and in plasma catecholamines did not differ between before and after ingesting alcohol. We concluded that the change in the extracellular Ca-Mg equilibrium may contribute to the mechanism of alcohol-induced variant angina.
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PMID:[Alcohol-induced variant angina and considerations of its mechanism: a case report]. 181 76

Ethanol in acute low doses is believed to be relatively nontoxic to the normal myocardium, despite data indicating low-level contractility impairment. In patients with myocardial disease, or as the serum ethanol concentration is increased to high levels, angina, myocardial infarction, and arrhythmia may be potentiated. Chronic ethanol use, at moderate doses, may be protective against coronary artery disease, despite increased rates of hypertension. Alcohol consumption at high doses may result in dilated cardiomyopathy and a dismal prognosis. Alcohol abuse is associated with increased mortality.
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PMID:Cardiac disease in the alcoholic patient. 222 86

A 66-year-old man having a long history of angina on effort has started to show frequent episodes of angina at rest since 6 months ago. He noticed that chest pain was uncommon after taking alcohol. A variant form of angina pectoris (variant angina) was diagnosed by documentation of typical ST elevation during anginal attack and also by inducing coronary arterial spasm with intracoronary administration of ergonovine maleate. Ambulatory ECG monitoring revealed frequent ST elevation during sleep. Since the history suggested that alcohol ingestion could be effective for preventing variant angina, this effect was examined by giving 540 ml of "sake" in the evening. Variant angina was inhibited, while plasma ethanol was detected. The plasma ethanol reached its peak value as 152 mg/dl at 10 o'clock pm and returned to zero after 12 hours. When ethanol disappeared in the plasma, variant angina recurred again. Although the precise mechanism for inhibition of variant angina by alcohol ingestion is not clear, alcohol or its metabolite such as acetaldehyde seems to be able to inhibit coronary arterial spasm.
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PMID:[Inhibition of vasospastic angina by alcohol ingestion]. 223 66

In order to ascertain the most effective index for predicting coronary sclerosis, the concentration of lipids, lipoproteins, and apoproteins in serum were determined in 45 males aged over 44 with angiographically diagnosed effort angina and in 153 male controls aged over 44 without ischemic heart disease (IHD) on physical examination. The results of our study are summarized as follows. 1) Alcohol intake of 25 g/day or more and smoking of 20 cigarettes/day or more showed significant odds ratios of 0.47 and 2.33, respectively. 2) By decrease of 10 mg/dl in HDLC level or of 10 mg/dl in Apo-AI level, the possibility of coronary sclerosis increases twofold after adjusting the effects of confounders. 3) LDLC/HDLC and Apo-B/Apo-AI are effective indices for predicting coronary sclerosis and, in particular, the probability of coronary sclerosis increases 3.8 times by increase of 0.5 in Apo-B/Apo-AI.
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PMID:Coronary sclerosis risk factors in males with special reference to lipoproteins and apoproteins: establishing an index. 228 5

Intravenous nitroglycerin is frequently used in the treatment of acute myocardial infarction for its vasodilating effect on lowering both preload and afterload and in the control of ischemic heart pain. The end point for doses of nitroglycerin infusion is either relief of persistent or recurrent angina or controlling congestive heart failure by lowering left ventricular end diastolic pressure and volume. Nitroglycerin accomplishes these end points primarily through its venodilating property. Intolerable headaches or symptomatic hypotension may prevent achieving the clinical end point. Nevertheless, high doses of intravenous nitroglycerin may need to be administered to achieve a desired hemodynamic and therapeutic effect. Changes in mental status, i.e., lethargy and confusion, should be a warning sign of possible ethanol intoxication. An alcohol blood level verifies the clinical impression and gradually withdrawing the intravenous nitroglycerin is all that is necessary to effect a total recovery from this reaction.
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PMID:An unusual complication of intravenous nitroglycerin. 309 6

Thirty male patients with ischemic heart disease and cardiomyopathy entered a controlled study of the acute effects of alcohol on cardiac function evaluated by right heart catheterization. Twenty patients, nine with angina pectoris and 11 with congestive heart failure, were studied during alcohol intoxication, and ten patients, five with angina pectoris and five with heart failure, served as a control group. The mean serum ethanol concentration in the alcohol group was 93 mg/100 ml (S.D. 17). The systemic arterial blood pressure was reduced by 6% in the alcohol group, P less than 0.05 compared with the control group. No significant changes occurred in the central venous pressure, the pulmonary artery pressure, the pulmonary capillary wedge pressure, or in cardiac output, stroke volume and total peripheral resistance. Alcohol intake in moderate doses has no measurable effect on pulmonary blood pressures or cardiac output in patients with ischemic heart disease and cardiomyopathy. Such an effect may, however, be masked by a reduction of afterload.
Alcohol Alcohol 1988
PMID:Cardiac function after alcohol ingestion in patients with ischemic heart disease and cardiomyopathy: a controlled study. 335 19

Ethanol produces in vitro vasoconstriction of coronary arteries and can precipitate angina in patients with coronary obstructive disease. To demonstrate the in vivo effect of ethanol on coronary dynamics, baseline measurements of left anterior descending (LAD) coronary artery dimension by quantitative angiography, hemodynamics, arterial and coronary sinus blood gases, and blood ethanol levels were obtained in 14 closed-chest mongrel dogs. Three ethanol levels were established by intravenous bolus followed by 1-hour maintenance infusions. All measurements made at baseline were recorded every 30 minutes. Phentolamine (5 mg i.v.) and nicardipine (0.15 mg/kg i.v.) were given to evaluate constrictor mechanisms. Blood ethanol levels achieved at 60, 120, and 180 minutes were 649 +/- 48, 1,285 +/- 81, and 2,546 +/- 130 micrograms/ml, respectively. LAD cross-sectional area was reduced significantly from control at the end of each of the three dosing periods (-24 +/- 5%, -40 +/- 3%, and -53 +/- 3%; p less than 0.004). alpha-Adrenergic blockade had no effect on LAD cross-sectional area, while nicardipine partially reversed the ethanol-induced vasoconstriction. No significant change in vessel cross-sectional area took place in control dogs. These data suggest that ethanol induces epicardial coronary artery vasoconstriction in dogs at clinically important blood levels. alpha-Adrenergic blockade does not alter or reverse ethanol-induced vasoconstriction, while calcium channel blockade appears to be an effective vasodilator of ethanol-constricted vessels.
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PMID:Ethanol causes epicardial coronary artery vasoconstriction in the intact dog. 338 1


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