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)

Changes in level of isoenzyme LDH1 seem to be a valuable criterion in differentiating acute myocardial infarction from active coronary insufficiency without infarction. LDH1 level increases noticeably within 48 hours after onset of pain from acute myocardial infarction but tends to decrease if the pain is due to active coronary insufficiency.
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PMID:Differential diagnosis of chest pain. Use of isoenzyme LDH1 level as a criterion. 76 85

Unstable angina is a syndrome which comprises a spectrum of symptomatic manifestations of coronary artery disease which lies between stable angina pectoris and acute myocardial infarction. Patients fall into three groups: angina of recent onset (4 weeks), angina of changing pattern, and angina occurring at rest (longer than 15 minutes). The syndrome may presage acute myocardial infarction or sudden death, or may itself be the manifestation of a myocardial infarction. The pathophysiology may involve primary cardiac events or extracardiac precipitating factors, and does not appear to be the consequence of a particular anatomic pattern of coronary artery disease. Pain may occur as a result of regional reduction of coronary flow to pressure-dependent areas of myocardium during states of increased myocardial oxygen demand. Persisting ischemia leads to infarction via a series of events which may include myocardial edema formation, increased beta-sympathetic tone, and others which have been experimentally modified by interventions designed to limit infarct size. Although the incidence of acute myocardial infarction and death was high in early studies, in recent reports acute infarction occurs in under 15.5 per cent and death in under 2 per cent. Patients at high risk are those pain persists with bed rest, and those with preceding stable angina pectoris or myocardial infarction. Prognostic differences among Groups 1, 2, and 3 may exist but cannot be assessed from available studies. Studies of the management of unstable angina have generally been uncontrolled. Hospitalization, bed rest, and short- and long-acting nitrates are generally employed in Groups 2 and 3 patients and the marked reduction in myocardial infarction rates from early to recent studies tends to support these approaches. Anticoagulants are less used now than formerly. Propranolol can produce a significant reduction of myocardial oxygen consumption and may redirect coronary flow to ischemic areas. The drug has effectively controlled pain in several studies and is now widely used to manage unstable angina. Aortocoronary bypass surgery has been extensively employed but there is only one preliminary report of a controlled study available. The role of surgery is not yet defined. The optimal approach to therapy may eventually involve the use of medical therapy, including beta-blockade to stabilize patients, with delayed semielective coronary angiography and surgery in those who respond. Emergency angiography and surgery might then be reserved for the high-risk group of patients whose pain persists during optimal medical therapy.
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PMID:Unstable angina pectoris. 78 21

Nitroglycerin (NTG) traditionally has bben avoided in the treatment of pain caused by acute myocardial infarction because of the belief that NTG-induced decrease in arterial pressure and concomitant reflex increase in heart rate might extend the ischemic process. However, recent experimental and clinical investigations cast doubt on this concept. For example, when the left anterior descending coronary artery is acutely occluded in normal dogs or in dogs when chronic coronary occlusions and extensive collaterals, NTG reduces ST-segment evevation (and presumably myocardial ischemia). This salutary effect occurs despite lowering of systemic arterial pressure, as long as excessive reflex tachycardia does not result; the magnitude of ischemia reduction is potentiated when methoxamine or phenylephrine are administered simultaneously to abolish the NTG -induced hypotension and reflex tachycardia. NTG and methoxamine treatment also results in 1) reduction of infarct size as (as assessed by gross morphologic examinations and myocardial CPK levels) in dogs subjected to 5 hours of coronary occlusion, and 2) increase in ventricular fibrillation (VF) threshold and reduction of the incidence of spontaneously occurring VF in dogs with acute coronary occlusion. Finally, the effectiveness of NTG during acute myocardial iinfarction (AMI) in man has been studied. Multiple precordial electrodes were used to measure changes in the degree of ST-segment elevation; these changes were used as an index of alterations in myocardial ischemic injury. Patients with normal pulmonary capillary wedge pressures ( less than 15 mm Hg) did not benefit consistently from NTG alone; however, when phenylephrine was administered with NTG (to abolish NTG-induced arterial pressure reduction and reflex increase in heart rate), ST-segment elevation diminished consistently. In patients with elevated wedge pressures ( greater than 15 mm Hg), NTG alone consistently reduced ischemia; addition of phenylephrine often partially reversed this benefit. Thus, administration of NTG, alone or with phenylephrine, appears to reduce myocardial ischemic injury during AMI in man; however, the response to phenylephrine depends upon the presence or absence of LV failure prior to treatment. These experimental and clinical results suggest this form of therapy may be use in reducing infarct size in man, although additional studies are necessary to determine the functional significance of these acute electrophysiologic alterations.
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PMID:Protection of ischemic myocardium by nitroglycerin: experimental and clinical results. 81 59

Six new cases of acute myocardial infarction with normal coronary arteriogram are presented and supplemented by 19 collected cases (group I). These are compared with 16 cases of myocardial infarction caused by occlusive coronary artery disease in a comparable population (group ii). The following significant differences between the two groups are established: patients in group I were younger (27.5 years vs 33.7 years, P less than 0.005); at least one risk factor was present in all patients in group II, but in only 40% of group I (P less than 0.0001). effort angina preceded the attack in ten patients of group II, but in none of group I (P less than 0.0001). The attack was unheralded in 24 of the 25 patients in group I, but was preceded by prodromes in 11 of 16 in group II (P less than 0.0001). Attacks of pain following myocardial infarction occurred in five patients of group 2 and II of group II) (P less than 0.001). Results are discussed in the light of the nature of myocardial infarction in group I. No support is found for the coronary spasm theory. The most likely mechanism for development of myocardial infarction in group I is thought to be a thromboembolic "accident." This accident is not necessarily related to atherosclerotic coronary disease and is presumed to be benign in nature.
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PMID:The nature and clinical features of myocardial infarction with normal coronary arteriogram. 83 99

Although there is no statistical proof of the efficacy of coumarin drugs in the therapy of acute myocardial infarction, the numbers of patients at risk from thromboembolism are sufficiently great and the favorable clinical and pathologic impressions are sufficiently strong that, conversely, the possibility of benefit cannot be excluded. This delicate balance is indeed a Hobson's Choice. In this therapeutic dilemma, we would interpret one acceptable course in regard to the use of anticoagulants among patients with acute myocardial infarction as follows: all patients with proved acute myocardial infarction should be treated with anticoagulants while hospitalized unless there are relative or absolute contraindications to the therapy or deficiencies in laboratory facilities. Patients with questionable infarcts should be treated with anticoagulants only until the diagnosis is established or rejected. If the latter occurs, the administration of the drug should be discontinued. When, in a patient suspected of having an acute myocardial infarction, there is reason to believe that the pain may be due to pericarditis, dissecting aneurysm, or gastrointestinal abnormalities, anticoagulant therapy should be withheld until this is resolved.
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PMID:Antithrombotic agents are indicated in the therapy of acute myocardial infarction. 84 87

In order to investigate the relation between the release of creatine kinase (CK) in acute myocardial infarction and the evolution of infarction, the appearance functions of CK (release of CK from the heart into the circulation) were calculated by the modified method of Sobel and associates from the serial determinations of serum CK activity in 50 patients with acute myocardial infarction. The relation of the time between the onset of infarction and the peak value of the appearance function to the duration of the evolution of abnormal Q waves in 14 patients with inferior infarction and to the duration of pain in all patients was investigated. The duration of CK release from the heart averaged 37-2+/-2-4 hours and correlated well with the total CK released (R=0.665) which represents the infarct size. The mean per cent of the total CK eventually released by the time of maximum sigmaQ (sum of the amplitude of Q wave in leads II, III, and aVF) was 80-0+/-6-4 per cent and that of CK released while pain persisted was 72-0+/-3-9 per cent. These results strongly suggest that the appearance function of CK reflects the evolution of myocardial infarction.
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PMID:Evaluation of evolution of myocardial infarction by serial determinations of serum creatine kinase activity. 86 Oct 91

This presentation has described the modern approach to the patient presenting with chest pain suspected as acute myocardial infarction. Noninvasive and invasive methods have been applied to estimate the extent of the myocardial damage and to monitor the electrical, hemodynamic and metabolic changes during the acute phase. In addition to the use of standard analgesics and antiarrhythmics, measurement of the determinants of left ventricular function by noninvasive and invasive techniques provides a physiologic basis for administration of available pharmacologic agents that can alter the afterload, contractile state, preload, heart rate, metabolic state and infarct size. Information from the Swan-Ganz catheter can describe hemodynamic categories that can be optimally managed by regulation of the left ventricular filling pressure. Patients managed in this manner can be identified for early hospital discharge at 7-10 days. Other patients less than 50 years of age or those experiencing recurrent arrhythmias, ischemic pain or evidence of left ventricular dysfunction may be candidates for coronary arteriography and left ventricular angiography before hospital discharge.
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PMID:Modern approach to the patient with acute myocardial infarction. 90

In 14 patients with hypertensive crisis treated with diazoxide, close monitoring of blood pressure, heart rate, and symptoms was performed. Standard 12-lead electrocardiograms were recorded before and after diazoxide. All patients showed a significant fall in blood pressure after drug administration. Seven patients (50%) showed significant ST-T changes after diazoxide. Six patients (43%) developed substernal discomfort demonstrated by substernal pain of tightness. Five patients (35%) had both chest discomfort and ST-T changes. One of these patients with substernal pain and ST elevation had evidence of acute myocardial infarction with serial enzyme studies. In the patients with significant ST-T changes, the average fall in blood pressure was significantly greater than the average fall in blood pressure in the patients without significant ST-T changes. These findings suggest that both ST-T changes and substernal discomfort were due to myocardial ischemia secondary to a sudden severe drop in blood pressure.
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PMID:Angina-like syndrome with diazoxide therapy for hypertensive crisis. 93 81

A 48 years old male developed acute cardiac pain manifested by prolonged P-R interval as the only electrocardiographic sign. Subsequently the electrocardiogram evolved an acute myocardial infarction with a normal P-R interval. Immediately therafter prolonged P-R interval reappeared to become established even after digitalis was long discontinued.
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PMID:Changes in P-R interval immediately before, during, and after acute myocardial infarction. 96 89

It is generally accepted that ST segment elevation is one of the characteristic electrocardiographic features of acute myocardial infarction. In experimental myocardial infarction the degree of ST segment elevation has been related to the degree of change in coronary flow. Surface mapping in patients of the electrocardiographic potentials gives an indirect representation of the epicardial ST segment change and in indication of the area of underlying myocardial damage. A number of patients who had sustained myocardial infar-tion within 72 hours were studied. All the patients had a history of prolonged ischaemic cardiac pain, electrocardiographic changes and a rise in serum enzymes. Electrocardiagrams were recorded from 72 points on the chest surface. Control maps were constructed from the ST segment changes measured at each of these points and plotted on a standard diagram. Electrocardiograms were recorded during a control period immediately before 20 mg of practolol was given intravenously over a period of five minutes. In all patients practolol produced a significant reduction in the area of ST segment elevation as represented by a reduction in the number of points with ST elevation of more than 2 mm. The significance of these findings is discussed.
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PMID:Electrocardiographic surface mapping of the heart following myocardial infarction and the influence of beta-blockade. 96 68


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