Background Left ventricular (LV) and right ventricular (RV) function are known predictors of morbidity and mortality after an acute myocardial infarction (MI). However, the prognostic use of a late evaluation of cardiac function after an MI remains unclear.Methods We analyzed echocardiograms obtained 1 year after MI in patients with LV dysfunction at baseline (ejection fraction [EF]<= 40%) from 291 patients enrolled in the SAVE echocardiographic substudy who did not develop heart failure (HF) or a recurrent MI during this first year. Left ventricular EF and RV fractional area change were assessed.Results After a median follow-up of 22 months after the 1-year echocardiogram, a low LVEF (<30%) at 1 year was associated with an increased risk of death and/or HF (hazards ratio [HR] 2.7, 95% CI 1.3-5.3). Presence of RV dysfunction was also associated with an increased risk of death (HR 8.9, 95% CI 3.5-22.1), development of HF (HR 7.1, 95% CI 3.4-15.0), and the composite end point of death or HF (HR 7.6, 95% CI 4.1-14.2). In multivariate analyses, both low LVEF and RV dysfunction remained independently predictive of the composite end point of death or HF. Patients with biventricular dysfunction were at the greatest risk of death and/or HIF (HR 19.4, 95% CI 8.2-46.0) in follow-up.Conclusions in a stable population of survivors of MI, impaired LV and RV function at I year after MI are independently and additively predictive of increased risk of HIF or death.

Whether antecedent systemic hypertension influences the risk of subsequent left ventricular (LV) dilation in patients after an acute myocardial infarction with LV systolic dysfunction is unclear. We assessed echocardiographic evidence of ventricular remodeling from baseline (mean +/- SD 11 +/- 3 days) to 2 years after an acute myocardial infarction in 122 hypertensive (defined as a history of treated hypertension, baseline systolic blood pressure > or =140 or baseline diastolic blood pressure > or =90 mm Hg) and 334 nonhypertensive patients in the Survival and Ventricular Enlargement echocardiographic substudy. Compared with nonhypertensives, baseline heart size, defined as the sum of the average short- and long-axis LV cavity areas, was similar (70.1 +/- 11.9 vs 68.8 +/- 11.2 cm(2), p = 0.33 at end-diastole; 50.1 +/- 11.3 vs 48.8 +/- 10.8 cm(2), p = 0.31 at end-systole), but short-axis LV myocardial area (24.7 +/- 4.3 vs 25.7 +/- 5.0 cm(2), p = 0.043) and wall thickness (1.15 +/- 0.16 vs 1.21 +/- 0.17 cm, p = 0.004) at end-diastole were greater among hypertensives. The myocardial infarct segment lengths were similar in the 2 groups (p = 0.22). Although LV cavity areas increased significantly in the 2 groups from baseline to 2 years (p < or =0.001), the increase was significantly greater in hypertensives than in nonhypertensives (+5.6 +/- 11.5 vs +2.2 +/- 10.7 cm(2), p = 0.005 at end-diastole; +6.23 +/- 12.75 vs +2.94 +/- 11.4 cm(2), p = 0.012 at end-systole). There was no concomitant difference in the change in LV myocardial area or LV wall thickness between the 2 groups (p >0.30). After adjusting for known confounders, antecedent hypertension was associated with a doubling of the risk of LV dilation (50.8% vs 37.7%, odds ratio 2.09, 95% confidence interval 1.27 to 3.45, p = 0.004). This association was not modified by diabetes mellitus, myocardial infarct segment length, or captopril use (all p values for interaction >0.10). We conclude that antecedent hypertension is associated with subsequent LV dilation in patients after acute myocardial infarction with LV systolic dysfunction.

Doppler echocardiography is commonly used to estimate systolic pulmonary artery pressure and to diagnose pulmonary hypertension, but data relating to its utility in patients with advanced lung disease are limited. In a cohort study of 374 lung transplant candidates, the performance characteristics of echocardiography compared with right heart catheterization in the determination of systolic pulmonary artery pressure and diagnosis of pulmonary hypertension were investigated. The prevalence of pulmonary hypertension was 25% in the study population. Estimation of systolic pulmonary artery pressure by echocardiography was possible in 166 patients (44%). The correlation between systolic pulmonary artery pressure estimated by echocardiography and measured by cardiac catheterization was good (r = 0.69, p < 0.0001). However, 52% of pressure estimations were found to be inaccurate (more than 10 mm Hg difference compared with measured pressure), and 48% of patients were misclassified as having pulmonary hypertension by echocardiography. Sensitivity, specificity, and positive and negative predictive values of systolic pulmonary artery pressure estimation for diagnosis of pulmonary hypertension were 85%, 55%, 52%, and 87%, respectively. In conclusion, despite a statistically significant correlation with directly measured values, estimation of systolic pulmonary artery pressure by echocardiography is frequently inaccurate in patients with advanced lung disease and leads to considerable overdiagnosis of pulmonary hypertension.

Background-The relation between left ventricular (LV) remodeling and ventricular arrhythmias after myocardial infarction is poorly documented. We investigated the relations between LV size, hypertrophy, and function and ventricular arrhythmias in 263 patients from the Survival and Ventricular Enlargement (SAVE) study, using quantitative 2D echocardiography and ambulatory ECG monitoring after myocardial infarction.Methods and Results-Transthoracic 2D echocardiograms and arrhythmia monitoring were performed at baseline ( mean, 11 days) and 1 and 2 years after infarction. LV size, short-axis muscle (mass) area (LVMA), and function were quantified from 2D echocardiograms. The prevalence of ventricular tachycardia (VT) and frequent ventricular ectopy (premature ventricular contractions [PVCs]>10/h) was assessed from ambulatory ECG. VT and PVCs>10/h occurred in 20% and 29% of patients at baseline, in 22% and 35% at 1 year and 23% and 39% at 2 years, respectively. VT and PVCs>10/h at baseline and 1 and 2 years were significantly related to LV size, LVMA, and function. Furthermore, changes in LV size and function from baseline to 2 years predicted both VT and PVCs>10/h. The study was underpowered to detect treatment effect of ACE inhibitors and beta-adrenergic receptor blockers but did not alter the relations between ventricular arrhythmias, LV size, and function.Conclusions-Quantitative echocardiographic assessment of LV size, LVMA, and function and changes in these measurements over time predict ventricular arrhythmias after infarction. Altered LV architecture and function during postinfarction LV remodeling provide an important substrate for triggering high-grade ventricular arrhythmias.

HomeCirculationVol. 108, No. 17Pulmonary Venous Aneurysms in Hereditary Hemorrhagic Telangiectasia Detected by 3-Dimensional Magnetic Resonance Angiography Free AccessReview ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessReview ArticlePDF/EPUBPulmonary Venous Aneurysms in Hereditary Hemorrhagic Telangiectasia Detected by 3-Dimensional Magnetic Resonance Angiography Victor A. Ferrari, MD, Nehal N. Mehta, MD, Michael Soulen, MD, David A. Roberts, MD, PhD and Martin St John Sutton, MBBS, FRCP Victor A. FerrariVictor A. Ferrari From the Adult Congenital Heart Disease Program, Division of Cardiovascular Medicine, Department of Medicine (V.A.F., N.N.M., M.S.J.S.), and the Department of Radiology (M.S., D.A.R.), Hospital of the University of Pennsylvania, Philadelphia. , Nehal N. MehtaNehal N. Mehta From the Adult Congenital Heart Disease Program, Division of Cardiovascular Medicine, Department of Medicine (V.A.F., N.N.M., M.S.J.S.), and the Department of Radiology (M.S., D.A.R.), Hospital of the University of Pennsylvania, Philadelphia. , Michael SoulenMichael Soulen From the Adult Congenital Heart Disease Program, Division of Cardiovascular Medicine, Department of Medicine (V.A.F., N.N.M., M.S.J.S.), and the Department of Radiology (M.S., D.A.R.), Hospital of the University of Pennsylvania, Philadelphia. , David A. RobertsDavid A. Roberts From the Adult Congenital Heart Disease Program, Division of Cardiovascular Medicine, Department of Medicine (V.A.F., N.N.M., M.S.J.S.), and the Department of Radiology (M.S., D.A.R.), Hospital of the University of Pennsylvania, Philadelphia. and Martin St John SuttonMartin St John Sutton From the Adult Congenital Heart Disease Program, Division of Cardiovascular Medicine, Department of Medicine (V.A.F., N.N.M., M.S.J.S.), and the Department of Radiology (M.S., D.A.R.), Hospital of the University of Pennsylvania, Philadelphia. Originally published28 Oct 2003https://doi.org/10.1161/01.CIR.0000092308.57590.8CCirculation. 2003;108:e122–e123A 38-year-old woman with a history of presumed multiple pulmonary arteriovenous malformations (PAVMs), epistaxis, and hereditary hemorrhagic telangiectasia (HHT) presented with a 2-year history of progressive dyspnea on exertion. She had no orthopnea, paroxysmal nocturnal dyspnea, edema, or exertional chest discomfort. She denied hemoptysis and seizure activity but complained of severe migraine headaches. Her medical history was otherwise unremarkable. Her family history was notable in that her mother died at age 44 from respiratory failure of unknown etiology; a sister has multiple PAVMs, and her daughter has recurrent epistaxis. In both the sister and daughter, the diagnosis of HHT has been confirmed.Physical examination was normal except for 3 telangiectasias—one on the palmar surface of the left fifth digit, one on the lower lip, and one on her left eyelid. Her oxygen saturation was 96% on room air. ECG was normal. Chest x-ray and a contrast-enhanced computed tomographic scan of the chest suggested multiple PAVMs. A time-resolved, ultrafast 3D gadolinium-enhanced magnetic resonance angiogram (MRA) was obtained to delineate the cardiopulmonary anatomy before referral for transcatheter embolotherapy. Coronal plane images demonstrated no abnormalities during the late arterial phase (Figure 1A) but during the venous phase identified large abnormal serpiginous pulmonary veins with multiple venous aneurysms (Figure 1B). The patient underwent pulmonary angiography, which confirmed the MRA findings (Figure 2). Download figureDownload PowerPointFigure 1. A, Three-dimensional reformatted MRA in the coronal plane demonstrates the late arterial phase of the contrast-enhanced scan with no abnormal arterial communications in either lung. The right atrium (RA) and the pulmonary artery (PA) are identified. B, Three-dimensional reformatted MRA in the coronal plane shows the venous phase with multiple abnormal pulmonary veins with large, grape-like aneurysmal venous malformations (arrows), seen particularly in the lower lobe of the right lung. The aneurysmal veins are seen to drain normally to the left atrium (LA). An asterisk (*) is placed at the ostium of the right superior pulmonary vein. The ascending aorta (A) is also identified.Download figureDownload PowerPointFigure 2. Digital-subtraction left pulmonary arteriogram showing normal early arterial phase (A), late arterial (parenchymal) phase (B), and venous phase images (C). The venous phase (C) demonstrates dilated serpiginous pulmonary veins (open arrows) with venous aneurysms (solid arrows).Because these vascular anomalies were confined to the venous side of the pulmonary circulation, they were not amenable to transcatheter embolotherapy treatment. To our knowledge, this is the first description of multiple aneurysmal malformations confined to the pulmonary venous circulation in HHT. The patient was managed conservatively, and her symptoms have not progressed.The editor of Images in Cardiovascular Medicine is Hugh A. McAllister, Jr, MD, Chief, Department of Pathology, St Luke's Episcopal Hospital and Texas Heart Institute, and Clinical Professor of Pathology, University of Texas Medical School and Baylor College of Medicine.Circulation encourages readers to submit cardiovascular images to the Circulation Editorial Office, St Luke's Episcopal Hospital/Texas Heart Institute, 6720 Bertner Ave, MC1-267, Houston, TX 77030.FootnotesCorrespondence to Victor A. Ferrari, MD, Hospital of the University of Pennsylvania, 3400 Spruce St, 9014 E Gates Pavilion, Philadelphia, PA 19104. E-mail [email protected] Previous Back to top Next FiguresReferencesRelatedDetailsCited By Shostak E, Ameer R, Gruden J and Jessurun J (2019) A Diagnostic Conundrum, Chest, 10.1016/j.chest.2019.02.318, 155:5, (e131-e135), Online publication date: 1-May-2019. Palkar A, Shah R, Greben C and Talwar A (2015) Pulmonary Venous Varix, American Journal of Respiratory and Critical Care Medicine, 10.1164/rccm.201506-1065IM, 192:12, (e59-e59), Online publication date: 15-Dec-2015. Restrepo C and Carswell A (2012) Aneurysms and Pseudoaneurysms of the Pulmonary Vasculature, Seminars in Ultrasound, CT and MRI, 10.1053/j.sult.2012.04.001, 33:6, (552-566), Online publication date: 1-Dec-2012. Loqman N, McGuire F and McLemore T (2008) Case Report: Identification of a Pulmonary Venous Aneurysm Using Radial Endobronchial Ultrasound and Electromagnetic Navigational Bronchoscopy, Journal of Bronchology, 10.1097/LBR.0b013e31816b6551, 15:2, (116-117), Online publication date: 1-Apr-2008. Goldman J (2005) MR Angiography of the Pulmonary Vasculature Magnetic Resonance Angiography, 10.1007/88-470-0352-0_9, (163-175), . Hung J, Papakostas L, Tahta S, Hardy B, Bollen B, Duran C and Levine R (2004) Mechanism of Recurrent Ischemic Mitral Regurgitation After Annuloplasty, Circulation, 110:11_suppl_1, (II-85-II-90), Online publication date: 14-Sep-2004. Edelstein S, Naidich T and Newton T (2004) The rare phakomatoses, Neuroimaging Clinics of North America, 10.1016/j.nic.2004.03.012, 14:2, (185-217), Online publication date: 1-May-2004. Bell D and Weerakkody Y (2012) Pulmonary venous varix Radiopaedia.org, 10.53347/rID-19541 October 28, 2003Vol 108, Issue 17 Advertisement Article InformationMetrics https://doi.org/10.1161/01.CIR.0000092308.57590.8CPMID: 14581389 Originally publishedOctober 28, 2003 PDF download Advertisement

Background— Diabetic patients are at increased risk for heart failure (HF) and other adverse events after myocardial infarction (MI). Left ventricular (LV) enlargement after MI is also associated with the same increased risk. We used data from the Survival and Ventricular Enlargement (SAVE) echocardiographic substudy to test the hypothesis that diabetes was associated with increased LV enlargement after MI. Methods and Results— Four hundred twelve nondiabetic and 100 diabetic patients underwent echocardiographic assessment at baseline and 3 months, 1 year, and 2 years after MI. HF developed in 30% of diabetic and 17% of nondiabetic patients during follow-up ( P <0.001). Baseline LV diastolic size, ejection fraction, and infarct segment length were similar between diabetic and nondiabetic patients. Diabetic patients demonstrated less LV enlargement between baseline and 2 years than nondiabetic patients (0.9±11.1 cm 2 versus 3.8±10.9 cm 2 , P =0.047). In patients who developed HF, LV diastolic dilatation (10.0±12.4 cm 2 versus 3.7±13.1 cm 2 , P =0.06) and systolic dilatation (4.6±11.8 versus 0.91±12.1, P =0.017) were greater in nondiabetic than in diabetic patients. LV dilatation between baseline and 2 years was a predictor of HF in nondiabetic patients, but not in diabetic patients, even after excluding patients with recurrent MI and adjusting for history of hypertension, prior MI, age, treatment group, and smoking. Diabetes modified the relationship between ventricular enlargement and the risk of HF ( P =0.011). Conclusions— The increased incidence of HF after MI in diabetic patients is not explained by a greater propensity for LV remodeling.

OBJECTIVES The purpose of our study was to evaluate patients with suspected anomalous pulmonary veins (APVs) and atrial septal defects (ASDs) using fast cine magnetic resonance imaging (MRI) and ultrafast three-dimensional magnetic resonance angiography (MRA). BACKGROUND Precise anatomic definition of anomalous pulmonary and systemic veins, and the atrial septum are prerequisites for surgical correction of ASDs. Cardiac catheterization and transesophageal echocardiography (TEE) are currently used to diagnose APVs, but did not provide complete information in our patients. METHODS Twenty consecutive patients with suspected APVs were studied by MRA after inconclusive assessment by catheterization, TEE or both. The MRI images were acquired with a fast cine sequence and a novel ultrafast three-dimensional sequence before and after contrast injection. RESULTS Partial anomalous pulmonary venous drainage was demonstrated in 16 of 20 patients and was excluded in four patients. Magnetic resonance imaging correctly diagnosed APVs and ASDs in all patients (100%) who underwent surgery. For the diagnosis of APVs, the MRI and catheterization results agreed in 74% of patients and the MRI and TEE agreed in 75% of patients. For ASDs, MRI agreed with catheterization and TEE in 53% and 83% of patients, respectively. CONCLUSIONS Fast cine MRI with three-dimensional contrast-enhanced MRA provides rapid and comprehensive anatomic definition of APVs and ASDs in patients with adult congenital heart disease in a single examination.

those without heart failure, with equivalent ventricular dysfunction. Assessment of left ventricular diastolic function in patients with heart failure has proved even more challenging; partly because diastolic function varies with age in normal subjects, and partly because most measurements of diastolic function are exquisitely sensitive to alterations in loading conditions. Moreover, measures of diastolic ventricular function have not correlated with severity of symptoms or with exercise capacity. Increased awareness of patients with primary diastolic heart failure and normal systolic left ventricular function stimulated investigation of a number of indices of diastolic function. Measurement of peak blood flow velocities during rapid filling (E wave) and artrial systolic contraction (A wave) represented the initial foray into the non-invasive assessment of diastolic ventricular function. Measurements of transmitral blood flow velocities provided qualitative description of prolonged or impaired myocardial relaxation in hypertrophy, but proved to be highly pre-load dependent. Deceleration time of transmitral blood flow velocity during rapid left ventricular filling (E wave deceleration time), estimation of filling pressures from pulmonary venous flow, flow propagation velocities and myocardial velocities by Doppler tissue imaging are less influenced by age and loading conditions but their respective predictive values require validation in large cohorts of heart failure patients. These new measurements of diastolic function are of interest as they can differentiate between the impact of altered loading conditions and intrinsic changes in myocardial diastolic relaxation on global left ventricular function. The ideal test for heart failure would be a noninvasive, integrated assessment of systolic and diastolic left ventricular function that did not artificially uncouple systolic from diastolic function and is independent of ventricular loading conditions and reproducible at serial follow-up. The Tei index fulfils some of these criteria in that it takes into account both systolic and diastolic function and appears to be independent of heart rate and blood pressure. This Doppler-derived index, also known as the myocardial performance index, is estimated as the sum of isovolumic contraction time and isovolumic relaxation time divided by ejection time. The Tei index is easily calculated in the majority of patients from Doppler blood flow velocity recordings from the left ventricular inflow and outflow tracts. It has already been demonstrated to predict morbidity and mortality See page 1888 for the article to which this Editorial refers

Epidemiological studies of patients with coronary heart disease have identified a number of risk factors for fatal and non-fatal myocardial infarction including diabetes, hypertension, tobacco use, elevated plasma lipids and a family history of precocious coronary artery disease. Of equal importance is the observation that the incidence of myocardial infarction can be favourably modulated by cessation of smoking, reduction in plasma cholesterol, optimal treatment of hypertension and appropriate glycaemic control. While primary prevention of coronary heart disease remains the ideal, the majority of clinical cardiovascular specialists treat patients who have already manifested coronary disease or related complications. In symptomatic or asymptomatic patients with evidence for coronary heart disease, another tier of information, regarding further long-term prognostic stratification is a prerequisite for optimal patient management. Clinical trials of survivors of acute myocardial infarction have been a rich substrate for prospective acquisition of baseline measurements of ventricular topography, ejection fraction, coronary anatomy, pulse pressure and ambulatory electrocardiographic evidence of ischaemia, and have all provided incremental prognostic information above that available from baseline demographics. The purpose of characterizing objective measures of prognosis is to identify individual patients at high, moderate and low risk of future adverse events and tailor treatment strategies to minimize risk of adverse events which include recurrent infarction, congestive heart failure and stroke. Attenuation of left ventricular remodelling with angiotensin converting enzyme inhibitors, beta adrenergic receptor blockade and aggressive reduction of plasma cholesterol in post-infarction patients represent three different treatment strategies that have proved efficacious in reducing the incidence of adverse cardiovascular events. The aim now and into the millennium is to anticipate adverse cardiovascular consequences of coronary artery disease and intervene rather than stratify risk after complications have occurred. Over the last decade, attention has focussed on the central vasculature and in particular upon assessing plaque stability, lipid content, biophysical properties of the fibrous cap and estimation of the shear forces necessary to trigger plaque rupture, thrombosis, vessel occlusion and myocardial infarction. The specific aim of these studies has been to recognize abnormal vessel structure and function early, so that consequent irreversible loss of cardiomyocytes can be avoided. The myocardium may be regarded as a target organ with limited ability to autoregulate its epicardial and intramural coronary blood flow when subjected to acute reduction in coronary flow by sudden thrombotic occlusion of a previously haemodynamically unimportant stenosis as well as during perturbations in systolic and diastolic load. Risk factors for coronary heart disease mediate their effect by altering the structure, properties and function of the medial and endothelial components of the arterial wall which vary among different vascular beds. In addition, age-related changes in the composition and material properties of the arterial wall in individuals without atheromatous disease are associated with increased systolic blood pressure and increased pulse pressure and reflect increased arterial stiffness or reduced arterial distensibility. Aortic stiffness: a predictor of acute coronary events?

In the current climate of cost containment, discontinuation of medications shown to have efficacy has taken on an urgency that may not appear appropriate to the individual clinician when applied to the individual patient. However, it is often in the patient's best interest to decrease the number of medications prescribed. Following a myocardial infarction, patients are usually discharged on multiple medications including β adrenergic receptor blockers, angiotensin converting enzyme (ACE) inhibitors, aspirin, and lipid lowering agents. Polypharmacy is a national health issue that increases the risk of medication errors in formulation or dosage by the prescriber, the pharmacist or the patient, and increases the likelihood of drug interaction. Polypharmacy also decreases patient compliance with the medical regimen.1 2 Cost is a factor for many patients and one that may be underappreciated by physicians. In addition, no drug is without side effects. Discontinuation of a medication removes the possibility of untoward side effects, although at the same time eliminates the possibility of any further therapeutic benefit. It is this risk benefit analysis that must be applied to each patient's situation to determine appropriate pharmacotherapy. Hitherto, no studies have specifically addressed the appropriate timing for discontinuation of ACE inhibitors or warfarin after myocardial infarction, nor are any likely to be performed in the future. Thus these recommendations are necessarily speculative and rely on inferences drawn from the large clinical trials, as well as on of the natural history of ventricular remodelling and thrombus formation. The case for ACE inhibition after myocardial infarction appears ironclad. A large meta-analysis established the efficacy of early administration with oral ACE inhibitors in the treatment of unselected patients with acute myocardial infarction.3 A 7% relative reduction in 30 day mortality was observed, with the higher risk subgroups …

The effect of inotropic stimulation on the pattern and magnitude of regional left ventricular contraction was studied using tagged magnetic resonance imaging to assess whether dobutamine exacerbates variation in regional contraction at rest. Dobutamine stress testing defines a normal response as a homogeneous increase in regional wall motion. In 8 normal subjects, 4 equally spaced left ventricular short-axis levels were imaged through systole using tagged magnetic resonance imaging. The baseline imaging sequence was repeated with 5-, 10-, 15-, and 20-μg/kg/min dobutamine infusion. Regional myocardial displacement, radial thickening, and circumferential shortening were measured. The left ventricle was analyzed by level (base to apex) and wall (septum, inferior, lateral, anterior). Dobutamine did not alter baseline regional functional heterogeneity. Dobutamine infusion resulted in a uniform increase in displacement, radial thickening, and circumferential shortening from baseline to 10-μg/kg/min infusion without additional increases at higher doses.

Coronary artery aneurysm is a rare disorder, characterized by abnormal dilatation of a localized portion or diffuse segments of the coronary artery. We studied clinical demographics, catheterization findings, and clinical outcomes in an Asian patient cohort with documented coronary artery aneurysms. Compared to a Caucasian adult population, our patient cohort had a lower incidence of coronary artery aneurysm (0.25% vs. 2.6%), and more patients with nonobstructive coronary artery aneurysms (70%); age, gender, and coronary distribution were comparable. The initial presentation of myocardial infarction occurred in five patients (5/17, 30%) with nonobstructive coronary artery aneurysms; however, none who were receiving preventive medications consisting of anticoagulant and antiplatelet agents subsequently developed myocardial infarction. We conclude that the incidence of coronary artery aneurysms with or without associated significant coronary stenosis seems to be lower in the Asian population. In contrast, the incidence of nonobstructive coronary artery aneurysms is considerably high and should not be thought of as a relatively benign disease entity if not treated with preventive medications. Rheumatoid arthritis-related vasculitis might be a cause of coronary artery aneurysm. Surgical intervention is based on the severity of coronary artery stenosis. The result of medical treatment has been compatible with long-term survival. Cathet. Cardiovasc. Intervent. 48:31-38, 1999.

Sinus of Valsalva aneurysm is a rare congenital anomaly which, if overlooked, may be associated with increased mortality and morbidity. Multiplane transesophageal echocardiography proved useful in identifying a variety of associated structural heart disease. This study sought to assess the accuracy of the surgical result on the basis of the multiplane transesophageal echocardiography findings and to describe patient-demographics and clinical outcome in an Oriental patient cohort. From July 1984 to December 1995, clinical, catheterization, echocardiographic, and surgical results were retrospectively studied in 23 patients with documented sinus of Valsalva aneurysm. Compared with previous reports of Oriental patients, our patient cohort was older (p < 0.025), had more associated aortic, mitral, and tricuspid regurgitation (p < 0.01), but had fewer coexistent ventricular septal defects (p < 0.01), and had more associated coronary artery disease (9%). Multiplane transeophageal echocardiography precisely showed three undiagnosed and/or ambiguous transthoracic echocardiographic studies, and the preoperative transesophageal echocardiography TEE findings were confirmed intraoperatively in the last eight consecutive patients. We concluded that multiplane trans esophageal echocardiography provides conclusive information and is the current technique of choice for diagnosis and clinical management of patients with sinus of Valsalva aneurysm; although the natural history of sinus of Valsalva aneurysm remains uncertain, it is likely that the incidence of unruptured sinus of Valsalva aneurysm is considerably higher in the elderly than has been previously reported.