[Variant (Prinzmetal) angina pectoris].
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Angina Pectoris, Variant↗
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[Prinzmetal variant of angina pectoris on coronarographic picture (author's transl)].
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Adult↗
[Prinzmetal's angina as a variant of the preinfarct state].
The clinical course of variant angina pectoris has been analyzed in 11 patients, in 5 of them acute myocardial infarction supervened while in hospital. The character of painful attacks, ECG changes in some patients fully resemble the clinical picture of unstable angina pectoris. The direct relationship has been established between the variant angina pectoris and the development of myocardial infarction which suggests that this state is an urgent one. Certain aspects of pathogenesis of variant angina pectoris and its treatment are discussed.
Aged↗
A comparative study of eccentric and concentric coronary stenosis vasomotion in patients with Prinzmental's variant angina and patients with stable angina pectoris.
BACKGROUND AND HYPOTHESIS: In patients with stable angina pectoris, eccentric stenoses have a greater potential for dynamic changes of caliber in response to vasoactive stimuli than concentric lesions. It is not known whether in patients with coronary artery spasm the degree of coronary vasoconstriction differs in eccentric versus concentric stenoses. Therefore, we examined the relationship between coronary stenosis morphology and the vasomotor response to vasoactive stimuli in patients with variant angina. METHODS: Computerized quantitative angiography was used to measure minimum luminal diameter of eccentric and concentric stenoses before and after the administration of ergonovine and isosorbide dinitrate in 22 patients with Prinzmetal's variant angina and in 20 patients with chronic stable angina. RESULTS: In patients with variant angina, mean stenosis diameter reduction with ergonovine was -0.85 +/- 0.38 and -1.12 +/- 0.69 mm in eccentric and concentric stenoses, respectively (p = NS). Isosorbide dinitrate promptly relieved spasm in all patients and increased the diameter of eccentric stenoses by 0.26 +/- 0.34 mm and that of concentric stenoses by 0.24 +/- 0.32 mm (p = NS). In patients with chronic stable angina, mean diameter reduction with ergonovine was -0.23 +/- 0.12 and -0.12 +/- 0.10 mm for eccentric and concentric stenoses, respectively (p < 0.05). Isosorbide dinitrate increased coronary diameter by 10% from baseline in 70% of eccentric and 38% of concentric stenoses (p < 0.01). CONCLUSION: In patients with variant angina pectoris, eccentric and concentric spastic stenoses react similarly in response to vasoactive stimuli. In patients with chronic stable angina, eccentric stenoses are more likely to show vasomotor responses than concentric stenoses.
Adult↗
Altered platelet alpha 2-adrenoceptors in patients with ischemic heart disease.
We evaluated the characteristics of platelet alpha 2-adrenoceptors in 12 patients with effort angina pectoris, 11 patients with variant angina pectoris and 11 normal control subjects. alpha 2-Adrenoceptors were quantified using a radioligand binding assay with radiolabelled rauwolscine, an alpha 2-selective antagonist. In addition, plasma norepinephrine concentrations were measured by high performance liquid chromatography. The mean value of the maximal number of binding sites (Bmax) in patients with effort angina (205.1 +/- 11.3 fmol/mg protein) was significantly lower than that in control subjects (293.0 +/- 10.2 fmol/mg protein). Bmax did not differ between patients with variant angina (322.9 +/- 45.4 fmol/mg protein) and control subjects. There was no significant difference in the dissociation constant (Kd) among the 3 groups. The plasma norepinephrine concentration tended to be higher in patients with effort angina or variant angina than in normal controls, but this difference was not statistically significant. In addition, studies in another group of young volunteers (n = 20) revealed a negative correlation (r = -0.50, p < 0.05) between the Bmax of 3H-rauwolscine binding to platelets and the percent change in the plasma norepinephrine concentration when subjects moved from the supine to the standing position. This suggests a functional correlation between platelet alpha 2-adrenoceptors and those located at presynaptic sites. If platelet alpha 2-adrenoceptors correlate with presynaptic alpha 2-adrenoceptors, the current findings of decreased alpha 2-adrenoceptor density in platelets from patients with effort angina could represent attenuated negative feedback of norepinephrine by presynaptic alpha 2-adrenoceptors.
Adult↗
Prinzmetal's variant angina.
Although the prevalence of variant angina pectoris is unknown, it appears to be substantially less common than typical, exertional angina and unstable angina at rest. The patient with variant angina typically complains of a pressure-like, squeezing retrosternal chest discomfort of several minutes duration. The diagnosis is secured by the occurrence of transient ST-segment elevation in association with chest pain, both of which resolve spontaneously or with nitroglycerin. After the diagnosis is made, the patient usually becomes symptom-free on calcium-channel blockers with or without long-acting nitrates. Although the long-term survival of these patients is excellent, an occasional individual with variant angina sustains a complication, most often myocardial infarction, a life-threatening arrhythmia, or sudden cardiac death.
Angina Pectoris, Variant↗
Two cases of variant form angina pectoris associated with myocardial bridge--a possible relationship among coronary vasospasm, atherosclerosis and myocardial bridge.
Myocardial bridge (MB) is a congenital anomaly of the coronary artery and may occur in 5 to 12% of the human population. However, the mechanism of MB-induced myocardial ischemia is still speculative. We report 2 cases of variant form angina pectoris associated with MB in which myocardial ischemia seemed to be related to the interaction between coronary perfusion and MB. In case 1, electrocardiography during anginal attack at rest showed ST elevation in the inferior leads and MB was observed after percutaneous transluminal coronary angioplasty at the site of the right coronary artery lesion following successful dilatation. In case 2, MB of the left anterior descending coronary was located in the identical portion where coronary vasospasm was induced by intracoronary acetylcholine injection, although ischemia during the spontaneous anginal attack was limited to the inferior area of myocardium. These 2 cases suggest that MB can be, at least in some patients, one of the possible causes of the endothelial damage which seems to be related to coronary vasospasm; this was documented in both cases.
Angina Pectoris, Variant↗
Phase changes caused by hyperventilation stress in spastic angina pectoris analyzed by first-pass radionuclide ventriculography.
To understand the effect of hyperventilation (HV) stress in patients with spastic angina, left ventricular (LV) contraction was analyzed by quantitative phase analysis. The study was performed on 36 patients with spastic angina pectoris, including vasospastic angina pectoris (VspAP: 16 patients) and variant angina pectoris (VAP: 20 patients). First-pass radionuclide ventriculography (first-pass RNV) was performed at rest and after HV stress, and standard deviation of the LV phase distribution (SD) was analyzed. The SD was lower in patients with VspAP than in VAP (12.8+/-1.4 degrees vs. 14.6+/-2.2 degrees, p < 0.005) at rest. After HV stress, the SD (HVSD) tended to increase in VspAP patients (62.5%), whereas the SD decreased in VAP patients (70%). Due to HV stress, the percentage change in SD (%SD) in VspAP patients was 8.9+/-23.7% whereas that in VAP patients was -9.1+/-17.3% (p < 0.01). Moreover, phase histograms were divided into HVSD increase and HVSD decrease groups. The HVSD increase group had a decrease of HVEF, but the HVSD decrease group tended to have more decreased HVEF than the HVSD increase group. These results indicate that spastic angina pectoris patients show various responses to HV stress. The HVSD increase group might have additional myocardial ischemia due to regional coronary spasm. In contrast, in the HVSD decrease group severe LV dysfunction or diffuse wall motion abnormality might have been generated, and this caused a reduction in the SD value. Phase analysis would therefore add new information regarding electrocardiographically silent myocardial ischemia due to coronary spasm, and HV stress might increase sensitivity for the detection of abnormalities in quantitative phase analysis, especially in VspAP patients.
Adult↗
Histological evaluation of coronary plaque in patients with variant angina: relationship between vasospasm and neointimal hyperplasia in primary coronary lesions.
OBJECTIVES: This study was designed to determine whether coronary vasospasm in patients with variant angina pectoris (VAP) may produce focal organic lesions at the site of vasospasm that would contribute to disease progression. BACKGROUND: Recent clinical angiographic and experimental studies have demonstrated the potential role of vasospasm in the worsening of organic coronary stenosis. METHODS: We studied histologically the coronary plaques obtained at atherectomy in 202 patients with moderate to severe coronary stenosis. This population included 22 patients with VAP, 100 patients with chronic stable angina and 80 patients with restenosis following angioplasty or atherectomy. Diagnosis of VAP was based on both the clinical feature of angina at rest associated with ST elevation and a positive response to acetylcholine provocation test. RESULTS: The most common histological appearance in 92% of patients with stable angina was hypocellular fibroatheromatous plaques, whereas neointimal hyperplasia was the characteristic feature of the plaque observed in 90% of patients with restenosis. The coronary specimens at the site of spasm in 15 of the 22 patients (68%) with VAP demonstrated intimal injuries such as neointimal hyperplasia (15), thrombus formation (2), and intimal hemorrhage (3). Neointimal hyperplasia was significantly more common in the patients with VAP as compared with those with stable angina (68% vs. 8%; p < 0.0001). A rapid progression of organic stenosis within three years was angiographically found in 5 of the 22 patients with variant angina. In all five cases, neointimal hyperplasia was the main contributor to the worsening of the organic lesion at the site of spasm. These histological findings in patients with VAP extremely resembled those in restenosis. Except for vasospasm, no factors significantly predicted the presence of neointimal formations in primary coronary lesions. CONCLUSIONS: Coronary vasospasm may provoke vascular injury that leads to the formation of neointima in VAP patients similar to that seen with restenosis. Coronary spasm may thus play a key role in the rapid coronary stenosis progression in certain patients with VAP.
Adult↗
Spectrum of coronary arterial spasm. Clinical, angiographic and myocardial metabolic experience in 29 cases.
A relationship of coronary arterial spasm to variant angina pectoris, subendocardial ischemia, major ventricular arrhythmias and myocardial infarction has been demonstrated. In 29 patients, spasm was angiographically observed in normal-appearing coronary arteries (7 patients) as well as superimposed on various degrees of coronary atherosclerotic obstruction (22 patients). All patients experienced an atypical anginal syndrome;16 patients also experienced typical exertional angina. Coronary spasm appeared to be a major contributory factor in eight occurrences of myocardial infarction and in 11 incidents of ventricular tachycardia, ventricular fibrillation and heart block. Coronary spasm in the 29 cases was distributed in the following fashion: left main trunk, 6 cases; right main trunk, 12 cases; proximal left anterior descending artery, 13 cases; proximal circumflex artery, 1 case; distal left anterior descending artery, 1 case; and distal circumflex artery, 2 cases. In 5 cases coronary spasm was noted at multiple sites.
Adult↗
Nifedipine in the treatment of Prinzmetal's (variant) angina.
The clinical response to therapy with the calcium-blocking agent nifedipine was assessed in 12 patients with variant angina pectoris who were 44 to 67 years old. Five patients had vasospasm of the left anterior descending coronary artery, and seven had spasm of a dominant right coronary artery. Before nifedipine therapy, the frequency of anginal attacks per 24 hour period ranged from 1 to 12, with ventricular tachycardia accompanying ischemic episodes in 7 of 12 patients and high grade atrioventricular block occurring in 2 patients. After therapy with nifedipine, 11 of 12 patients had initial relief of symptoms, and 7 of the 11 had long-term relief. Withdrawal of nifedipine led to recurrence of angina on six occasions in four patients. Provocative testing in the cardiac catheterization laboratory by means of the cold pressor test in one patient and ergonovine maleate in another before and after nifedipine administration showed that this agent can block both alpha adrenergic- and regonovine-induced vasospasm. Nifedipine may have a significant role in the therapy of angina caused by coronary spasm.
Adult↗
Aminophylline termination of dipyridamole stress as a trigger of coronary vasospasm in variant angina.
Dipyridamole testing represents an alternative to exercise stress testing for documentation of ischemia related to coronary artery disease (CAD). In such a case, ischemia is attributed to maldistribution of coronary flow during dipyridamole-induced vasodilation. The present study evaluated the potential role of dipyridamole testing in producing ischemia through a vasospastic mechanism, following rapid withdrawal of vasodilation induced by aminophylline. The possibility was tested in 36 in-hospital patients with variant angina pectoris who underwent dipyridamole infusion (up to 0.84 mg/kg over 10 minutes) with continuous 12-lead electrocardiographic and 2-dimensional echo monitoring. Medications were withdrawn from all patients. The test was pharmacologically stopped with the dipyridamole antidote (aminophylline, 80 to 240 mg intravenously over 1 to 3 minutes) in all patients. Two to 6 minutes after starting aminophylline infusion, 10 patients (28%) developed (greater than 0.10 mV) ST-segment elevation (2.9 +/- 0.8 mm from baseline), always accompanied by obvious asynergy detected by echocardiography, in the same electrocardiographic leads showing spontaneous or ergonovine-induced ST-segment elevation. Nitrates promptly resolved ischemia in all patients. At coronary angiography, 5 of these 10 patients showed significant CAD (greater than 70% lumen diameter reduction of at least 1 major coronary artery), whereas 5 had nonsignificant CAD. The rate pressure product at the onset of ST-segment elevation (after dipyridamole plus aminophylline) was considerably less than that recorded at peak exercise stress test in these patients (9,600 +/- 2,200 vs 18,400 +/- 4,900, p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Three-vessel coronary artery spasm in a patient with variant angina and normal coronary arteries.
Variant angina with two or more electrocardiographic or angiographic localizations has seldom been reported [1-4]. We present a case of variant angina pectoris and normal coronary arteries with three different and independent electrocardiographic localizations.
Angina Pectoris, Variant↗
Myocardial imaging in a patient with reproducible variant angina.
A unique case is presented of variant angina pectoris with reproducible chest pain and S-T segment elevation in the immediate postexercise period and with normal coronary arteries. Coronary arterial spasm was deomnstrated with arteriography after intravenous administration of ergonivine maleate. Thallium-201 imaging during the pain reproducibility demonstrated malperfusion in the region supplied by the artery with documented spasm.
Adult↗
Prinzmetal's variant angina: electrocardiographic and angiographic correlations.
Thirty patients with variant angina pectoris (VAP) were analyzed for electrocardiographic features during episodes of VAP. Twenty-nine of these patients had cardiac catheterization, and an autopsy study was performed in one. The patients showed predominantly concave upright T-waves during pain. An increase of R wave amplitude (expressed as delta R) of more than 10% was seen in 17/30 patients (57%). The primary ST-T changes produced by the VAP episodes were conspicuous in two patients with pre-existent complete left and right bundle branch block. Serious dysrhythmias, including ventricular fibrillation (VF), ventricular tachycardia (VT), ventricular premature beats (VPBs) (more than five/min, multifocal and R on T phenomenon), and 2 degrees atrioventricular block were found in thirteen patients (43%). The development of dysrhythmias was related to the duration of VAP episodes. The average time to onset of dysrhythmias was 3.54 min. The dysrhythmias were not contingent upon pre-existing coronary artery anatomy (defined by Friesinger's coronary score), left ventricular ejection fraction or left ventricular segmental abnormalities. The location of the ST-segment elevation and the presence of dysrhythmias during the episodes of VAP (A-V blocks, ventricular tachycardia and fibrillation) were not predictive factors of the coronary anatomy. Eight patients (27%) developed myocardial infarction (MI). Five of them had nontransmural MIs and three developed transmural MIs. The development of MI was not related to the severity of the VAP attacks (appreciated by the magnitude of ST-segment elevation and R wave changes) but showed a relation to the development of an unstable pattern which preceded the infarction. Sixteen patients underwent exercise testing. In eight of them, the coronary arteriograms were normal (Group I); in the remaining eight, significant proximal coronary artery obstructive disease was found (Group II). Group I patients displayed a normal ST-segment response and functional aerobic capacity (FAI = 4.4 +/- 14) as well as normal heart rate (HR) and double product (SBP X HR) responses (HR = 154 +/- 21; SBP X 21; SBP X HR = 290 +/- 71). During exercise, a normal delta R was observed. With one exception, Group II patients showed an abnormal ST-segment response with an overall low exercise capacity (FAI = 57 +/- 17) and decreased hemodynamic response (HR = 27; SBP X HR = 130 +/- 40). FAI, HR, SBP X HR Group I vs. Group II = P less than .005/less than .02/less than .005. The abnormal ST-segment response included elevation in four patients and depression in three. During exercise, Group I with ST-elevation displayed a normal (negative) delta R response; while Group II with ST-depression displayed an abnormal delta R response (positive or no change). There was no difference in the coronary score between Group II patients with ST-segment elevation or depression.
Adult↗
Cardiac arrest related to coronary spasm in patients with variant angina: a three-case study.
We present three patients with variant angina pectoris and episodes of cardiac arrest. All of them had typical clinical symptoms, ST-segment changes in electrocardiogram, and coronary artery spasm confirmed by arteriography. They were treated with high doses of calcium antagonists and nitrates. An automatic cardioverter-defibrillator was implanted in the patient who developed ventricular fibrillation despite therapy with calcium antagonists. In another patient a DDD pacemaker was implanted because of high-degree atrioventricular block.
Amiodarone↗
Calcium antagonists in the treatment of individuals with ischemic heart disease.
The so-called calcium antagonists--verapamil, nifedipine, diltiazem, and perhexiline--are pharmacologic agents that will have a dramatic impact on the medical therapy of individuals with ischemic heart disease. They have been used extensively in Europe and Japan for over 15 years, and more recent studies from this country have demonstrated their efficacy in the treatment of patients with Prinzmetal's "variant" angina pectoris, stable (exertional) angina pectoris, and unstable angina pectoris. In addition, they appear effective in protecting ischemic myocardium both in patients with acute myocardial infarction as well as in those undergoing cardiopulmonary bypass. The purpose of this review is twofold: (a) to describe the mechanism of action and pharmacology of these agents and (b) to delineate their role in the treatment of individuals with ischemic heart disease.
Angina Pectoris↗
Acute myocardial infarction provoked by a cold pressor test.
Coronary artery spasm is a well documented cause of variant angina pectoris. It has also been postulated to cause acute myocardial infarction. The diagnosis of coronary artery spasm is frequently made by means of ergonovine provocation during cardiac catheterization. Spasm of the coronary arteries may also be provoked by the cold pressor test. We describe a patient in whom an acute myocardial infarction evolved after his chest pain was reproduced with a cold pressor test. We suggest that the cold pressor test should be performed with caution, and perhaps should be limited to the cardiac catheterization laboratory.
Angina Pectoris, Variant↗