Angiographic demonstration of spontaneous diffuse three vessel coronary artery spasm

The spontaneous occurrence of diffuse three vessel coronary artery spasm was documented during routine coronary angiography in three patients with a history of variant angina. Quantitative angiographic analysis of 18 arterial segments demonstrated that the mean luminal diameter of 1.47 mm during spasm increased to 2.47 mm after the administration of nitroglycerin (p less than 0.0001). The underlying coronary arteries were normal or near normal. Although multivessel spasm has previously been considered to be uncommon and its spontaneous occurrence during angiography only rarely documented, these cases suggest that it may be more common than previously recognized. In addition to important diagnostic considerations, this phenomenon may have important implications regarding the pathophysiologic role of endothelium in coronary artery spasm.     

Exercise-induced coronary arterial spasm: Angiographic demonstration,documentation of ischemia by myocardial scintigraphy and results of pharmacologic intervention

Exercise-induced coronary arterial spasm is an infrequently recognized phenomenon whose mechanism and management are not well established. In two patients with reproducible exercise-induced S-T segment elevation and angina pectoris thallium-201 scintigraphy showed areas of reversible anteroapical hypoperfusion, and gated radionuclide ventriculography revealed anteroapical hypokinesia with a decrease in left ventricular ejection fraction at peak exercise. During coronary arteriography, supine exercise provoked occlusive spasm of the left anterior descending coronary artery, which at rest had only minimal plaques'. Consequently, treadmill testing was performed with five different pharmacologically provoked interventions: direct vasodilatation (nitrates), alpha adrenergic blockade (phenoxybenzamine), beta adrenergic blockade (propranolol), calcium flux blockade (verapamil), and prostaglandin inhibition (indomethacin). Exercise-induced coronary arterial spasm, manifested as S-T segment elevation and angina, was prevented by nitrates, but was not eliminated by short-term oral administration of an alpha or beta blocking agent, a calcium antagonist or a prostaglandin inhibitor. Further, beta adrenergic blockade appeared to be detrimental. Thus, this study demonstrates (1) that coronary arterial spasm may be the underlying mechanism of at least some cases of exertional angina associated with transient perfusion deficits and left ventricular dysfunction, and (2) that it may be prevented by oral nitrates.     

Nifedipine blockade of ergonovine-lnduced coronary arterial spasm: Angiographic documentations

To determine whether calcium-flux blockade with nifedipine blunts coronary vasospasm, four patients with angiographically demonstrable coronary arterial spasm in the absence of Significant fixed coronary arterial stenosis were evaluated with coronary arteriography before and after treatment with nifedipine. After initial coronary arteriography, ergonovine was administered in successive doses of 0.05, 0.1 and (when necessary) 0.2 mg intravenously at 3 minute intervals. Three patients had symptomatic high grade focal coronary arterial spasm with electrocardiographic changes, and the fourth exhibited asymptomatic 60 percent constriction of the left anterior descending coronary artery. A maximal ergonovine challenge was repeated 30 minutes later after each patient had been pretreated with a 20 mg sublingual dose of nifedipine. Under these conditions, no patient had chest pain or electrocardiographic changes. Furthermore, neither focal nor diffuse coronary arterial spasm was demonstrable angiographically after the second challenge. Thus, in each case, a single dose of nifedipine precluded the angiographie expression of ergonovine-provoked coronary arterial spasm.     

Angiographic presentation of coronary artery spasm in heart transplant recipients

We describe the angiographic characteristics of coronary artery spasm observed in 12 out of 247 (4.9%) patients who underwent 808 coronary angiographies after heart transplantation. Coronary artery spasm was diagnosed when localized and reversible narrowing of the coronary lumen was identified. After coronary artery spasm identification all patients were followed-up clinically for a mean period of 5.1 years. Coronary artery spasm was documented 1-3 years after heart transplant. Coronary artery spasm affected 1 main coronary artery in 10 patients and 2 in 2 patients; in 3 patients 1 or more secondary branches were also affected. The right coronary artery was affected by coronary artery spasm in 8 patients and the anterior descending coronary artery in 6 patients. In 6 patients coronary artery spasm was mechanically induced by the catheter tip. The degree of luminal narrowing due to coronary artery spasm ranged from mild to almost complete occlusion. Coronary artery spasm appeared as a single tubular smooth and concentric stenosis in 8 patients, was discrete in 2 patients and multiple on the same vessel in 2 patients. In 1 patient coronary artery spasm was erroneously interpreted as an organic lesion and percutaneous transluminal coronary angioplasty was planned. During follow-up 3 patients out of 4 who had shown multiple coronary artery spasm died and 2 patients developed critical organic stenosis. In conclusion coronary artery spasm after heart transplant is less rare than commonly believed. Although it usually has a peculiar appearance, it can be misinterpreted as an organic lesion. Multiple coronary artery spasm appears to carry a poor prognosis.     

Arteriographic demonstration of coronary artery spasm during thrombolysis

A 60-year-old man with an acute inferior-wall myocardial infarction was noted, on arteriography, to have an occluded distal right coronary artery. The vessel was reopened with intravenous tissue plasminogen activator; during resolution of the clot, spasm was observed arteriographically but was successfully treated with intracoronary nitroglycerin. Follow-up arteriography showed a normal right coronary artery. The significance of this case lies in the fact that we were able to document the occurrence of spasm during coronary thrombolysis; such documentation supports the hypothesis that spasm may be a factor in the initiation of coronary thrombosis.     

Angiographic assessment of the infarct-related residual coronary stenosis after spontaneous or therapeutic thrombolysis

The severity of the infarct-related residual coronary stenosis after spontaneous or therapeutic thrombolysis was quantitatively assessed in 91 patients with an acute myocardial infarction who were allocated to treatment in the acute stage with either a thrombolytic agent (100 mg of recombinant tissue-type plasminogen activator given over 3 h, 49 patients) or a placebo (42 patients). Heparin and aspirin were given to both groups until angiography was performed. Digital subtracted images of the infarct-related coronary vessel were obtained 10 to 14 days after hospital admission and were subsequently analyzed with the use of a computer-assisted coronary stenosis measurement system. Neither treatment group differed significantly in age, gender or location of the culprit coronary lesion. Median values (90% range) in the thrombolysis and control groups were, respectively, 1.95 (0.9 to 5.3) mm versus 1.7 (0.9 to 3.4) mm for stenosis length; 1.4 (0.8 to 2.7) mm versus 1.4 (0.9 to 1.8) mm for minimal luminal diameter; 57% (36% to 75%) versus 58% (44% to 71%) for diameter obstruction; 82% (59% to 95%) versus 82% (68% to 92%) for geometric area obstruction; and 78% (58% to 91%) versus 79% (66% to 90%) for densitometric area obstruction. The difference between the two groups was not statistically significant for any of these measurements. Thus, in this study no significant differences in anatomy or severity of residual coronary stenosis could be demonstrated at 10 to 14 days after an acute myocardial infarction in patients with a recanalized infarct-related vessel, whether or not thrombolytic therapy was given on admission. These results indicate that with effective antithrombotic treatment, gradual endogenous fibrinolysis or more rapid lysis induced by the infusion of a thrombolytic agent results in a similar infarct-related coronary lesion at the time of hospital discharge.     

Prolonged catheter-induced coronary artery spasm mimicking fixed stenosis

Two cases of prolonged catheter-induced right coronary artery spasm, mimicking fixed stenoses, are presented. In one case, the spasm appeared at the same place in sequential catheterizations. This angiographic finding may be easily misinterpreted as a fixed lesion, leading to unnecessary attempts at angioplasty. Cathet. Cardiovasc. Diagn. 41:170–173, 1997. © 1997 Wiley-Liss, Inc.     

Relation of coronary arterial spasm to sites of organic stenosis

Among 63 patients with Prinzmetal's variant angina, coronary arterial spasm responsible for attacks of variant angina was documented arteriographically in 9 patients. In each observed episode (11 attacks in nine patients), coronary spasm producing myocardial ischemia occurred at and was superimposed on a site of preexisting organic stenosis. Measurements of normal portions of "spastic" and "nonspastic" vessels suggested a generalized uniform constriction of all major coronary arteries during attacks, with "spasm" limited to the site of an organic lesion in most cases. In two cases the magnitude of constriction in all vessels was consistent with generalized coronary hypercontractility or spasm. Among 104 patients with organic coronary artery disease and documented single vessel coronary spasm (foregoing 9 patients combined with 95 others from published reports), there were 70 patients with essentially single vessel organic coronary disease in 90 percent of whom the spasm involved the diseased vessel. Of 60 cases abstracted from the literature in which the relation of coronary spasm to the site of organic disease was described, 88 percent had the spasm causing ischemia localized to the site of an organic lesion. Hypotheses attempting to describe the pathophysiologic aspects of coronary spasm in variant angina must account for the intimate association of spasm with sites of organic stenosis in the majority of cases.     

Angiographic characteristics of the infarct-related coronary artery in patients with angina pectoris after myocardial infarction

To elucidate the pathophysiology of angina pectoris after myocardial infarction, we analyzed the coronary stenoses in 45 subjects (28 men, 17 women, aged 33 to 67 years) with recent (less than or equal to 60 days) infarction, significant narrowing of only the infarct-related artery, and residual anterograde flow in this artery. Postinfarction angina was absent in 19 (group I) and present in 26 (group II). The groups were similar in age, left ventricular function, incidence with which each coronary artery was involved, as well as stenosis diameter (1.0 +/- 0.3 vs 0.9 +/- 0.4 mm [mean +/- standard deviation], respectively, difference not significant), stenosis area (0.9 +/- 0.4 vs 0.8 +/- 0.8 mm2, respectively, difference not significant), percent diameter narrowing (65 +/- 5 vs 66 +/- 9, respectively, difference not significant), and stenosis eccentricity. However, those with postinfarction angina had longer stenoses (group I, 4.3 +/- 1.4 mm; group II, 10.3 +/- 4.0 mm; p less than 0.001). Thus, patients with postinfarction angina and residual anterograde flow in the infarct artery may have angina due to a marked reduction in anterograde flow, caused by a long stenosis. There is no apparent relation between stenosis eccentricity and postinfarction angina.     

Relationship between coronary atherosclerotic stenosis and cerebral atherosclerotic stenosis

To investigate the relationship between severity of cerebrovascular atherosclerosis stenosis and that of coronary atherosclerosis stenosis.Methods Cerebral angiography and coronary angiography were performed in 34 patients who had coronary disease with cerebral ischemia.Patients were divided into 3 subgroups according to the degree ofstenosis on angiography,concomitant diseases,risk factors and biochemical data.Results The follow-up study showed that the incidence of cardiac and cerebrovascular death increased significantly in patients with moderate to severe stenosis of coronary and cerebral arteries;the severity of stenosis in the coronary artery parallels that in the solitary carotid artery,or dual carotid and vertebral arteries.Conclusions Patients with coronary and cerebral artery stenosis,especially those with multi-risk factors,such as hypertension,diabetes and cigarette smoking,should receive intensive treatment to reduce cardiac and cerebrovascular events.(J Geriatr Cardiol 2008;5:227-229)     

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     

冠状动脉粥样硬化狭窄与脑动脉粥样硬化狭窄的关系

目的探讨颈动脉和（或）脑动脉粥样硬化狭窄与冠状动脉狭窄的关系。方法选择34例心内科住院伴有脑缺血症状、接受冠状动脉造影并颈动脉造影或全脑血管造影的患者。根据造影动脉管腔狭窄的程度分别分成三个亚组,冠状动脉狭窄分为轻度狭窄组（5例）、中度狭窄组（4例）、重度狭窄组（25例）;脑血管狭窄分为轻度狭窄组（6例）、中度狭窄组（4例）、重度狭窄组（24例）。结果冠状动脉狭窄与颈动脉或椎动脉狭窄程度分布一致,冠状动脉血管重度狭窄者25例,脑血管重度狭窄者24例,二者间差异无统计学意义;冠状动脉Califf危险记分≥2分者,脑血管中、重度狭窄的比例高达92％,且随着冠状动脉狭窄程度的加重,颈动脉及脑血管狭窄的程度亦加重。随访发现中重度双重狭窄（冠状动脉狭窄同时伴有脑动脉狭窄）病变的心脑事件发生明显增多,其中双重度狭窄死亡3例。结论颈动脉或椎动脉粥样硬化性狭窄的发生率及程度与冠状动脉狭窄是平行的。故对冠状动脉狭窄合并颈动脉和（或）椎动脉粥样硬化狭窄者,尤其伴有高血压、糖尿病、吸烟等多重危险因素时,应给予积极强化的联合治疗以减少心脑血管事件的发生。     

Coronary artery spasm associated with a moderately severe atherosclerotic stenosis in the proximal LAD

Treatment of coronary artery spasm can be difficult; up to 25% of patients continue to have episodes of chest pain despite maximal therapy with calcium antagonists and nitrates. We describe the case of a 42-year-old female with severe coronary artery spasm associated with a moderately severe atherosclerotic stenosis of the proximal left anterior descending coronary artery. We discuss the diagnostic value of intravascular ultrasound and treatment options for spasm associated with atherosclerotic plaques.     

Complex coronary artery disease due to coronary spasm and atherosclerotic lesions - a case report

We present a case of 55-year old man with a complex form of ischaemic heart disease. Except a significant narrowing of the circumflex coronary branch, a spasm of several branches of left coronary artery was found. The percutaneous balloon angioplasty and a modification of pharmacological treatment (introduction of nitrates and Ca-blockers) was effective. Clinical aspects and possible mechanisms of coronary artery spasm are discussed.     

Angiographic morphology and intraluminal coronary artery thrombus in patients with angina pectoris: clinical correlations

A prospective study was conducted in 104 consecutive patientswho underwent coronary angiography for the evaluation of anginapectoris. 50 patients experienced unstable symptoms, while therest of them were stable. Coronary lesions reducing the luminaldiameter by at least 50% were compared between both groups accordingto localization, grade, length, type and collateralization.Eccentric irregular lesions (EIL) appeared more frequently inthe unstable group of patients (27% vs 3%, P<0.01), whilethe incidence of concentric lesions was higher in stable group(45% vs26%, P <0.02). There was no significant differencein localization, grade, length, or collateralization. EIL weremost frequently identified as spontaneous AP producing lesions(55%, P <0.001) in 29 patients in the unstable group. Spontaneousangina was associated in 86% with EIL, occlusions, or fillingdefects— all of these lesions might contain occlusiveor nonocclusive thrombi. EIL with a narrow neck appeared onangiograms earlier than EIL with a wall irregularity. We concludethat EIL is a sensitive and very specific angiographic markerof unstable AP. The morphologic details of EIL may help oneto choose appropriate therapy.