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A 55-year-old man demonstrated typical reflux esophagitis, not esophageal spasm, by esophageal manometry, although he demonstrated classic migraine, positive Raynaud's scan, and proven coronary artery spasm. He suffered from severe chest pain by medication of ergotamine tartrate. Ergot alkaloids should be avoided in patients with symptomatic coronary artery spasm.
A 55-year-old man came to the hospital because of chest pain, mostly occurring in the early morning at rest. He had to get isosorbide dinitrate intravenously with continuous infusion. Following ergonovine provocation test, total occlusion of mid-left anterior descending artery was identified with marked elevation of ST segment as exercise test showed despite isosorbide dinitrate.
Calcium channel blockers are active in variant angina principally by preventing coronary vasospasm. However, a direct antiischemic effect may also occur. In open-chest dogs, an attack of variant angina was mimicked by a 2-min critical coronary stenosis, and the following reversible myocardial ischemia was assessed by measuring the decrease of segmental shortening. We compared the antiischemic mechanism of mibefradil, a T and L calcium channel blocker, with that of amlodipine, a pure L channel blocker. Both drugs showed a similar relationship between the decrease of the rate-pressure product and the antiischemic effect, but only mibefradil reduced heart rate. Amlodipine and mibefradil at the highest doses tested (20 and 70 micrograms/kg/min, respectively) restored 68 +/- 8 and 76 +/- 5% of segmental shortening in the ischemic area, respectively, as compared with preischemic values. Matching blood pressure (by intraaortic balloon) or heart rate (by atrial pacing) to predrug values showed that the antiischemic effect was mainly afterload-dependent for amlodipine and heart rate-dependent for mibefradil. We conclude that in variant angina, in addition to their antivasospastic effects, calcium channel blockers may be antiischemic by a direct myocardial effect associated with a decrease of the rate pressure product. Blockade of the T channel does not seem to participate in the direct antiischemic effect of mibefradil but could explain the decrease of heart rate.
We studied 57 patients admitted to hospital with ischaemic heart disease, including nine patients with variant angina, to evaluate platelet reactivity and its dependence on alpha-adrenergic receptor function. The threshold concentration for biphasic platelet aggregation in response to adrenaline and adenosine diphosphate was measured in fresh platelet rich plasma. There were age related alterations in platelet responsiveness to adrenaline. In 27 age matched control subjects platelets showed adrenaline induced aggregation at a concentration higher than 0.1 mumol. The threshold concentrations for adrenaline and adenosine diphosphate were 0.91 mumol and 4.68 mumol. In 16 patients with acute infarction, 14 with old infarction, nine with effort angina, and nine with rest angina, mean values of platelet aggregation threshold for both adrenaline and adenosine diphosphate were not altered significantly when compared with control subjects. In contrast, the values for adrenaline and adenosine diphosphate in nine patients with variant angina were 0.012 mumol and 2.24 mumol and seven of them showed obvious platelet hyperactivity to adrenaline at a concentration lower than 0.1 mumol. The threshold concentration for adrenaline induced aggregation did not correlate with serum cholesterol and triglyceride levels.
Chest pain is a common complaint in adolescents. It is mostly from musculoskeletal origin. Variant angina is a rare cause of chest pain in adolescents. Here we report a 17-year-old male with severe chest pain accompanied by transient ST-segment elevation in leads II, III, avF of the electrocardiogram showing/revealing variant angina associated with acute myocardial ischaemia. Data obtained from laboratory tests, including serial cardiac markers, were normal and subsequent cardiac catheterization revealed a normal coronary anatomy. The patient has been asymptomatic since discharge, and treatment with calcium channel antagonists with nitrate seems to assure a good prognosis.
Coronary artery spasm has been described as occurring frequently in Prinzmetal variant angina. The relatively poorer results obtained after aorto-coronary by pass grafting carried out in patients with Prinzmetal angina may be due to recurrence of spasm despite the grafts. Accordingly it has been our recent policy since February 1973 to carry out cardiac denervation in all patients with Prinzmetal variant angina. The patients fall into two groups depending on the presence or absence of organic disease in the coronary vessel. The technique of cardiac denervation (plexectomy) as described by Arnulf is fully described and the early and late results of this procedure in the two groups are documented and discussed.
The revival of the concept of coronary spasm has stimulated research into coronary artery disease. Observations in patients with variant angina have substantially contributed to the appreciation of painless myocardial ischemia. However, the presence or absence of pain during ischemic episodes is not related to the cause of ischemia, because painless ischemia can be observed in variant angina (caused by spasm), in effort-induced angina (caused by increased myocardial demand) and in myocardial infarction (caused by thrombosis). Continuous monitoring initially of patients with variant angina and subsequently of patients with unstable and stable angina proved that often painful and painless ischemic episodes are caused by a transient impairment of regional coronary blood flow rather than by an excessive increase of myocardial demand. The transient impairment of coronary flow appears to be caused by dynamic stenosis of epicardial coronary arteries. This most often occurs at the site of atherosclerotic plaques encroaching on the lumen to a variable extent. Dynamic stenosis can be caused by 1) "physiologic" increase of coronary tone, as in stable angina, 2) spasm, as in variant angina, and 3) thrombosis, usually in combination with "physiologic" changes in tone or with spasm, or both, as in unstable angina. The mechanisms of spasm, as typically observed in variant angina, are different from those of "physiologic" increase of tone; they appear to be related to a local alteration that makes a segment of coronary artery hyperreactive to a variety of constrictor stimuli causing only minor degrees of constriction in other coronary arteries. The nature of this abnormality, which may remain stable for months and years, is yet unknown.
We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.
Malignant ventricular arrhythmias appearing during acute myocardial ischaemia, are the most frequent mechanism of sudden death. ST-T alternans is the result of an intraischaemic conduction delay and is frequently associated with those potentially lethal arrhythmias. In fact, such a phenomenon was seen in 35% of 46/86 patients with Prinzmetal's variant angina who showed ventricular arrhythmias during ischaemia, while it was never observed in the remaining 40 patients without arrhythmias during ischaemia. Therefore ST-segment alternans should be considered a reliable marker of the possible occurrence of ventricular arrhythmias during myocardial ischaemia. ST-T-segment alternans is associated with R alternans, as clearly demonstrated by thoracic maps, and this phenomenon is due to a 2:1 intraischaemic block. The patients with Prinzmetal's variant angina who present ventricular arrhythmias during ischaemia, show a more prominent increase of the positive area of the QRS (411.75 +/- 102.5 vs 294.05 +/- 80.3 mu volts ms), that is, a more relevant intraischaemic conduction delay. The effects of different pretreatments (lidocaine, propranolol and diltiazem) on arrhythmias related to vasospastic myocardial ischaemia induced by ergonovine maleate, were evaluated in four patients with Prinzmetal's variant angina. As in experimental observations, neither a 'pure' antiarrhythmic agent like lidocaine, nor a betablocking agent like propranolol, prevented acute ischaemic ventricular arrhythmias. Only the calcium antagonist, diltiazem, seemed to prevent such arrhythmias. However, these findings necessitate further confirmation.
Plasma levels of thromboxane B2 (TXB2) and 6-keto PGF1 alpha in the blood samples taken at the coronary sinus and ascending aorta from twenty-one Japanese patients with variant angina and twenty with effort angina were measured by radioimmunoassay, the objective being to search for the contribution of prostanoids in coronary spasm. The data were compared with data on thirteen subjects free from coronary artery diseases. In coronary sinus blood, plasma TXB2 in patients with effort angina exhibited statistically significant high levels, as compared with data in the controls. These with variant angina also had high levels, albeit without a statistically significant difference. Eight patients with variant angina and for whom the coronary angiogram showed more than 50% of narrowing had statistically significant high levels of TXB2, and the other thirteen with variant angina and normal coronaries or less than 50% of narrowing had the same plasma levels of TXB2 as the controls. In contrast to TXB2, the plasma levels of 6-keto PGF1 alpha in both coronary sinus and aortic blood of patients with variant angina were very low, as compared with normal controls. Statistically significant low levels of 6-keto PGF1 alpha were noted in the coronary sinus blood of patients with variant angina with normal coronaries and in the aortic blood of those with variant angina, as compared with data on the normal controls. Neither ergonovine test nor spontaneous attacks in patients with variant angina revealed characteristic changes in levels of TXB2 and 6-keto PGF1 alpha in the coronary sinus. These data suggest that high levels of TXB2 in patients with atherosclerotic coronaries may be one factor leading to spasm, while low levels of PGI2 may be a contributing factor.
A 67-year-old man, who was previously diagnosed with vasospastic angina and treated with standard therapy, was admitted to our hospital because of recurrent chest pain refractory to sublingual nitroglycerin. Admission electrocardiography revealed ST segment elevation in II, III and aV(F), and his symptoms were relieved by intravenous bolus administration of nicorandil. He was diagnosed to have active variant angina, and remained symptomatic even after treatment with calcium antagonists and nitrates at optimal doses. Intravenous bolus administration of nicorandil was consistently effective to relieve his symptoms. Anginal attack was finally prevented by massive oral nicorandil in addition to conventional treatment.
Thallium-201 myocardial scintigraphy with quantitative analysis of emission computed tomography was performed during episodes of angina in 19 patients with variant angina and nearly normal coronary arteriographic findings. Eleven patients (group I) were shown by arteriography to have spasm in 2 or more large coronary arteries. Eight patients (group II) had spasm in only 1 coronary artery. In 7 patients in group I, significant diffuse perfusion defects simultaneously appeared in multiple coronary artery regions on the scintigram (group IA). The extent and severity of the perfusion defect as measured by thallium-201 tomography were significantly greater in group IA than in group II (p less than 0.001 and p less than 0.01, respectively). The duration of transient ST-segment elevation during the attack in group IA was significantly longer than in group II (p less than 0.001). The incidence of ventricular arrhythmias, including ventricular tachycardia, or complete atrioventricular block during the anginal attack was significantly higher (p less than 0.05) in group IA than in group II. In all study patients, neither attack nor scintigraphic perfusion defect appeared on the repeat test after oral administration of nifedipine. In conclusion, multivessel coronary artery spasm simultaneously appears and causes the attack in many patients with variant angina and nearly normal coronary arteriographic findings, and myocardial ischemia due to simultaneous multivessel coronary spasm is likely to be more extensive and severe, persist longer and have a higher frequency of potentially dangerous arrhythmias than that due to spasm of only 1 coronary artery.
BACKGROUND: Clinical characteristics and outcome of patients with variant angina were assessed in the 1970-1980s of the past Century. The recent progress in prevention, diagnosis and treatment of coronary artery disease may have significantly modified clinical characteristics and prognosis of these patients. METHODS: From January 1991 to December 2002, 202 patients (57.1+/-12 years; 166 men) were diagnosed to have variant angina at our Institute. Detailed clinical findings and clinical events were prospectively collected for each patient. RESULTS: The median time from the first angina attack to diagnosis was 2 months (range 1-276), with diagnosis requiring >6 months in 31.7% of patients. Coronary angiography (n=183) showed normal coronary arteries in 42.1% of patients and significant coronary stenoses (>50%) in 44.3%, with multi-vessel disease in 8.7%. Diagnosis of variant angina was done during coronary angiography in 3% of cases during the first half of the study period, but in 42% of patients in the second half of the study period. Major cardiac events (MCE, i.e., death, resuscitation from cardiac arrest, myocardial infarction) occurred in 41 patients (20.3%), with 43.9% of events occurring within 1 month of symptom onset. The only variable significantly associated with MCE was the detection during angina of ST segment elevation in both anterior and inferior ECG leads (odds ratio 3.24; 95% confidence interval 1.43-7.36; P=0.005). CONCLUSION: Our data suggest that variant angina is still a frequently overlooked diagnosis, and a timely diagnosis would be crucial to prevent early life-threatening events. Patients with diffuse ST segment elevation on ECG are those at the highest risk of MCE, independently of angiographic findings.
Authors report an unusual case of variant angina associated with unconsciousness. They were able to prove by coronary angiography the vasospasm of the circumflexus artery which was responsible for the morning attacks of the 35 year old patient with unconsciousness, ST segment elevation and high degree AV block. Unconsciousness was the first and earliest sign of the coronary vasospasm.
A 45-year-old woman with almost normal coronary arteries suffered from acute inferior myocardial infarction after taking 2 tablets (2.0 mg) of ergotamine tartrate for headache. She had had attacks of variant angina and spasm of the right coronary artery had been demonstrated during the attack. After the recovery from myocardial infarction the intravenous injection of ergonovine maleate 0.05 mg induced spasm of the right coronary artery again. We conclude that acute myocardial infarction in this patient was probably caused by coronary arterial spasm induced by ergotamine tartrate.
BACKGROUND: Serotonin, a major product of platelet activation, has potent vasoactive effects in animal models, but its role in human coronary artery disease remains largely speculative. METHODS: Using quantitative coronary angiography, we compared the effects of the intracoronary infusion of graded concentrations of serotonin (10(-7) to 10(-4) mol per liter) on coronary vessels in two groups of patients with different clinical presentations of coronary disease (nine with stable angina and five with variant angina), with the effects in a control group of eight subjects with normal vessels on angiography. RESULTS: Normal coronary vessels had a biphasic response to intracoronary serotonin: dilation at concentrations up to 10(-5) mol per liter, but constriction at 10(-4) mol per liter. Vessels in patients with stable angina constricted at all concentrations, with mean (+/- SEM) maximal decreases in diameter of 23.9 +/- 3.6, 33.1 +/- 3.9, and 41.7 +/- 3.1 percent from base line in proximal, middle, and distal segments at a serotonin concentration of 10(-4) mol per liter. Smooth segments constricted more than irregular segments (42.0 +/- 4.6 vs. 21.1 +/- 1.6 percent). Four patients with stable angina had a marked reduction in collateral filling. All the patients with stable angina had angina during the intracoronary infusion of serotonin, and electrocardiographic changes were noted in six. All the patients with variant angina had angina, electrocardiographic changes, and localized occlusive epicardial coronary-artery spasm at concentrations of 10(-6) (n = 2) or 10(-5) (n = 3) mol per liter. CONCLUSIONS: Patients with stable coronary disease do not have the normal vasodilator response to intracoronary serotonin, but rather have progressive constriction, which is particularly intense in small distal and collateral vessels. Patients with variant angina have occlusive coronary-artery spasm at a dose that dilates normal vessels and causes only slight constriction in vessels from patients with stable angina. These findings suggest that serotonin, released after the intracoronary activation of platelets, may contribute to or cause myocardial ischemia in patients with coronary artery disease.
The giant R wave syndrome is characterized by giant R wave accompanied by widening of the QRS complex, marked ST segment elevation, QRS axis deviation, and the formation of monophasic QRS-ST complex with obliteration of S wave in leads facing the ischemic zone. This report describes a 65-year-old-man with variant angina who had a transient giant R wave syndrome during an exercise treadmill test. Initially, at peak exercise, there was a convex ST segment elevation ending in a negative T wave in the same (inferior) leads which showed giant R waves. Later, in the recovery period and coinciding with an amelioration of myocardial ischemia, there was a less marked increase of R wave amplitude associated with concave ST segment elevation and positive T wave in the inferolateral leads. Subsequently, a ST segment depression in the inferolateral leads preceded the ECG normalization. The patient had also a concave ST segment elevation and positive T wave in inferolateral leads during a spontaneous episode of variant angina at rest. An emergency coronary arteriography showed a dominant right coronary artery with an 80% and a 75% diameter stenosis of the middle and distal segment, respectively; the other arteries and left ventriculogram were normal. The underlying mechanisms of the different shapes of ST segment elevation and T waveform in the setting of acute transmural myocardial ischemia are discussed.
BACKGROUND: Vasospastic angina usually responds well to medical treatment. HYPOTHESIS: The present study describes our experience in patients who received a coronary stent because of recurrent variant angina refractory to medical treatment and evaluates stent implantation as an alternative treatment. MATERIALS AND METHODS: Between March 1998 and February 2005, recurrent variant angina was diagnosed in 22 patients admitted to our coronary care unit. Of these, five patients (22.7%), were refractory to pharmacologic treatment. Coronary angiography and coronary stents were indicated. Clinical follow-up was 29 +/- 6 months. RESULTS: Stenting was performed during diagnostic coronary angiography in two patients. In the other three patients, the stent was implanted 24-48 h later. We observed coronary spasm recurrences proximal or distal to the stent in four patients-two during the stent implantation procedure and the other two in the coronary care unit within 48 h post angioplasty. Three patients where treated with additional stenting and the fourth patient improved with pharmacologic treatment. During follow-up three patients remained asymptomatic. The fourth patient had diffuse in-stent restenosis in the third month, and the fifth patient showed a de novo lesion in the treated segment 2 years later. CONCLUSIONS: Stent implantation in patients with recurrent variant angina refractory to medical treatment may be an alternative treatment in carefully selected, clinically unstable patients. Spasm recurrences may occur in other segments of the treated artery, probably due to the diffuse nature of the disease. Immediate and continued surveillance is recommended because of the risk of adverse clinical events.