Cefuroxime-induced coronary artery spasm manifesting as Kounis syndrome

Allergic angina and allergic myocardial infarction (Kounis syndrome) occurring during the course of a drug-induced allergic reaction in the absence of angiographically stenosed coronary arteries, is rare in clinical practice. This paper reports the case of a 70-year-old woman with no significant risk factors for coronary artery disease who developed coronary artery spasm after intravenous injection of cefuroxime. A subsequent coronary angiogram revealed normal coronary arteries (type I variant of the syndrome). The allergic reaction following cefuroxime administration seems to have triggered the development of coronary artery spasm. Susceptible individuals expressing an amplified mast cell degranulation effect may be more vulnerable to coronary artery spasm. The clinical implications of this syndrome are also discussed.     

Acute myocardial infarction induced by ergotamine tartrate: possible role of coronary arterial spasm

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.     

Kounis syndrome with Samter–Beer triad treated with intracoronary adrenaline

Kounis syndrome is a well‐described clinical condition characterized by the simultaneous occurrence of chest pain and an allergic reaction accompanied by clinical and laboratory findings of angina caused by inflammatory mediators released during an allergic insult. We present the case of a 50‐year‐old male with the Samter–Beer triad of asthma, nasal polyps, and salicylate intolerance with an ST elevation myocardial infarction complicated with cardiac arrest due to multi‐vessel coronary artery spasm secondary to aspirin anaphylaxis. Adrenaline is recommended during anaphylaxis but is controversial in Kounis syndrome as it may worsen coronary spasm. We report the use of intracoronary adrenaline in successfully reversing coronary artery spasm in this hemodynamically unstable patient. © 2015 Wiley Periodicals, Inc.     

Role of coronary artery spasm in ischemic heart disease. Therapeutic implications

The term coronary artery spasm should not be used interchangeably with the specific clinical syndrome "variant angina" since it does occur in other acute and chronic ischemic heart disease syndromes. The term coronary artery spasm should not be applied to patients with ischemic heart disease unless there is clinical, angiographic, and physiologic evidence of its presence. The diagnosis of coronary artery spasm is confirmed by angiography, i.e. change in caliber of the coronary arteries plus evidence of ischemia. Probable diagnosis is in patients who have the syndrome of variant angina, i.e. rest angina associated with ST segment elevation on the electrocardiogram. One can be highly suspicious that the spasm is at work in patients who have rest angina, especially those with unstable angina. One can be suspicious of patients who have variable effort angina or walk-through angina. Coronary artery spasm is a possibility in patients with an acute myocardial infarction or acute re-infarction and is also possible that sudden death in patients with normal coronary arteries can be related to coronary artery spasm. Coronary artery spasm is the usual cause of myocardial ischemia in patients with rest angina without effort angina. This has also commonly been documented in patients with rest and effort angina. There are isolated reports suggesting that patients with effort angina pectoris also develop coronary artery spasm. Coronary artery spasm has been documented to occur in association with acute myocardial infarction. Whether coronary artery spasm is the cause or the result of myocardial infarction has not been determined at this time. However, the recent combined use of intracoronary nitroglycerin and intracoronary streptokinase in patients with acute myocardial infarction has shown reversal of totally obstructed arteries and suggests the relationship between coronary artery disease, coronary artery spasm, and in situ coronary thrombosis. The incidence of sudden death in patients with documented coronary artery spasm is unknown. But, since complete heart block and/or ventricular tachycardia occur during episodes of coronary artery spasm, it is not unreasonable to assume that some patients have died as a result of these rhythm disturbances. The prognosis of patients with coronary artery spasm seems to depend on the presence or absence of severe coronary atherosclerosis, i.e. those with severe disease have a worse prognosis. Current therapy of patients with coronary artery spasm involves the use of nitrates and calcium antagonists.(ABSTRACT TRUNCATED AT 400 WORDS)     

A case of variant angina with normal coronary arteriogram who developed acute myocardial infarction and cerebral embolism

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.     

冠脉痉挛与变异型心绞痛和急性心肌梗死的关系

目的 探讨冠脉痉挛与变异型心绞痛(VA)和急性心肌梗死(AMI)的关系。方法 对30例AMI和14例VA患者施行冠状动脉造影(CAG),以冠脉狭窄>50％为CAG阳性。结果 在30例AMI患者中有4例CAG正常,在14例VA中,CAG正常2例,狭窄程度在50％～90％的12例。结论 本文结果提示,冠脉痉挛在VA和AMI的发病中起着十分重要的作用。冠脉痉挛不仅可以发生在有严重狭窄的冠状动脉,亦可以发生于造影正常的冠状动脉。     

Left coronary artery spasm causing severe left ventricular dysfunction without myocardial infarction

This report describes a patient with persistent, recurrent left anterior descending coronary artery spasm, which causes marked left ventricular dysfunction in a clinical course that is typical of acute myocardial infarction with hyperacute electrocardiographic changes. However, after emergency coronary artery bypass surgery, the patient had complete reversal of left ventricular dysfunction, with no residual evidence of acute myocardial infarction by electrocardiograph or gated blood pool imaging and no CPK enzyme rise. The patient therefore demonstrates that coronary spasm in some instances clearly precedes the sequence of pathophysiologic events leading to acute myocardial infarction. Our report also demonstrates for the first time in man that massive left ventricular dysfunction may occur in this intermediate coronary syndrome, presenting clinically as impending myocardial infarction. With aggressive surgical intervention and emergency bypass surgery, left ventricular function was restored to normal. Despite the semantic problems of categorizing such patients as having impending myocardial infarction, the severe left ventricular dysfunction and alarming course of this patient's illness was resolved by emergency surgery, suggesting that, in some instances, aggressive therapy is warranted.     

Kounis syndrome (allergic acute coronary syndrome): different views in allergologic and cardiologic literature

The clinical picture of myocardial ischemia accompanying allergic reactions is defined in the cardiologic literature as Kounis syndrome (KS) or allergic angina/myocardial infarction. In PubMed, a search for ??Kounis syndrome??, ??allergic angina?? or ??allergic myocardial infarction?? retrieves more than 100 results (among case reports, case series and reviews), most of which are published in cardiology/internal medicine/emergency medicine journals. In allergologic literature, heart involvement during anaphylactic reactions is well documented, but Kounis syndrome is hardly mentioned. Single case reports and small case series of angina triggered by allergic reactions have been reported for many years, and involvement of histamine and others mast cell mediators in the pathogenesis of coronary spasm has long been hypothesized, but the existence of an allergic acute coronary syndrome (ACS) is still questioned in the allergologic scientific community. Putative mechanisms of an allergic acute coronary syndrome include coronary spasm or heart tissue-resident mast cell activation (precipitating coronary spasm or inducing plaque rupture and coronary or stent thrombosis) due to systemic increase of allergic mediators, or heart tissue-resident mast cell activation by local stimuli. Indeed, the pathogenic mechanism of an ACS after an allergic insult might be related to direct effects of mast cell mediators on the myocardium and the atherosclerotic plaque, or to exacerbation of preexisting disease by the hemodynamic stress of the acute allergic/anaphylactic reaction. Which of these mechanisms is most important is still unclear, and this review outlines current views in the cardiologic and allergologic literature.     

Kounis综合征研究进展

Kounis综合征是一种由严重过敏反应诱发的急性冠状动脉综合征。常在过敏体质患者接触过敏原或易致过敏反应的药物时诱发。Kounis综合征的临床特征是急性心肌缺血及急性过敏反应的临床表现共存。它与肥大细胞激活、脱颗粒,释放出大量生物胺、活性酶、及细胞因子等炎性介质,诱发冠状动脉痉挛、冠状动脉斑块糜烂、破裂和冠状动脉支架内血栓形成等相关。根据冠状动脉造影结果 Kounis综合征可以分三型:Ⅰ型冠状动脉正常型,Ⅱ型冠状动脉粥样硬化型,和Ⅲ型冠状动脉支架内血栓型。Kounis综合征患者的治疗,需兼顾急性心肌缺血和急性过敏性反应两种病因,至今尚缺乏相关的循证医学研究,仅能依据各自的诊疗指南及以往的病例报道经验进行诊治。在急性过敏反应及急性冠脉综合征发病机制中有相同的炎症细胞及炎症因子参与,两者有着共同的通路。因此能够稳定肥大细胞或阻止肥大细胞内容物释放的药物,可能为防治急性冠脉事件提供了新的思路。     

Spontaneous coronary artery dissection after a natural course for 10 years--a case report.

We encountered a patient with spontaneous coronary artery dissection complicated by acute inferior myocardial infarction. A 58-year-old male was admitted to our hospital due to acute inferior myocardial infarction in 1979. Coronary angiography performed 4 weeks after the onset showed a double lumen divided by a linear intimal flap in the right coronary artery, suggesting coronary artery dissection, but no apparent occlusion. Subsequently, he had been medicated with nitrates without any recurrent infarction. In February, 1989, 10 years after the first examination, coronary angiography was again performed and showed that the dissection had remained unchanged. Acetylcholine infusion into the right coronary artery induced coronary spasm. The prognosis of this condition seems to be better than has been generally considered, particularly in patients such as ours in whom the involvement of coronary spasm in the development of coronary artery dissection and myocardial infarction is suggested. When coronary spasm in controlled by treatment with nitrates or calcium antagonists, an uneventful course may be expected.     

Automatic implantable cardioverter defibrillator for the treatment of ventricular fibrillation following coronary artery spasm: a case report

Coronary artery spasm is an infrequently recognized condition that causes Prinzmetal's angina and specific electrocardiographic changes. A 50-year-old man who suffered a spontaneously aborted acute inferior myocardial infarction is presented. He underwent cardiac catheterization, which initially showed a normal coronary artery. The coronary angiogram was repeated shortly after a second presentation of acute coronary syndrome and ventricular fibrillation. Coronary spasm of very proximal right coronary artery was present, which was reversed completely with intracoronary nitroglycerin. The spasm segment was first stented. Subsequently, an automatic implantable cardioverter defibrillator was inserted because of the uncertainty of future spasm recurrence. The patient was discharged with oral isosorbide dinitrate and Amlodipine. In further follow-up, the patient had two separate shocks within 4 months of implantation. Ventricular fibrillation was the trigger for the shock therapy in both occasions.     

Coronary spasm in acute myocardial infarction

A 30 year old man had an acute anterolateral myocardial infarction following which he developed unstable angina requiring percutaneous transluminal coronary angioplasty. He subsequently developed further angina with recurrence of coronary artery lesions that were reversed by intracoronary nitrate. A diagnosis of prinzmetal (vasospastic) angina was made and this had been the apparent cause of his myocardial infarction. He was treated with a calcium antagonist and an oral long acting nitrate with resolution of symptoms. He remained well and symptom free, and was reviewed in the outpatient clinic six weeks after discharge without problems.

Keywords: coronary spasm; acute myocardial infarction; syndrome X; prinzmetal's angina     

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.

In contrast to findings in patients manifesting only typical exertional angina, the hemodynamic findings during spasm were those of a hypodynamic state. Left ventricular systolic pressure decreased from 138.9 ± 6.0 (mean ± standard error of the mean) to 113.2 ± 6.2 mm Hg; left ventricular end-diastolic pressure did not change significantly. Myocardial lactate extraction during spasm was invariably markedly reduced: −53.19 percent ± 15.44 (P < 0.001). However, the effect of coronary sinus pacing on myocardial lactate extraction was not significantly abnormal: +15.74 percent ± 6.66.

The respective roles of medical and surgical intervention are uncertain. Only 3 patients had a completely satisfactory pharmacologic response to nitrates alone or in combination with propranolol, and the condition of 5 others was partially improved; the remaining 21 patients were judged intractable to medical management. Coronary bypass surgery was performed as the ultimate recourse in 18 patients. However, short-term results reveal that only nine (50 percent) showed improvement, four (22 percent) had myocardial infarction during or after surgery and four (22 percent) died.

These studies confirm that coronary arterial spasm is a definite pathogenetic factor in a variety of acute myocardial ischemic syndromes. The incidence and full clinical significance of this functional disorder remain to be determined.     

Coronary artery spasm in the genesis of myocardial ischemia

Angina pectoris that is mainly caused by coronary artery spasm (coronary spastic angina) has 1 or more of the following characteristics: (1) the attack occurs at rest, (2) the attack is associated with ST-segment elevation on the electrocardiogram (not necessarily so in case of old myocardial infarction), (3) the attack has a variable exercise threshold, and (4) the attack is suppressed by calcium antagonists but not by beta-adrenergic blocking agents. By this criteria, coronary artery spasm is involved in the development of most angina pectoris in patients with 1-vessel disease. The role of coronary artery spasm in the development of acute myocardial infarction is still controversial. However, in this study, injection of nitroglycerin, 0.2 mg, into the totally or subtotally occluded coronary artery either released the occlusion or improved the patency in 13 of the 69 patients (18.8%) with acute transmural myocardial infarction in whom coronary arteriography was performed within 4.0 +/- 1.9 hours of the onset of symptoms. Thus, coronary artery spasm appears to play a role in the production of acute myocardial infarction in these patients.     

Acute myocardial infarction after anaphylactic reaction to amoxicillin]

A 62-year-old man was admitted to the hospital in a state of shock with electrocardiographic signs of inferior-wall acute myocardial infarction. He was initially diagnosed of cardiogenic shock. An urgent coronary angiography showed an irregular stenosis of 90% in the right coronary artery. Coronary angioplasty was performed, and a stent was placed in this lesion. In-depth questioning of the family revealed that the patient had taken an oral dose of amoxicillin 15 minutes before the onset of the symptoms. Further tests proved that he was allergic to amoxicillin, and was diagnosed of anaphylactic shock, complicated with acute myocardial infarction. There are several reports of myocardial infarction as a complication of anaphylactic reaction. We have found very few cases related to antibiotics, and none associated with amoxicillin. The most frequently quoted mechanism in these cases is coronary artery spasm due to the mediators of anaphylaxis. In the case reported herein, the irregular lesion suggests that disruption of an atherosclerotic plaque and platelet aggregation have occurred.     

Lethal presentations of coronary artery spasm after an event-free period of six years following initial diagnosis

Isolated coronary artery spasm without atherosclerotic obstruction is an unusual cause of myocardial infarction (MI). A middle-aged woman presented to our institution in 2001 with acute inferior MI due to coronary artery spasm at the mid segment of the dominant left circumflex coronary artery. After being well for 6 years, she was readmitted again in 2007 with the same type of severe retrosternal chest pain. Electrocardiography (ECG) showed ST-segment elevation over the inferior leads. The chest pain resolved with sublingual nitroglycerin and emergency diagnostic coronary angiography showed normal coronary arteries. Two months later, the patient developed another episode of severe retrosternal chest pain at home, followed by cardiac arrest. An onsite ECG showed ventricular fibrillation and immediate defibrillation was carried out. She was readmitted to the hospital and recovered over the next few days. In view of the recurrent coronary artery spasm causing myocardial infarction and ventricular fibrillation, an implantable cardioverter defibrillator was implanted. The patient was well at 2-month follow up.     

Myocardial bridge of the left anterior descending coronary artery and myocardial infarction: does coronary spasm play a part?]

The association of a myocardial bridge of the left anterior descending (LAD) coronary artery and myocardial infarction is rare. The mechanisms by which the myocardial bridge could predispose to myocardial infarction are tachycardia (reducing the duration of diastolic coronary filling), thrombosis at the site of the myocardial bridge, and coronary spasm which, however, has never been demonstrated in the context of infarction. The aim of this study was to detect coronary spasm by provocative ergometrine testing in 4 patients, all male, aged 21 to 49 years, average 39 years old, who had anterior myocardial infarction associated with myocardial bridging of the LAD artery without atheromatous coronary stenosis. The ergometrine tests were performed during (2 cases) or after coronary angiography (2 cases). The systolic narrowing due to the myocardial bridge ranged from 25 to 95% (average 70%). The ergometrine test was strongly positive in 1 patient and negative in the other 3. Repermeabilisation of a thrombus was suggested in these 3 patients by the recording of an accelerated idioventricular rythm in the acute phase of infarction (2 cases) or by the demonstration of abnormal platelet aggregation (1 case). This is the first report of coronary spasm in a patient with myocardial bridging associated with infarction. However, it is not possible to determine the respective roles of spasm and myocardial bridging in the genesis of the infarct. We suggest systemic provocative ergometrine testing in this situation to orientate the most appropriate treatment.     

Arteriographic evidence of coronary arterial spasm in acute myocardial infarction.

Coronary arteriography was performed before and after the intracoronary injection of nitroglycerin to determine the presence or absence of spasm in patients within the first 12 hours of acute myocardial infarction. Coronary arterial spasm was demonstrated in six of fifteen (40%) acute myocardial infarctions associated with coronary artery disease. In five of the six instances the interval from the onset of symptoms to arteriography was less than 6 hours. Spasm was superimposed on a high-grade atherosclerotic obstruction and was separated from the catheter tip by a segment of normal vessel in each instance. The coronary artery remained patent (following the initial relief of spasm) in two patients maintained on sublingual nitrates and heparin. Spasm, superimposed on an atherosclerotic obstruction, may be the primary event or a secondary occurrence in the pathophysiology of acute myocardial infarction. Catecholamines could play an important role in the early pathophysiology of acute myocardial infarction by producing spasm and/or platelet aggregation at the site of an atherosclerotic obstruction. A dynamic interaction between spasm, platelet aggregates and the atherosclerotic plaque may precede coronary thrombosis.     

Ergonovine maleate provocative test for coronary arterial spasm

Ergonovine maleate was evaluated as a provocative agent for inducing coronary spasm during coronary arteriography. The study group consisted of 98 patients with either mild fixed obstructions of coronary luminal diameter (less than 50 percent) or normal coronary arteriograms. The test was considered positive if the drug precipitated severe coronary spasm. A positive ergonovine test occurred in 10 of 11 patients with Prinzmetal's variant angina (P < 0.02). Two of these patients had a transmural myocardial infarction in the distribution of the spastic artery. Ergonovine tests were negative in (1) the 15 control patients with no clinically suspected coronary artery disease (P < 0.001), (2) 63 of 66 patients with angina-like chest pain (P < 0.001), and (3) all 6 patients with myocardial infarction and no history of Prinzmetal's variant angina (P < 0.05). No major complications occurred as a result of this test.Thus, ergonovine maleate test is a safe, sensitive and specific method for reproducing coronary spasm in patients with Prinzmetal's variant angina and no major coronary obstructions. The results suggest that coronary spasm can be implicated as a cause of myocardial infarction in patients with normal coronary arteriograms who also have Prinzmetal's variant angina. Coronary spasm was not demonstrated in patients who had normal coronary arteriograms and a history of myocardial infarction as an isolated clinical event. Also, coronary spasm could not be demonstrated in the majority of patients who had angina-like chest pain and no major coronary obstruction.