Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 65 years old woman with an acute myocardial infarction, as it was judged by serial enzyme changes, developed transitory Q waves in V2-V4 and II, III and AVF during the attack of chest pain. These Q waves were not present 12 hours later. It is suggested that these changes represent a focal block in the septal fibers of the left bundle system. This defect could explain the transient right precordial Q waves seen in myocardial infarction or ischemia, as well as the fixed Q waves of many patients without septal infarction at autopsy.
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PMID:Transient abnormal Q waves during acute myocardial infarction. 31 75

Fifteen patients with frequent anginal chest pain underwent diagnostic cardiac catheterization. After coronary arteriography a specially designed cardiac catheter was seated in the aortic root, permitting the continuous infusion of krypton-81m into the right and left aortic sinuses. A gamma camera, areas of interest and a visual display unit were used to record images and the regional myocardial equilibrium of activity before, during and after a standarized atrial pacing test. The unique physical properties of krypton-81m allowed the continuous imaging and recording of moment to moment changes in regional myocardial perfusion. This investigation revealed that when the coronary arteriogram was normal or revealed lumonal stenosis of less than 50 percent, regional myocardial perfusion was uniform at rest and during stress. Two patients with a previous history of myocardial infarction had defects of regional perfusion at rest and during stress. Krypton scintigraphy demonstrated reversible regional defects in myocardial perfusion during stress in seven patients with greater than 70 percent stenosis of one or more coronary arteries. Alterations in regional myocardial perfusion occurred within 30 seconds of the start of atrial pacing in all the patients and preceded the onset of electrocardiographic signs of ischemia or chest pain.
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PMID:Krypton-81m in the physiologic assessment of coronary arterial stenosis in man. 42 Jan 4

Sixteen patients with significant two and three vessel coronary artery disease but without clinical congestive heart failure were studied during rapid atrial pacing before and after infusion of 0.015 mg/kg of ouabain. Seven patients with a decreased (less than 50 percent) ejection fraction and nine patients with a normal ejection fraction had a significant (P less than 0.05) increase in resting arterial systolic pressure after the administration of ouabain. However, resting values for coronary sinus flow, coronary vascular resistance, myocardial oxygen consumption and myocardial lactate extraction did not change significantly in either group. During pacing, patients with a decreased ejection fraction demonstrated more ischemia than patients with a normal ejection fraction; however, the administration of ouabain did not significantly alter pacing-related changes in coronary sinus flow, myocardial oxygen consumption, myocardial lactate extraction, ischemic electrocardiographic changes or onset of chest pain in either group. The administration of ouabain has a negligible effect on coronary hemodynamics, myocardial metabolism or clinical signs of ischemia in patients with coronary artery disease with normal or abnormal left ventricular function.
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PMID:Lack of ouabain effect on pacing-induced myocardial ischemia in patients with coronary artery disease. 43 84

When exercise testing 159 patients with prior myocardial infarction, we identified 39 who were limited by fatigue. This group was all in sinus rhythm; none were taking drugs likely to impair the chronotropic response of the heart; none experienced chest pain or developed ischemic ECG changes. In 18 of this group, maximal heart rate achieved with exercise was 2SD or more below the age predicted value, and their heart rate response to exercise was reduced compared to that of the other 21 whose maximal exercise heart rates were within 2SD of age predicted values. A subgroup of 8 subjects with reduced exercise heart rates was studied before and after vagal blockade. In the 4 subjects whose infarction was inferior, the reduction in heart rate response was more profound and persisted after vagal blockade, suggesting either reduced pacemaker responsivness, due to ischemia or infarction, or autonomic imbalance as possible mechanisms. All 8 showed alinear increases in ventilation at higher power outputs and mean blood lactate postexercise was 7.5 mM/I without vagal blockade. Our findings suggest that a reduced heart rate response to exercise, already shown to imply added coronary risk, may be subdivided aetiologically and possibly prognostically. The use of a "Target Heart Rate" in such patients offers no safety margin, and maximal exercise capacity will be grossly over-estimated if extrapolated from the submaximal heart rate response. A cardiovascular limitation to exercise may be detected by an alinear increase in ventilation.
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PMID:Reduced heart rate response to exercise in ischemic heart disease: the fallacy of the target heart rate in exercise testing. 52 31

99mtechnetium diphosphonate was used in 81 patients for myocardial imaging. 46 of the patients suffered, 2-6 days prior to the test, from an acute transmural infarction provided by clinical, ECG, and enzymatic evidence; the scintigram was definitely positive in 43, equivocal in 2, and negative in 1. In 16 patients with subendocardial infarctions, in 9 the scintigram showed a positive result, in 1 it was equivocal, and in6 patients negative. In 6 other patients who suffered from acute chest pain, followed by enzyme changes, but no ECG evidence of infarction throughout the hospitalization period, the scan was positive in all. In 13 patients with acute ischemia (unstable 'crescendo' angina), 9 had a positive, 1 an equivocal, and 3 a negative scan. We conclude that radionuclide imaging is a valuable addition to the methods already available for diagnosis of myocardial infarction. With the use of diphosphonate as the tracer, we found that acutely ischemic myocardium that later may recover, gives also positive imaging.
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PMID:Radionuclide imaging of the heart in myocardial infarction and acute ischemia by 99mtechnetium diphosphonate. 59 Feb 93

Patients with mitral valve prolapse (MVP) frequently experience chest pain which may, expecially in older subjects and males, be difficult to differentiate from angina pectoris. Electrocardiographic (ECG) changes, ventricular arrhythmias, metabolic abnormalities and rare reports of myocardial infarction and sudden death further suggest the presence of an ischemic process in these patients. The recognition of accompanying coronary artery disease (CAD) and exclusion of other causes of ischemia, therefore, may be important in determining the prognosis and appropriate therapy for such patients.
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PMID:Myocardial perfusion scintigraphy in patients with mitral valve prolapse: Its advantage over stress electrocardiography in diagnosing associated coronary artery disease and its implications for the etiology of chest pain. 61 88

First heart sound (S1) energy spectra in isovolumic systole, hemodynamics, and angiographic left ventricular wall motion (LVWM) at rest and with atrial pacing were compared in 27 patients who underwent diagnostic cardiac catheterization and angiography because of chest pain. Eighteen patients were found to have coronary artery disease (CAD) and nine patients, normal coronary arteries. Eleven of the 18 CAD patients (61%) had a mean reduction in the spectral energy of S1 of 6.5 +/- 1.4 (SEM) dB below control (-52%), during interruption of ischemic stress of rapid atrial pacing, compared to only one of nine patients without CAD (P less than 0.05). Only five CAD patients (28%) had an abnormal rise (greater than or equal to 5 mm) in left ventricular end-diastolic pressure (LVEDP) either during or upon interruption of pacing, and six (33%) had ischemic ST-segment depression greater than or equal to mv in the ECG. Similarly two patients free of CAD (22%) had an abnormal increase in LVEDP, and none had ECG evidence of ischemia. Seventeen CAD patients (94%) had segmental LVWM abnormalities at rest or with interruption of pacing, while three patients with normal coronary arteries (33%) had abnormal angiographic LVWM (P less than 0.01). Thus, reduction is S1 spectral energy is a common accompaniment of myocardial ischemia. In the present study, it was more frequently observed than abnormalities in either the ECG or LVEDP, but was not was consistently seen as segmental left ventricular wall motion abnormalities.
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PMID:Spectral energy of the first heart sound in acute myocardial ischemia. A correlation with electrocardiographic, hemodynamic, and wall motion abnormalities. 62 70

51 patients with coronary heart disease had exercise tests on a bicycle ergometer (86 +/- 32 watts). Compared to a normal control group, only 13 patients had normal contractile reserve (group 4.1). In 32 patients the increase in contractility during exercise was reduced (max dP/dt below 3200 mm Hg/s, group 4.2). Patients with reduced contractile reserve were graded according to the height of left ventricular enddiastolic pressure during exercise: In patients with grade 1, enddiastolic pressure was normal. In patients with grade 2, enddiastolic pressure increased between + 4 and + 15 mm Hg and in the patients with grade 3a a above + 15 mm Hg. Contractile and relaxation reserve decreased along with a rise in enddiastolic pressure and an increase in the complaints of the patients. Severe chest pain led to termination of exercise in patients of grade 3b. Enddiastolic pressure increased above + 15 mm Hg. During ischemia, peak-measured velocity of contractile elements (dP/dt/P) and the maximal rate of left ventricular pressure fall (min dP/dt) decreased. In conclusion, with increasing chest pain a decrease of contractile reserve was observed. Left ventricular enddiastolic pressure rose excessively. This has to be taken as a sign of myocardial failure due to ischemic dyskinesia and impeded relaxation.
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PMID:[Contractile and relaxation reserve of the left ventricle. IV. Patients with coronary heart disease (author's transl)]. 62 71

Serial blood pressure recordings were taken for 72 hours in 112 patients with acute myocardial infarction and in 96 patients with cardiac ischemia, admitted to hospital no more than 6 hours after the onset of chest pain. During the first hour of admission 66 (31.7%) had a blood pressure recorded 160/100 or greater. By the sixth hour, without specific antihypertensive therapy, this number had fallen to 13 (6.3%). This fall was subsequently maintained with very similar trends for both acute myocardial infarction and cardiac ischemia. Such an early blood pressure fall in acute myocardial infarction may indicate that this is too labile a measurement to determine the need for, or efficacy of, antihypertensive therapy aimed at the preservation of myocardium. The hospital course and mortality rate of patients with acute myocardial infarction and early hypertension, as defined, did not differ significantly from the non-hypertensive group.
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PMID:Blood pressure levels in acute myocardial infarction. 69 68

Serial 72-point precordial mapping of ECG has been recorded to describe the natural history of changes in the precordial areas of ST segment elevation and the development of Q waves in 51 patients with acute uncomplicated anterior myocardial infarction. Eight patients have been studied in the same way but received 25 mg/kg of methylprednisolone sodium succinate as a single intravenous injection within 6 hours from the onset of chest pain. There was a linear relationship between the stable precordial area of Q waves at 24 hours and the rapidly changing precordial areas of ST segment elevation at 2--3 hours, 5--6 hours and 12 hours after the onset of pain in the untreated patients. When methylprednisolone was given, the treated patients developed a smaller precordial area of Q waves at 24 hours than was predicted from the precordial area of ST elevation recorded before the drug was given. This study has introduced a technique that can provide a qualitative assessment of the relationship between ECG evidence of ischemia and infarction in each patient.
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PMID:Electrocardiographic precordial mapping in anterior myocardial infarction. The critical period for interventions as exemplified by methylprednisolone. 69 56


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