Silent myocardial infarct as a main manifestation of systemic lupus erythematosus

Myocardial infarction has rarely been reported in patients with systemic lupus erythematosus but may develop late in the disease usually as a result of severe and accelerated atherosclerosis or coronary arteritis. A 32-year-old man with untreated and unrecognized systemic lupus erythematosus, in the absence of conventional coronary risk factors (except family predisposition) and definite extracardiac manifestations of systemic lupus erythematosus had a silent myocardial infarction early in the course of the disease. A coronary arteriogram revealed multiple stenosis of the left anterior descending artery and critical stenosis of the right coronary artery. It is our belief that lupus vasculitis is a likely contributing factor in the development of obstructive coronary disease in this patient.     

Multiple coronary aneurysms in a case of systemic lupus erythematosus.

A 29-year-old woman with active systemic lupus erythematosus (SLE) sustained an anterior myocardial infarction and demonstrated angiographic evidence of multiple, diffuse coronary aneurysms. Coronary artery aneurysms have been reported in 11 prior cases of patients with SLE. A Medline search of the literature revealed no prior reports of extensive aneurysmal dilatations involving all three main coronary arteries (left anterior descending, left circumflex, and right coronary arteries).     

Unusual coronary artery aneurysm and acute myocardial infarction in a middle-aged man with systemic lupus erythematosus

A 55-year-old man developed acute myocardial infarction (AMI) related to a large coronary artery aneurysm and a distal coronary stenotic lesion after steroid therapy for systemic lupus erythematosus (SLE). Only 13 SLE patients with AMI caused by coronary artery aneurysms have been reported, 11 of whom were young or middle-aged women and the 2 remaining were young men. This is the first report of a middle-aged man with multiple coronary lesions.     

Acute myocardial infarction associated with systemic lupus erythematosus documented by coronary arteriograms

A 19-year-old man with untreated systemic lupus erythematosus had an acute myocardial infarction. A coronary arteriogram five hours after the onset of symptoms revealed total occlusion of the left anterior descending coronary artery. Reperfusion was achieved by coronary thrombolytic therapy with urokinase. Four weeks later, a coronary arteriogram showed only minimal luminal irregularities at the original site of occlusion, where significant reduction in diameter could be induced by ergonovine maleate. This case suggests that coronary arterial involvement in systemic lupus erythematosus may be related to coronary arterial spasm.     

Thrombolytic therapy for a patient with systemic lupus erythematosus and acute myocardial infarction

A young patient with systemic lupus erythematosus was admitted to our hospital because of acute myocardial infarction, and treated by thrombolysis. Coronary angiography revealed a significant stenosis of the left anterior descending artery, together with an intraluminal thrombus. Clotting studies demonstrated an anticoagulant factor suggestive of lupus erythematosus. We conclude that thrombolytic therapy can be useful in patients with systemic lupus erythematosus who present with acute myocardial infarction, although some caution is needed in treatment.     

Myocardial infarction due to coronary atherosclerosis in three young adults with systemic lupus erythematosus

Three patients, 24, 24 and 25 years of age, with systemic lupus erythematosus had signs of myocardial infarction. Two had serial electrocardiographic changes indicative of infarction without any cardiac symptoms. The third patient had clinical evidence of an acute massive myocardial infarction, which was proved at autopsy to be due to coronary atherosclerosis. This case is presented in detail and the association between systemic lupus erythematosus and myocardial infarction is reviewed. It is postulated that the relation between lupus erythematosus and coronary atherosclerosis is more than coincidental.     

Coronary artery disease in systemic lupus erythematosus: A review of the literature

CONTEXT: Coronary artery occlusive disease is a common though underappreciated complication of systemic lupus erythematosus (SLE), typically a disease of young women. A case of a premenopausal patient with SLE and an acute myocardial infarction is presented, and the etiology and management of coronary artery disease in SLE reviewed. OBJECTIVES: To review the incidence, risk factors, pathology and treatment of coronary artery disease in systemic lupus erythematosus. DATA SOURCES: MEDLINE search of articles in English-language journals from 1980 to 2000. The index words "systemic lupus erythematosus" and the following co-indexing terms were used: "coronary artery disease," "atherosclerosis," "vasculitis," "anticardiolipin antibodies," "antiphospholipid syndrome." SELECTION SYNTHESIS AND ABSTRACTION: Papers identified were reviewed and abstracted by the authors with a presentation of a summary. RESULTS: The prevalence of coronary artery disease among women with SLE between the ages of 35 and 44 years is at least 50-fold greater than among age-matched control subjects. Of these, coronary atherosclerosis accounts for the vast majority of cases; vasculitis of the coronary arteries and other causes generally believed to be more typical of SLE are comparatively rare. CONCLUSIONS: The evidence suggests that SLE is a significant risk factor for coronary atherosclerosis independent of the classic risk factors of hypertension, tobacco use, and hyperlipidemia.     

Myocardial perfusion abnormalities in asymptomatic patients with systemic lupus erythematosus

Accelerated coronary artery disease and myocardial infarction in young patients with systemic lupus erythematosus is well documented; however, the prevalence of coronary involvement is unknown. Accordingly, 26 patients with systemic lupus were selected irrespective of previous cardiac history to undergo exercise thallium-201 cardiac scintigraphy. Segmental perfusion abnormalities were present in 10 of the 26 studies (38.5 percent). Five patients had reversible defects suggesting ischemia, four patients had persistent defects consistent with scar, and one patient had both reversible and persistent defects in two areas. There was no correlation between positive thallium results and duration of disease, amount of corticosteroid treatment, major organ system involvement or age. Only a history of pericarditis appeared to be associated with positive thallium-201 results (p less than 0.05). It is concluded that segmental myocardial perfusion abnormalities are common in patients with systemic lupus erythematosus. Whether this reflects large-vessel coronary disease or small-vessel abnormalities remains to be determined.     

Angiographic progression of coronary artery disease and the development of myocardial infarction

There are few data on angiographic coronary artery anatomy in patients whose coronary artery disease progresses to myocardial infarction. In this retrospective analysis, progression of coronary artery disease between two cardiac catheterization procedures is described in 38 patients: 23 patients (Group I) who had a myocardial infarction between the two studies and 15 patients (Group II) who presented with one or more new total occlusions at the second study without sustaining an intervening infarction. In Group I the median percent stenosis on the initial angiogram of the artery related to the infarct at restudy was significantly less than the median percent stenosis of lesions that subsequently were the site of a new total occlusion in Group II (48 versus 73.5%, p less than 0.05). In the infarct-related artery in Group I, only 5 (22%) of 23 lesions were initially greater than 70%, whereas in Group II, 11 (61%) of 18 lesions that progressed to total occlusion were initially greater than 70% (p less than 0.01). In Group I, patients who developed a Q wave infarction had less severe narrowing at initial angiography in the subsequent infarct-related artery (34%) than did patients who developed a non-Q wave infarction (80%) (p less than 0.05). Univariate and multivariate analysis of angiographic and clinical characteristics present at initial angiography in Group I revealed proximal lesion location as the only significant predictor of evolution of lesions greater than or equal to 50% to infarction. This retrospective study suggests that myocardial infarction frequently develops from previously nonsevere lesions.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cardiac rupture following acute myocardial infarction in systemic lupus erythematosus: case report

A thirty-three year-old woman with systemic lupus erythematosus (SLE) suffered from acute myocardial infarction. Prednisolone 20 mg/day was used because the signs of SLE, such as fever and decreased serum C3, levels, became aggravated on the fifth hospital day of acute myocardial infarction. Fatal cardiac rupture occurred on the twenty-second hospital day. At autopsy, extensive myocardial infarction with coronary artery thrombi and diffuse coronary arteritis were revealed. The rare clinical picture of a fatal cardiac rupture in the later phase of acute myocardial infarction and the precise dosage of prednisolone for her SLE are described.     

Myocardial infarction secondary to premature coronary artery disease as the initial major manifestation of systemic lupus erythematosus

A 32-year-old woman admitted to the emergency department was diagnosed with acute anterior myocardial infarction, treated with thrombolytics and referred for angiography on the basis of her age. The patient was then referred for angioplasty with the diagnosis of an atherosclerotic lesion in the left anterior descending (LAD) coronary artery. Successful treatment of the lesion by primary stenting ensued. Laboratory findings revealed a state of hypercoagulability as well as some collagen fibre disease. The final diagnosis, confirmed by a rheumatologist, was systemic lupus erythematosus (SLE) with premature atherosclerosis of the LAD in addition to hypercoagulability. A Medline search of the literature revealed limited previous reports of myocardial infarction due to premature coronary artery disease as the first manifestation in SLE.     

A case of myocardial infarction in a young man with systemic lupus erythematosus]

Apparently the incidence of coronary artery disease in systemic lupus erythematosus (SLE) has been increasing. However, most of the cases had been treated with corticosteroids, and had atherosclerotic lesions in the coronary arterial tree. A 21-year-old man with latent and untreated SLE had an attack of acute myocardial infarction. Coronary arteriography showed eccentric stenotic lesion at the proximal segment of the right coronary artery. One week later, in the 2nd coronary arteriography, this stenotic lesion was not able to be recognized. We supposed that the coronary artery occlusion was due to thrombus formation, and was not related to atherosclerosis, arteritis and embolus. He had no coronary risk factors. Laboratory data showed lymphocytopenia, proteinuria, positive antinuclear antibody, and positive LE cell, and the case was diagnosed as SLE. Subsequent investigations showed the presence of antibodies to cardiolipin. It was suggested that anticardiolipin antibody and other thrombogenic factors were the causes of the coronary occlusive thrombosis in this patient with SLE.     

Incidence and age distribution of patients with myocardial infarction and normal coronary arteriograms

Over a 41 month period selective coronary arteriography was performed on all patients age 35 and under seen at our hospital with a documented myocardial infarction. In these 25 patients, 4 (16%) demonstrated no arteriographic evidence of coronary artery disease. One-hundred and fifty-two patients over age 35 with a documented myocardial infarction underwent selective coronary arteriography during the same period. In each of the 152 cases, obstructive coronary artery disease was demonstrated. The generally favorable prognosis of patients with myocardial infarction and normal coronary arteriograms has been previously documented. On the basis of our experience and a review of the literature, it is recommended that all patients age 35 and under sustaining a myocardial infarction should undergo selective coronary arteriography, in order to establish prognosis.     

Revisiting the culprit lesion in non-Q-wave myocardial infarction. Results from the VANQWISH trial angiographic core laboratory

OBJECTIVE: We sought to determine the underlying coronary anatomy and characterize the culprit lesion after non-Q-wave myocardial infarction (NQWMI). BACKGROUND: Although the culprit lesion and infarct-related artery often are easily identified with coronary angiography after Q-wave MI, the culprit lesion after NQWMI has not been well characterized. Small retrospective studies have suggested that the absence of Q-waves on an electrocardiogram is due to incomplete occlusion of the infarct-related artery. METHODS: Coronary angiograms from 350 patients randomized to the early invasive strategy in the Veterans Affairs Non-Q-Wave Infarction Strategies in-Hospital (VANQWISH) trial were systematically analyzed in an angiographic core laboratory. A consensus panel identified the culprit lesion and the infarct-related artery using prespecified criteria for complex lesion morphology and acute versus chronic occlusions. Severity of angiographic disease and left ventricular function also were analyzed. Patients with a single identified culprit lesion were compared with those who had multiple apparent culprits and those without an identifiable culprit lesion. RESULTS: A single culprit lesion was identified in only 49% of patients undergoing early angiography after NQWMI. The majority of patients either had no identifiable culprit (37%) or multiple apparent culprit lesions (14%). A single incomplete occlusion of the infarct-related artery was found in only 36% of patients, and an isolated acute occlusion of the infarct-related artery occurred in 13%. Patients without an identifiable culprit lesion had severe coronary disease (obstructive coronary artery disease [CAD] in 84%) but no complex lesion morphology. There was no difference in angiographic severity of disease comparing patients with and without identifiable culprit lesions. Patients with a single incomplete occlusion of the infarct-related artery were more likely to undergo percutaneous transluminal coronary angioplasty than other patients, whereas patients with multiple culprit lesions were more frequently treated with coronary artery bypass grafting. CONCLUSIONS: Coronary angiography early after NQWMI frequently identifies severe obstructive CAD, but a single identifiable culprit lesion was identified in <50% of patients. Multiple culprit lesions were seen in 14% of patients. An angiographic culprit lesion could not be identified in more than one-third of patients undergoing coronary angiography as part of an invasive strategy.     

30岁以下急性心肌梗死患者的临床和冠状动脉病变特点

目的 探讨30岁以下急性心肌梗死(AMI)患者的临床和冠状动脉病变特征.方法 2007年1月至2009年12月共360例因胸痛或胸部不适就诊于北京协和医院行急诊冠状动脉造影确诊AMI患者,对其中7例(1.9%)年龄≤30岁患者[男性4例,年龄(25±5)岁]进行回顾性分析并电话随访.平均随访时间为(12±9)个月.结果 6例为急性ST段抬高型心肌梗死,1例为非ST段抬高型心肌梗死.冠状动脉造影发现5例患者罪犯血管为前降支,左主干和右冠状动脉各1例.3例女性患者均合并先天性血管异常或自身免疫性疾病,包括1例左前降支瘤样扩张,1例大动脉炎和1例系统性红斑狼疮;4例男性患者中3例为吸烟者.2例患者进行了经皮再血管化治疗.随访期间,无患者死亡或因心脏事件再住院者.结论 30岁以下AMI患者多为急性ST段抬高型心肌梗死,以单支、非阻塞性病变常见,前降支为最常见的罪犯血管.女性患者常合并有先天性血管异常或自身免疫性疾病.短期预后较好.     

Collateral circulation to the diagonal artery from the infundibular coronary artery in obstructive coronary arterial disease

We report an unusual collateral pathway from the isolated infundibular (third coronary) artery to the diagonal artery in a young adult male with a history of recent anteroseptal myocardial infarction and apparently angiographically normal left and right coronary arteries. The isolated infundibular (conus) artery is an important source of collateral pathways in obstructive coronary arterial disease. Its selective arteriography is essential for complete angiographic evaluation of these patients.     

Angiographic morphology of coronary lesions in various syndromes of ischemic cardiopathy

The angiographic morphology of coronary lesions is often completely ignored in the prognostic and decision-making process related to patients with coronary disease. We performed this study to evaluate the possibility of identifying complex or complicated atherosclerotic lesions by means of routine diagnostic coronary arteriography, and to assess their prevalence in the different syndromes of ischaemic heart disease. From an overall group of 200 successive cases studied using coronary angiography, 111 patients with significant coronary artery disease in whom a "culprit lesion" could be identified were retrospectively selected. The angiographic morphology of coronary lesions was defined according to an original classification as: 1) simple stenosis, 2) complex lesion, 3) thrombosis. Of the 111 patients, 36 had been studied for stable angina, 31 for unstable angina, 10 for a non-Q wave myocardial infarction, 34 for transmural infarction. The clinical groups did not show any significant differences when compared on the basis of number of vessels involved and degree of narrowing of the ischaemia-producing artery. Significant differences were found when angiographic morphology was analyzed. In stable angina 78% of ischaemia producing lesions appeared as simple stenoses, while 92% of the unstable or more severely ischaemic patients exhibited complicated lesions (p less than 0.001). In unstable angina and non-Q infarction a complex lesion was present respectively in 71% and 60% of the cases; clear-cut intraluminal thrombosis was demonstrated in 23% of unstable angina, in 30% of non-Q wave infarction and in 39% of transmural infarction (p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Atteinte coronarienne et syndrome néphrotique au cours du lupus systémique : à propos d’une observation

IntroductionHeart failure during systemic lupus erythematosus has various causes.Case reportA 29-year-old female presented with a systemic lupus flare and a nephrotic syndrome, followed by cardiogenic shock requiring extra-corporeal membranous oxygenation. Ventricular dysfunction was related to massive myocardial infarction due to an anterior interventricular artery thrombosis and an underlying atheroma. The young age and the absence of chest pain were not suggestive of coronary artery disease initially. Coronary thrombosis was probably favored by the nephrotic syndrome, in which the arterial thrombotic risk is increased.ConclusionCoronary artery disease should be systematically evoked in the presence of ventricular dysfunction in patients with systemic lupus, including when they are young and in the absence of chest pain. Nephrotic syndrome should be identified as a risk factor for arterial thrombosis.     

Angiographic assessment of the culprit coronary artery lesion before acute myocardial infarction

Serial angiographic studies of patients with myocardial infarction and unstable angina suggest that the culprit plaque underlying a thrombus need not have produced severe luminal obstruction before onset of the event. An atherosclerotic coronary artery lesion can, therefore, have 2 important characteristics. First, it may be obstructive. Second, it may be "vulnerable" in that it has the potential to become thrombogenic if exposed to the appropriate triggering stimulus. A lesion need not be obstructive to become thrombogenic, nor do all obstructive lesions have thrombogenic potential. The cause of an infarction may thus be rupture of a nonobstructive plaque leading to occlusive thrombus formation. Because it may be difficult to predict the site of a subsequent occlusion from a coronary angiogram, coronary bypass surgery or angioplasty directed only at discernible stenotic lesions may not be effective for preventing subsequent myocardial infarctions. Appropriate therapy may need to be directed at the entire coronary tree. Such therapy might include cholesterol lowering, beta blockade and aspirin.     

Spontaneous Coronary Artery Dissection in a 35 Year-Old Woman with Systemic Lupus Erythematosus Successfully Treated by Angioplasty

Spontaneous coronary artery dissection (SCAD) is an unusual cause of acute myocardial ischaemia with complex pathophysiology; it has been associated with several conditions such as atherosclerosis, connective tissue disorders and the peripartum period. SCAD has exceptionally been reported (three published cases) in patients with systemic lupus erythematosus (SLE). In this work, we report the original case of a 35 year-old woman with a known history of SLE who presented with an acute coronary syndrome caused by an extensive dissection of the left anterior descending artery (LAD) and the diagonal and who was successfully treated by an intravascular ultrasound (IVUS)-guided percutaneous angioplasty.