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)

Numerous disorders can mimic chronic coronary disease either clinically or electrocardiographically. Particularly noteworthy are Wolff-Parkinson-White syndrome, asymmetric septal hypertrophy, floppy mitral valve syndrome, angina pectoris with normal coronary arteries, hyperventilation syndrome, neurogenic T wave abnormalities, vasoregulatory abnormality, cervicoprecordial angina, hyperkalemia or hypokalemia, left ventricular hypertrophy, and left anterior fascicular block.
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PMID:Mimics of coronary heart disease. 14 66

Technetium-99m stannous pyrophosphate (99mTc-PYP) myocardial imaging was performed in 436 consecutive patients for the evaluation of chest pain and suspected acute myocardial infarction (AMI). Scintigrams were assessed independently by three observers with a 90% interobserver agreement. In 134 patients with documented AMI (97 TRANSMURAL, 37 NONTRANSMURAL), THE SENSITIVITY OF 99MTc-PYP imaging was significantly lower in patients with nontransmural AMI (41%) than in patients with transmural AMI (78%), 99mTc-PYP imaging correctly localized the site of transmural infarction in 53 patients (70%). A diffuse 99mTc-PYP uptake was found in nine (10%) of 91 patients with positive scintigrams: six of these had a transmural AMI and three nontransmural AMI. In 226 patients without AMI, the specificity of infarct imaging was 95%. A false-positive scintigram was found in 0%, 8%, 9%, and 2% of patients with unstable angina, progressive angina, stable angina, and noncardiac chest pain, respectively. A diffuse uptake was found in six (54%) of 11 patients with false-positive scintigrams. No patient with the clinical diagnosis of noncardiac chest pain showed discrete uptake. In 76 patients with uncertain diagnosis for AMI, 99Tc-PYP imaging was considered of value in 11 patients with ventricular conduction defects (two patients with WPW syndrome, nine patients with LBBB). These data suggest that: 1. 99mTc-PYP imaging is moderately sensitive in detecting and localizing transmural AMI and is insensitive in detecting nontransmural AMI; 2. A discrete 99mTc-PYP uptake is highly specific for AMI; 3. a diffuse uptake is neither sensitive to, nor specific for AMI. Myocardial imaging with 99m-Tc-PYP is of clinical value when the standard electrocardiographic and enzymatic techniques are inadequate for an accurate diagnosis of AMI.
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PMID:Value and limitations of technetium-99m stannous pyrophosphate in the detection of acute myocardial infarction. 49 27

A 7-year-old black boy with sickle cell disease, Wolff-Parkinson-White syndrome, mild left ventricular dysfunction, and normal coronary arteries developed angina pectoris five months after cessation of hypertransfusion therapy. Exercise-induced ECG ST segment depression associated with angina disappeared following transfusion therapy.
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PMID:Angina pectoris in a child with sickle cell anemia. 67 56

Verapamil is a new anti-anginal and anti-arrhythmic drug whose pharmacological actions can be related to its specific blocking effect on the transmembrane transport of calcium ions. Intravenous verapamil slows the ventricular rate in atrial fibrillation and flutter with an occasional patient reverting to sinus rhythm. The drug promptly terminates most cases of paroxysmal supraventricular tachycardias. It is likely to become the initial agent of choice in the acute treatment of this arrhythmia. Verapamil is not effective in ventricular tachycardia or in atrial fibrillation complicating the WPW syndrome. Few side effects are encountered following intravenous verapamil expecially when the drug is given slowly. Verapamil is also effective in angina in a dose of 120mg tds orally. Little is known of the metabolism and pharmacokinetic of verapamil but the available experience in arrhythmias clearly justifies further study.
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PMID:Verapamil and the heart: Pharmacological and Therapeutic Considerations. 106 88

Without treatment, about 60% of atrial arrhythmia patients suffer a relapse within 3 months and 70% within one year. Antiarrhythmic treatment intended to reduce this percentage is therefore justified, on condition that it is well tolerated. Several preliminary questions have to be settled before this medical prophylaxis: 1) Justification of antiarrhythmic treatment (sometimes pointless to deal with very occasional episodes); 2) Treatment of the underlying heart disease (valve disease, cardiothyrotoxicosis, etc.) or promoting factors (potassium depletion etc.); 3) Accurate assessment of any associated conduction abnormalities, which may constitute a contraindication to antiarrhythmic treatment (WPW syndrome in the case of verapamil and the digitalis-like drugs) or require additional treatment (pacemaker); 4) Definition of the mechanism (vagal or sympathotonic) inducing arrhythmia; 5) Evaluation of the hemodynamic parameters of the underlying heart disease (size of the atria, ventricular function, coronary or valvular lesions) which may limit the efficacy of the treatment. Once these parameters have been identified, the primary treatment should be type la or lb antiarrhythmics, which have been shown to be effective, despite the fact that they are not without arrhythmic risks (the Ib antiarrhythmics are less effective and have a poor safety profile). The beta-blockers have preferential indications (hypersympatheticotonia, hyperthyroidism, hypertrophic myocardiopathy, mitral prolapse, angina etc.) and can be replaced by verapamil or bepridil if there are non-cardiac contraindications (ulcers, asthma, diabetes). Amiodarone is extremely effective, but its poor extracardiac safety restricts its long-term use. Complementary treatments (digitalis-like, anticoagulants or anti-PAF and cardiostimulant drugs) should be added if necessary. Recurrences (to be confirmed by ECG or Holter) should lead to rigorous confirmation of therapeutic compliance and observance of simple hygienic and dietary measures (no excessive exertion, elimination of stimulants etc.). With strict clinical and ECG monitoring, it would then be possible either to increase the dose levels (accompanied by plasma determinations if possible) or to switch to a treatment with more effective, but more aggressive drugs (amiodarone, flecainide) or to use drug associations (la and lb, la and II etc.). Repeated failure of such attempts should lead to a non-medical approach to treatment.
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PMID:[Preventive drug therapy of recurrence of atrial fibrillation]. 129 92

During the past 28 months, 16 cases of WPW syndrome were operated on at Hiroshima University Hospital. Two cases were complicated by other cardiac disorders which accelerated tachycardia, making diagnosis difficult. One of these cases showed serious mitral regurgitation, due to infective endocarditis and the patient suffered cardiac failure accompanied by paroxysmal tachycardia not responsive to medical therapy or cardioversion. A complex rhythm with atrial fibrillation and antegrade conduction rhythm through the accessory pathway made diagnosis and therapy quite difficult. The condition of the other patient was associated with myocardial bridging which caused angina pectoris during paroxysmal tachycardia. Myocardial scintigraphy showed myocardial ischemia in the antero-lateral area of the left ventricle. In the former case, mitral valve replacement and interruption of the accessory pathway were undergone simultaneously. In the latter case, myotomy of the muscle on segment 7 was conducted, following interruption of the accessory pathway.
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PMID:WPW syndrome complicated by another cardiac disorder. 186 67

Myocardial bridging causes myocardial ischemia during supraventricular tachycardia. We present a case of Wolff-Parkinson-White syndrome combined with myocardial bridging. The patient complained of angina pectoris during paroxysmal supraventricular tachycardia because of severe constriction of the left anterior descending coronary artery during systole. A myocardial scintigram revealed myocardial ischemia in the anteroseptal wall during paroxysmal supraventricular tachycardia. Myotomy to prevent myocardial bridging and interruption of the accessory conduction pathway was successfully accomplished in a one-stage operation.
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PMID:Surgical repair of Wolff-Parkinson-White syndrome complicated with myocardial bridging. 198 50

In a patient with Wolff-Parkinson-White syndrome and an inferior-posterior bypass tract, transient restoration of normal conduction occurred during an attack of angina. The ECG pattern of inferior posterior ischemia was present when the conduction was normal. Thallium scintigraphy showed a reversible posterolateral perfusion defect. The possible mechanisms for production of intermittent preexcitation are discussed.
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PMID:Alternating Wolff-Parkinson-White syndrome associated with attack of angina. 238 30

Prevention of sudden arrhythmic cardiac death must be preceded by identification of the high-risk patient to whom appropriate therapy can be given. The most common disease state associated with sudden cardiac death is coronary artery disease. Factors which identify a high-risk subset include: left ventricular dysfunction; frequent and complex arrhythmias on Holter monitoring; abnormal signal-averaged electrocardiograms; angina, ST depression, and exertional hypotension or ventricular arrthythmias on exercise testing; inducible sustained arrhythmias at electrophysiologic testing, or a combination of these factors. Other conditions which are known to be associated with sudden death include: dilated or congestive cardiomyopathy, hypertrophic cardiomyopathy, mitral valve prolapse, valvular heart disease, Wolff-Parkinson-White syndrome, myocarditis, congenital heart disease, electrolyte abnormalities, long QT syndromes, proarrhythmic effects of drugs, and less common conditions such as myocardial tumors and pulmonary hypertension. If the primary abnormality responsible for the tendency toward arrhythmias cannot be corrected, appropriate therapy should be administered to attempt to reduce the patient's risk of sudden arrhythmic cardiac death.
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PMID:Definition of patients at high risk of sudden arrhythmic cardiac death. 327 Nov 94

A patient with Wolff-Parkinson-White syndrome and variant angina developed progressive ST-segment elevation in the inferior leads after hyperventilation-induced right coronary artery spasm. At the same time, increasing pre-excitation ("concertina effect") developed with gradual prolongation of the AH interval on His bundle ECG. The ECG changes promptly disappeared after sublingual nitroglycerin, with termination of the chest pain. Transient ischemia induced by coronary artery spasm can be an etiology of increasing pre-excitation.
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PMID:Increasing pre-excitation ("concertina effect") during vasospastic angina. 374 56


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