Aspirin, clopidogrel, and warfarin: is the combination appropriate and effective or inappropriate and too dangerous?

OBJECTIVE: To review the rationale, clinical practice guideline recommendations, and clinical trial data describing bleeding and clinical outcomes associated with the use of the combination of aspirin, a thienopyridine, and warfarin. DATA SOURCES: An English-language literature search was conducted using MEDLINE (1966-March 2008) and the search terms aspirin, clopidogrel, ticlopidine, thienopyridine, warfarin, antiplatelet, anticoagulant, myocardial infarction, atrial fibrillation, and percutaneous coronary intervention (PCI). Additional references were identified by reviewing reference citations of articles retrieved. STUDY SELECTION AND DATA EXTRACTION: Applicable data were extracted from published reports and studies that included either clinical outcomes or adverse events. DATA SYNTHESIS: Clinical guidelines recommend the combination of antiplatelets and anticoagulants based largely on writing committee consensus. To date, only one randomized clinical trial has evaluated the safety and efficacy of adding warfarin to dual antiplatelet therapy (ie, triple antithrombotic therapy). Other published data are from case series, observational studies, and case-controlled studies primarily of patients undergoing PCI with intracoronary stent placement. Four of 12 studies reported no increased risk of major bleeding events. In the other 8 studies, a 3- to 6-fold increase in bleeding events was reported with triple antithrombotic therapy. Ischemic events were reported in only 6 of the studies. Only 2 studies observed an additional benefit in the reduction of ischemic events, and 1 study reported worsened ischemic outcomes with the triple antithrombotic regimen compared with dual antithrombotic therapy. CONCLUSIONS: Available guidelines pertaining to the concomitant administration of aspirin, a thienopyridine, and warfarin are based on limited trial data and consensus judgment. Overall, selection of triple antithrombotic therapy for patients with vascular disease is considered a matter of clinical judgment for an individual patient based on the prescriber's perceived balance between the patient's risk for recurrent ischemic events, expected duration of treatment, and patient's risk for bleeding.

Rationale and design of ACTIVE: the atrial fibrillation clopidogrel trial with irbesartan for prevention of vascular events.

BACKGROUND: Atrial fibrillation (AF) is the most frequently occurring cardiac arrhythmia with often serious clinical consequences. Many patients have contraindications to anticoagulation, and it is often underused in clinical practice. The addition of clopidogrel to aspirin (ASA) has been shown to reduce vascular events in a number of high-risk populations. Irbesartan is an angiotensin receptor-blocking agent that reduces blood pressure and has other vascular protective effects. METHODS AND RESULTS: ACTIVE W is a noninferiority trial of clopidogrel plus ASA versus oral anticoagulation in patients with AF and at least 1 risk factor for stroke. ACTIVE A is a double-blind, placebo-controlled trial of clopidogrel in patients with AF and with at least 1 risk factor for stroke who receive ASA because they have a contraindication for oral anticoagulation or because they are unwilling to take an oral anticoagulant. ACTIVE I is a partial factorial, double-blind, placebo-controlled trial of irbesartan in patients participating in ACTIVE A or ACTIVE W. The primary outcomes of these studies are composites of vascular events. A total of 14000 patients will be enrolled in these trials. CONCLUSIONS: ACTIVE is the largest trial yet conducted in AF. Its results will lead to a new understanding of the role of combined antiplatelet therapy and the role of blood pressure lowering with an angiotensin II receptor blocker in patients with AF.

Influence of infarct-related artery patency on the indexes of parasympathetic activity and prevalence of late potentials in survivors of acute myocardial infarction.

OBJECTIVES: The purpose of this study was to determine whether infarct-related coronary artery patency influences myocardial electrical stability as measured by the prevalence of late potentials or heart rate variability. BACKGROUND: Several studies have suggested that loss of vagal activity is associated with an increased incidence of arrhythmic death after myocardial infarction. METHODS: A short-duration, high resolution electrocardiogram (ECG) was performed before hospital discharge in 175 patients with a first myocardial infarction. Seventy-three patients received thrombolytic therapy. All patients underwent coronary angiography. Coronary occlusion was defined as minimal or no anterograde flow. Eighty-eight patients (50.3%) had an occluded infarct-related artery. Sixty-two healthy subjects served as control subjects to determine the normal range of heart rate variability. RESULTS: Comparison between the control group and patients without patency of the infarct-related artery in the time domain and spectral analyses revealed in the latter patients a reduced heart rate variability (p < 0.0001) and a lower power spectrum density in both the 0.05- to 0.15-Hz band (p < 0.0001) and the 0.15- to 0.35-Hz band (p < 0.0001). The heart rate variability in patients with late potentials was lower than in those with a normal signal-averaged ECG. Those patients with spontaneous or thrombolysis-induced reperfusion have less occurrence of late potentials and higher parasympathetic activity than do patients with a closed artery. CONCLUSIONS: This study suggests that the patency of the infarct-related artery determines both the absence of late potentials and the preservation of vagal tone and may explain the reduction in mortality induced by thrombolytic therapy in myocardial infarction.

Differences in heart rate variability between cardioinhibitory and vasodepressor responses to head-up tilt table testing.

BACKGROUND: Patients with syncope show different responses to head-up tilt (HUT) test, which may be due to different pathophysiological mechanisms. METHODS: HUT (70 degrees) was performed in 24 patients who experienced recurrent syncope. Nine patients had a cardioinhibitory (CI) response, 7 patients had a vasodepressor (VD) response, and 8 patients had a mixed (MX) response. Heart rate variability was analyzed at 60-sec periods during HUT. RESULTS: Total spectrum (TS) was greater at rest and 1 min after syncope in the CI and MX groups as compared to the VD group. Low frequency spectrum (LF) was significantly greater during rest and the first minute after syncope in the CI groups as compared with the VD group. After the rest period, the CI and MX groups showed more elevated high frequency spectrum (HF) values than the VD group (p < 0.01). One minute after syncope, the HF increased in the CI and MX groups but not in the VD group (p < 0.01). The VD group showed higher LF/HF ratio from the beginning of rest (3.9 +/- 4.1) as compared to the CI and MX groups (p < 0.01). This difference was most significant 2 min before syncope occurred. The CI and MX groups showed greater pNN50 and rMSSD as compared to the VD group. CONCLUSIONS: Our results suggest that vagal tone is higher in subjects showing cardioinhibitory and mixed responses to HUT. In contrast, patients with a vasodepressor response showed predominantly sympathetic activity. These findings suggest that there are different pathophysiological mechanisms underlying syncope.

Repeatability of heart rate variability during simple cardiovascular reflex tests on healthy subjects.

BACKGROUND: Our purpose was to determine the repeatability, after 2 weeks, of frequency domain measures of heart rate variability (HRV) during simple cardiovascular reflex tests. METHODS: Twenty healthy volunteers aged 29.3 +/- 2.5 years were assessed twice (at weeks 0 and 2). Continuous electrocardiogram and minute-to-minute blood pressure were recorded during spontaneous and metronome-paced breathing (0.2 Hz). Under paced breathing, two tests were performed: 1) active change of posture: 5 min supine position, 5 min seated upright, and 5 min standing up, and 2) cold pressor test: the right hand was immersed in cold water (5 degrees C) for 2 min. RESULTS: Paced breathing elicited a significant increase of the high-frequency (HF) component of HRV. This effect was repeatable on 95% of the subjects. Active change of posture induced a significant increase of the heart rate with an increase of the low-frequency/high-frequency ratio of HRV. Although repeatability was better for the response to being seated upright than for the response to being standing up, it was always higher than 90%. The cold pressor test induced a significant increase of the heart rate and blood pressure, but with variable changes on the HRV measurements (either a decrease or an increase). Repeatability of responses was evident for 95-100% of the subjects. Although repeatability of HRV measurements in the same subject during the tests was higher than 95%, coefficients of repeatability reflected large differences among the subjects. CONCLUSIONS: The results suggest that it is not advisable to use isolated HRV changes to interpret the response to simple cardiovascular reflex tests in groups of healthy subjects.

Risk stratification for malignant arrhythmic events in patients with an acute myocardial infarction: role of an open infarct-related artery and the signal-averaged ECG.

BACKGROUND: There is increasing evidence that an open infarct-related artery results in increased electrical stability of the heart and that this effect is at least in part responsible for the favorable outcome of these patients. In the thrombolytic era the optimal strategy for risk stratification remains controversial. This study examined the predictors of serious arrhythmic events during the first year after myocardial infarction. METHODS: A total of 222 patients with acute myocardial infarction, 41.4% of whom were treated with thrombolysis, were studied. At hospital discharge, signal-averaged electrocardiography was performed on 196 subjects and Holter monitoring on 200. One hundred and ninety-seven patients underwent coronary angiography. Left ventricular ejection fraction was determined in 201 subjects. RESULTS: An open infarct-related artery was documented in 106 patients. The incidence of late potentials was 34% (66 patients). Twenty-four patients (10.8%) had an arrhythmic event during follow-up (sudden death in seven, sustained ventricular tachyarrhythmias in 15, unexplained syncope in two). Signal-averaged electrocardiography had a sensitivity of 94% and a specificity of 72% for prediction of arrhythmic events. An occluded infarct-related artery was 78% sensitive and 58% specific, a left ventricular ejection fraction below 40% had a sensitivity of 71% and specificity of 80%, and Holter monitoring was only 38% sensitive and 92% specific. A combination of late potentials plus an occluded infarct-related artery was 68% sensitive and 84% specific. Positive predictive value was low for all variables examined, but could be improved by the combination of several risk factors. The highest positive predictive value was provided by the combination of an abnormal signal-averaged ECG and complex ventricular arrhythmias on ambulatory ECG. On multivariate analysis, in rank order, presence of late potentials, ejection fraction below 40%, high-grade ventricular ectopic activity and an occluded infarct-related artery were predictive of arrhythmic events. CONCLUSION: Among patients surviving an acute myocardial infarction, the occurrence of malignant arrhythmic events can be reliably predicted by the combination of an abnormal signal-averaged ECG, left ventricular dysfunction, complex ventricular arrhythmias on Holter monitoring and an occluded infarct-related artery at the time of hospital discharge.

Effects of delayed recanalization of an occluded acute myocardial infarction-related artery using coronary angioplasty on late potentials.

BACKGROUND: Recent evidence suggests that late reperfusion of an occluded infarct-related artery after an acute myocardial infarction may reduce the frequency of subsequent arrhythmic events. Late mechanical reperfusion by percutaneous transluminal coronary angioplasty (PTCA) under these circumstances has a high success rate. The present study was performed to test the hypothesis that the late mechanical restoration of anterograde flow in an occluded infarct artery after an acute myocardial infarction causes a resolution of late potentials. METHODS: Twenty subjects (10 men, one woman; aged 32-77 years) suffering a first acute myocardial infarction, with signal-averaged electrocardiographic (ECG) recordings and a severely occluded infarct-related artery, were prospectively identified. RESULTS: Eighteen patients underwent successful PTCA of the occluded artery 6-32 days after a first acute myocardial infarction. Late potentials were observed in 14 patients 5-22 days after the infarction. A follow-up signal-averaged ECG was performed 1-8 days later. In the subgroup of 12 patients with successful reperfusion and an abnormal signal-averaged ECG before PTCA, seven (58.3%) showed resolution of the late potentials at follow-up; in these patients the filtered QRS duration showed a significant reduction (112.1 +/- 14.2 to 96.7 +/- 12.7 ms, P = 0.02), the root-mean-square voltage increased (9.8 +/- 6.5 to 33.1 +/- 15.5 microV, P = 0.017), and the duration of low-amplitude signals < 40 microV decreased after angioplasty (46.3 +/- 11.0 to 28.5 +/- 6.5 ms, P < 0.022). In contrast, two patients with late potentials before PTCA and unsuccessful reperfusion had no significant changes in signal-averaged ECG. CONCLUSIONS: In some patients with an acute myocardial infarction, late mechanical reperfusion of the culprit vessel may reduce the incidence of abnormalities on the signal-averaged ECG. Whether this will improve long-term survival has yet to be confirmed in a large trial.

Relationship between the site of a myocardial infarction and signal-averaged electrocardiogram indices.

We evaluated the relationship between the site of a myocardial infarction (MI) and signal-averaged electrocardiogram (SAECG) indices in both time-domain (TDA) and spectral turbulence (STA) analyses, and their implications in the prediction of infarct-related artery (IRA) patency, in 114 survivors of a first MI. They were divided into two groups based on MI location (57 anterior and 57 inferior). Patients with bundle branch block were not included. Fifty patients had been treated with thrombolytic therapy (TT). The STA was done in both XYZ-leads and in vector magnitude. Forty patients had an abnormal SAECG in TDA and 37 in STA, but only 22 (19%) in both (71% of agreement, kappa=0.35). Fifty-four patients (47%) had an occluded IRA. The best predictors from multivariate analysis of having an occluded IRA in the inferior MI group were: an abnormal Y-lead in STA (odds ratio 4.9; P=0.005); an abnormal RMS40 in TDA (odds ratio, 4.8; P=0.02); absence of TT (odds ratio, 9.15; P=0.001). Conversely, in the anterior MI group they were: an abnormal SAECG in TDA (odds ratio 6.83; P=0.005); absence of TT (odds ratio, 4.3; P=0.02). The multivariate receiver operator characteristic curves clearly showed the effect of MI location on the SAECG indices. This study suggests that the myocardial infarction site is an important factor for the variability and poor concordance between TDA and STA. Such differences may alter the predictive accuracy of SAECG. TDA and STA should be complementary methods, and the exploration in each orthogonal lead appears to be better than in vector magnitude.

Orthostatic hypotension, 2001.

Upright posture requires rapid and effective circulatory and neurologic compensations to maintain blood pressure and consciousness. Although it has been recognized over the past 100 years or more that the act of standing may cause hypotension in patients with autonomic dysfunction, only recently several of the pathophysiologic mechanisms resulting in orthostatic intolerance have been discovered. In patients with orthostatic hypotension, failure of reflex vasoconstriction causes pooling of blood in the legs during standing. Not everyone with a postural blood pressure drop requires treatment, nor does everyone with posturally induced symptoms have orthostatic hypotension. This review will discuss current knowledge of a broad, heterogeneous group of disturbances in the autonomic nervous system, each of which is manifested by hypotension, orthostatic intolerance, and often syncope.

Tilt testing in neurocardiogenic syncope: isosorbide versus isoproterenol.

OBJECTIVE: To compare the diagnostic value of pharmacological stimulation with sublingual isosorbide dinitrate and intravenous isoproterenol during tilt testing in patients with neurocardiogenic syncope and with a negative tilt test without pharmacological provocation. METHODS AND RESULTS: One hundred and twenty patients with a history of neurocardiogenic syncope (aged 15 to 77 years) and 50 healthy volunteers (aged 25 to 70 years) were prospectively submitted to head-up tilt (HUT). Those who did not develop syncope or presyncope during passive HUT for 30 minutes underwent repeated HUT with isoproterenol infusion at 4 microg/min (ISOP HUT), for 10 minutes, and, subsequently, were tilted after sublingual administration of 5 mg of isosorbide dinitrate (ISDN HUT) for another 12 minutes. ISDN HUT was always performed after ISOP HUT. Sensitivity and specificity of passive HUT were 41% (95% C.I. 32.9% to 51.0%) and 100%, respectively. Sensitivity of ISOP HUT was 51.4% (95% C.I. 39.2% to 63.6%) and specificity 70% (95% C.I. 55.4% to 82.1%) and for ISDN HUT were 70% (95% C.I. 57.9% to 80.4%) and 88% (95% C.I. 75.7% to 95.5%), respectively. The accuracy of ISDN HUT was significantly higher than the accuracy of ISOP HUT 77.5% (95% C.I. 68.9% to 84.6%). There were fewer side effects during ISDN HUT. CONCLUSION: Sublingual isosorbide dinitrate is at least as sensitive as isoproterenol to assess patients with suspected neurocardiogenic syncope and with a negative tilt test without provocation. The low rate of side effects and the higher accuracy of ISDN HUT, along with the simplicity of this challenge compared to ISOP HUT, suggest that sublingual isosorbide dinitrate should be preferred as a provocative agent to evaluate neurocardiogenic syncope after a negative passive tilt test.

Evidence of a linkage between neurocardiogenic dysfunction and reactive hypoglycemia.

OBJECTIVE: Reactive hypoglycemia is a common medical problem whose pathophysiology is not completely understood. The objective of this study was to investigate the prevalence of autonomic nervous system abnormalities in patients with reactive hypoglycemia compared with controls. METHODS: Six women, mean age 31 +/- 5 years, with reactive hypoglycemia, and 5 healthy controls women aged 24 +/- 4 years were studied. We investigated the heart rate variability and blood pressure changes after an upright tilt with and without an isoproterenol infusion. A positive result was defined as syncope or presyncope associated with bradycardia, hypotension or both. RESULTS: In response to the orthostatic stress alone or in conjunction with a 4 micrograms isoproterenol infusion, 5 of 6 patients had a positive test as did one of the five control subjects. Patients had a baseline hyperadrenergic tone, with a sympathetic to parasympathetic ratio of 2.3 +/- 0.8 under basal conditions and 10.1 +/- 4.1 during the isoproterenol infusion, compared to 0.7 +/- 0.3 (p = 0.06) and 0.5 +/- 0.1 (p < 0.01) respectively, in the control group. CONCLUSION: Patients with reactive hypoglycemia may be at the extreme end of a spectrum of normal biologic variability, they may have an hyperadrenergic tone and, after a provocative stimulus, sympathetic nerve firing and or synaptic release of NE may not be sufficient to maintain an adequate vascular tone. Alternatively, the vascular response to NE may be impaired. An excessive and paradoxic vasovagal or parasympathetic response was not observed.

[Clinical diagnosis of dyslexia]. / Diagnóstico clínico de dislexia.

In 5 years of experience at the Instituto Nacional de la Comunicacion Humana, 302 clinical histories showed the diagnosis of dyslexia. The following parameters were studied: age, sex, heredofamilial history, gestation, psychomotor development, clinical picture, examination of the language (type, reading, spontaneous writing, dictation, mathematic concepts), laterality, scholarship, scholar failures, psychological study. The following results were obtained: Dyslexia was more important or frequent between 5 to 8.9 years of age. Males predominated 3:1. The heredofamilial history was important. Dyslexia prevailed in products of the first gestations. A high disturbance was found in the psychomotor development of a large percent of dyslexic patients. Examination of language was also important. Dyslexia was more frequent in right-handed patients. Scholar failures in one or more instances were found. The psychological study must be done. If dyslexia is diagnosed on time, it may be prevented and all unwanted sequelae may be avoided.

Autonomic dysfunction in diffuse scleroderma vs CREST: an assessment by computerized heart rate variability.

OBJECTIVE: Autonomic dysfunction has been described in scleroderma. Heart rate variability gives information about sympathetic-parasympathetic autonomic balance, therefore it can provide insight into which division of the system is most affected. Our purpose was to determine whether the neural control of heart rate in patients with CREST syndrome differed from that in patients with diffuse scleroderma. Since low heart rate variability in some diseases is associated with an increased risk for malignant ventricular arrhythmias, assessment of patients with scleroderma with this technique might establish a marker of adverse outcome. METHODS: A short time analysis of heart rate variability was performed in 9 patients with diffuse scleroderma, 8 with CREST and 17 age/sex matched healthy controls. RESULTS: An abnormal heart rate variability was found in patients with CREST: There was a reduced standard deviation of the mean of beat-to-beat R-R intervals and a low power spectrum density in both the 0.05 to 0.15 Hz band and the 0.15 to 0.35 Hz band, a significant reduction in their total power (p < 0.05), a reduction in the high frequency to total power ratio (p < 0.05), and a reduction in the ratio between high and low frequency components of their spectrum. CONCLUSION: It is suggested that patients with CREST have a decreased parasympathetic control of heart rate, significantly different from those with diffuse disease. Whether this finding is pertinent to the differences between these subsets of patients remains to be established.

[Myocardial infarct without pathologic Q waves]. / Infarto del miocardio sin ondas Q patológicas.

Neither the presence nor the absence of pathological Q waves are related to the transmural or subendocardial localization of an acute myocardial infarction. The prognosis of an acute myocardial infarction without pathological Q waves is controversial. We studied 23 hospitalized patients with prolonged, typical chest pain, enzymatic elevation, an EKG without pathological Q waves but with changes in ventricular repolarization and a positive scintigraphy with radioactive pyrophosphates. The patients were classified in two groups according to the pattern of pyrophosphate uptake; group A had grade 2+ focal uptake (N = 13) and group B with grade 2+ diffuse uptake (N = 10). The level of serum glutamic transaminase was significantly greater in group A as compared to group B (p less than 0.05). However, levels of creatine kinase and lactic dehydrogenase were no different. The clinical hospital course was similar in both groups. Eleven patients were followed by 31.7 months: 30.4% had chronic angina, one underwent coronary bypass surgery, another suffered a recurrent myocardial infarction and there were no deaths. The diagnosis of acute myocardial infarction should be suspected in patients with prolonged angor pectoris, electrocardiographic changes in ventricular repolarization, increased enzymatic levels and a positive scintigraphy with a grade 2+ diffuse myocardial uptake of Tc 99m pyrophosphates. The diagnosis is certain if the uptake has a focal distribution.

Positive head-up tilt table test in patients with the long QT syndrome.

AIMS: Syncope in patients with the long QT syndrome is commonly attributed to a ventricular arrhythmia (torsades de pointes). The susceptibility of patients with the long QT syndrome (LQTS) to neurally mediated syncope is currently unknown. METHODS AND RESULTS: Head-up tilt table testing (70 degrees) was performed in six patients with the long QT syndrome and a history of syncope. All patients had syncope with a mixed response. The RR interval was significantly decreased 2 min before the onset of syncope (980 +/- 125 ms vs 630 +/- 91 ms, P=0.003), and significantly increased during syncope (983.17 +/- 224.71; P=0.006). Non-significant changes in QT intervals were observed. Baseline QT was 513 +/- 86 ms and decreased to 450 +/- 59 ms 2 min before the onset of syncope (P=0.11). Although not statistically significant, QT intervals during syncope were longer than at 2 min before syncope (485 +/- 85 ms vs 450 +/- 59 ms; P=0.29). CONCLUSION: Our results suggest that patients with the LQTS are susceptible to neurally mediated syncope. Whether this susceptibility differs from control populations remains unresolved. From a clinical standpoint, neurocardiogenic syncope should be considered a diagnostic alternative in patients with LQTS.

Successful radiofrequency ablation of an accessory pathway during pregnancy.

The preexcitation syndrome is a rare entity during pregnancy. We present a 20-week pregnant patient with Wolff-Parkinson-White syndrome and recurrent episodes of tachycardia with hemodynamic compromise refractory to medical treatment that required electrical cardioversion several times. Due to the poor evolution we performed a successful radiofrequency ablation of a right posteroseptal accessory pathway using 70 seconds of total fluoroscopy time without complications. We consider this is an alternative and safer treatment in those cases in which the tachyarrhythmias compromise the hemodynamic state during pregnancy.

Circadian studies of autonomic nervous balance in patients with fibromyalgia: a heart rate variability analysis.

OBJECTIVE: To determine the accumulated 24-hour cardiovascular autonomic modulation and its circadian variations in patients with fibromyalgia, by means of heart rate variability analysis. METHODS: Thirty patients with fibromyalgia and 30 age- and sex-matched controls were studied prospectively. Assessments included a 24-hour ambulatory recording of heart rate variability, time-domain analysis of the accumulated 24-hour R-R interval variations, and power spectral analysis to determine the sympatho/ vagal balance at different hours (calculated as the power spectral density of the low-frequency [0.04-0.15-Hz] sympathetic band divided by the power of the high-frequency [0.15-0.50-Hz] parasympathetic band). RESULTS: Fibromyalgia patients had diminished accumulated 24-hour heart rate variability, manifested by a decreased standard deviation of all R-R intervals (mean +/- SD 126 +/- 35 ms, versus 150 +/- 33 ms in controls; P = 0.008) and a decreased ratio of pairs of adjacent R-R intervals differing by >50 ms (mean +/- SD 12.0 +/- 9.0% versus 20.1 +/- 18.0%; P = 0.031). Patients lost the circadian variations of sympatho/vagal balance, with nocturnal values significantly higher than those of controls at time 0 (mean +/- SD 3.5 +/- 3.2 versus 1.2 +/- 1.0; P = 0.027) and at 3 hours (3.3 +/- 3.0 versus 1.6 +/- 1.4; P = 0.01). CONCLUSION: Individuals with fibromyalgia have diminished 24-hour heart rate variability due to an increased nocturnal predominance of the low-frequency band oscillations consistent with an exaggerated sympathetic modulation of the sinus node. This abnormal chronobiology could explain the sleep disturbances and fatigue that occur in this syndrome. Spectral analysis of heart rate variability may be a useful test to identify fibromyalgia patients who have dysautonomia.

The dysautonomia of fibromyalgia may simulate lupus.

Some overlap between features of fibromyalgia and systemic lupus erythematous (SLE) is well-recognized. Our objective is to describe eight patients with an original diagnosis of SLE, in whom, after re-evaluation, the multi-system symptoms could be explained on the basis of the dysautonomia that occurs in fibromyalgia.Seven of the eight patients were females. Their mean age was 31 years. All of them fulfilled the American College of Rheumatology criteria for fibromyalgia. Their lupus-like features that could later be explained by dysautonomia were the following: diffuse arthralgias with subjective feeling of swelling, malar erythema, syncopal episodes, profound fatigue, and distal vasospastic changes. Six patients had low titer ANA. None of the patients had signs of organic damage. Autonomic dysfunction was demonstrated by means of circadian studies of heart rate variability (6 patients) and/or tilt table testing (3 patients). We conclude that autonomic dysfunction may be an explanation for the lupus-like symptoms present in some patients with FM.