Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exposure to cold causes a vasoconstriction and a tachycardia, both resulting in a rise of blood pressure and cardiac work. This last effect may have a deleterious influence on people suffering from ischaemic heart disease (IHD). Moreover, coronary artery spasm could occur if vasoconstriction extends to the heart vessels. Epidemiologic studies have shown that mortality from IHD was correlated to the ambient temperature. There will be more deaths per day in the winter, and fewer in the summer. However, the daily number of deaths also increases during the heat waves. During a cold test, the coronary blood flow remains normal or slightly increased in normal subject. There is never a coronary artery spasm. Subjects who suffer from angina but have normal coronary arteries behave in the same way as normal subjects. Patients with IHD show a decrease in coronary blood flow. In a few cases, those patients may exhibit a coronary spasm with chest pain and even myocardial infarction. It is concluded that people with normal cardiovascular function are unaffected by cold stress whereas those with IHD may be crippled, although rarely, by exposure to cold, especially if they perform a physical work.
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PMID:Cold exposure and ischemic heart disease. 148 67

Associations between ischaemic heart disease and psychiatric morbidity in hospital recruited samples may be confounded by differential referral of patients with co-morbidity. Associations of angina, past history of myocardial infarction, blood pressure, and electrocardiographic evidence of ischaemia with psychiatric disorder can best be examined in community samples as reported here in 2204 middle-aged men from the Caerphilly Collaborative Study. There was a strong association between past history of myocardial infarction, non-specific chest pain, Angina Grade II and psychiatric disorder measured by the 30-item General Health Questionnaire. Electrocardiographic evidence of ischaemia alone was not significantly associated with psychiatric disorder. It is suggested that non-specific chest pain is a symptom of psychiatric disorder; conversely in severe angina psychiatric disorder is secondary to the pain, restricted activity and threat to life which angina implies.
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PMID:A population survey of ischaemic heart disease and minor psychiatric disorder in men. 148 89

This study prospectively evaluates the long-term prognosis of patients admitted with chest pain under suspicion of acute myocardial infarction (AMI) with and without confirmed diagnosis. All patients below 76 years of age, free of other severe diseases and alive at discharge, who were admitted to a coronary care unit of a well-defined region during 1 year, constituted the study population. In all, 275 patients with and 257 patients without confirmed AMI (non-AMI) were included. During 7 years of follow-up, 122 cardiac events (96 cardiac deaths and 26 nonfatal AMI) occurred in the AMI patients, and 69 (44 cardiac deaths and 25 nonfatal AMI) were observed in the non-AMI patients. Using univariate analysis, the following risk variables were significantly related to an impaired prognosis of non-AMI patients: age, a history of previous AMI, angina pectoris, clinical heart failure, diabetes and ST or T changes in the electrocardiogram (ECG) on admission. By multivariate analysis, the following risk factors contained independent prognostic information for non-AMI patients: (1) a history of angina pectoris and (2) ST and T changes on the ECG on admission. We conclude that a subset of non-AMI patients at high risk for cardiac events even in the long term can be identified from the medical history and the ECG on admission. These patients should be carefully evaluated prior to discharge, whereas patients without signs of ischemic heart disease have an excellent prognosis.
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PMID:Risk factors related to the 7-year prognosis for patients suspected of myocardial infarction with and without confirmed diagnosis. 151 76

The clinical features of congestive heart failure in the elderly were investigated in 104 patients (57 males, 47 females, mean age of 79.2). Patients were divided into two subgroups, the readmission group, 33 patients who were readmitted within 6 months after discharge, and the non-readmission group. Chief complaints were dyspnea, edema, chest pain, loss of appetite, chest compression, and palpitation. Heart failure was caused by infection, myocardial ischemia, arrhythmia, inappropriate drug usage including poor drug compliance, the use of beta-blockers, excessive intake of sodium, and anemia. Careful use of drug was essential especially in the readmission group. Major underlying heart disease were ischemic heart disease (39.4%), valvular disease (26.9%), hypertensive heart disease (9.6%), with cardiomyopathy, congenital heart disease seen in the minority. There was no statistically significant difference in underlying heart diseases between the two groups. Supraventricular arrhythmias such as atrial fibrillations, paroxysmal atrial fibrillations, paroxysmal supraventricular tachycardias, and premature atrial contractions were noted in 85.3% of the cases. Drugs for treatment were diuretics, digitalis, isosorbide dinitrate, calcium antagonists. ACE inhibitors and alpha-blockers were also used, showing that vasodilators were more extensively used than before. The major complications were hypertension (39.4%), renal dysfunction (27.9%), cerebrovascular disease (26.9%), diabetes mellitus (16.5%), arteriosclerosis obliterans (7.7%). Renal dysfunction, arteriosclerosis obliterans was seen significantly more frequently in the readmission group. The prognosis at one year after admission was significantly worse in the readmission group. In summary, the major underlying diseases were ischemic heart disease, valvular disease, and hypertensive heart disease. Ischemic heart disease was seen more frequently than in previous investigations at our hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Congestive heart failure in elderly readmitted patients]. 152 7

The operating characteristics of thallium stress testing for detection of significant epicardial coronary artery disease (CAD) in hypertensive subjects with chest pain or electrocardiographic (ECG) ischemia have not been previously defined. This becomes important because of the high prevalence of both hypertensive heart disease and CAD. Ninety-two hypertensives with a history of typical or atypical chest pain or ECG myocardial ischemia underwent coronary arteriography, 2D-guided echocardiography, and thallium-201 stress testing, combined with intravenous dipyridamole if the rate-pressure product was less than 20,000. Patients with myocardial infarction, prior revascularization procedure, valvular heart disease, and chronic ethanol abuse were excluded. The mean age was 54.8 +/- 9.9 years with 55% blacks and 46% women. Eighteen patients (19.6%) had significant (greater than or equal to 50% luminal diameter narrowing) epicardial CAD at catheterization, of whom 17 had positive thallium scans. Overall, there were 17 true positives, 47 true negatives, 27 false positives, and one false negative resulting in 94.4 +/- 5.4% sensitivity (95% confidence limits [95% CL] 71 to 100%), 63.5 +/- 5.6% specificity (95% CL 51 to 74%), 38.6 +/- 7.3% positive predictive value (95% CL 25 to 54%), 97.9 +/- 2.1% negative predictive value (95% CL 88 to 100%), and 69.6 +/- 4.8% overall accuracy (95% CL 59 to 79%). For hypertensive patients with chest pain or ECG myocardial ischemia, the high sensitivity and negative predictive value and low false negative rate support the role of thallium stress testing +/- dipyridamole as an exclusion test for significant CAD.
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PMID:A negative thallium (+/- dipyridamole) stress test excludes significant obstructive epicardial coronary artery disease in hypertensive patients. 153 15

Myocardial function was assessed by stress echocardiography in 28 patients before and after successful elective coronary angioplasty. Dobutamine stress echocardiography was performed using up to 40 micrograms/kg/min, followed by the addition of atropine in 20 patients to achieve 85% of the predicted maximal exercise heart rate. The initial studies were performed 1 day before and the second ones within 3 days (mean 1.3) after angioplasty. Peak heart rates and systolic blood pressures were the same for the 2 studies. The frequency of dobutamine-induced new wall motion abnormalities decreased from 20 (71%) before to 4 (14%) after angioplasty (p less than 0.0001). Before angioplasty, wall motion score index (an indicator of left ventricular wall motion, an increase in which indicates impaired wall motion due to myocardial ischemia) increased from 1.06 at rest to 1.23 at peak stress (p less than 10(-6)), but there was no significant increase in this index in the study after angioplasty. Before angioplasty, 14 patients (50%) developed chest pain during the stress test compared with 6 (21%) after angioplasty (p = 0.05), and before angioplasty, the stress test was stopped before the target heart rate was achieved, because of symptoms, ST-segment change or severe new wall motion abnormality in 14 patients compared with 7 after angioplasty (p = 0.09). Thus, early after angioplasty there is a reduction in myocardial ischemia as assessed by dobutamine stress echocardiography.
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PMID:Dobutamine stress echocardiography before and after coronary angioplasty. 154 47

Nursing care for Mr J evolved around his actual and potential problems. The actual problems were: an alteration in comfort (chest pain) related to myocardial ischemia, decreased cardiac output related to reperfusion dysrhythmias, and knowledge deficit regarding treatment with thrombolytic therapy. The potential problems were: fluid volume deficit related to lysis of clots in the cerebral vasculature, and alteration in myocardial tissue perfusion related to reocclusion of the coronary artery. Objectives focused on relief of chest pain, prompt initiation of thrombolytic therapy, maintenance of hemodynamics and cardiac output with early interventions, prevention of bleeding and initiation of patient education.
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PMID:Thrombolytic therapy: a case study. 155 84

The pathogenesis of acute myocardial ischemia or infarction following cocaine abuse is not known. Cocaine causes an increase in circulating catecholamines. Therefore alpha-adrenergic mediated focal or generalized coronary artery spasm has been presumed to be the likely mechanism to induce ischemia. However, coronary vasospasm in chronic cocaine abusers has not been demonstrated angiographically. Moreover, it has been observed that patients commonly manifest ischemic changes hours up to a week after abusing cocaine. In order to evaluate direct effects of cocaine on coronary vasculature, 6 chronic cocaine abusers admitted with prolonged chest pain and electrocardiographic ST- and T-wave changes were studied. Cocaine administered intravenously (maximum 32 mg) produced subjective sensation of central nervous stimulation (the "high") in all patients. However there was no significant change in coronary artery diameter (assessed by computer-assisted quantitative technique), myocardial perfusion (assessed by contrast echocardiography) or left ventricular wall motion (assessed by two-dimensional echocardiography) as compared with the baseline values. Coronary sinus flow (thermodilution) showed an upward trend, a probable reflection of a significant increase in cardiac output (average 62%, p less than 0.007). Despite a significant elevation in heart rate (average 56%, p less than 0.007), mean systemic arterial pressure (average 12%, p less than 0.05) and rate-pressure product (average 69%, p less than 0.005), no symptomatic or acute electrocardiographic changes were observed. It is concluded that recreational doses of cocaine do not cause focal or generalized coronary vasospasm or reduced myocardial perfusion in patients who present with chest pain temporally related to cocaine.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Does cocaine cause coronary vasospasm in chronic cocaine abusers? A study of coronary and systemic hemodynamics. 156 28

One hundred and eight consecutive patients admitted urgently for the first time with chest pain were interviewed to assess psychiatric symptoms prior to admission, at admission and three months later. Seventy-one patients had ischaemic heart disease, 19 had non-specific chest pain and 18 patients were excluded because of other organic causes for the pain. Compared to the ischaemic heart disease subjects, the non-specific chest pain patients tended to have more psychiatric disorder which increased over the three assessments; at follow up 33% of ischaemic heart disease patients and 59% of non-specific chest pain patients had psychiatric disorder. Chest pain was reported by 71% of the non-specific group at three months but this was not related to presence of psychiatric disorder. Unlike previous studies which 'have assessed out-patients with normal coronary angiograms', this study has shown that males predominate among patients admitted urgently with non-specific chest pain. In addition, these subjects use greater amounts of cigarettes and alcohol, and experience significantly more psychiatric disorder compared to patients admitted with ischaemic heart disease. The factors which lead to some of these patients developing chronic non-specific chest pain need to be investigated in further studies.
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PMID:The course of psychiatric disorder associated with non-specific chest pain. 159 8

Esophageal distention, motor abnormalities, or exposure of the esophageal mucosa to acidic gastric juice can cause chest pain indistinguishable from that of myocardial ischemia in patients with and without coronary artery disease. In these situations the exact cause of the symptom needs to be established prior to any surgical therapy. An antireflux procedure relieves chest pain in patients with increased esophageal acid exposure more reliably than medical therapy. The best results are obtained in patients in whom a direct correlation of the symptom with reflux episodes can be documented on 24-hour esophageal pH monitoring. Ambulatory 24-hour esophageal motility monitoring shows that esophageal motor disorders are a less frequent cause of noncardiac chest pain than suggested by standard manometry or provocation tests. Furthermore, chest pain episodes in patients with esophageal motor abnormalities are not associated with single contractions of excessively high amplitude or duration. Rather, the symptom appears to be triggered by an increased frequency of simultaneous, multipeaked, and repetitive motor activity. In appropriately selected patients with chest pain and dysphagia secondary to an esophageal motor abnormality, a long esophageal myotomy eliminates the ability of the esophagus to produce these contractions, reduces or eliminates dysphagia, and decreases the frequency and severity of chest pain episodes.
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PMID:Therapy of noncardiac chest pain: is there a role for surgery? 159 57


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