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.     

Catheter-induced spasm during spontaneous attack of variant angina

The simultaneous occurrences of spontaneous spasm and catheter-induced spasm during coronary angiography were obtained in 3 patients. Catheter-induced spasm was seen in the right coronary artery in 3 patients: 1 patient had spontaneous spasm in the distal right coronary artery and 2 patients had spontaneous spasm in the proximal left anterior descending coronary artery. These findings suggest that patients with variant angina may be susceptible to mechanical induction of spasm.     

Stent implantation in variant angina refractory to medical treatment

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.     

Ischaemia related ventricular arrhythmias in patients with variant angina pectoris

Twenty-three patients with variant angina were studied by Holtermonitoring both to assess the incidence of serious ventriculararrhythmias (a risk factor of sudden death in variant angina),during ischaemic episodes and to examine the time-relation ofthe arrhythmias to ST changes. Serious ventricular arrhythmias were observed in 12/23 patients(52%). In the 23 patients, a total of 491 episodes of ST segmentelevation were recorded during 954 h of Holter monitoring; seriousventricular arrhythmias were found in only 46 ischaemic episodes(9.4%). Six out of 12 patients showed serious ventricular arrhythmiasat the onset of ischaemic episodes or during maximal ST elevation(phase 1), one patient during return or immediately after returnof ST to baseline (phase 2) and five patients during both phases.Thirty-three out of 46 ischaemic episodes (76%) showed seriousventricular arrhythmias during phase 1, eight (17%) during phase2, and five (11%) during both phases. Serious ventricular arrhythmias were neither related to previousmyocardial infarction nor to the presence of serious ventriculararrhythmias during inter-crisis periods, whereas a good relationshipwith severity of ischaemic episodes, as assessed by the magnitudeand duration of ST elevation, was found. A modest relationshipwith anterior ST elevation was also found. In conclusion: (1) serious ventricular arrhythmias occur ina high percentage of variant angina patients, but in only asmall proportion of ischaemic episodes; (2) serious ventriculararrhythmias are related to the severity of ischaemia and occurpredominantly at the onset of ischaemic episodes and/or duringmaximal ST elevation; in only a few cases do they occur duringresolution of ischaemic episodes.     

Limitations of ergonovine testing in patients with variant angina

Fourteen patients with variant angina underwent ergonovine testing during diagnostic coronary angiography. The clinical electrocardiographic or angiographic manifestations of coronary artery spasm could not be reproduced in six of these patients. Five patients had chest pain and transient ST-segment elevation within 4 days of the ergonovine study, including three who developed coronary spasm in the catheterization laboratory. It appears that the sensitivity of ergonovine testing in the diagnosis of coronary spasm is lower than previously emphasized.     

Once daily felodipine in preventing ergonovine-induced myocardial ischaemia in Prinzmetal's variant angina

The efficacy of extended-release felodipine in preventing ergonovine-inducedmyocardial ischaemia was assessed in 14 patients (12 male, twofemale, aged 56±7 years) with Prinzmetal's variant angina.Four of the patients had normal coronary arteries, eight hadone-vessel and two had two-vessel disease. The ergonovine testwas performed once in basal conditions and twice 5 days afterbeginning the oral administration of felodipine 20 mg o.d.,4 and 24 h after the last administration. During a continuous6-lead ECG recording, ergonovine was injected at doses of 25,50, 100, 200, and 400 µg at 5 min intervals. Blood samplesfor felodipine plasma concentrations were drawn at the timeof the tests. The basal ergonovine test was positive in all 14 patients (sevenwith anterior and seven with inferior ST segment elevation >0•1m V) at a mean ergonovine dose of 162±138 µg. Thetest was repeated 4 h after the last felodipine administrationand was negative in 13 patients (93%), but 24 h after the lastdrug administration, eight patients (57%) had a positive testresponse (five with anterior, three with inferior ST segmentelevation) at a higher ergonovine dose than at baseline (150vs 97 µg, P=0•042). The only dtfferences betweenpatients with a negative and a positive test were the mean valuesof the left ventricular end-diastolic pressure (9•3 vs14•9 mmHg, P=0•002) and the ergonovine doses usedin the baseline tests (250 vs 97 µg, P=0•034). Themean felodipine plasma level 4 h after dosing was 18•0±12•2nmol. l^–1; 24 h post-dosing plasma concentrations weregenerally very low (<3 nmol. l^–1 in eight cases). Noacute side effects were observed during the trial. In conclusion, extended-release felodipine, given once daily,appears to be highly effective in preventing ergonovine-inducedischaemia in patients with Prinzmetal's variant angina, maintaininggood efficacy even 24 h post-dosing.     

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.     

Fragmented QRS as a risk marker for the occurrence of ventricular fibrillation in patients with variant angina

BackgroundVariant angina (VA) is caused by reversible coronary artery spasm, which is characterized by chest pain with ST‐segment elevations on standard 12‐lead electrocardiogram (ECG) at rest. Ventricular fibrillation (VF) is often caused by VA attack, but the risk stratification is not well understood. The purpose of this study was to evaluate the impact of fragmented QRS (fQRS) on VF occurrence in VA patients.MethodsNinety‐four patients who showed ST elevation on 12‐lead ECGs with total or nearly total occlusion in response to coronary spasm provocation test were enrolled. Among them, 16 patients had documented VF before hospital admission (n = 12) or experienced VF during provocation test (n = 4) (VF occurrence group). The fQRS was defined as the presence of spikes within the QRS complex of two or more consecutive leads.ResultsThe prevalence of fQRS was more often observed in the VF occurrence group than in the non‐VF occurrence group (63% [10/16] vs. 27% [21/78], p = 0.009). Univariate analyses revealed that age, history of syncope, QTc, and the presence of fQRS were associated with VF occurrence (p = 0.004, 0.005, 0.029, and 0.008, respectively). Furthermore, upon multivariate analyses using those risk factors, age, QTc, and fQRS predicted VF occurrence independently (p = 0.007, 0.041, and 0.014, respectively).ConclusionsThe present study demonstrated that fQRS in VA patients is a risk factor for VF. The fQRS may be a useful factor for the risk stratification of VF occurrence in VA patients.     

Autonomic antecedents to variant angina exacerbation after beta-blockade withdrawal

We describe a patient with nonsignificant coronary artery disease who experienced variant angina after beta -blockade withdrawal. Standard therapy with nifedipine and nitrates aimed at suppressing symptoms and typical transient ST-segment elevations was superseded by the reinstitution of metoprolol. The autonomic alternations before and after readministration of metoprolol were analyzed by time and spectral indices of heart rate variability (HRV). Metoprolol reduced the HRV and reversed the low-frequency/high-frequency power ratio toward a more physiological autonomic balance. We conclude that the reinstitution of beta -blocker acted protectively by preventing surges of sympathetic activity on an underlying basis of parasympathetic predominance.     

变异性心绞痛58例临床研究

目的 了解变异性心绞痛临床特点.方法 观察心绞艰发作时心电图变化.其中42例做冠状动脉造影,其中男性46例,女性12例,年龄29～68岁.凌晨熟睡时发作44例,午睡时发作14例.结果 发作时ST段伴T波高尖26例占44.8%,仅ST段抬高22例占37.9%,仅有T波高尖10例占17.2%.42例冠状动脉造影结果:冠状动脉狭窄≥70%有27例,侵犯1支8例占19.0%,侵犯双支19例占45.2%;冠状动脉狭窄<50%7例占16.8%;正常8例占19.0%.随访12～18个月,因药物不能理想控制心绞痛发作行PTCA 25例占43.1%,2例作了CABG,猝死1例,其余30例占57.7%,经药物治疗后症状消失.结论 变异性心绞痛主要是在冠状动脉狭窄基础上冠状动脉痉挛引起,夜间发作者可能为交感神经张力增高致冠状动脉痉挛.     

High remnant lipoprotein levels in patients with variant angina

BACKGROUND: Dyslipidemia with increased oxidative stress but without elevation of low-density lipoprotein cholesterol has been recently implicated in the pathogenesis of coronary vasospasm. HYPOTHESIS: Disordered triglyceride-rich lipoprotein metabolism may be linked to the genesis of coronary artery spasm. METHODS: Both serum remnant lipoprotein (RLP) and alpha-tocopherol levels were determined in 18 patients with the active stage of variant angina (VA), in 16 patients with the inactive stage of variant angina (IVA), and in 19 control subjects (CONTROL). RESULTS: The RLP levels were significantly (p < 0.05) higher in VA (6.4 +/- 2.7 mg/dl) than in IVA (4.4 +/- 1.5 mg/dl). In contrast, alpha-tocopherol levels were significantly lower in VA than that in CONTROL. Serum trigyceride levels were not significantly different among the study groups, although serum high-density lipoprotein cholesterol levels were significantly lower in VA than in CONTROL. Smoking was significantly (p < 0.05) more prevalent in VA (72%) than in IVA (25%) and CONTROL (37%). Serum RLP levels correlated positively with triglyceride levels (R = 0.73) and correlated inversely with alpha-tocopherol levels (R = -0.31) significantly in all study subjects. CONCLUSIONS: Patients with active stage of variant angina had higher RLP levels than inactive patients with variant angina and lower alpha-tocopherol levels than control subjects. Disordered triglyceride-rich lipoprotein metabolism with increased oxidative stress appears to be linked to the activity of coronary vasospasm, suggesting a possible role in its pathogenesis.     

Prinzmetal's variant angina induced only by alcohol ingestion

Prinzmetal's variant angina occurred in a 52-year-old man 10–11 h after the ingestion of alcohol, when blood levels of alcohol decreased almost to the zero level. Coronary arteriograms revealed significant narrowing in the left circumflex artery and the left anterior descending artery and minimal wall irregularity in the right coronary artery; however, both exercise and pharmacologic stress tests were negative. A withdrawal from an acute exposure to alcohol was discussed as a possible causative mechanism of the alcohol-induced Prinzmetal's variant angina in this case.     

Insulin resistance relates to acetylcholine-induced microvascular vasoconstriction in a patient with vasospastic angina: potential implication of causalities between hyperinsulinemia and coronary microcirculation failure

Coronary vasomotor response to acetylcholine infusion was studied in a 69-year-old currently smoking man with enhanced insulin response to oral glucose load. Coronary angiogram showed no significant stenoses. Immediately after 20µg acetylcholine infusion in the right coronary artery, angiographic no-flow, ischemic electrocardiographic changes, and anginal pain developed in the absence of epicardial coronary obstruction. While intracoronary infusion of isosorbide dinitrate was only partially effective, intracoronary infusion of nicorandil, an agent known to improve coronary microcirculation, completely resolved these changes. This is the first case reported so far suggesting that enhanced insulin response may be associated with acetylcholine-induced microvascular vasoconstriction. Microvascular vasoconstriction must be considered when a patient with insulin resistance presents with chest pain.     

Angiographic documented coronary arterial spasm in absence of critical coronary artery stenoses in a patient with variant angina episodes during exercise and dobutamine stress echocardiography

Dobutamine stress echocardiography is widely performed as a useful diagnostic tool in patients with known or suspected coronary artery disease. Dobutamine induced myocardial ischaemia is frequently associated with ST segment depression. ST segment elevation is uncommon and is almost always associated with prior myocardial infarction or transient total coronary occlusion. Dobutamine induced ST segment elevation in absence of significant coronary artery disease is a rare condition and is supposed to be a consequence of severe coronary artery spasm. The case of a 58 year old man with variant angina episodes at rest, during exercise test, and dobutamine stress echocardiography is reported, in whom coronary spasm without significant coronary artery stenoses was documented angiographically.


Keywords: coronary spasm; variant angina; Prinzmetal angina; dobutamine stress echocardiography; exercise test     

Multivessel coronary spasm as a cause of ischemic syncope in angina at rest

Two patients with vasospastic angina at rest developed ST segmentelevation both in the anterior and inferior leads during spontaneousand ergonovine-induced attacks. In both cases the acute myocardialischemia secondary to multivessel coronary spasm led to reversibleelectromechanical dissociation. Coronary arteriography showednormal coronary arteries in one case and severe three-vesseldisease in the other; spasm of the right coronary artery wasdemonstrated in both patients. These cases show that in patientswith vasospastic angina coronary spasm may simultaneously involvedifferent arteries and lead to ischemic electromechanical dissociation.Ergonovine testing is contraindicated in those patients withsuspected or proved multivessel coronary spasm.     

单中心192例变异型心绞痛的临床分析

目的探讨变异型心绞痛的临床特点及发病机制。方法回顾性分析5年内我院住院患者中192例确诊为变异型心绞痛患者(未行激发试验)的临床资料。结果变异型心绞痛临床上少见,好发于男性,占85.9%,合并危险因素包括吸烟、高血压、饮酒,有过敏史16.7%。心绞痛的好发时间为夜间及凌晨。35例(18.2%)心绞痛发作时合并心律失常,其中室性心动过速11例(5.7%)、心室颤动6例(3.1%)、窦性心动过缓7例(3.6%)、三度房室传导阻滞6例(3.1%);56.9%患者存在冠状动脉固定狭窄,17例(8.9%)合并冠状动脉肌桥。结论变异型心绞痛是冠状动脉痉挛导致的心肌缺血,常合并恶性心律失常,可导致急性心肌梗死甚至猝死。对于狭窄程度严重者应行支架置入术。     

Efficacy of amoldipine besilate therapy for variant angina: Evaluation by 24-hour Holter monitoring

Summary The efficacy of amlodipine, a calcium antagonist, was investigated in 12 patients with variant angina. Amlodipine was administered at a dose of 5 mg once daily, and efficacy was assessed from the frequency of anginal attacks, the frequency of ST elevation or depression, and the extent of ST segment changes [ST segment elevation or depression (mm) × duration (seconds)] on the Holter ECG before and after treatment. The frequency of ST elevation during the observation period was 1.67 ± 0.33 times/day (symptomatic attacks: 1.17±0.21/day; asymptomatic attacks: 0.50±0.19/day), and this significantly decreased to zero per day (both symptomatic and asymptomatic attacks) after treatment (p<0.05). The extent of ST segment elevation during the observation period was 507.5±156.6 mm·sec/day (symptomatic: 382.5±102.9 mm·sec/day; asymptomatic: 125.0±62.0 mm·sec/day), and such changes were completely suppressed (both symptomatic and asymptomatic) by treatment (p<0.05). The frequency of ST depression was 2.08±0.42 times/day (symptomatic: 0.25±0.13/day; asymptomatic: 1.83±0.37/day) during the observation period, while it was 1.50±0.36 times/day (symptomatic: 0.25±0.13/day; asymptomatic: 1.25±0.30/day) after treatment. Although anginal attacks remained unchanged, asymptomatic attacks tended to decrease (p=0.07). The extent of ST depression during the observation period was 632.5±239.4 mm·sec/day (symptomatic: 105.0±64.4 mm·sec/day; asymptomatic: 527.5±189.5 mm·sec/day), and this significantly decreased to 333.8±111.4 mm·sec/day (symptomatic: 50.0±31.2 mm·sec/day; asymptomatic: 283.8±102.6 mm·sec/day) after treatment (p<0.05). The frequency of anginal attacks during the observation period was 1.27±0.18 times/day, and this significantly decreased to 0.40±0.12/day after 1 week of treatment and to 0.22±0.07/day after 2 weeks of treatment (p<0.05). These results suggest that amlodipine is effective for treating variant angina at a daily dose of 5 mg.     

Exercise-induced vasospastic angina after left atrial catheter ablation: A case report

Introduction

Left atrial catheter ablation (LACA) is routinely used in the management of recurrent atrial fibrillation.

Case presentation

We report a patient suffering from vasospastic angina 2 months after a LACA procedure. Typical clinical symptoms, ST-segment changes during exercise test and successful treatment with nicorandil led to the diagnosis. According to our hypothesis, destruction of autonomic ganglia in the left atrium and resulting autonomic nerve tone imbalance might be the main determinants that have caused this phenomenon.

Conclusion

Coronary spasms even weeks after LACA should draw attention to a possible association with the procedure.     

变异型心绞痛研究进展

<正>变异型心绞痛(variant angina,VA),也称血管痉挛性心绞痛(vasospastic angina,VSA),其本质是冠状动脉痉挛(coronary artery spasm,CAS)。1959年,Prinzmetal描述一种与普通心绞痛显著不同的心绞痛,其在静息状态下发作且不能由运动诱发,发作时心电图ST段抬高,但长期以来这种心绞     

Role of percutaneous transluminal coronary angioplasty in patients with variant angina and coexistent coronary stenosis refractory to maximal medical therapy

Percutaneous transluminal coronary angioplasty (PTCA) was performed with initial success in 7 patients with variant angina and significant (greater than 60%) coronary stenosis. The mean degree of stenosis was reduced from 77 +/- 12% to 29 +/- 15% and the mean systolic pressure gradient from 78 +/- 18 to 25 +/- 9 mmHg. Apart from a reversible spasm in one patient, PTCA was free of acute complications. Despite long-term treatment with nifedipine, nitrates, and warfarin (patients 1 to 5) or aspirin (patients 6 and 7) restenoses occurred in 4 of 7 patients. An aortocoronary bypass was necessary in 2 patients, 3 respectively 6 weeks after PTCA because of tighter restenoses than before PTCA. Another patient underwent successful repeat angioplasty after 6 weeks and remained improved. During a mean follow-up observation of 21 months (6 to 30 months), 4 patients were asymptomatic, even without medication. In one of these patients, the follow-up angiography (6 months after PTCA) demonstrated a restenosis. These results suggest that PTCA demonstrated a restenosis. These results suggest that PTCA can be performed without a higher risk of acute complications in patients with variant angina. Although the recurrence rate is high in these patients, sustained clinical improvement was achieved in a substantial percentage of patients in our study.