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)

Nifedipine is a non-nitrate vasodilator which has proved effective, in oral form, in Europe, Japan, and the USA for treatment of Prinzmetal Angina. The drug has not been used before in Australia. We report a patient with Prinzmetal's variant angina, complicated by recurrent syncopal episodes due to ventricular arrhythmias. The attacks were resistant to standard therapy except sublingual nitroglycerin but ceased completely during treatment with nifedipine.
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PMID:Nifedipine in the treatment of life threatening Prinzmetal angina. 28 97

A case of Prinzmetal variant angina with transient complete atrioventricular block and syncopal episodes following an anteroseptal myocardial infarction is described. The syncopal attacks were not prevented by demand cardiac pacing and were presumably caused by transient severe ischaemia of the left ventricle, with a consequent reduction in cardiac output. The left ventriculogram showed a large anterior dyskinetic area corresponding to the high grade proximal obstruction in the left anterior descending artery demonstrated by coronary angiography. All other coronary vessels appeared free of disease and it is suggested that the anginal episodes were caused by transient proximal segmental spasm of the right coronary artery. The anginal episodes were successfully prevented by a regimen of two-hourly coronary arterial vasodilator therapy.
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PMID:Syncope in association with Prinzmetal variant angina. 115 86

We investigated the clinical and pathophysiologic characteristics in patients with vasospastic angina who developed syncope and/or experienced aborted sudden death (SD). Vasospastic angina was diagnosed using the methylergonovine test. Syncope was found in 32 (10.4%) patients among 309 who were admitted to our institute in a one-year period. The most frequent cause of syncope was ventricular tachycardia which was found in 10 (31.2%) of the 32 patients. The next important cause of syncope was vasospastic angina which was found in 7 patients (21.8%). Among the 7 patients with vasospastic angina who experienced one or more syncopal episodes, there were 3 patients with aborted SD, 3 with syncope and one with shock. Cardiovascular collapse was observed in 4. Interior wall ischemia was found in 5 and anterior wall ischemia in 2 during the methylergonovine test. None of the 7 patients had significant coronary stenosis. Two patients had no prodromal symptom such as chest pain. Our results suggest that coronary artery spasm may be one of the most frequent cardiovascular diseases that causes syncope which is not always accompanied by a prodromal symptom. Therefore, coronary spasm should be distinguished in patients with unexplained syncope or aborted SD.
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PMID:Clinical characteristics and possible role of coronary artery spasm in syncope and/or aborted sudden death. 207 44

This study analyses the long-term prognosis of 210 patients with coronary spasm documented at coronary angiography. All patients with a previous history of myocardial infarction or who had undergone coronary angioplasty were excluded. The average follow-up was 55 months and only 11 patients were lost to follow-up. The actuarial survival figures showed the 1 year, 2 year and 5 year survival rates to be 95, 92 and 89 per cent respectively. Extracardiac mortality was mainly related to smoking (lung cancer, laryngeal cancer, etc.) and was higher than cardiac mortality. More than half of the cardiovascular events (sudden death, myocardial infarcts) occurred during the first year of follow-up. Ten patients (4.7%) died suddenly. The predictive factors of this event were: previous syncopal episodes or syncopal angina due to coronary spasm, percritical arrhythmias and the documentation of multiple spasms at coronary angiography. Myocardial infarction was observed in 10.6 per cent of patients. Only those with significant coronary arterial lesions developed this complication. At the end of the follow-up period, 75 per cent of patients were asymptomatic or had only atypical chest pain. No significant differences were observed between the two groups treated medically, by aortocoronary bypass or by the association of coronary bypass and plexectomy with the exception of non-lethal myocardial infarcts being significantly less common in patients treated medically. Therefore, the long-term prognosis of patients with coronary spams is relatively satisfactory.
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PMID:[Long-term prognosis of coronary artery spasm]. 211 66

Management of patients with chest pain and hypothyroidism is a clinical dilemma. Thyroid replacement therapy may exacerbate angina pectoris. Administration of a beta blocker such as propranolol (Inderal) concomitantly with thyroid replacement therapy is useful in treatment of angina. However, beta blockers can induce variant angina owing to increased norepinephrine secretion and enhanced alpha-mediated responsiveness in the hypothyroid state. Hypotension and syncopal episodes may develop in the hypothyroid patient after administration of nitrates. Cardiac catheterization and revascularization are well tolerated by myxedematous patients with angina. After surgery, full thyroid replacement therapy should be initiated gradually and with caution.
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PMID:Hypothyroidism with angina pectoris. A clinical dilemma. 308 77

Aortic valvular dilatation with a balloon catheter was performed in 44 patients, 20 men and 24 women, most of whom were very elderly (average age 77 years). The indication for valvular replacement had not been retained in these cases because of surgical contra-indications or a very high operative risk and in 3 cases because of patient refusal. Twenty-nine patients were in functional classes III or IV of the NYHA classification; 12 had syncopal episodes and 18 had invalidating angina. The dilatation was performed by a femoral arterial approach in 34 cases, and by a brachial arterial approach in 10 cases. MEDI-TECH catheters with 15, 18 or 20 mm diameters when inflated were used in the majority of cases. Several inflations lasting 10 to 240 seconds were performed in each case with balloons of increasing size. This was well tolerated in all but one patients who had a sharp syncope. The immediate results confirmed valvular dilatation. The average transvalvular pressure gradient fell from 76 +/- 25 mmHg to 30 +/- 13 mmHg (p less than 0.001). The aortic valve surface area calculated by the Gorlin formula increased from 0.5 +/- 0.18 cm2 to 1 +/- 0.42 cm2 (p less than 0.01). After dilatation the gradient was less than or equal to 40 mmHg in 37 cases; aortic valve surface area was greater than or equal to 1 cm2 in 14 cases and less than or equal to 0.7 cm2 in only 5 cases. The left ventricular ejection fraction increased immediately after valvuloplasty from 44 +/- 16 p. 100 to 49 +/- 15 p. 100 (p less than 0.01). In the 18 cases in which it was less than 40 p. 100 before valvuloplasty, it increased from 30 +/- 6 p. 100 to 36 +/- 9 p. 100 (p less than 0.02). Residual aortic regurgitation was only observed in one case. Two patients died in the hospital period (4.6 p. 100). There were no other serious complications. During an average follow-up period of 60 days (3 weeks to 6 months) there was a big improvement in symptoms in the great majority of cases and, in particular, syncopal and anginal attacks disappeared. Only 4 patients remained in functional classes III or IV after valvuloplasty. Percutaneous aortic valvuloplasty is a new, relatively simple, low risk, economic and very effective therapeutic procedure in all cases in which aortic valve replacement is contra-indicated or refused by the patient.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Percutaneous transluminal aortic valvuloplasty using a balloon catheter. A new therapeutic option in aortic stenosis in the elderly]. 310 79

Thirty-seven patients with coronary artery spasm and minor coronary atherosclerosis (34) or normal coronary arteries (3) were followed up long-term. All had angina at rest, 32 had nocturnal angina, and 13 had a positive exercise test with S-T elevation. Three had a previous subendocardial infarction; 10 had had serious arrhythmias, which caused syncope in 7. At last review, 21 months (range 1 to 61) after starting therapy, 27 patients continued on verapamil, 314 (120 to 600) mg/day; 4 who did not respond to verapamil were taking nifedipine, 58 (30 to 80) mg/day; and 16 were also taking isosorbide dinitrate, 41 (20 to 80) mg/day. Of the 31 patients on therapy, 21 were asymptomatic, 9 were improved (1 to 4 attacks/month), and 1 had an average of 8 anginal attacks/month; the remaining 6 had stopped therapy and 5 were asymptomatic a mean of 10 (3 to 18) months after stopping. The exercise test became negative in all 12 patients tested on therapy, although 3 required nitrates in addition to verapamil or nifedipine. In 26 supervised treatment withdrawals in the hospital, a mean of 15 (1 to 55) months on therapy, 10 developed angina in less than 48 hours. Angina recurred in all 6 unsupervised, patient-initiated withdrawals. Failure to stop smoking was positively associated with recurrence of angina on treatment withdrawal (p less than 0.02). Long-term treatment of coronary artery spasm with verapamil or nifedipine together with isosorbide dinitrate was well tolerated and effectively relieved angina. No documented serious arrhythmias, syncopal episodes, myocardial infarction, or death occurred during follow-up.
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PMID:Long-term follow-up of verapamil and nitrate treatment for coronary artery spasm. 681 5

We describe the case of a 44-year-old man, with a history of recurrent syncopal episodes and effort angina, the latter attributed to cardiac syndrome-X, who was admitted to our department because of a syncopal episode. During his hospitalization laboratory investigations including haematologic and blood chemical findings, head C/T scan, electroencephalogram, 48-hour Holter monitoring, electrophysiologic testing and echocardiographic study disclosed no abnormalities. On the contrary, a passive upright tilt testing was found to be positive, resulting, approximately, in a 10-seconds time interval of asystole accompanied by syncope. The association in the same patient of cardiac syndrome-X and neurocardiogenic syncope, although never described before, might be explained by a similar pathophysiological mechanism, which is a sympathovagal imbalance.
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PMID:Recurrent syncopal episodes of neurocardiogenic origin in a patient suffering from cardiac syndrome-X. 1037 20

Bernardo O'Higgins was a very apprehensive individual regarding his health and ailments. This fact is clearly reflected in his letters, that provide valuable anamnestic data. During his youth, while living is Spain, he suffered of yellow fever and later in Chile, he probably had an acute phase of a rheumatic fever. Since his adolescence, he was affected by a chronic hlepharo-conjunctivitis. During the Chilean independence revolution, he suffered several battle wounds. The most severe was a shot that affected both his right arm and elbow (1818). While living in Peru (1823-1842) he suffered of dysentery and malaria. The latter was an endemic disease in the valleys of Peru. Being previously asymptomatic, he started experiencing extensional dyspnea, angor pectoris and syncopal episodes in 1840. At that time, physicians diagnosed a hypertrophic cardiomyopathy. Analyzing his symptoms and taking into account their short term evolution, the author concludes that they were a consequence of either an aortic stenosis or coronary insufficiency. These led him to a heart failure that was his immediate cause of death in 1842.
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PMID:[A medical history of Bernardo O'Higgins (1778-1842)]. 1066 97

Brugada Syndrome and Vasospastic Angina. We present two patients with vasospastic angina and Brugada-type ECG abnormalities. The first patient complained of chest pain, and transient ST segment elevation was confirmed on ECG. Coronary angiogram showed no organic stenosis. The second patient had syncopal episodes following anginal chest pain, and the same symptoms were reproduced by intracoronary acetylcholine injection that induced vasospasm. In both patients, ECG at rest showed ST segment elevation in leads V1 and V2 and a right bundle branch block pattern that were accentuated by a Class I antiarrhythmic drug. Ventricular fibrillation also was induced by programmed electrical stimulation. Susceptibility to ventricular fibrillation can be modulated by the interaction of coronary vasospasm with Brugada syndrome or vice versa; therefore, it is important to study the clinical implications of the coexistence of the two diseases in such patients.
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PMID:Vasospastic angina accompanied by Brugada-type electrocardiographic abnormalities. 1120 72


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