Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030193 (pain)
 261,466 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A double-blind study including three different cardioselective beta-blockers, practolol, H 87/07 and metoprolol, was performed in 54 patients with acute myocardial infarction and chest pain shortly after onset of symptoms. Transmural infarctions were found in 42 patients while 12 patients had nontransmural infarctions. Chest pain and the product of heart rate and systolic blood pressure were significantly reduced in the beta-blocker groups whereas no changes were seen after saline. All patients with nontransmural infarctions and 14 out of 29 with transmural infarctions got pain relief lasting for at least 30 min. None of the patients developed signs of left ventricular backward failure, shock, or bradycardia. A decrease in ST segment elevation was observed in all the transmural infarctions after beta-blockade. No changes in ST segment elevation were found after analgesics when given after saline, but in some cases an increase was seen in this parameter when analgesics were given due to insufficient pain relief after beta-blockers or due to return of chest pain. It is suggested that pain relief by beta-blockers indicates decrease of myocardial ischemia.
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PMID:Double-blind study of the effect of cardioselective beta-blockade on chest pain in acute myocardial infarction. 0 98

Acute myocardial infarction is associated with pain, tissue damage and circulatory impairment. As a result of these changes, there is increased sympathetic drive to the heart in the form of increased sympathetic nerve activity and increased circulating catecholamines.
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PMID:The role of long term beta-blockade after myocardial infarction: Paper 2. 3 Apr 42

Twelve patients aged 33--70 years (mean 49.5) underwent nightly recordings in the ICU and subsequently on the ward following acute myocardial infarction. Sleep patterns were analyzed according to night after infarct and ICU versus ward environment. Significant differences in nocturnal sleep patterns from matched controls initially after infarction included greater wakefulness, low REM sleep per cent, long REM latency, fewer REM periods, more awakenings, more stage shifts and decreased sleep efficiency. The usual circadian variation in HR was absent, and there was an estimated 8--10 h of unrecorded daytime sleep, which together suggested a quite generalized disruption of biological rhythms. With time, there was loss of daytime sleep, lowered nocturnal wakefulness and increased REM sleep. Slow-wave sleep (sometimes with very long duration delta waves) increased above normal over post-infarction nights 3--9, and sleep was otherwise renormalized by post-infarction night 9. No sudden sleep changes occurred with transfer from ICU to ward. The altered sleep patterns appeared mainly attributable to infarction itself. Twelve nocturnal anginal attacks occurred. Ten began in NREM sleep and two in REM periods without particularly intense phasic activity. Post-infarction nocturnal angina therefore appears to differ in pathogenesis from angina outside this period, which usually occurs in REM sleep. ECG changes could occur during sleep before awakening with pain, and overall decrease in ECG amplitude sometimes accompanied angina. Most attacks (10 of 12) occurred on post-infarction nights 4 and 5, indicating that undetermined that undetermined factors produce a secondary period of heightened risk at that time.
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PMID:Sleep patterns in the intensive care unit and on the ward after acute myocardial infarction. 7 74

In cardiac failure unresponsive to digoxin and diuretics, afterload reduction brings about a dramatic increase in cardiac output, renal perfusion and responsiveness to diuretics; furthermore, the decrease in venous pressure relieves the dyspnoea. Intravenous vasodilators should only be used when sophisticated haemodynamic monitoring equipment and experienced physicians are at hand. Indications for the use of these agents are severe cardiac failure, acute myocardial infarction complicated by left ventricular failure, persistent ischaemic pain and limitation of infarct size. A wide variety of oral vasodilator agents is available, all having different sites of action; the choice of vasodilator agents should be tailored to the needs of the patient. Treatment with these agents is indicated in patients in whom cardiac failure becomes refractory to conventional therapy with digoxin and diuretics. The utmost care must be taken to avoid further impairment of cardiac output by excessive reduction of the left ventricular end-diastolic pressure (LVEDP) and hypotension, which will jeopardize myocardial, renal and cerebral perfusion.
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PMID:The use of vasodilator agents in the treatment of heart failure. 15 2

Technetium-99m-stannous pyrophosphate (99mTc-PYP) accumulates in acutely infarcted myocardium and can be detected by scintiscanning. The clinical value of 99mTc-PYP scintiscanning was studied in 83 patients 6 hours to 21 days after the onset of acute chest pain. In 12 patients with normal electrocardiograms and serum enzyme values no uptake of 99mTc-PYP was detected on the scintigrams. Of 44 patients with electrocardiographic or enzyme evidence, or both, of acute myocardial infarction the scintigrams were positive in 31, "questionable" in 2 and negative in 11; no positive scan was obtained within 12 hours of the onset of pain, and the scans generally remained positive for up to 5 days. In 24 patients with evidence of prolonged myocardial ischemia the scans were positive in 2, questionable in 4 and negative in 18. The scans were negative in each of three patients with acute or constrictive pericarditis. Localization by electrocardiography and scintiscanning correlated nearly perfectly for transmural infarcts but subendocardial infarcts could not always be localized precisely by scintiscanning. The infarct area (total area of 99mTc-PYP uptake) correlated well with the peak serum value of creatine phosphokinase.
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PMID:Technetium pyrophosphate scanning in the detection of acute myocardial infarction: clinical experience. 18 87

To determine the sensitivity of myocardial scintigraphy with technetium-99m pyrophosphate during the early phase of acute myocardial infarction, 31 patients admitted to the coronary care unit with prolonged ischemic pain underwent imaging within 4 to 8 hours and again at 24 hours after the onset of symptoms. In 11 of 15 patients with documented acute myocardial infarction, increased focal myocardial uptake was demonstrated on early myocardial scintigraphy. Focal uptake was observed in only 2 of 16 patients with unstable angina pectoris. Three or four patients with normal early scintigrams had massive transmural myocardial infarction. Normal early scintigrams in these three patients may have reflected poor perfusion because the images were abnormal at 24 hours. In four patients the extent of technetium-99m pyrophosphate uptake increased more than 20 percent at 24 hours without other evidence of infarct extension. In the other seven patients, there was no significant change in the area of the abnormal radioactive uptake between early and delayed scintiscans. This study suggests that technetium-99m pyrophosphate scintigraphy can defect acute myocardial infarction as early as 4 hours after the onset of symptoms although the sensitivity rate (73 percent) is less than that at 24 hours.
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PMID:Myocardial scintigraphy with technetrium-99m pyrophosphate during the early phase of acute infarction. 20 76

Scintigraphy with pyrophosphate 99mTc was performed in 230 patients with various forms of ischemic heart disease and in 15 persons with pain in the region of the heart caused by osteochondrosis of the cervical and thoracic spinal segments or vegetovascular dystonia (control group). It was found that labelled purophosphate accumulated in the myocardium in necrosis of the heart muscle or when coronary insufficiency takes a course in which necrosis of the myocardial cells is quite possible. Positive results of scintigraphy with pyrophosphate 99mTc are not a strict criterion of acute myocardial infarction because they are also encountered in a chronic course of ischemic heart disease and are evidence in this case that "a state of risk" has occurred during the disease.
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PMID:[Importance of pyrophosphate-99mTc scintigraphy in the diagnosis of acute myocardial infarct]. 22

Twenty-one patients with postinfarction angina (2 to 15 days after acute myocardial infarction) unresponsive to medical therapy were treated by intra-aortic balloon pumping (IABP). Anginal pain and electrocardiographic (ECG) ST-segment changes were prevented in all patients. Coronary angiograms were obtained during IABP without complication and confirmed severe coronary artery disease. Of the four nonoperated patients, three had reinfarction and two died of cardiogenic shock. Seventeen patients underwent aorta-coronary bypass grafting, associated with aneurysmectomy in two patients and closure of a ventricular septal defect in one. Sixteen patients survived the operation. All survivors are in clinically improved condition and 14 are pain free from 9 to 28 months postoperatively, but three have mild heart failure.
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PMID:Treatment of post-myocardial infarction angina by intra-aortic ballon pumping and emergency revascularization. 30 68

Two grams of methylprednisolone was administratered to ten patients with acute myocardial infarction at an average of 13 hours from the onset of symptoms; pain in the chest was not relieved in six of the ten patients. In one hour, no significant improvement was noted in the function of the ischemic segments (examined using a multiaxis echocardiographic method) or in the S-T segments of the 12-lead electrocardiogram. Left ventricular filling pressure soon increased by an average of 4 mm Hg (P less than 0.005), without ventricular dilatation or a Frank-Starling response, suggesting a decrease (ischemic?) in myocardial compliance. Cardiac output by Swan-Ganz thermodilution later increased by 21 percent (P less than 0.01) when a decrease in peripheral vasoconstriction was evident. In contrast, small-dose beta-adrenergic blockade using 0.2 mg of pindolol intravenously after administration of methylprednisolone immediately relieved pain in the chest in all six patients. Elevation of the S-T segments was reduced by 34 percent (P less than 0.05) within 15 minutes, and the contractile function of the ischemic segments improved markedly, by 3 mm or to 34 percent of normal, from the 4 percent of normal before administration of pindolol (P less than 0.005). Hemodynamic function did not deteriorate in the eight patients with uncomplicated infarction or moderate left ventricular failure. Therapy with pindolol thus reduced clinical, electrocardiographic, and myocardial mechanical signs of acute ischemia safely, while administration of methylprednisolone had no short-term protective effect.
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PMID:Failure of methylprednisolone to protect acutely ischemic myocardium: a contrast with subsequent beta-adrenergic blockade in man. 34 14

The efficacy of a non-narcotic analgesic is evaluated in a double-blind randomized series of patients with acute myocardial infarction (AMI). Levomepromazine or pethidine were given in 328 consecutive cases to 316 patients within 24 hours after the onset of symptoms. Levomepromazine, 12.5 mg, appeared as effective as pethidine, 50 mg, in the alleviation of pain, though the initial dose had to be higher. Nausea and vomiting were half as frequent in the levomepromazine group as in the pethidine group (p less than 0.001). The incidences of arrhythmias, lung oedema, hypotension and thromboembolic complications did not differ between the groups. The mortality rate in the first 4 weeks was 22% in the levomepromazine group and 37% in the pethidine group (p less than 0.005), and after one year 39 and 50% (p less than 0.05), respectively. It is concluded that levomepromazine is better tolerated than pethidine in AMI. This suggests that the present management of pain in AMI should be reconsidered.
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PMID:Analgesic treatment with levomepromazine in acute myocardial infarction. A randomized clinical trial. 37 39


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