Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis
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Risk for Systemic Embolization of Atrial Fibrillation Without Mitral Stenosis Henry S. Cabin, MD, K. Soni Clubb, BS, Cynthia Hall, MD, Robin A. Perlmutter, MPH, and Alvan R. Feinstein, MD trial fibrillation (AF) has often been associated The risk for systemic embolixation was studied in with systemic embolization.*-I’ In studies of ce- 272 patients wlthout mitral stenosis or prosthetic A rebrovascular events, 6 to 23% of strokes have valves who were referred to the echocardlography been attributed to cardiogenic emboli,8~12+13almost half laboratory with atrial fibrillation (AF). During a of which were in patients with AF.‘*Y’~Although it was mean follow-up perfod of 33 months (range <I to reportedly highest in patients with mitral stenosis and 83), 27 (10%) patients had a systemic embolic AF,3,4,15,16the risk of systemic embolization has also event, which was cerebral in 23 patients (85%) and been suggestively increased when AF occurred without peripheral in 4 (15%). In the analysis of individual mitral stenosis.4v’5T17The increasedrisk of embolization variables, the risk of embolixation was increased by has been reported in patients with AF alone* and in female sex, underlying heart disease and left atrial those with associatedcoronary artery disease,4thyro- she 14.0 cm, but not by age, hypertension or type toxicosis,* 8 systemic hypertensionl 9 or dilated left of AF (paroxysmal vs chronic). In multivariable atria.*O Patients with AF have seldom been followed, analysis, left atrial size 14.0 cm was the single however,to identify risk factors for subsequentsystemic strongest predkitor of htcreased risk for embolixa- embolization. We present such a study in a consecutive tion (p <O&01), but female sex (p = 0.014) and un- group of patients, referred for echocardiographicexami- derlying heart disease (p = 0.027) also contributed. nation and having AF without mitral stenosis. When each of these 3 factors was assigned 1 point in a risk score, embolii events were found to occur METHODS in none (0%) of 24 patients with a risk score of 0, Sturly population: The basic population consistedof in 2 (3%) of 83 patients with a risk score of 1, in all patients with AF who were referred to the echocardi- 13 (11%) of 118 patients with a risk score of 2 ography laboratory at Yale-New Haven Hospital from and in 12 (26%) of 47 patients with a risk score of January 1, 1981, to September 1, 1983. Patients with 3. The score allows patients with AF and without technically inadequate echocardiogramswith prosthetic mitral stenosis to be stratified into high-, medium- cardiac valves or with a clinical diagnosisor echocardio- and low-risk groups for systemic embolixation. graphic evidenceof mitral stenosiswere excluded from such information couki be useful in decision making analysis, leaving 320 patients eligible for the study. for antkoagulation in patients with AF. Follow-up: Follow-up information about possible (Am J Cardiol1990;65:1112-1116) systemic embolic events was obtained by review of the patients’ hospital records and by telephone communica- tion with physicians, patients or their families. If the patient had a cerebrovascularaccident, we tried to de- termine the time course of development of neurologic deficits, presence of carotid arterial bruits, previous transient ischemic attacks and results of scansor carotid angiography. If the patient had a peripheral embolic event, the solicited data included results of peripheral angiography and embolectomy, if performed. In patients who died during the follow-up period, the circumstancesof death were appraised.A sudden death without a prior embolic event was not consideredto be an embolic event. The follow-up was consideredadequate if it was > 12 months or if the patient died or had an embolic event From the Yale University School of Medicine, Section of Cardiology, <I2 months after the echocardiogram. New Haven, Connecticut. Manuscript received November 21, 1989; Of the 320 eligible patients, 5 refused to participate revised manuscript receivedand acceptedDecember 27,1989. Address for reprints: Henry S. Cabin, MD, Yale University School and 43 had inadequate follow-up data. The age, sex, left of Medicine, Section of Cardiology, 333 Cedar Street, PO Box 3333, atria1 size and frequency of underlying heart diseasedid New Haven, Connecticut 06510. not differ significantly in these 48 patients from the re- 1112 THE AMERICAN JOURNAL OF CARDIOLOGY VOLUME 65 maining 272 patients who comprised the group under In an embolic risk score constructed from the multi- analysis. variable results, patients were assigned 1 point for each Echocardiography: Echocardiography was done risk factor identified by Cox regression.Life tables for with an HP 77-020 phased array real time echocardio- each risk group were constructed by the Kaplan-Meier gram machine. Left atria1 size was measured from the method and were statistically compared using the gen- M-mode tracing using the American Society of Echo- eralized Savage log-rank test. cardiography standards.*’ Measurements were made at end-systole using leading edge echoes.The atria1 sizes RESULTS measured at the time of the original examination were Of the 272 patients under analysis after the index used in all but 15 patients, for whom the measurement echocardiogram,27 (10%) had a systemic embolic event had not been recorded. In those patients, the echocar- during the follow-up period, which ranged from <l to diogram was reviewed and atria1 size was measured 83 months (mean 33). All study patients were followed without knowledge of the clinical outcome. for 112 months unless they had an embolic event or Systemic embolic events: The criteria establishedby died <12 months after the echocardiogram. Hart et al** were used to classify strokes as embolic, Table I lists the results of bivariate analysis of di- indeterminate or nonembolic. The embolic and indeter- verse demographic and clinical factors as predictors for minate categorieswere counted as embolic in the analy- systemic embolization. The frequency of systemic em- sis. The nonembolic strokes had 21 of the following cri- bolic events did not differ significantly between the pa- teria: ipsilateral carotid bruit; previous ipsilateral tran- tients above and below the median age of 70 years; sient ischemic attack; hypertension and evidence of a mean age was 68. Women had a higher frequency of lacunar infarction; nonsudden onset of the neurologic embolic events than men (14 vs 6%, p = 0.02) and pa- deficit while awake; evidence of ipsilateral cerebrovas- tients with underlying structural heart diseasehad em- cular stenosis by angiography or noninvasive testing; bolic events more often than those without structural prior ipsilateral carotid endarterectomy; or nonembolic heart disease (14 vs 5%, p = 0.02). Systemic embolic stroke at autopsy.22 Patients having a transient cerebral events occurred in 13% of patients with coronary artery ischemic event without a persistent deficit were consid- disease (myocardial infarction or angina pectoris), in ered embolic unless they had evidence of ipsilateral ca- 16% of patients with valvular heart disease(aortic ste- rotid diseaseor prior transient ipsilateral deficits. nosis or regurgitation or mitral regurgitation) and in Peripheral ischemic events were considered embolic 23% of patients with cardiomyopathy (dilated or hyper- unless there was evidence of associatedatherosclerotic trophic) when compared to 5% of patients with no un- peripheral vascular disease.All peripheral systemic em- derlying heart disease(p = 0.07, p = 0.06, p = 0.05, bolic events had either surgical embolectomyto confirm respectively). The frequency of embolic events did not the diagnosis or had associatedembolic events in other show a statistically significant difference according to locations. the type of AF (chronic [15%] vs paroxysmal [9%]). Strokes that occurred before the index echocardio- The presenceof systemic hypertension also did not sig- gram were not analyzed as a risk factor for subsequent nificantly alter the frequency of embolization. systemic embolization, becauseinformation was rarely There was a striking difference in embolic frequency available to allow the strokes to be categorized as em- according to left atria1 size. Of the 180 patients whose bolic or nonembolic. left atrium measured 24.0 cm, 25 (14%) had systemic Paroxysmal versus chronic atrial fibrillation: embolic events compared with only 2 of 92 patients Chronic AF was defined as >-2 documented episodesof (2%) whose left atrium was <4.0 cm (p = 0.003). AF, at least 1 month apart, with no documented inter- Of the 27 embolic events,23 (85%) were cerebrovas- vening or subsequentepisodes of normal sinus rhythm. cular and 4 (15%) were peripheral. A history of 2 1 Paroxysmal AF was defined as AF followed by an epi- month of therapeutic anticoagulation at some point be- sode of normal sinus rhythm. Thus, a patient was con- fore the embolic event was noted in 5 patients (19%) in sidered to have paroxysmal AF if a single episodeof AF the embolic group and in 37 patients (15%) in the non- was followed by normal sinus rhythm or if there were embolic group. Of the 5 patients who embolized with a multiple episodesof AF with intervening normal sinus history of therapeutic anticoagulation, only 3 were re- rhythm. The status of the AF was consideredunknown ceiving a therapeutically effective dosage(prothrombin if there was a single episodeof AF with no subsequent time 11.3 X control) at the time of the embolic event. documentation of either normal sinus rhythm or persis- To determine the relative contributions of the embol- tent AF. ic risk factors identified by bivariate analysis, Cox re- Statistical analysis: Bivariate analysis of clinical gression was performed. As listed in Table II, the fol- variables was performed using Pearson’schi-square test lowing 3 variables contributed significantly to the model for categorical data and Student’s t test (2-tailed) for predicting risk of embolization: left atria1 size 14.0 cm; continuous data. Cox regressionanalysis was then used female sex; and the presenceof structural heart disease.