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 61-year-old man was admitted to our hospital with complaints of cough and left back and chest pain. He had suffered from left tuberculous pleurisy at the age of 20 years. Chest X-ray film and CT revealed atelectasis of the left lung, a left hilar mass and an irregular left atrial wall. Depressed P-Ta segment in the inferior limb and anterior chest leads and an abnormal P wave were found on ECG. Transbronchial lung biopsy showed squamous cell carcinoma. After radiation therapy, the patient complained of chest oppression. ECG revealed a normalized P-Ta segment deviation, markedly elevated ST segment in the inferior limb and lateral chest leads and a depressed ST segment in the anterior chest leads. These findings persisted until his death. An obscure appearance of the pericardium and an echogenic intramyocardial mass in the posteroinferior and lateral wall were evident by echocardiography. The patient died due to heart failure. Postmortem needle biopsy showed scattered intramyocardial tumor cell nests with keratinization. CPK, GOT and LDH were within normal limits throughout the course, but CPK-MB was slightly increased. Cardiac metastasis with an ECG appearance similar to that of acute myocardial infarction has been rarely reported. Our present case showed peculiar feature including 1) ECG findings similar to atrial and ventricular myocardial infarction, and 2) an echogenic intramyocardial mass and an ill-defined pericardium on echocardiography. These findings suggested direct invasion of squamous cell carcinoma of the lung to the ventricular myocardium.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Report of a case of lung cancer with metastasis to the myocardium which showed electrocardiographic findings similar to acute myocardial infarction and intramyocardial mass on echocardiography]. 274 Jun 46

The activities of cyclic 3',5'-nucleotide phosphodiesterases which hydrolyze cyclic 3',5'-nucleotides were measured in sera from patients with an acute myocardial infarction, angina pectoris and other heart diseases. Cyclic AMP and cyclic GMP phosphodiesterase activities were significantly elevated in acute myocardial infarction, but not in angina pectoris and other cardiovascular diseases. The peak activity appeared approximately within 24 hours following the acute attack of chest pain, and then gradually decreased as the patient recovered. The observed changes of cyclic 3',5'-nucleotide phosphodiesterase activity were similar to that of the other enzyme activities such as GOT, CPK and LDH in sera of acute myocardial infarction. These data reflect damage of myocardial cells during myocardial infarction.
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PMID:Serum cyclic 3',5'-nucleotide phosphodiesterase activity in myocardial infarction. 300 9

In order to discuss the mechanism of onset in myocardial infarction (MI), clinical cases were reviewed and various clinical findings were analyzed according to the premise that the onset of MI requires both a predisposition and a trigger. The majority of subjects did present conditions that constituted predispositions for MI, including a history of angina pectoris (especially unstable angina), poor therapeutic results for angina pectoris, organic stenosis of the coronary artery, life changes, and overwork. Patients with multiple factors tended to develop MI without a definite trigger, i.e., onset during sleep or rest whereas, in patients with fewer predisposing factors, it was obvious effort, excitation or stress that triggered MI. However, not a few of the patients presented with no organic stenosis of the coronary artery or no history of angina pectoris. There were patients without ST segment elevation at onset of MI, and patients in whom ST elevation was recorded after onset. These findings suggest the existence of mechanisms other than coronary occlusion in onset of MI. Occlusion of the coronary artery distributed to the infarct region occurred frequently among patients with delayed CPK efflux as well as prolonged chest pain and ST segment elevation. These lines of evidence suggest extension of infarction due to secondary coronary occlusion.
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PMID:Evaluation of clinical factors involved in onset of myocardial infarction. 372 78

A 26-year-old black woman presented with a febrile illness and subsequently sustained an inferior myocardial infarction with chest pain. CPK-MB elevation and ECG changes. Left ventriculography revealed inferior wall hypokinesis, and coronary angiography demonstrated multiple aneurysms of the coronary arteries. Findings on visceral angiography of multiple organs was normal. Various etiologies were considered; however, her clinical course was felt to be most consistent with periarteritis nodosa and steroid therapy was instituted.
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PMID:Myocardial infarction in a young woman with isolated coronary arteritis. 612 46

The hour of day of primary ventricular tachycardia (VT) in the acute phase of myocardial infarction was studied in 63 consecutive patients without cardiac failure or antiarrhythmic therapy, admitted to hospital less than 6 hours after the onset of chest pain. There were 19 women and 44 men, with an average age of 63 years. The site of infarction was anterior in 23 cases, posterior in 34 cases and circumferential in 6 cases. The cardiac rhythm was analysed from the 6th hour following the onset of chest pain for 4 days, using a HP 98220 A computerised analyser CPK levels were measured daily. Ventricular tachycardia occurred in 73% of cases with no significant difference between daytime (18 patients) and night time (28 patients). The patients developing VT did not differ from the remainder with respect to age, sex, or site of ECG changes, but peak CPK levels were significantly higher than in patients without VT. The risk of VT decreased slowly as the interval from the onset of chest pain increased and fell practically to zero after the 40th hour. Diurnal and nocturnal VT were independent of age, sex or site of infarct. However, nocturnal VT correlated independently of the time of onset of chest pain to high values of CPK. There was no difference with respect to age, sex, location of infarct or incidence of ventricular tachycardia between infarcts with pain starting during the day, and infarcts with pain starting at night. However, when the pain started during the day, the peak CPK was significantly higher and there were significantly more attacks of nocturnal ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Time of occurrence of primary ventricular tachycardia in the acute phase of myocardial infarction]. 643 67

Emergency coronary angiography and intracoronary thrombolysis were performed on 47 patients who were hospitalized within 12 hours from onset of chest pain. It revealed either a severe stenosis (14 pts: stenosed group) or complete occlusion (33 pts) of infarct-related coronary artery. In 25 out of 33 patients (76%) with complete occlusion, reperfusion was achieved after 10 to 20 minutes of intracoronary urokinase (UK) infusion at a rate of 500IU/kg/min (thrombolysed group). The failure to open coronary artery in remaining 8 patients may have been caused by the occlusion of atheroma itself (unsuccessful group). Left ventricular angiography was performed at one month after attack. In unsuccessful group, the mean age was younger and infarct-nonrelated vessel disease was lower frequency compared to other two groups. Ejection fraction in stenosed, thrombolysed and unsuccessful groups were 56.6 +/- 12, 47.5 +/- 14 and 44.3 +/- 5.1%, respectively. Wall motion assessed by point-score system were 6.7, 5.9 and 3.6, respectively (p less than 0.05 in each group). These facts suggest that early recanalization may result in greater reversal of cardiac function. The time to the peak CPK was shortened in stenosed and thrombolysed groups, but, the values of CPK was maximum in thrombolysed group. Rethrombosis was recognized in 2 patients during 1 to 30 months follow-up. No death and no remarkable complications were seen during this intervention, but 4 late deaths were recognized. Thus, early reperfusion by intracoronary UK infusion is effective therapy to improve cardiac function and reduction of death in AMI.
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PMID:Effects and limitation of CCU--prevention of evolving myocardial infarction. 647 48

This study was carried out on patients of a coronary unit to evaluate the diagnostic efficiency of total CPK and CPK-MB by using different analytical techniques: catalytic, immunoassisted, cellulose acetate electrophoresis, radioimmunoassay and immunoradiometric assay. The behaviour of the enzyme was studied in all patients with reference to the localization and extent of the infarct. In all cases a diagnostic algorithm was followed based on the combined use of CPK and its MB isoenzyme; the activity was measured twice, at three-hour intervals after admission. In this way the utilization of total CPK and MB isoenzyme allows almost complete diagnostic efficiency within the first 9 hours from onset of chest pain, together with the possibility of calculating the slope of the curve of MB isoenzyme release useful for calculating infarct size. Maximum diagnostic efficiency is also obtained in cases of small infarcts, with silent ECG, and those difficult to classify clinically.
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PMID:CPK and CPK-MB in the early diagnosis of acute myocardial infarction and prediction of infarcted area. 651 51

In order to evaluate differences between the initial manifestations of acute myocardial infarction (AMI) in diabetics (DM) and non-diabetics (N-DM), 94 consecutive AMIs (DM 40, N-DM 54) were studied over a four-year period. Cases with abrupt onset associated with chest pain and/or discomfort in the areas of the chest and back were classified as the typical group (I). All other cases were classified as the atypical group (II). In subjects over the age of 60, 12 out of 33 DM had atypical manifestations, but only 3 out of 29 N-DM (p less than 0.05). In subjects aged 59 or less, the incidence of atypical cases was similar in the DM and N-DM groups. The initial symptoms of AMI were not correlated with type or location of infarction, nor with the type of treatment or presence of the ankle jerk reflex. Pre-infarction symptoms were present in 69% of Group I and 74% of Group II DM subjects. In Group II, 5 out of 16 patients had a history of typical angina, but had no chest pain at the onset of infarction. The post-AMI mortality within one month was 15% in the DM and 18% in the N-DM group. It was 14% in Group I and 25% in Group II. Mean CPK did not differ statistically between Group I and Group II. However, the Peel prognostic index was 11.0 +/- 5.1 for Group I and 15.5 +/- 5.0 for Group II (p less than 0.05) in subjects over the age of 60.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Painless myocardial infarction in diabetics. 668 May 31

Platelet scintigraphy with radioactive indium-111 may be used both to identify and to reflect the activity of thrombin in vivo in man. Forty-one patients with acute myocardial infarction were studied for active left ventricular thrombosis by platelet scintigraphy and followed until in-hospital death, discharge, or same-admission cardiac surgery for evidence of systemic embolization. A total of 4.7 +/- 2.4 X 10(9) platelets (mean +/- 1 SD) labelled with 381 mu Ci +/- 51 mu Ci of indium-111 was injected intravenously at 91 +/- 88 hours following the onset of chest pain. Patients were imaged in multiple views on the day of and three to four days after injection of the platelet suspension. Group 1 (n = 29) had transmural myocardial infarctions, of which 21 were anterior (peak total level of creatine phosphokinase [CPK], 2,272 +/- 2,026 IU; mean +/- 1 SD) and eight were inferior (CPK level, 1,673 +/- 589 IU). Group 2 (n = 12) had subendocardial myocardial infarctions (CPK level 799 +/- 751 IU). Those with subendocardial and transmural inferior myocardial infarctions had neither left ventricular thrombosis nor emboli. Ten (48 percent) of 21 with anterior transmural myocardial infarctions had left ventricular thrombosis by platelet scintigraphy. Three with and one without such thrombosis by scintigraphy had acute neurologic episodes. In the group with anterior myocardial infarctions, seven of ten patients with and four of 11 without left ventricular thrombosis received heparin subcutaneously (chi 2 = 1.22 [Yates correction]; p greater than 0.30). We conclude that platelet scintigraphy may be used to monitor antiplatelet and anticoagulant therapy in patients with anterior transmural myocardial infarctions who are at risk for left ventricular thrombosis and systemic embolization.
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PMID:Detection of active left ventricular thrombosis during acute myocardial infarction using indium-111 platelet scintigraphy. 673 89

A bolus of 1000 mg of 5-FU intravenously was given to a 54-year-old patient with adenocarcinoma of colon, a month after hemicolectomy. He had not received irradiation therapy. Five hours later he complained of severe chest pain; after 24 hours ecg. changes of pericarditis were seen and on heart auscultation a pericardial friction rub was heard. After 6 day the ecg. returned to the pattern of that on day of admission to the ICCU. Two further injections of 1000 mg of 5-FU were also followed by severe precordial pain and the same ecg. pattern. The pulmonary edema 14 hours after the second injection and the slight elevation of CPK value after the third injection strongly suggest myocardial cell damage. For the strictly temporal relationship between the clinical and electrocardiographic pattern with 5-FU administration intravenously, we are of the opinion that the perimyocarditis was due to the direct toxic action of 5-FU on pericardium and myocardium.
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PMID:[Early cardiotoxicity of 5-fluorouracil]. 734 80


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