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)

Forty-eight consecutive patients (37 men, 11 women, mean age 49 +/- 8 years) were followed up regularly for a mean period of 7 years. All presented with spontaneous angina, documented coronary spasm and no stenosis greater than 50 p. 100 at coronary arteriography. The first attack of pain had taken place 3 days to 9 years previously; exertion angina was also present in 47 p. 100 of the cases and severe arrhythmia in 17 p. 100. Treatment was based on calcium antagonists in doses and combinations that varied with the course of the disease. The follow-up period lasted from 16 to 122 months (mean 85 +/- 24 months). 3 patients are now known to be alive but were lost sight of after 12 to 21 months. Major cardiac complications were 1 death (2 p. 100) and 3 cases of myocardial infarction (6.6 p. 100). None of the patients died suddenly. 70 p. 100 of the remaining 41 patients became asymptomatic; angina persisted in 15 p. 100 and 14 p. 100 had episodes of severe angina but with remissions of at least one year. No predictive factor of functional deterioration or major cardiac complications could be elicited. The long-term prognosis of vasospastic angina in patients with little or no coronary stenosis is favourable, but there is a very small risk of myocardial infarction or death.
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PMID:[Long-term prognosis of spastic angina with normal or irregular coronary arteries. Apropos of 48 cases]. 250 60

We studied seven patients with Prinzmetal's angina and three patients with unstable angina pectoris type III (according to the criteria of Conti) during and after a spontaneous attack of angina pectoris by two-dimensional echocardiography. All patients underwent coronary angiography. The echocardiographic studies were performed during the attack (phase I), immediately after the attack (phase II), and 24 h after the attack (control). Left ventricular ejection fraction was significantly decreased during the attack (38.1 +/- 11% vs 59.8 +/- 7%), while left ventricular end-diastolic volume was increased (71.9 +/- 28 ml/m2 vs 50.3 +/- 13 ml/m2). The double product of heart rate and systolic blood pressure was equal at the 3 different examination times. In all patients transient regional disturbances of left ventricular contraction could be observed. In six patients the wall motion disturbances had already disappeared at phase II, while in four patients hypokinetic regions could still be found. At control, nine patients showed a normal left ventricular contraction pattern, while one patient with previous anterior myocardial infarction showed a small region of anterior akinesia. In all patients coronary artery obstructions were found in the same region of the left ventricle, where transient wall motion abnormalities occurred. Thus, two-dimensional echocardiography performed during an attack of angina pectoris in patients with Prinzmetal's angina and unstable angina pectoris type III can evaluate the localization, as well as the extent of transient myocardial wall motion abnormalities.
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PMID:[Echocardiography detection of reversible regional disorders of contraction in patients with unstable angina pectoris and Prinzmetal angina during an attack]. 250 59

Stress T1-201 myocardial SPECT was performed and evaluated quantitatively by Bull's eye method in 54 patients with single vessel coronary artery disease (33 angina pectoris, 21 myocardial infarction) who underwent successful PTCA. As the index of myocardial ischemia and viable muscle that was not affected by work load and others, relative washout rate (rW-R) was calculated from the formula: washout rate (W-R) of ischemic area was divided W-R of normal area. The purpose of this study was to examine the significance and usefulness of rW-R. Good correlation was recognized between grade of coronary artery stenosis, severity score (Sv-S) and rW-R in 28 patients with effort angina pectoris (EAP). Therefore, rW-R was regulated with coronary flow in EAP. On the other hand, in 5 patients with vasospastic angina (VSA), there was a tendency that rW-R showed low value compared with Sv-S. It was suggested that rW-R in patients with VSA was regulated not only coronary flow but also other factors. As a result of study before and after successful PTCA, rW-R foresaw the improvement of coronary perfusion and work load capacity by successful PTCA exactly. It was concluded that W-R reflected myocardial ischemia and myocardial viability accurately, and rW-R was a useful clinical index.
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PMID:[Assessment of relative washout rate (rW-R) in stress T1-201 myocardial SPECT]. 252 66

Experimental data in animals indicate that coronary vasoconstriction occurs following blockade of the beta-adrenergic receptors or alpha-receptors activation. The vasomotor effects of these maneuvers in man are unclear. Therefore we investigated whether and to which extent alpha-stimulation (cold pressor test: CPT) and beta-blockade (propranolol) cause coronary vasoconstriction; whether this effect involves the resistance arterioles as well as the large epicardial branches, and, within these, whether the normal and stenotic tracts are involved. Patterns in patients with effort angina were compared with those in patients with Prinzmetal angina. We studied 19 cases with classic and 15 cases with Prinzmetal angina. The systemic, pulmonary and coronary hemodynamics (pressure, flow and resistance) and the vasomotor pattern of normal and stenotic epicardial branches (quantitative angiography) were evaluated in the baseline condition, during CPT, after propranolol (5 mg iv) and during CPT repeated after propranolol. We observed that: changes of the coronary flow due to beta-blockade and to CPT are related to the variations of the myocardial oxygen consumption, induced by the inhibition and activation of adrenergic receptors and not to the concomitant vasomotor reaction of the stenotic vascular tract; beta-blockade does not affect homogeneously the lumen of the stenotic lesions in effort angina and invariably increases the lumen in the Prinzmetal form; influences of CPT, in the absence as well as in the presence of beta-receptor blockade, on the lumen diameter of both normal vessels and stenotic lesions are minimal in either form of angina.
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PMID:[Activation and inhibition of adrenergic effects on the coronary vessels of patients with different forms of angina pectoris]. 255

Calcium antagonists are among the most potent and efficacious drugs used in the treatment of angina pectoris. Amlodipine, a new member of this family of dihydropyridines, has a unique pharmacokinetic profile with high bioavailability and an extended period of pharmacodynamic activity. In formal randomized, double-blind, placebo-controlled trials with exercise tests carried out 24 hours after administration, amlodipine was significantly more effective than the placebo and comparable in efficacy with the calcium antagonist diltiazem and the beta-blocking drug nadolol. In addition to extending exercise capacity in patients with angina pectoris, amlodipine significantly reduces ECG evidence of myocardial ischemia. Amlodipine has also been found to be effective in reducing the anginal attack rate in patients with vasospastic angina. From the evidence available, it is concluded that once-daily treatment with amlodipine in the dose range of 5 to 10 mg is effective in improving exercise capacity and reducing anginal attack rate in patients with chronic stable angina pectoris and also those with vasospastic angina.
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PMID:The efficacy of amlodipine in myocardial ischemia. 257 66

Calcium antagonists block the entry of calcium into vascular smooth muscle cells, producing pharmacological vasodilation. Thus, it is not surprising that these drugs are effective in treating unstable angina that is often characterized by increased vasomotion and dynamic obstruction at the site of atheromatous plaques. Nifedipine, diltiazem, and verapamil are all highly and equally effective in reducing painful and painless ischemic episodes in Prinzmetal's variant angina. In patients with unstable angina who have known or suspected significant underlying coronary artery disease, a multipharmacological approach to therapy is warranted. Nifedipine used with beta-blocker drugs is more effective than nifedipine as monotherapy. Diltiazem and verapamil have been shown to be effective when given without beta-blockers in unstable angina patients. In many patients, thrombus formation rather than vasospasm is the major pathophysiological event resulting in progression of the syndrome to infarction or sudden death. In these patients, antiplatelet, antithrombotic, or antiplatelet and antithrombotic therapy is of utmost importance to maintain adequate coronary flow. Nonresponders to medical therapy with unstable angina have a high prevalence of eccentric and multiple coronary stenoses with a high incidence of thrombi. The best responders to calcium antagonist therapy are patients with concentric coronary stenoses. In summary, calcium antagonists are highly effective in reducing ischemic episodes in patients with Prinzmetal's angina and effective for therapy for unstable angina when used in conjunction with other forms of medical treatment aimed at the processes of platelet activation and thrombus formation.
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PMID:Calcium antagonists in the treatment of Prinzmetal's angina and unstable angina pectoris. 257 42

A case is reported of the variant form of Prinzmetal angina, occurring two months after effort angina, in which the electrocardiogram revealed a Q wave in V2 in addition to ST segment elevation in precordial leads all of which disappeared in a few minutes. Several hours later, the ECG changes were suggestive of antero-septal infarction. However, four days later an R wave was present in lead V2, and 12 days after the acute episode, the tracing became entirely normal. Cinecoronary angiography revealed severe obstruction of the anterior descending artery, and a moderate obstruction of the left circumflex artery. The possibilities of spasm and/or coronary thrombosis, of spontaneous recanalization and of reperfusion due to thrombolysis are discussed, in addition to interpreting the abnormal Q waves as presumably due to severe myocardial ischemia resulting from acute coronary insufficiency. The present case exemplifies the concept that the syndromes of acute coronary heart disease cannot always be precisely differentiated, since they often overlap and are difficult to identify.
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PMID:[Unstable angina, Prinzmetal's variant and transient Q waves. Report of a case]. 259 1

Impedance to flow due to coronary spasm is currently interpreted as the mechanism of Prinzmetal angina. Flow impedance, probably of vasomotor origin, superimposed on severe coronary stenosis is also viewed as the trigger for the spontaneous component of mixed angina. The major question that we attempted to answer in this study was whether mixed angina may be considered a variant of the Prinzmetal form, or a particular manifestation of the classic effort form. For these purposes we investigated the acute vasomotor response to calcium channel blockade (nifedipine 10 mg sl) of both significant (greater than 50%) stenotic lesions and of normal coronary vessels in 22 patients with mixed angina and in 14 patients with Prinzmetal angina, and correlated it with the clinical response to treatment (nifedipine 20 mg qid). Calcium channel blockade, in fact, is considered as a specific remedy in the presence of an altered coronary vasomotility. The clinical response was evaluated through ambulatory Holter monitorings of 48 hour duration, while on placebo, nifedipine and placebo again. In mixed angina an angiographic evaluation showed that the residual lumen diameter of significant lesions was unchanged in 2, enhanced in 11 and reduced in 9 patients after sl nifedipine; lumen variations from base line ranged from +1.5 to -1.3 mm. Acute stenosis widening or narrowing correlated closely with the efficacy or not of the treatment. In the Prinzmetal group the vast majority of the lesions had compliant portions which invariably responded with dilatation (the residual coronary lumen increased by an average of 69% of base line); 100% of patients in this group responded favourably to treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Various clinical and vasomotor coronary responses to calcium block in mixed angina and Prinzmetal's angina, expression of various physiopathologic mechanisms]. 263 84

To examine whether intracoronary injections of acetylcholine induce coronary artery spasm in patients with vasospastic angina, incremental doses (20, 30 and 50 micrograms) were injected directly into the coronary arteries in 12 patients with variant angina (Group A: rest angina with electrocardiographic ST-segment elevation during attacks), 19 with vasospastic angina (Group B: rest angina and/or effort angina with variable threshold in the treadmill exercise stress test), 11 with organic coronary artery stenosis but without angina (Group C), and 14 without coronary artery disease (Group D). A temporary cardiac pacemaker was positioned in the right ventricle. Coronary artery spasm was defined as severe vasoconstriction (greater than or equal to 90% of reduction in the luminal diameter) with chest pain and/or ischemic changes in the electrocardiogram. Intracoronary injection of acetylcholine induced spasm of at least one coronary artery in all 12 patients (100%) of Group A, in 18 (95%) of Group B, in two (18%) of Group C, and in two (14%) of Group D. Thus, the sensitivity of this method for inducing coronary spasm was 100% in group A, 95% in Group B, and 97% in Group A plus Group B. The specificity for inducing spasm was 86% in Group D, and 84% in Group C and Group D. When acetylcholine was injected separately into the left and right coronary arteries, spasm of both the coronary arteries was observed in two (40%) of Group A, in five (33%) of Group B, and none (0%) of Group C and Group D. Acetylcholine (20 micrograms) induced coronary spasm in 10 (83%) of Group A and only in nine (47%) of Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Induction of coronary arterial spasm by intracoronary administration of acetylcholine in patients with vasospastic angina]. 264 69

During ergonovine-induced vasospastic angina, U wave inversion without significant ST segment deviation on the precordial electrocardiograms was documented in four patients. Coronary angiography revealed incomplete spastic obstruction of the left anterior descending artery without delayed filling and runoff in three patients. In the remaining patient, the proximal left anterior descending artery was totally occluded and there were well-developed collaterals from the non-spastic artery. Thus, ergonovine-induced U wave inversion was related to the presence of coronary vasospasm, and angiography demonstrated less severe myocardial ischemia in such patients than in cases with ST segment elevation or depression, which is usually associated with subtotal or total obstruction of a major coronary artery without adequate collaterals. In their clinical courses, two patients had episodes of angina with ST segment elevations or depressions. It was suggested that vasospastic angina with U wave inversion alone is one aspect of a continuous spectrum of vasospastic myocardial ischemia.
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PMID:[Coronary angiography in patients with U wave inversion during coronary artery spasm]. 264 70


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