The effects of cinacalcet on blood pressure, mortality and cardiovascular endpoints in the EVOLVE trial.

Patients with end-stage renal disease often have derangements in calcium and phosphorus homeostasis and resultant secondary hyperparathyroidism (sHPT), which may contribute to the high prevalence of arterial stiffness and hypertension. We conducted a secondary analysis of the Evaluation of Cinacalcet Hydrochloride Therapy to Lower Cardiovascular Events (EVOLVE) trial, in which patients receiving hemodialysis with sHPT were randomly assigned to receive cinacalcet or placebo. We sought to examine whether the effect of cinacalcet on death and major cardiovascular events was modified by baseline pulse pressure as a marker of arterial stiffness, and whether cinacalcet yielded any effects on blood pressure. As reported previously, an unadjusted intention-to-treat analysis failed to conclude that randomization to cinacalcet reduces the risk of the primary composite end point (all-cause mortality or non-fatal myocardial infarction, heart failure, hospitalization for unstable angina or peripheral vascular event). However, after prespecified adjustment for baseline characteristics, patients randomized to cinacalcet experienced a nominally significant 13% lower adjusted risk (95% confidence limit 4-20%) of the primary composite end point. The effect of cinacalcet was not modified by baseline pulse pressure (Pinteraction=0.44). In adjusted models, at 20 weeks cinacalcet resulted in a 2.2 mm Hg larger average decrease in systolic blood pressure (P=0.002) and a 1.3 mm Hg larger average decrease in diastolic blood pressure (P=0.002) compared with placebo. In summary, in the EVOLVE trial, the effect of cinacalcet on death and major cardiovascular events was independent of baseline pulse pressure.

The role of early and sufficient isolated venovenous ultrafiltration in heart failure patients with pulmonary and systemic congestion.

Hypervolemia, present in at least 70% of patients with decompensated heart failure, results in renal dysfunction due to increased renal venous pressure, impaired renal autoregulation, and decreased renal blood flow that are associated with increased morbidity and mortality. Loop diuretics, widely used in congested patients, result in the production of hypotonic urine and neurohormonal activation. In contrast, ultrafiltration (UF) removes isotonic fluid without increasing renin secretion by the macula densa. Simplified devices that permit us to perform UF with peripheral venous access, adjustable blood flows, and small extracorporeal blood volumes make this therapy feasible at most hospitals and in less acute care settings. Conflicting results on the effects of UF in heart failure patients underscore the challenges of patient selection and choice of fluid removal rates. Unfavorable outcomes in patients undergoing UF in the midst of cardiorenal syndrome type 1 are in contrast with the sustained benefits of UF initiated before unsuccessful use of high-dose intravenous (IV) diuretics. UF rates should be based on a precise knowledge of the degree of hypervolemia and careful assessment of blood volume changes, so that extracellular fluid gradually refills the intravascular space and volume depletion is avoided. Poor outcomes are likely to occur if fluid removal rates are not tailored to individual patients' clinical characteristics. A large trial is ongoing to determine if a strategy of early UF, initiated before renal function is worsened by other therapies, is superior to IV diuretics in reducing 90-day heart-failure-related hospitalizations in patients with pulmonary and systemic congestion.

Troponin I levels and postoperative myocardial infarction following renal transplantation.

BACKGROUND: The relationship of routine postoperative troponin I (TnI) monitoring in kidney transplant recipients and in-hospital myocardial infarction (MI) is not known. METHODS: This observational study evaluated the prevalence of abnormal postoperative TnI (Ortho Clinical Diagnostics assay) in 376 consecutive kidney or kidney/pancreas transplant recipients. In-hospital MI was adjudicated using the universal definition. Rates of death and coronary revascularizations at 1 year were studied. Logistic regression analysis was performed to identify independent predictors of abnormal TnI. RESULTS: Ninety-five (25%) recipients had abnormal TnI (>0.04 ng/ml) following transplantation. Abnormal TnI levels were more common in older (mean age: 52.2 ± 13.4 vs. 48.3 ± 13.2 years, p = 0.01), diabetic (57.9 vs. 45.6%, p = 0.04), and prior coronary artery disease (31.6 vs. 20.3%, p = 0.02) patients. In-hospital MI occurred in 6 patients (1.6%). All subsequent in-hospital cardiovascular events occurred in the abnormal postoperative TnI group; most in those with TnI levels >1 ng/ml. Previous coronary artery disease was the only independent predictor of a postoperative TnI level >1 ng/ml in multivariate analysis (odds ratio 4.61, 95% confidence interval 1.49-14.32). At 1 year there was no significant difference in death (3.2 vs. 1.8%, p = 0.42) and borderline significant difference in coronary revascularization (5.3 vs. 1.4%, p = 0.049) in abnormal versus normal TnI groups. CONCLUSIONS: In-hospital MI was infrequent, but abnormal TnI highly prevalent following renal transplantation. Normal TnI levels following renal transplantation had a high negative predictive value in excluding patients likely to develop subsequent postoperative MI. The role of a higher TnI cut-off for screening for postoperative MI in high-risk subgroups deserves future prospective evaluation.

Cardiac biomarkers in the new millennium.

Cardiac disease is the major cause of death in patients with end-stage renal disease (ESRD), accounting for about 45% of all deaths. In dialysis patients about 20% of cardiac deaths are attributed to acute myocardial infarction (AMI). The survival of dialysis patients after AMI is poor, with nearly three-quarters of patients dead at 2 years after AMI. The definition of AMI is based on symptoms, electrocardiography, and cardiac biomarkers. In the non-ESRD population, it has been recognized that sensitive markers of myocardial injury (cardiac troponin I and troponin T) define a group of patients who are increased risk for adverse cardiac outcomes and who are more likely to benefit from treatment. Elevated cardiac troponin levels in nonhospitalized ESRD patients without other evidence of ongoing myocardial ischemia may also prospectively identify a subgroup of ESRD patients at increased risk for death. This editorial is an overview of cardiac biomarkers (specifically troponin I and troponin T) in the management of acute coronary syndromes in ESRD patients. A potential role of cardiac troponin testing for risk stratification in the outpatient dialysis unit is also presented.

Clinical outcomes of PTCA in chronic renal failure: a case-control study for comorbid features and evaluation of dialysis dependence.

We compared clinical outcomes following percutaneous transluminal coronary angioplasty (PTCA) for 77 chronic renal failure (CRF) (dialysis and nondialysis) patients and a control group matched for history of myocardial revascularization, specific revascularization procedure, gender, age, diabetes, number of native vessels diseased, number of vessels dilated, and the specific vessel(s) dilated. CRF patients had a higher incidence of peripheral vascular disease, hypertension, and more complex PTCA target lesion types than controls: 5% vs. 16% Type A, 12% vs. 28% Type B1, 44% vs. 41% Type B2, 39% vs. 15% Type C (p < 0.001). The primary success rate for PTCA in CRF patients and controls was 89% and 97% (p < 0.05). Survival analysis 24 months following PTCA showed a lower composite cardiac event-free survival (angiographic restenosis, myocardial infarction, coronary artery bypass surgery, and cardiac death) for those with CRF than controls, 54% vs. 69% (p = 0.002). Over the study period, 26 CRF patients died (11 from cardiac causes) compared to only 3 control patients (one from a cardiac cause); p < 0.001 for all cause and p < 0.003 for cardiac mortality. We also compared PTCA results between two categories of CRF patients. The first consisted of 49 end-stage renal disease (ESRD) patients on dialysis and the second included 28 patients not on dialysis (13 with creatinine > 2. 0 mg/dL and 15 with ESRD post-renal transplant). Both subgroups had similar coronary anatomy, including PTCA, target lesion type, and acute and long-term outcomes. In conclusion, we observed acceptable primary success and complication rates for PTCA in CRF patients compared with controls matched for comorbid features despite more complex target lesion morphology. Poorer long-term outcomes, however, were apparent for those with CRF regardless of dialysis dependence and likely relate to more extensive atherosclerosis and complex target coronary lesions at index PTCA as well as other features related to CRF.

Long-term survival of renal transplant recipients in the United States after acute myocardial infarction.

Cardiac disease is a major cause of death in renal transplant recipients. One third of the cardiac deaths are attributed to acute myocardial infarction (AMI). Few data exist on predictors of long-term survival of renal transplant recipients after AMI. The purpose of this study is to determine predictors of survival (including treatment era) for renal transplant recipients in the United States after AMI. The US Renal Data System database of 783, 171 patients was used to retrospectively examine outcomes of renal transplant recipients hospitalized during 1977 to 1996 for a first AMI after initiation of renal replacement therapy. Long-term survival was estimated by life-table method, and independent predictors of survival were examined in a comorbidity-adjusted Cox model. There were 4,250 renal transplant recipients with AMI. The in-hospital death rate was 12.8%. Overall 2-year cardiac and all-cause mortality rates were 11.8% +/- 0.6% (SE) and 33.6% +/- 0. 8%, respectively. The poorest survival after AMI occurred in patients with diabetic end-stage renal disease (ESRD), with 2-year cardiac and all-cause mortality rates of 14.9% +/- 1.1% and 40.5% +/- 1.4%, respectively. In the Cox model, the risks for cardiac and all-cause death from AMI were 51% (P = 0.0003) and 45% less (P < 0. 0001) in 1990 to 1996 compared with 1977 to 1984, respectively. The long-term survival of renal transplant recipients in the United States after AMI has markedly improved in the modern treatment era. Patients with diabetic ESRD experience the worst outcome.

Acute myocardial infarction in patients with end-stage renal disease.

BACKGROUND: Ischemic heart disease is the major cause of death in dialysis patients, with 22% of cardiac deaths attributed to acute myocardial infarction (AMI). Few data exist on survival of dialysis patients after AMI. METHODS: The United States Renal Data System (USRDS) database of 627,983 patients was used to examine outcomes of dialysis patients hospitalized from 1977 to 1995 for AMI. Long-term survival was estimated by life-table method and independent predictors of survival were examined in a comorbidity-adjusted Cox model. In preliminary analyses we examined the utilization of thrombolytic therapy for AMI in 1991 to 1995 and separately analyzed outcomes of dialysis patients hospitalized 1977 to 1994 at our own institution. RESULTS: There were 34,189 dialysis patients with AMI. The in-hospital death was 26%. The all-cause mortality was 59% at one year and 73% at two years. The one- and two-year cardiac mortality was 41% and 52%, respectively. Patients with AMI 1990 to 1995 (vs. 1977 to 1984) had decreased mortality with RR (relative risk) 0.87 (0.83, 0.90). There were 16,063 patients with AMI 1991 to 1995 receiving no reperfusion therapy, and only 95 patients received intravenous thrombolytics, of whom 16 received concurrent coronary revascularization. At our institution, the in-hospital death for 113 dialysis patients with AMI was 29% (52% mortality for transmural MI, 16% mortality for nontransmural MI). CONCLUSION: We conclude that dialysis patients with AMI suffer dismal long-term survival. Based on preliminary data, thrombolytic therapy appears to be under-utilized in dialysis patients with AMI in the United States.

Long-term outcome of dialysis patients in the United States with coronary revascularization procedures.

BACKGROUND: The optimal method of coronary revascularization in dialysis patients is controversial, as previous small retrospective studies have reported increased cardiac events after percutaneous transluminal coronary angioplasty (PTCA) compared with coronary artery bypass (CAB) surgery. The purpose of this study was to compare the long-term survival of chronic dialysis patients in the United States following PTCA or CAB surgery. METHODS: Dialysis patients hospitalized from 1978 to 1995 for first coronary revascularization procedure after initiation of renal replacement therapy were retrospectively identified from the United States Renal Data System database. Survival for the endpoints of all-cause death, cardiac death, myocardial infarction, and cardiac death or myocardial infarction was estimated by the life-table method and was compared by the log-rank test. The impact of independent predictors on survival was examined in a Cox regression model with comorbidity adjustment. RESULTS: The in-hospital mortality was 5.4% for 6887 PTCA patients and 12.5% for 7419 CAB patients. The two-year event-free survival (+/-SE) of PTCA patients was 52.9 +/- 0.7% for all-cause death, 72.5 +/- 0.7% for cardiac death, and 62.0 +/- 0.7% for cardiac death or myocardial infarction. In CAB patients, the comparable survivals were 56.9 +/- 0.6, 75.8 +/- 0.6, and 71.3 +/- 0. 6%, respectively (P < 0.02 for PTCA vs. CAB surgery for all endpoints). After comorbidity adjustment, the relative risk of CAB surgery (vs. PTCA) performed 1990 to 1995 for all-cause death was 0. 91 (95% CI, 0.86 to 0.97); cardiac death, 0.85 (95% CI, 0.78 to 0. 92); myocardial infarction, 0.37 (95% CI, 0.32 to 0.43); and cardiac death or myocardial infarction 0.69 (95% CI, 0.64 to 0.74). CONCLUSIONS: In this retrospective study, dialysis patients in the United States had better survival after CAB surgery compared with PTCA, but our study does not exclude the possibility of more unfavorable coronary anatomy in the PTCA patients at baseline. Our data support the need for prospective trials of newer percutaneous coronary revascularization procedures in dialysis patients.

Dobutamine stress echocardiography for the detection of significant coronary artery disease in renal transplant candidates.

Prophylactic coronary revascularization may reduce the risk for cardiac events in diabetic renal transplant candidates. No published data exist on the accuracy of dobutamine stress echocardiography (DSE) for the diagnosis of angiographically defined coronary artery disease (CAD) in renal transplant candidates. The purpose of this study is to examine the accuracy of DSE for the detection of CAD in high-risk renal transplant candidates compared with coronary angiography. Fifty renal transplant candidates with diabetic nephropathy (39 patients) or end-stage renal disease (ESRD) from other causes (11 patients) underwent prospectively performed DSE, followed by quantitative coronary angiography (QCA) and qualitative visual assessment of CAD severity. Twenty of 50 DSE tests were positive for inducible ischemia. Twenty-seven patients (54%) had a stenosis of 50% or greater by QCA, 12 patients (24%) had a stenosis of greater than 70% by QCA, and 16 patients (32%) had a stenosis greater than 75% by visual estimation. The sensitivity and specificity of DSE for CAD diagnosis were respectively 52% and 74% compared with QCA stenosis of 50% or greater, 75% and 71% compared with QCA stenosis greater than 70%, and 75% and 76% for stenosis greater than 75% by visual estimate. On long-term follow-up (22.5 +/- 10.1 months), 6 of 30 patients (20%) with negative DSE results and 11 of 20 patients (55%) with positive DSE results had a cardiac death, myocardial infarction (MI), or coronary revascularization. Six of 27 patients (22%) with a QCA stenosis of 50% or greater had a cardiac death or MI compared with none of the 23 patients (0%) with QCA stenosis less than 50% (P = 0.025). We conclude that DSE is a useful but imperfect screening test for angiographically defined CAD in renal transplant candidates.

The prevalence of cardiac valvular insufficiency assessed by transthoracic echocardiography in obese patients treated with appetite-suppressant drugs.

BACKGROUND: After case reports of cardiac-valve abnormalities related to the use of appetite suppressants were published, we undertook a study to determine the prevalence of the problem using transthoracic echocardiography. METHODS: We examined patients who had taken dexfenfluramine alone, dexfenfluramine and phentermine, or fenfluramine and phentermine for various periods. We enrolled obese patients who had taken or were taking these agents during open-label trials from January 1994 through August 1997. We also recruited subjects who had not taken appetite suppressants and who were matched to the patients for sex, height, and pretreatment age and body-mass index. The presence of cardiac-valve abnormalities, defined by the Food and Drug Administration and Centers for Disease Control and Prevention as at least mild aortic-valve or moderate mitral-valve insufficiency, was determined independently by at least two cardiologists. Multivariate logistic-regression analysis was used to identify factors associated with cardiac-valve abnormalities. RESULTS: Echocardiograms were available for 257 patients and 239 control subjects. The association between the use of any appetite suppressant and cardiac-valve abnormalities was analyzed in a final matched group of 233 pairs of patients and controls. A total of 1.3 percent of the controls (3 of 233) and 22.7 percent of the patients (53 of 233) met the case definition for cardiac-valve abnormalities (odds ratio, 22.6; 95 percent confidence interval, 7.1 to 114.2; P<0.001). The odds ratio for such cardiac-valve abnormalities was 12.7 (95 percent confidence interval, 2.9 to 56.4) with the use of dexfenfluramine alone, 24.5 (5.9 to 102.2) with the use of dexfenfluramine and phentermine, and 26.3 (7.9 to 87.1) with the use of fenfluramine and phentermine. CONCLUSIONS: Obese patients who took fenfluramine and phentermine, dexfenfluramine alone, or dexfenfluramine and phentermine had a significantly higher prevalence of cardiac valvular insufficiency than a matched group of control subjects.

Poor long-term survival after acute myocardial infarction among patients on long-term dialysis.

BACKGROUND: Cardiovascular disease is common in patients on long-term dialysis, and it accounts for 44 percent of overall mortality in this group. We undertook a study to assess long-term survival after acute myocardial infarction among patients in the United States who were receiving long-term dialysis. METHODS: Patients on dialysis who were hospitalized during the period from 1977 to 1995 for a first myocardial infarction after the initiation of renal-replacement therapy were retrospectively identified from the U.S. Renal Data System data base. Overall mortality and mortality from cardiac causes (including all in-hospital deaths) were estimated by the life-table method. The effect of independent predictors on survival was examined in a Cox regression model with adjustment for existing illnesses. RESULTS: The overall mortality (+/-SE) after acute myocardial infarction among 34,189 patients on long-term dialysis was 59.3+/-0.3 percent at one year, 73.0+/-0.3 percent at two years, and 89.9+/-0.2 percent at five years. The mortality from cardiac causes was 40.8+/-0.3 percent at one year, 51.8+/-0.3 percent at two years, and 70.2+/-0.4 percent at five years. Patients who were older or had diabetes had higher mortality than patients without these characteristics. Adverse outcomes occurred even in patients who had acute myocardial infarction in 1990 through 1995. Also, the mortality rate after myocardial infarction was considerably higher for patients on long-term dialysis than for renal-transplant recipients. CONCLUSIONS: Patients on dialysis who have acute myocardial infarction have high mortality from cardiac causes and poor long-term survival.

Reversible myocardial contraction abnormalities in patients with an acute noncardiac illness.

STUDY OBJECTIVES: Reversible myocardial contraction abnormalities are usually observed in patients with acute ischemic syndromes caused by coronary artery disease. In this study, we report the occurrence of reversible anterior-apical contraction abnormalities in patients with an acute noncardiac illness. SETTING: This was a retrospective study of 22 patients with the following characteristics: (1) hospitalization for an acute noncardiac illness; (2) appearance of deep T-wave inversion in the precordial leads of the ECG; and (3) presence of an anterior wall motion abnormality on an echocardiogram. Standard clinical information was collected together with results of serial ECGs, echocardiograms, and coronary angiograms. RESULTS: The primary diagnoses for the 22 acutely ill patients included CNS injury (n=6); sepsis (n=3); acute pulmonary disease (n=3); drug overdose or metabolic abnormality (n=7); and post noncardiac surgery (n=3). An initial echocardiogram revealed an anterior apical wall motion abnormality. At follow-up, all patients had progressive improvement in anterior wall motion with return of normal wall motion in 16 patients (73%). All patients evolved deep T-wave inversion (average, 7.8 mm) and QT interval lengthening in the precordial leads. Coronary angiography revealed a significant stenosis in the likely culprit artery (left anterior descending) in only one patient. CONCLUSION: A reversible cardiac contraction abnormality of the anterior wall and apex of the left ventricle can complicate the clinical course of critically ill patients in the absence of significant coronary artery disease. This phenomenon is associated with striking T-wave inversion and QT interval lengthening. Mechanisms other than myocardial ischemia may lead to the occurrence of reversible regional myocardial contraction abnormalities.

Cardiac troponin I, cardiac troponin T, and creatine kinase MB in dialysis patients without ischemic heart disease: evidence of cardiac troponin T expression in skeletal muscle.

Serum cardiac troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and cardiac troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.

Diagnosis and treatment of ischemic heart disease in dialysis patients.

Ischemic heart disease is the major cause of death in dialysis patients. Efforts at coronary artery disease detection in end-stage renal disease patients have primarily focused on the cardiac evaluation of 'high-risk' renal transplant candidates. Despite their high cardiac risk, no data exist on the results of reperfusion therapy in dialysis patients with acute myocardial infarction, and the outcome of coronary revascularization procedures remains controversial. This review highlights recent work on the diagnosis and treatment of coronary artery disease in dialysis patients.

A comparison of coronary angioplasty and coronary artery bypass grafting outcomes in chronic dialysis patients.

The objective of this study was to compare the outcomes of angina, myocardial infarction (MI), cardiac death, and all-cause death following percutaneous transluminal coronary angioplasty (PTCA) or coronary artery bypass grafting (CABG). The study design was based on retrospective, nonrandomized analysis and was set in referral teaching hospitals and community hospitals. Eighty-four chronic dialysis patients with symptomatic coronary artery disease without prior revascularization were included in the study. Twenty-four patients underwent PTCA of one or more vessels, and 60 patients underwent CABG. Recurrence of angina, MI, cardiac death, and all-cause death following revascularization as well as the number of inpatient days preprocedure and postprocedure were recorded. The two patient groups were comparable in terms of age, sex, history of MI, left ventricular mass and function, and angina severity. Diabetes mellitus was more prevalent in the PTCA group. The CABG group had more severe coronary artery disease. The 2-year survival rate of the CABG patients (66%; 95% confidence interval = 53.79) did not differ from that of the PTCA patients (51%; 95% confidence interval = 27.65). Thirteen PTCA patients were restudied 106 +/- 108 days after recurrence of angina; nine (69%) of these patients were found to have angiographic restenosis. The postprocedure risk of angina and the combined endpoints of angina, MI, and cardiovascular death were significantly greater following PTCA than CABG. Percutaneous transluminal coronary angioplasty was the only consistent predictor of outcomes; the adjusted relative risks (compared with CABG) of postprocedure angina and combined endpoints were 16.4 and 10.2, respectively, and were several-fold higher than the unadjusted risks. We conclude that in chronic dialysis patients with symptomatic coronary disease, patients undergoing PTCA have a higher risk of subsequent angina and combined angina, MI, and cardiovascular death than those undergoing CABG. The optimal approach to coronary revascularization in this patient population remains to be determined.

Echocardiography in the evaluation of cardiac sources of emboli: the role of transthoracic echocardiography.

Cardioembolism is responsible for a significant number of systemic emboli including approximately 15% of all ischemic strokes. Transthoracic echocardiography has contributed to the understanding of cardioembolism and has been used to detect specific and potential cardiac sources of systemic emboli and risk stratify patients with specific clinical findings for subsequent cardiovascular events. Findings from transthoracic echocardiography indicate that stasis is an important prerequisite for intracardiac thrombosis while reversal of stasis and thrombolysis appear operative in embolism of existing thrombus. Transthoracic echocardiography allows a sensitive and specific noninvasive means to detect left ventricular thrombus, valvular vegetation, and intracardiac tumor, lesions that are directly responsible for cardioembolism. Transthoracic echocardiography can also detect lesions that could potentially contribute to cardioembolism but are not specific causes. Examples of these potential lesions include mitral valve prolapse, patent foramen ovale, and interatrial septal aneurysm. Finally, population-based studies and prospective clinical trials have indicated that the results of transthoracic echocardiography have predictive value for subsequent cardiovascular events and hence provide a means for stratification of patients at risk for cardioembolism. The latter is most notable for the group of patients with nonvalvular atrial fibrillation where left ventricular dysfunction and increased left atrial size are independent predictors for subsequent stroke.