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)

Survival for patients with advanced head and neck carcinoma and esophageal carcinoma is poor with radiotherapy and/or surgery. Obviously, there is a need for effective chemotherapy. In the present study, cis-platin (80-120 mg/m2BSA) and 5-FU (1000 mg/m2BSA daily as a continuous infusion during 5 days) were given to 76 patients before radiotherapy and surgery. The aim of the study was to clarify the incidence and severity of adverse cardiac effects to this treatment. Before treatment all patients had a cardiac evaluation and during treatment serial ECG recordings were performed. In the pre-treatment evaluation, signs of cardiovascular disease were found in 33 patients (43%). During treatment, adverse cardiac effects were observed in 14 patients (18%). The mean age of these patients was the same as for the entire group, 64 years. The incidence of cardiotoxicity was not higher in patients with signs of cardiovascular disease than in those without in the pre-treatment evaluation. The most common signs of cardiotoxicity were chest pain, ST-T wave changes and atrial fibrillation. This was followed by ventricular fibrillation in one patient and sudden death in another. It is concluded that patients on 5-FU treatment should be under close supervision and that the treatment should be discontinued if chest pain or tachyarrhythmia is observed.
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PMID:Adverse cardiac effects during induction chemotherapy treatment with cis-platin and 5-fluorouracil. 318 73

The emergency physician's disposition of patients with suspected myocardial ischemia is currently debated; some physicians believe that a subgroup of patients can be managed safely outside the coronary care unit. Clinical predictors are needed in assessing the patient with suspected myocardial ischemia to help identify this subgroup. Through a retrospective cohort study, we investigated the value of the initial emergency department ECG in discriminating between chest pain patients with low and high risk for immediately life-threatening complications. Two hundred eleven initially uncomplicated consecutive coronary care unit admissions with suspected unstable angina or myocardial infarction were studied. Patient outcome, including the incidence of myocardial infarction, complications, and mechanical and pharmacologic interventions, was reviewed. Immediately life-threatening complications included ventricular fibrillation, ventricular tachycardia, shock, 2 degrees and 3 degrees block, and death. Mechanical interventions included electrocardioversion or defibrillation, endotracheal intubation, intra-aortic balloon pump, Swan-Ganz catheter, or pacemaker insertion. Pressors, antiarrhythmics, and vasodilators were the reviewed pharmacologic interventions. A positive ECG was defined by the presence of ST elevation or depression, T wave inversion, left ventricular hypertrophy, left bundle branch block, paced rhythm, or new Q waves. All other ECG interpretations were considered negative. Patients were divided into two groups based on this initial emergency physician ECG interpretation and their complication incidences compared. Of the 211 patients, 96 had a positive ECG; 115 had negative ECGs. Patients with positive ECGs were older, had a greater history and concurrent incidence of myocardial infarction, and more complications and intensive interventions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The emergency department ECG and immediately life-threatening complications in initially uncomplicated suspected myocardial ischemia. 334 14

Out-of-hospital ventricular fibrillation (OHVF) is the most common cause of sudden cardiac death. Of 1,070 patients with OHVF who entered this study, 150 were discharged alive. Of this group, 120 were free of anoxic brain damage. Of these survivors, 67 (57%) had no previously demonstrated anginal symptoms. Treadmill stress testing revealed painless ST depression in 76% of these neurologically intact patients. Exercise ventriculography in a subset of 9 patients without angina before OHVF and in 6 patients with typical anginal symptoms revealed marked left ventricular dysfunction with ST depression in the absence of chest pain in all 15 patients. Sublingual nitroglycerin reversed this evidence of ischemia in the asymptomatic patients. Patients were followed for 6 years after discharge. No statistical difference in mortality could be demonstrated for patients who had previous anginal symptoms vs those who did not, nor was age a predictor of mortality. Women had the same risk of death as men at 2 years after OHVF, but a significantly higher risk by year 6. Myocardial infarction associated with OHVF did not predict lower mortality throughout the study.
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PMID:Six-year survival of patients with and without painless myocardial ischemia and out-of-hospital ventricular fibrillation. 335 59

The variability of chest pain is described in 389 patients with acute myocardial infarction. Whereas 17% were free from severe pain after arrival in hospital, 11% required more than 10 analgesic injections. In 27% of the series analgesics were given more than 24 h after arrival in hospital. Predictors for the severity of chest pain were the rate-pressure product and degree of chest pain soon after arrival in hospital as well as electrocardiographic signs of myocardial infarction at entry. Patients with more severe chest pain had a higher 2-year mortality rate and a higher incidence of ventricular fibrillation and congestive heart failure during hospitalization.
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PMID:Variability, prediction and prognostic significance of chest pain in acute myocardial infarction. 351 82

In a randomized controlled study examining the value of an intramuscular injection of lidocaine in the prehospitalization phase of suspected acute myocardial infarction, paramedics used an automatic injector to administer 400 mg of the drug into the patient's deltoid muscle before transport to the hospital. In a 33-month period, 7026 patients with acute chest pain were seen. Of the 6024 patients randomized (2987 to the lidocaine group and 3037 to the control group), 1935 (32 per cent) proved to have an acute myocardial infarction. In the entire 60-minute period of observation by continuous electrocardiography, primary ventricular fibrillation was observed in 8 treated and 17 control patients (P = 0.08). However, from 15 minutes after randomization onward, when plasma lidocaine levels were in the therapeutic range, only 2 cases of ventricular fibrillation occurred in the treated group, as compared with 12 in the control group (P less than 0.01). Ventricular tachycardia terminated a mean of 10 minutes after injection in six of nine lidocaine-treated patients with acute myocardial infarction but in none of five control patients with infarction (P less than 0.02). Mean plasma lidocaine levels were 3 micrograms per milliliter 11 to 20 minutes after injection in 369 consecutive patients. In 65 patients, levels were below 2 micrograms per milliliter, and in 15 patients, levels were above 6 micrograms per milliliter. Side effects were rare and did not contribute to mortality. We conclude that intramuscular lidocaine may be useful if given by a paramedic, another person, or the patient himself when acute myocardial infarction is suspected outside the hospital.
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PMID:Intramuscular lidocaine for prevention of lethal arrhythmias in the prehospitalization phase of acute myocardial infarction. 390 Jul 27

A 74 years old man was admitted as an emergency for syncopal attacks due to recurrent ventricular fibrillation (VF). These attacks were observed at the height of myocardial ischaemia as shown by ST elevation in Leads II, III and RV without associated anginal pain. Inferior myocardial infarction occurred during recurrent VF on the 4th day; the outcome was favourable. Coronary angiography was performed on the 10th day and showed double vessel disease; ergometrine (0.2 mg) induced anginal pain and ST elevation in Leads II, III and AVF. A good clinical result was obtained by calcium antagonists with an 18 months follow-up. Coronary spasm, documented in this case by the ergometrine provocation test, is now recognised as a cause of resting angina, effort angina and also some cases of myocardial infarction. This report suggests that coronary spasm may also induce apparently isolated severe ventricular arrhythmias without associated chest pain, which raises the question as to whether arrhythmias induced by spasm could play a primary role in aggravating myocardial ischaemia, leading to myocardial infarction.
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PMID:[Pure arrhythmic form of the pre-infarction syndrome or spasm responsible for myocardial necrosis]. 392 41

A specific search for intramyocardial platelet aggregates was made in 90 patients who died suddenly of ischemic heart disease. Platelet aggregates in small intramyocardial vessels were found in 27 (30%). There was a significant difference (p less than .05) in the incidence of platelet aggregates in patients with chest pain of recent onset (unstable angina) before death (16/36, 44.4%) and that in those without it (11/54, 20.4%). Multifocal microscopic necrosis with involvement of the full thickness of the ventricular wall, including the subpericardial zone, was significantly more common (p = less than .005) in the patients with platelet emboli (55.6% vs 12.7%). With one exception, aggregates were confined to the segment of myocardium immediately downstream of a major epicardial coronary artery containing an atheromatous plaque that had undergone fissuring and on which mural thrombus had developed. The results support the view that platelet aggregates in the myocardium represent an embolic phenomenon and are a potential cause of unstable angina. The association of myocardial necrosis with such emboli could precipitate sudden death from ventricular fibrillation.
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PMID:Intramyocardial platelet aggregation in patients with unstable angina suffering sudden ischemic cardiac death. 394 52

A 54-year-old man with mitral valve prolapse syndrome diagnosed by echocardiography complained of anginal pain associated with ventricular tachyarrhythmia. One day he suddenly lost consciousness, and ECG at that time revealed ventricular fibrillation. Thereafter, he developed ST elevation, sporadic premature ventricular contractions, and R on T phenomenon leading to ventricular fibrillation during the attack of anginal pain. His coronary arteriogram was normal. This case implies that coronary artery spasm may be one of the causes of chest pain and ventricular tachyarrhythmias in patients with mitral valve prolapse syndrome.
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PMID:Mitral valve prolapse syndrome with coronary artery spasm: a possible cause of recurrent ventricular tachyarrhythmia. 399 4

Several controlled studies with long-term administration of beta blockers in postinfarction patients have demonstrated a reduction in cardiac events and mortality. During acute myocardial infarction (AMI), conventional treatment is directed mainly at such complications as pump failure and arrhythmias. Another approach attempts to influence the natural evolution of impending myocardial necrosis by interrupting the process in its reversible phase. In a double-blind trial with metoprolol in suspected or definite AMI, 1,395 patients were studied, 698 of whom received metoprolol and 697 placebo. The 3-month mortality was 36% lower in the metoprolol group (p = 0.024). A reduction in severe ventricular arrhythmias (ventricular fibrillation and tachycardia) was also seen. Chest pain was reduced and there was less need of analgesic drugs in the metoprolol group. Intervention within 12 hours resulted in a limitation of infarct size, a decreased need for furosemide and a shortened hospital stay. A significant reduction in mortality was maintained after 2 years of follow-up despite the same treatment in both groups between 3 and 24 months. Early institution of metoprolol in AMI has resulted in reduced mortality and morbidity.
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PMID:Early intervention with a beta-blocking drug after acute myocardial infarction. 615 Jun 31

Propafenone, a new class I antiarrhythmic drug, given as a bolus injection followed by oral medication, or lidocaine were given to 20 consecutive patients admitted with chest pain suggesting acute myocardial infarction and showing high grades, i.e. multiform, pairs or R-on-T premature ventricular complexes or short runs of ventricular tachycardia. Before institution of therapy the mean number (+/- 1 SD) of premature ventricular contractions (PVCs) per hour was 169 +/- 123 in the lidocaine group and 324 +/- 440 in the propafenone group. During the next 24 hours lidocaine reduced the numbers of PVCs by 73% and propafenone by 75%. The mean number (+/- 1 SD) of 5-minute periods with high grade PVCs was 4.3 +/- 2.9 in the lidocaine group and 5.8 +/- 4.5 in the propafenone group. During therapy this number was equally reduced in both groups to 2.4. One patient in the lidocaine group developed ventricular fibrillation and three patients in the propafenone group were excluded because of increasing numbers of PVCs. One patient in the propafenone group showed a torsade-de-pointes ventricular tachycardia.
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PMID:Comparative investigation of the antiarrhythmic effect of propafenone (Rytmonorm) and lidocaine in patients with ventricular arrhythmias during acute myocardial infarction. 639 42


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