Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002962 (angina)
21,142 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The patient with unstable angina (angina of recent onset, of changing pattern or occurring at rest) is at high risk of myocardial infarction and sudden death. Patients with simple angina of recent onset can generally be managed out of hospital. Those with progressive angina or angina at rest should be admitted to a coronary care unit, kept at bed-rest, and given propranolol and long-acting nitrates when such therapy is indicated. With these approaches the rate of infarction within 1 to 3 months after the onset of unstable angina is about 12% (as compared with 40% before 1970); the mortality in the same period is less than 2% (as compared with 17% before 1970), though during the first year it is about 17%, much higher than in patients with stable angina and in survivors of acute myocardial infarction.Urgent aortocoronary bypass grafting has proven to be unnecessary and probably undesirable for most patients with unstable angina, and is now generally reserved for patients who continue to have angina in hospital while receiving full medical therapy. The ongoing management of patients whose angina is controlled during the acute phase remains controversial. The main options are to operate on every possible patient, to operate only on those with certain distributions of coronary artery lesions, and to operate only on those who have recurrent symptoms. Further studies are required to delineate the etiology and the Optimal management of unstable angina.
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PMID:Current management of unstable angina. 9 24

Thallium--201 myocardial perfusion scanning has been evaluated in Australia in patients with coronary artery disease. Myocardial scans reliably detect both acute myocardial infarction and the transient myocardial ischaemia of angina pectoris. The non-invasive nature, ease of study, and the ability to scan patients with conventional cameras makes thallium--201 an attractive additional diagnostic agent for patients with suspected coronary artery disease. Although thallium--201 reliably indicates perfusion defects in the myocardium, its diagnostic use at the moment should be reserved to clarify such diagnostic problems in patients with coronary artery disease which cannot be satisfactorily explained by conventional investigation.
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PMID:Myocardial perfusion scanning with thallium--201 for the non-invasive diagnosis of coronary artery disease. 73 45

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

Analysis of questionnaire responses of 70208 persons undergoing multiphasic health checkups showed a greater proportion of cigarette smokers than nonsmokers (excesses averaging 1.6-fold in white men, 1.3-fold in white women) admitting to nine types of chest pain. This excess in smokers was greater in younger individuals, and applied about equally to anginalike and nonanginalike pain. The smoking/chest pain association was not explained by greater alcohol or coffee consumption, diminished pain tolerance, or less reliability among smokers; nor did it appear to be mediated chiefly by excess cough, shortness of breath, coronary disease, or musculoskeletal complaints in smokers. Although smokers averaged more complaints than nonsmokers, chest pain resembled clearly smoking-related symptoms, such as cough, when the number of each subject's complaints was considered. Although more smokers had chest pain no type of pain was unique to smokers, suggesting that the "tobacco angina" concept be discarded or reserved for rare patients with coronary heart disease in whom smoking clearly provokes angina pectoris.
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PMID:Cigarette smoking and chest pain. 114 21

The preoperative assessment of the high risk patient undergoing noncardiac surgery has traditionally been based on history, physical examination, and preoperative testing. We propose a method of assessing preoperative risk based on the presentation of coronary artery disease, exercise tolerance, and extent of the surgical procedure. Since this is an evolving field, as new information and perioperative management techniques become available, the preoperative evaluation of the high risk patient will change. We have presented one approach based on our interpretation of data from the current anesthesiology and cardiology literature. In the patient with a recent MI, the predischarge symptom-limited stress test and the electrocardiographic classification can be used to better stratify risk. In the patient with angina, testing should be reserved for those patients who are candidates for coronary revascularization or alternative surgical procedures. In the patient at risk of but without overt symptoms of coronary artery disease, the number of clinical risk factors can determine the probability of coronary artery disease in the individual patient. The decision to perform preoperative revascularization should be based on its anticipated improvement of both the short- and long-term prognosis of the patient considering the risk of such procedures. The objective assessment of LVEF should be performed in patients with a poor exercise tolerance with either a high risk of perioperative ischemia or a suspicion of cardiomyopathy.
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PMID:Preoperative cardiac evaluation for noncardiac surgery: a functional approach. 155 27

In the context of peripheral vascular disease, the clinical history provides a means of evaluating coronary risk. The key features are: age, previous myocardial infarction especially when recent (under 6 months), anginal pain, smoking, diabetes and ventricular arrhythmias. Treadmill testing, often limited by symptoms of claudication, may reveal severe coronary ischemia and thereby the patients at very high risk. Upper limb exercise stress testing gives results similar to standard protocols of non-atherosclerotic patients when correctly performed and a reliable detection and evaluation of coronary lesions. Thallium dipyridamol myocardial scintigraphy is a very useful diagnostic method but requires special radionuclide facilities. This technique demonstrates the site of ischemia. Coronary angiography should be reserved for special cases because the risks of the procedure are always greater in patients with peripheral vascular disease.
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PMID:[Which coronary investigation should be performed in patients with peripheral arterial diseases?]. 176 87

The goals in the treatment of hypertension have been outlined previously. The antihypertensive drugs should achieve as many of these criteria as possible. 1. Efficacious as monotherapy in more than 50% of all patients (demographics) 2. 24-hour blood pressure control during all activities 3. Once per day dosing 4. Hemodynamically logical and effective: reduces SVR, improves arterial compliance, preserves CO and maintains perfusion to all vital organs 5. Lack of tolerance or pseudotolerance: no reflex volume retention or stimulations of neurohumoral mechanisms 6. Favorable biochemical and metabolic effects 7. Reverses the structural, vascular smooth muscle, cardiac hypertrophy, LVH, and improves systemic and diastolic compliance, LV contractility and function, and reduces ventricular ectopy if present 8. Reduces all end-organ damage: cardiac, cerebrovascular, renal, retinal and large artery 9. Maintains normal hemodynamic response to aerobic and anerobic exercise 10. Low incidence of side effects and good quality of life 11. Good compliance with drug regimen 12. Good profile in concomitant diseases or problems The drugs that come closest to these characteristics include CCB, ACEI, CAA, and alpha blockers. All of these agents are effective as monotherapy and should be given as initial therapy to the maximum dose shown in Table 10 or until the advent of side effects, whichever occurs first. Combination therapy should be the next step, using the principal of go low, go slow, using additive or synergistic drug combinations. Therapy should be individualized using the subsets of hypertension approach: Diuretics in particular, especially high-dose diuretics, and BB to a lesser extent, should be reserved as second- or third-line drugs and used for specific indications and in the lowest dose possible to achieve clinical results. For example, diuretics would be reserved for volume overload states, systolic CHF, and volume-resistant hypertension. Beta blockers would be reserved for patients after a Q-wave myocardial infarction, those with obstructive angina, specific cardiac arrhythmias, and other like conditions. Long-term, prospective, clinical trials will be needed to confirm that CCB, ACEI, CAA, and alpha blockers reduce end-organ damage more effectively than diuretics, BB, direct vasodilators, and older antihypertensive drugs. Until then, one must rely on scientific evidence, discussed here, that strongly suggests that reduction in risk factors for end-organ damage will reduce the end-organ damage in heart, brain, kidney, and large arteries.
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PMID:Hypertension strategies for therapeutic intervention and prevention of end-organ damage. 194 95

The definition, pathogenesis, incidence and characteristics, detection, treatment, and prognosis of silent myocardial ischemia (SMI) are reviewed. SMI is the occurrence of myocardial ischemia for which there is objective evidence (electrophysiological, hemodynamic, and metabolic changes) but no angina. Patients with SMI are classified as type 1 (completely asymptomatic), type 2 (SMI after myocardial infarction), and type 3 (both symptomatic and silent ischemia). Episodes of SMI are true ischemic events. The absence of pain may be due to defects in pain perception, an altered physiological response to ischemia, or a lesser degree of ischemia. The incidence of SMI is 2-5% in totally asymptomatic patients, 20-30% in patients who have suffered myocardial infarction, and 44-84% in patients who have symptomatic ischemia. SMI can be detected by exercise testing, portable electrocardiographic monitoring, or imaging techniques. Patients with SMI have more frequent adverse cardiac events (except death) than patients without SMI. The frequency of adverse cardiac events is similar in patients with angina and patients with SMI. SMI has been treated with nitrates, calcium-channel blockers, and beta blockers. Beta blockers appear to be the most consistent in reducing the number and duration of episodes. Combination therapy with beta blockers and nifedipine may be more effective than therapy with either agent alone. Because of the limited number of studies and the possible contribution to the results of spontaneous variability in the occurrence of SMI, no definite conclusions can be drawn about drug efficacy. There is no evidence that the prognosis of patients with SMI is altered by drug therapy; routine treatment with anti-ischemic drugs cannot be recommended. Patients must be evaluated individually, with aggressive management being reserved for those at high risk for myocardial infarction or other serious cardiac events.
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PMID:Current concepts of silent myocardial ischemia. 197 45

PTCA is a widely used technique in patients post-acute myocardial infarction (AMI) as well as in unstable angina (UA). The precise timing of its application and some aspects of the indication nowadays remains a matter of controversy. Primary PTCA is not generally considered to be the initial treatment of AMI. In contrast, immediate PTCA after thrombolysis has been proposed attempting to decrease the incidence of early reocclusion, improve myocardial salvage, decrease the incidence of postinfarction angina and improve survival. Nevertheless, three recent controlled studies (TAMI, TIMI II and ECSG) have demonstrated that an "aggressive" strategy with obligatory, invasive intervention following thrombolysis does not provide any advantage in terms of survival, rate of reocclusion or improved ventricular function and is, in fact, likely to be harmful. Emergent coronary arteriography after AMI should be reserved for unstable patients with continued or recurrent ischemia in the CCU. In elective basis it should be indicated in all patients with spontaneous or provocable ischemia prior to hospital discharge. If high grade coronary stenoses are identified, the patient should be considered for PTCA or surgical revascularization. In our own experience with coronary arteriography 24 hours to 15 days after intravenous thrombolysis with SK, PTCA is anatomically feasible in 44% of all the patients and in 60% of those showing a patent vessel. However, when indicated because of postinfarction angina or a positive stress test, PTCA was performed only in 22%, some of them presenting with a totally occluded vessel. In case of stenosis lesser than 100% the dilation success rate is slightly lower than that of out entire series (84% vs 88%), but the incidence of acute occlusion is significantly higher (10% vs 6%), particularly in patients with angiographic evidence of intracoronary thrombi. The incidence of "non-significant" (less than 70%) stenosis spontaneously increases when the coronary arteriography is performed late during hospitalization (34% vs 17% when the patient is studied in the first 24-48 hours).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Coronary angioplasty in acute coronary syndrome]. 220 92

During the last years, medical interest has focused on sleep related diseases, especially the sleep apnea syndrome (SAS) and the nocturnal breathing abnormalities associated with broncho-pulmonary diseases. It now appears that SAS is far more prevalent than previously believed. In this review article we present the clinical features, the investigations and the current therapeutic methods. We also discuss the recent developments in our understanding of the SAS pathophysiology and their implications in the disease's management. Clinical importance of sleep related disorders of breathing is appreciated when one looks at some of the secondary effects including hypertension, angina pectoris, cardiac insufficiency and worsening of a broncho-pulmonary disease (hypoxemia, hypercapnia); these are associated with a high degree of morbidity. The recent advent of ambulatory screening systems allows an easier evaluation of patients at risk, such as obese or hypertensive snorers and patients with hypersomnolence; then the diagnostic polysomnographic studies can be reserved for subjects in whom home recording is abnormal. A precise and early diagnosis is important to allow the initiation of treatment such as Continuous Positive Airway Pressure (CPAP) or naso-pharyngeal surgery.
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PMID:[The sleep apnea syndrome. A general review]. 265 45


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