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We report a case of a 44-year-old male with variant angina who developed acute anterior myocardial infarction 2 weeks following demonstration of normal left coronary artery. This experience provides inferential evidence that myocardial ischemia resulting from coronary spasm may progress into myocardial infarction.
A case of severe ventricular ischaemia induced by hyperventilation which occurred in a woman aged 44 years is presented. The ischaemia was confirmed by echocardiography and scintigraphy and coronary arteriography revealed spasm in the proximal segment of the anterior descending branch of the left coronary artery.
BACKGROUND: Coronary artery spasm induces activation of the coagulation system. Turnover and maintenance of thrombus depend not only on formation but also on lysis. The relation between coronary spasm and fibrinolytic system has not been elucidated. OBJECTIVE: To examine whether there is impairment of or a circadian variation in fibrinolytic activity in patients with variant angina. METHODS: Plasminogen activator inhibitor (PAI) activity and concentrations of tissue plasminogen activator (t-PA) antigen were measured in venous plasma samples taken at 2200, 0600, and 1400 and 24 h Holter tapes were recorded in 15 patients with variant angina, 12 patients with stable exertional angina, and 12 controls. RESULTS: There were significant circadian variations in PAI activity and t-PA antigen with peak values at 0600 in all three groups. Mean (SEM) PAI activity (IU/ml) at 2200, 0600, and 1400 was 6.1 (1.1), 11.0 (1.3), and 4.4 (0.6) in the variant angina group; 1.8 (0.7), 5.6 (1.1), and 1.2 (0.3) in the stable exertional angina group; and 1.1 (0.5), 4.5 (0.8), and 0.7 (0.3) in the control group. Furthermore, both plasma PAI activity and t-PA antigen concentrations were significantly higher in the variant angina group than in the stable exertional angina group and the control group at each sampling time. CONCLUSIONS: In patients with variant angina there was a circadian variation in fibrinolytic activity, which was lowest in the early morning, and impaired fibrinolytic activity particularly in the early morning, when attacks of angina occur most frequently.
OBJECTIVES: The purpose of this study was to clarify clinical and angiographical characteristics of acetylcholine (ACh)-induced spasm in the right and left coronary artery. METHODS AND RESULTS: We performed 557 consecutive procedures of spasm provocation tests of ACh from January 1991 to December 2000 in patients without significant stenosis. ACh was injected in incremental doses of 20, 50 and 80 microg into the right coronary artery and in incremental doses of 20, 50 and 100 microg into the left coronary artery if spasm had not been provoked. Coronary spasm was defined as positive with more than 99% transient luminal narrowing. Proximal spasm was defined as that of segments 1, 2, 5, 6, 7 and 11 and distal spasm as that of segments 3, 4, 8, 9, 12, 13 and 14. Low-ACh-dose-induced spasms showed the clinical findings and angiographical characteristics of higher incidence of variant angina, proximal spasms, focal spasms, more ST elevation and ischemic heart disease. In contrast, angiographical characteristics of high-Ach-dose-induced spasms were distal spasms and diffuse spasms and there was less variant angina and less ST elevation. CONCLUSIONS: Lower ACh doses induced spasms more proximally and focally in the coronary artery, while higher doses of ACh provoked spasms more distally and diffusely.
3 patients with co-existing effort angina and Prinzmetal's variant angina are described, who had also 'atypical' manifestations of variant angina, i.e. chest pain and S-T segment elevation also during treadmill exercise testing. Because of these unusual manifestations the proper diagnosis was delayed and the patients continued with inappropriate therapy (propranolol and only low-dose nitrates). After the correct diagnosis of variant angina with 'atypical' manifestations was made, application of high-dose nitrates and nifedipine resulted in complete relief of symptoms. Repeat treadmill testing during this therapy did not provoke attacks of chest pain with S-T elevation.
BACKGROUND: In experimental models, ischemic preconditioning of the heart protects against ischemic damage and ventricular arrhythmias during subsequent coronary occlusion. In this study, we investigated whether protection against ischemic suffering and ischemia-induced arrhythmias may occur after spontaneous transmural ischemia in humans. METHODS AND RESULTS: We performed 24-hour Holter monitoring in 10 patients with variant angina who developed complex ventricular arrhythmias (CVAs, more than five premature ventricular beats per minute or repetitive ventricular arrhythmias) during episodes of ST-segment elevation. A total of 150 episodes of ST-segment elevation were detected on Holter monitoring, 21 (14%) of which showed CVAs. Episodes separated from the previous one by a time interval of < or = 30 minutes or by a time interval of > 30 minutes did not differ in either magnitude or duration of ST-segment elevation, but CVAs occurred more frequently in the second group (3% versus 29%, P < .0001). The time interval from the preceding ischemic episode was longer for the episodes with compared with those without CVAs (197 +/- 275 versus 57 +/- 87 minutes, P < .001), but these two groups of episodes also had similar severities and durations of ST-segment elevation. Finally, when we analyzed 13 clusters of two to six ischemic episodes, CVAs were found much more frequently in the first (92%) than in the last (23%, P = .009) episode of the clusters, while ST-segment elevations were similar (2.1 +/- 1.6 versus 2.2 +/- 1.1 mm) and ischemia durations shorter in the first than in the last episode (3.9 +/- 3.6 versus 6.1 +/- 1.7 minutes, P = .03). CONCLUSIONS: Our data indicate that preconditioning by transient ischemia induces a significant protection against ischemia-induced CVAs in patients with variant angina. This beneficial effect was not related to a reduction in either severity or duration of ischemia, suggesting that arrhythmic protection was a direct consequence of preconditioning rather than an epiphenomenon of ischemic protection.
Angina pectoris results from an imbalance between the oxygen supply and the oxygen needs of the myocardium. While the classic form of angina is usually caused by demands exceeding supply, a primary and transient decrease in coronary blood flow is more and more often recognised as an aetiological factor of myocardial ischaemia. Calcium antagonists, although new in cardiovascular therapeutics, are already recognised as the treatment of choice for some forms of angina and as useful therapeutic adjuncts in others. Few contraindications to their use exist. They are potent vasodilators and they can prevent the occurrence of coronary artery spasm responsible for the Prinzmetal's variant form of angina. They can also reduce coronary artery tone, which if high, can compromise flow through a narrowed coronary artery. Nifedipine, diltiazem and verapamil can also influence the various determinants of myocardial oxygen consumption to reduce myocardial oxygen needs. Their effects on heart rate, blood pressure and on the inotropic state of the left ventricle is, in vivo, the balance between their direct effects on the vascular wall and myocardial muscular cells and their indirect effects represented by the reflex physiological responses. Significant variations in these effects exist between the 3 calcium antagonists such that treatment can be individualised to a particular patient's needs. Precautions with their use as well as most of their side effects can be understood from a knowledge of their direct and indirect properties. Other pharmacological effects of these drugs include a regional redistribution of coronary blood flow, cardioprotection, delay in cell death and possibly in the progression of atherosclerosis. The clinical significance of these properties remains to be investigated.
It is not known whether coronary vasospasm is associated with coronary thrombosis. In this study, plasma levels of fibrinopeptide A during anginal attacks in 24 patients with variant angina were examined. A hyperventilation test was used to induce angina. Hyperventilation induced angina and ST segment elevation (AST: 0.32 +/- 0.14 mV, p less than 0.01) in eight patients with variant angina. Fibrinopeptide A increased from 0.75 +/- 0.27 at control to 7.8 +/- 4.4 ng/ml (p less than 0.01) during anginal attacks in these eight patients. In addition, four patients had spontaneous attacks of angina; they also had elevated levels of fibrinopeptide A during attacks (from 2.0 +/- 1.2 at control to 21.9 +/- 18.0 ng/ml [p less than 0.01] during attacks). Hyperventilation did not induce either angina or ST segment elevation in 12 of the patients with variant angina. Fibrinopeptide A levels did not change with hyperventilation in these patients. To determine whether elevated plasma levels of fibrinopeptide A were associated with angina, the plasma levels of fibrinopeptide A were examined during exercise-induced angina in seven additional patients with stable effort angina. They all developed angina with treadmill exercise; however, plasma fibrinopeptide A did not change. Therefore, only the patients with variant angina demonstrated elevated levels of fibrinopeptide A during anginal attacks. These findings suggest that coronary vasospasm associated with myocardial ischemia may induce stasis of blood, resulting in fibrinogen-fibrin conversion in the coronary vessels.
BACKGROUND: Angiotensin converting enzyme (ACE) perhaps plays roles in regulating coronary vasomotor tone by producing angiotensin II and degrading bradykinin. OBJECTIVES: We sought to investigate the role of ACE gene polymorphism in the pathogenesis of variant angina and to compare it with that of other clinical risk factors for male patients with variant angina and age-matched and sex-matched control subjects. METHODS: We studied 78 male patients with variant angina who exhibited spontaneous or provoked coronary spasms during coronary angiography and compared prevalences of ACE gene genotype (deletion D and insertion I) and other risk factors between this group of patients with variant angina and age-matched and sex-matched control subjects whose angiograms were normal and in whom the ergonovine test did not cause spasms (n = 80). RESULTS: Smokers were more prevalent in the group of patients with variant angina (P < 0.05). Genotype and allele prevalences of the group of patients with variant angina (0.14, 0.53 and 0.33 for DD, DI and II and 0.41 and 0.59 for D and I, respectively) were no different from those of the control group (0.16, 0.49 and 0.35 for DD, DI and II and 0.40 and 0.60 for D and I). Multiple logistic regression analysis showed that smoking was a significant risk factor for variant angina (odds ratio 2.61, 95% confidence interval 1.03-6.66) whereas ACE genotype was not. CONCLUSIONS: Variant angina is associated with an environmental factor, such as smoking, rather than a genetic factor, such as ACE gene polymorphism.
We report about the sudden death of a 45-year-old woman with anomalous origin of both coronary arteries from a single ostium in the right sinus of Valsalva, the left coronary artery running between the aorta and the pulmonary trunk. The clinical picture was that of Prinzmetal's form of variant angina, and it preceded death of inferior myocardial infarction. Coronary spasm and the anatomical anomaly were demonstrated by coronary angiography. There was no atheromatous plaque or other obstructive lesion in the dominant right coronary artery which could have explained the inferior myocardial infarction seen at autopsy. This is the first detailed report in which this rare coronary anomaly has been associated with Prinzmetal's variant angina. The demonstration of spasm in the dominant coronary artery and of an infarct in that part of the myocardium supplied by it in the absence of any anatomical obstruction suggests that this patient's death resulted from coronary spasm.
Prinzmetal's variant angina is a rare entity. When angina-like symptoms occur at rest, mostly at a specific hour in the early morning, together with transient ST segment elevations and angiographically normal arteries, provocative tests with ergonovine or acetylcholine should be performed. Endothelial dysfunction, a strong thrombotic tendency, an increased platelet aggregation together with changes in autonomic tone can trigger coronary vasospasms. Once treated with calcium antagonists and nitrates the prognosis is excellent and severe complications such as arrhythmias, myocardial infarction or sudden death are extremely rare. Coronary stenting can be useful for refractory coronary spasm, CABG can be used for important coronary atherosclerosis. This review is illustrated with three typical presentations of variant angina: a myocardial infarction without significant organic coronary atherosclerosis, an ergonovine-induced coronary spasm with a non-significant coronary lesion and a multivessel spasm complicated by ventricular arrhythmia. All these three patients became asymptomatic after a treatment with calcium antagonists and nitrates.
In 3 patients with Prinzmetal's variant angina there were inferior epicardial injury patterns on the electrocardiogram, corresponding to right coronary artery narrowing. Attacks were provoked by beta-adrenergic blockade and stopped by nitroglycerine and atropine. Spasm of the right coronary artery was demonstrated in the 2 patients who had high parasympathetic activity. In all 3 cases attacks disappeared on verapamil. We suggest that calcium-antagonists, which dilate the coronary arteries, should be used in the treatment of Prinzmetal's angina pectoris rather than beta-adrenergic blockers, which do not have this property.
A patient had attacks of Prinzmetal's angina, resistant to sublingual nitrates in high doses and to a calcium antagonist. All the crises wee resolved by sodium nitroprusside therapy. This report suggests that nitroprusside merits further evaluation in the treatment of Prinzmetal's angina, particularly in cases resistant to usual therapy in which the evolution towards myocardial infarction is very likely.
The response of the coronary artery to a small dose (0.01 mg) of ergonovine was observed in nine patients without variant angina and in 10 patients with variant angina. Coronary angiograms were obtained before and after small and larger (routinely used) doses of ergonovine. With the larger dose, all 10 patients with variant angina had total or subtotal spastic occlusion accompanied by angina and ECG changes. Excluding the site of spastic occlusion produced by the larger dose of ergonovine, diameters of proximal, middle, and distal segments in each major coronary artery were measured before and after a small dose of ergonovine. The mean percentage of change in diameter (diameter before - diameter after a small dose of ergonovine)/diameter before a small dose of ergonovine X 100% in patients without variant angina was not significantly different from that in patients with variant angina (5.2 +/- 9.5% vs 7.0 +/- 11.9%, respectively). However, in patients with variant angina, a small dose of ergonovine produced a percentage of change in diameter of 39.8 +/- 15.3% at the site of spastic occlusion included by a larger dose of ergonovine, compared with that of 7.0 +/- 11.9% in the remaining non-spastic coronary arteries (p less than 0.05). These results indicate that patients with variant angina have local segments which respond differently to ergonovine from the remaining segments of coronary arteries. Clinically, this observation might be helpful in determining the angiographic positivity to ergonovine.
To determine the factors influencing the prognosis of variant angina, the clinical characteristics and long-term prognosis of 158 consecutive Japanese patients were examined and compared with those in previous major western studies (Pisa, Montreal, and Duke studies). The Japanese patients were characterized by relatively low prevalences of coronary risk factors, significant coronary stenoses and previous myocardial infarction. Survival and survival without myocardial infarction for the entire group or for the subpopulation with significant coronary artery disease were significantly better in the Japanese population than in the western populations; however, in the subpopulation without significant coronary artery disease, the prognosis was excellent in all four studies. If the prevalence of coronary artery disease was corrected for the Japanese population, there would be no difference in the prognosis between the Japanese and the western populations. It is concluded: (1) the overall prognosis of variant angina may be better in Japanese patients, and (2) coronary artery disease appears to be the strongest prognostic factor for assessing the differences in the prognosis between the Japanese and the western populations.
OBJECTIVE: The purpose of this study was to assess whether the plasma levels of soluble adhesion molecules including E-selectin, intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are elevated in patients with variant angina and whether they are released in the coronary circulation. METHODS: Antecubital venous plasma samples were collected from 33 patients with variant angina, 22 patients with stable effort angina and 20 control subjects. Samples were also collected from the aortic root (AO) and the coronary sinus (CS) in 18 patients with variant angina before and after left coronary spasm induced by intracoronary injection of acetylcholine. The soluble adhesion molecules were assayed by enzyme immunoassay. RESULTS: Antecubital venous plasma soluble E-selectin (P < .05), ICAM-1 (P < .01) and VCAM-1 (NS) levels were higher in the variant angina group than in the control group, respectively. The plasma soluble ICAM-1 level was also higher (P < .01) in the variant angina group than in the stable effort angina group. In the variant angina group, both soluble ICAM-1 (P < .05) and VCAM-1 (P < .01) levels were significantly lower in CS than AO at baseline. In contrast, after the spasm the plasma soluble ICAM-1 level was (P < .05) higher in CS than AO and the CS-AO differences of soluble ICAM-1 (P < .05) and VCAM-1 (P < .05) increased as compared with the baseline, respectively. These values were remained unchanged in the stable effort angina group after rapid atrial pacing and in the control group after administration of acetylcholine. CONCLUSIONS: Circulating plasma levels of both soluble E-selectin and ICAM-1 were elevated in patients with variant angina, indicating an association of an inflammatory reaction with coronary spasm. Both soluble ICAM-1 and VCAM-1 appeared to be trapped in the coronary circulation at baseline and released into the coronary circulation following coronary spasm and reperfusion in the patients.
We studied 109 consecutive patients with variant angina who underwent cardiac catheterization over an 11 year period. All patients were followed for at least 6 months or until death, and 46 patients (22 treated medically and 24 treated surgically) were followed for 5 years or more. Of the 62 patients initially treated medically, 14 had nonfatal myocardial infarctions (12 within 1 month of catheterization) and 12 died (six within 6 months). Survival probabilities at 1, 3, and 5 years were 0.88, 0.84, and 0.77, respectively. Of the 48 surgically treated patients (including four patients initially treated medically and one initially treated with coronary angioplasty), four had nonfatal infarctions (three in the perioperative period) and three died (all in the perioperative period). The survival probability in these patients at 1 year was 0.94 and remained unchanged at 3 and 5 years. Only one nonfatal infarction and no deaths have occurred in the group of surgically treated patients subsequent to hospital discharge. Three additional patients were treated with coronary angioplasty. The single most important prognostic factor in medically treated patients was the presence or absence of fixed obstructive coronary artery disease. Infarction-free survival probabilities at 1 and 3 years in the 23 patients without significant coronary artery disease were 1.0 and 0.89, compared with 0.51 and 0.46 in the 39 patients with significant coronary disease. Analysis by the Cox model showed that variant angina patients had a higher probability of death and nonfatal infarction than did those with nonvariant angina coronary disease if other important prognostic variables were held constant.(ABSTRACT TRUNCATED AT 250 WORDS)
BACKGROUND: Serotonin, released by aggregating platelets, may contribute to or cause myocardial ischemia by constricting epicardial vessels. Experimental studies suggest that this constriction is mediated by two distinct serotonin receptor subtypes: 5-hydroxytryptamine1-like (S1-like) and 5-hydroxytryptamine2 (S2). METHODS AND RESULTS: To determine the relative contribution of S1-like and S2 receptors to the vasoconstrictor effects of serotonin, we studied the effect of ketanserin (0.75 mg, intracoronary), a selective S2 receptor antagonist, on the constrictor response of human coronary vessels to intracoronary infusions of serotonin. In control patients (n = 7), serotonin (10(-4) mol/l) caused significant (p less than 0.05) constriction only in distal segments, which was significantly (p less than 0.05) inhibited by ketanserin. In stable angina patients (n = 8), serotonin (10(-4) mol/l) caused significant constriction in proximal (p less than 0.01) and distal (p less than 0.01) segments, which was significantly inhibited by ketanserin in proximal (p less than 0.05) but not distal (p = 0.30) segments. In patients with variant angina (n = 3), epicardial occlusion at the site of preexisting stenoses in proximal locations occurred at infused concentrations of 10(-6) (one patient) or 10(-5) (two patients) mol/l. The infusion of the same concentration of serotonin after ketanserin again caused epicardial occlusion. CONCLUSIONS: Our results suggest that functionally important S1-like receptors that mediate vasoconstriction exist in the epicardial vessels of patients with stable or variant angina. Their activation, either at hyperreactive sites in patients with variant angina or in the distal epicardial vessels of patients with chronic stable angina, may contribute to or cause myocardial ischemia when serotonin is released after the intracoronary activation of platelets.