Severe Left Ventricular Dilatation Research Articles

Cardiac resynchronization therapy may improve symptoms of congestive heart failure in patients without electrical or mechanical dyssynchrony

Cardiac resynchronization therapy (CRT) has reportedly not been effective in the absence of electrical or mechanical dyssynchrony. We present six patients with severe left ventricular (LV) dilation, mitral regurgitation (MR), and non-ischaemic cardiomyopathy who underwent CRT. We assessed the effects of CRT on LV ejection fraction (EF), LV dimensions, mitral valve regurgitant fraction (RF), pulmonary arterial pressures (PAP), and serum levels of B-natriuretic peptide (BNP). All patients had severe LV dilation (>/=6.8 cm) and no electrical or mechanical dyssynchrony. All patients underwent CRT-D (with defibrillator) without complications. Average echocardiographic follow-up was 4.6 months. Mean LVEF increased significantly from 20.8 +/- 3.4 to 28.3 +/- 2.9% after CRT (P < 0.01). Mean LV end-diastolic dimension decreased significantly from 6.9 +/- 0.15 to 6.45 +/- 0.33 cm after CRT (P = 0.03); mean BNP serum level decreased from 1738 +/- 526 to 1040 +/- 768 pg/mL (P = 0.07). Baseline RF decreased from 45 +/- 12.2 to 20 +/- 10.9% after CRT-D (P = 0.009). Mean PAP decreased from 48.5 +/- 5.8 to 42.6 +/- 5.2 (P = 0.03). In five patients, New York Heart Association class symptoms improved by at least one level. No patients required assist devices or transplantation. One patient was hospitalized during follow-up. We describe six patients with severe LV dilation without evidence of electrical or mechanical dyssynchrony who improved with CRT, possibly due to improvement in MR.

Continuous Aortic Flow Augmentation in a Chronic Heart Failure Patient With Peripheral Arterial Disease

Continuous Aortic Flow Augmentation in a Chronic Heart Failure Patient With Peripheral Arterial Disease

Combined surgery for ischemic cardiomyopathy: Report of a case

A 65-year-old female with catecholamine-dependent ischemic cardiomyopathy was admitted to our hospital. Preoperative examination revealed severe triple vessel coronary artery disease, severe mitral valve regurgitation and left ventricular (LV) dilatation associated with low ejection fraction. Coronary artery bypass grafting with four distal anastomoses, mitral valve plasty using original papillary muscle application method, LV volume reduction using overlapping method and biventricular pacing were performed. Postoperative course was uneventful and quality of life at 2 years after surgery was good. Active combined surgery has the possibility of improving the outcome of patients with severe ischemic cardiomyopathy.

Xanthine Oxidase Inhibition Improves Left Ventricular Dysfunction in Dilated Cardiomyopathic Hamsters

Background Oxidative stress is implicated in cardiac remodeling and failure. We tested whether xanthine oxidase (XO) inhibition could decrease myocardial oxidative stress and attenuate left ventricular (LV) remodeling and dysfunction in the TO-2 hamster model of dilated cardiomyopathy. Methods and Results TO-2 hamsters were randomized to treatment with the XO inhibitor, allopurinol, or vehicle from 6 to 12 weeks of age. F1B hamsters served as controls. TO-2 hamsters treated with vehicle progressively developed severe LV systolic dysfunction and dilation between 6 and 12 weeks. Marked cardiac fibrosis was apparent in these hamsters at 12 weeks in comparison with F1B controls. The ratio of reduced to oxidized glutathione (GSH/GSSG) was decreased and malondialdehyde levels were increased in the hearts of vehicle-treated TO-2 hamsters. Treatment with allopurinol from 6 to 12 weeks attenuated LV dysfunction and dilation as well as myocardial fibrosis and the upregulation of a fetal-type cardiac gene. Allopurinol also inhibited both the decrease in GSH/GSSG ratio and the increase in malondialdehyde levels in the heart. Conclusions These results indicate that chronic XO inhibition with allopurinol attenuates LV remodeling and dysfunction as well as myocardial oxidative stress in this model of heart failure. Allopurinol may prove beneficial for the treatment of heart failure.

Follow-up outcomes 10 years after arterial switch operation for transposition of the great arteries: comparison of cardiological health status and health-related quality of life to those of the a normal reference population

The purpose of this study was to investigate the cardiological health status and health-related quality of life after the arterial switch operation (ASO) for transposition of the great arteries (TGA) in comparison with a normative reference group. Chart review and cross-sectional systematic follow-up, including echocardiography, exercise testing, and electrocardiography, were performed on all survivors of ASO for TGA between 1990 and 1995. Health-related quality of life (HRQOL) was assessed using a standardized questionnaire. A normative reference group was included. Forty-nine survivors [median age at operation 13 days, mean age at follow-up 11 +/- 2 years (37/49 with intact ventricular septum] were identified. Thirty-three of 49 patients (67%) [22/33 TGA with intact ventricular septum (IVS)] participated in cross-sectional follow-up. Cumulative 10-year event-free survival was 88% and the re-intervention rate 6%. Aortic root dilatation occurred in 70% of patients; none had severe aortic regurgitation. Left ventricular function was normal. Exercise performance (85% of reference capacity, p = 0.02), maximal oxygen uptake (85%, p < 0.01) and peak heart rate (95%, p < 0.01) were decreased. Exercise electrocardiogram was normal as was rhythm status. Unfavourable outcomes on HRQOL were found for motor functioning and positive emotional functioning. Overall there were no significant differences between TGA/IVS and TGA/VSD. We conclude that at mid- to long-term follow-up after ASO, major events and re-interventions (6%) occur infrequently. Exercise capacity and maximal oxygen uptake are lower than those in a reference population, which could not be related to diminished ventricular function. Aortic root dilatation is frequent, irrespective of the anatomical subgroup. Severe aortic regurgitation or left ventricular dilatation was not found. The unfavourable health-related quality of life deserves further attention.

Fetal and Neonatal Presentation of Noncompacted Ventricular Myocardium: Expanding the Clinical Spectrum

Noncompaction of the ventricular myocardium (NCVM) is a rare cardiomyopathy characterized by varying degrees of ventricular dysfunction and numerous, prominent trabeculations with deep intertrabecular recesses caused by arrest in myocardial embryogenesis. NCVM is rarely described in fetal and neonatal patients, and only isolated reports exist to date. We conducted a review of clinical and echocardiographic data from 6 neonates found to have NCVM to elucidate aspects of prenatal manifestations, initial presentations, and clinical course/outcome. Six neonates met criteria for diagnosis of NCVM. Five were initially evaluated during fetal life, whereas one patient presented for initial cardiology examination as a neonate. Three of the 5 fetuses had NCVM recognized at the initial examination. Both unrecognized fetuses also had severe prenatal left ventricular dilation and dysfunction. Left ventricular enlargement or increased wall thickness with decreased ejection fraction was evident in all patients at presentation. Mean ejection fraction at presentation was 36% and improved to 57% during an average follow-up of 2 years. Associated congenital cardiac anomalies were noted in 3 patients. After initial improvement, two patients had transient, late decreases in ejection fraction, which improved with medication adjustment. There have been no deaths. Fetuses with enlarged and poorly functioning left ventricles should be evaluated for NCVM, which may not be easily recognized on initial fetal studies. Unlike previous reports of neonatal NCVM, all 6 neonates, including the 3 requiring inotropic support, showed significant early recovery of cardiac function with aggressive therapy.

Guidelines for Performing a Comprehensive Epicardial Echocardiography Examination: Recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists

TABLE OF CONTENTSIntroduction 921General Guidelines 922Training and Certification 922Indications for TEE 923Management of Patient Sedation 927Sedation and Anesthesia 929Probe Insertion Techniques 930Instrument Controls 930Instrument Manipulation 931Comprehensive Imaging Examination 932ME Views 932TG

When should we close ventricular septal defects?

With the advent of catheter-based cardiac intervention, we are now capable of doing things that used to require open heart surgery in a less invasive manner. This progress has also allowed a thought process of potentially closing smaller and smaller ventricular septal defects (VSD). Important questions emerge about the appropriate indications for closure of VSD. In this issue of The Journal, Kleinman et al address these issues by reporting on a study of the natural history of unoperated patients with a moderate to large VSD and with left ventricular (LV) dilation. They found that most patients with pressure-restrictive VSDs, with moderate to large severe LV dilation, without heart failure, failure to thrive, or pulmonary hypertension will spontaneously decrease LV dilation over time without intervention. In an accompanying editorial, Beekman puts these findings in clinical perspective. He emphasizes that just because we can close VSDs without surgery, does not mean we should close them. He indicates that studies like that of Kleinman et al help to provide the evidence base we can use to make rational decisions about when to intervene. In most asymptomatic children with pressure restricted VSDs, even when they are relatively large, trans-catheter intervention is not needed to result in a favorable outcome. Spontaneous Regression of Left Ventricular Dilation in Children with Restrictive Ventricular Septal DefectsThe Journal of PediatricsVol. 150Issue 6PreviewTo test the hypothesis that left ventricular (LV) dilation associated with pressure-restrictive ventricular septal defect (VSD) often remains stable or regresses spontaneously, calling into question the role of interventional management for such defects. Full-Text PDF Closing the Ventricular Septal Defect Because You Can: Evidence-Averse Care?The Journal of PediatricsVol. 150Issue 6Preview“What this patient needs is a doctor.”—Eugene A. Stead, Jr, MD Full-Text PDF

Guidelines for Performing a Comprehensive Epicardial Echocardiography Examination: Recommendations of the American Society of Echocardiography and the Society of Cardiovascular Anesthesiologists

Scott T. Reeves, MD, FASE, Kathryn E. Glas, MD, FASE, Holger Eltzschig, MD, Joseph P. Mathew, MD, FASE, David S. Rubenson, MD, FASE, Gregg S. Hartman, MD, and Stanton K. Shernan, MD, FASE, for the Council for Intraoperative Echocardiography of the American Society of Echocardiography, Charleston, South Carolina; Atlanta, Georgia; Tubingen, Germany; Durham, North Carolina; La Jolla, California; and Lebanon, New Hampshire

Severe Left Ventricular Dysfunction in Left Atrial Myxoma

We report 2 patients with left atrial (LA) myxoma with associated severe left ventricular (LV) dysfunction. Both presented with progressive effort intolerance without a history suggestive of acute coronary event. LA myxoma was diagnosed by transthoracic echocardiography, which also detected severe systolic dysfunction and LV dilatation. Regional wall motion abnormality and thinning were absent. Coronary angiograms also showed no occlusive disease, but distal ectasia was seen in 1 patient. Metabolic and endocrine causes of reversible LV dysfunction were excluded. Cardiac function improved following surgery for myxoma in 1 patient. LV dysfunction, thus far, has not been directly attributed to myxoma. Coronary embolization leading to myocardial infarction and coexisting coronary atherosclerosis are the recognized methods by which LV dysfunction manifests in myxoma. Our report suggests the possibility of reversible severe global LV dysfunction due to cardiodepressant effect of myxoma through as yet unclear mechanisms.

NNOS Gene Deletion Exacerbates Pathological Left Ventricular Remodeling and Functional Deterioration After Myocardial Infarction

The neuronal isoform of nitric oxide synthase (nNOS) has been implicated in the regulation of basal and beta-adrenergic inotropy in normal and chronically infarcted hearts. Furthermore, myocardial nNOS expression and activity increase in failing hearts, raising the possibility that nNOS may influence left ventricular (LV) remodeling progression and functional deterioration after myocardial infarction (MI). We compared LV remodeling at 1, 4, and 8 weeks after MI in nNOS-knockout mice (nNOS(-/-)) and their wild-type (WT) littermates matched for infarct size by using a highly accurate 3-dimensional echocardiographic technique. Basal LV hemodynamics and the inotropic response to dobutamine infusion (4 and 16 ng.g(-1).min(-1)) were also evaluated 8 weeks after MI. Sham-operated nNOS(-/-) mice showed enhanced basal LV contractility (P<0.03 versus WT, as evaluated by preload-recruitable stroke work) but an attenuated inotropic response to dobutamine infusion (P<0.01 versus WT). Both basal and beta-adrenergic LV relaxations were significantly impaired in nNOS(-/-) mice. Survival after MI did not differ between groups. However, nNOS(-/-) mice developed a faster and more severe LV dilation compared with WT mice (P<0.05 for both end-systolic and end-diastolic volume indices). WT mice maintained a positive inotropic response to dobutamine 8 weeks after MI. In contrast, infarcted nNOS(-/-) mice responded to dobutamine with a dramatic fall in LV contractility (P<0.01 for preload-recruitable stroke work). nNOS plays a crucial role in preventing adverse LV remodeling and maintaining myocardial beta-adrenergic reserve after MI. Taken together, our findings suggest that upregulation of myocardial nNOS in infarcted hearts may be an important adaptive mechanism.

Beating Heart Surgery for Patients with Poor LV Function

Beating heart surgery expand the surgical indications to the old patient and serious case. We present a favorable outcome of beating heart surgery for the valvular disease and the aortic aneurysm patient with low cardiac function. In every cases, we use antegrade worm blood perfusion to coronary artery. First case of a 56-year-old man with a preoperative diagnosis of severe aortic stenoinsufficiency, Fractional shortening (FS=10%) is reduced, the left ventricle is dilated (LVDd=66mm), and severe tricuspid regurgitation was detected by echocardiogram. Aortic valve replacement and tricuspid annuloplasty was performed on baeating heart. At postoperative day 1, maximal CK-MB activity was 32(10.9%)IU/I. At postoperative day 7, Fractional shortening (FS=18%) was recovered. Second case of a 77-year-old man with thoracic aorta aneurysm, At preoperative echocardiogram, poor LV function (FS=27%, E/A=0.54, LV tei index=0.81) was pointed out. Total arch replacement with elephant trunk procedure was performed on beating heart. At postoperative day 1, maximal CK-MB activity was 23(7.0%)IU/I. Postoperative LV function was almost the same (FS=21%, E/A=0.88, LV tei index=0.86). Third case of a 71-year-old man with non-ischemic dilated cardiomyopathy, severe heart failure (FS=7%) and left ventricular dilatation (LVDd=90mm), and severe mitral regurgitation was detected by echocardiogram. Left ventricular reduction surgery (Batista procedure) and mitral valve plasty was performed on beating heart. We got an early postoperative recovery of LV function in every cases.

Multipotent Adult Progenitor Cells (MAPCs) Improve Cardiac Function after Ischemic Injury.

MAPCs are pluripotent cells derived from mesenchymal stromal cells (MSCs) in adult bone marrow. In contrast to MSCs, MAPCs differentiate into various lineages of mesodermal, ectodermal and endodermal origin, and contribute to numerous terminally differentiated tissues in the recipients. This capacity is enhanced in the setting of injury, suggesting a possible role of MAPCs in repair and regeneration in disease states. We aimed to investigate the capacity of MAPCs to aid in myocardial repair in hearts with postinfarction remodeling. We reasoned that as MAPCs differentiate to both endothelium and cardiomyocytes in vitro and as engraftment of delivered cells depends on establishing adequate blood flow in the ischemic region, MAPCs may represent the optimal cell type to contribute to both angiogenesis and the parenchymal tissue to regenerate function of injured myocardium. To study engraftment and survival of MAPCs, we labeled adult murine C57BL/6 MAPCs with firefly luciferase and DsRed2 fluorescent protein using non-viral Sleeping Beauty transposons, and injected them into myocardium of C57BL/6 adult mice with acute myocardial infarction (AMI). Mice were anesthetized, intubated and mechanically ventilated using a small-animal respirator. Under a stereomicroscope the heart was accessed via left thoracotomy. The left anterior descending coronary artery was ligated at mid-level between apex and base with a 9-0 surgical suture to produce AMI. Twenty minutes later, intramyocardial injections of labeled MAPCs in saline, or saline alone were administered at five distinct injection sites at boarder zone of AMI (total MAPC dose = 106/mouse). Chest was closed in layers and animals were allowed to recover. Mice were followed with echocardiography and in vivo whole body bioluminescent imaging. Seventy days after AMI, MAPCs recipients (N=6) had significantly less severe left ventricular (LV) dilatation evidenced by a smaller LV end-diastolic and LV end-systolic dimensions when compared to control mice infused with saline (N=4) (average±standard deviation, 4.7±0.2 mm versus 5.3±0.5 mm, p=0.05; and 3.7±0.2 mm versus 4.4±0.6 mm, p=0.03, respectively). In addition, ejection and shortening fractions were significantly higher in MAPC recipients (36±2% versus 30±3%, p=0.004; and 20±1% versus 16±2%, p=0.004, respectively). Luciferase signals emitted from donor MAPCs were easily detectable in MAPC recipients 100 days after MAPC infusion, at which point the animals were harvested. Analyses are ongoing to determine whether MAPCs and their progeny contributed to expansion of coronary vasculature (capillary density), or formed or modified injured myocardial tissue. Alternatively, both populations of repair cells could have been derived from donor (DsRed2+) MAPCs, or donor MAPCs could have provided permissive local environment to recruit recipient cells and enhance endogeneous regeneration. In summary, these findings provide evidence that MAPCs persist long term in injured myocardium and document the potential of MAPCs for improvement of cardiac function after ischemic myocardial injury. Jakub Tolar and Xiaohong Wang contributed equally to this study.

Impaired Endothelium-Dependent Forearm Vasodilation in Idiopathic Dilated Cardiomyopathy Is Related to Severe Left Ventricular Dysfunction and Elevated Serum Tumor Necrosis Factor Levels

Endothelial dysfunction has been found in patients with idiopathic dilated cardiomyopathy (IDC), but its mechanism remains unknown. Our aim was to investigate whether forearm endothelium-dependent vasoreactivity correlates with cardiac disease severity or neurohormonal activation. We studied 23 patients with IDC and 10 healthy sex- and age-matched controls using brachial artery ultrasound to assess flow-mediated dilation (FMD) and nitroglycerin-induced vasodilation (NIV). In the IDC group, we determined plasma neurohormone and cytokine levels at the same time. FMD was significantly less in the IDC group compared with the control group [--0.06 (2.8)% vs 4.4 (4.6)%, respectively; P<.01], whereas NIV was similar in both groups [15.0 (6.4)% vs 14.0 (7.4)%, respectively; P=NS]. FMD was significantly less in patients with poorer left ventricular (LV) function and more severe LV dilatation, and in those with a higher tumor necrosis factor-alpha (TNF-alpha) level. NIV was similar in all patient subgroups. There was a significant inverse correlation between the TNF-alpha plasma level and FMD (r=-0.75; P<.01). No correlation was found between the plasma levels of other neurohormones and FMD. FMD, but not NIV, was impaired in patients with IDC compared with control subjects. In patients, there were significant associations between FMD impairment and the severity of LV dilatation, the severity of LV systolic dysfunction, and the plasma TNF-alpha level. The strongest correlation was observed between TNF-alpha plasma level and FMD. These data suggest that TNF-alpha may be implicated in endothelial dysfunction in patients with IDC.

The effects of biventricular pacing on mitral coaptation point displacement in patients with heart failure

Purpose In recent years cardiac resynchronisation therapy (CRT) is an established treatment in selected patients with heart failure. Furthermore it has been shown that the displacement of the mitral leaflet coaptation point (CPMA) towards the LV apex correlates with the degree of left ventricular (LV) dysfunction. The purpose of this study is to find the acute effects of biventricular pacing in the mitral apparatus and LV function in heart failure patients. Methods We studied 16 patients (pts) 15 men, 1 woman aged 56±25 years in NYHA class III or IV and left ventricular ejection fraction (LVEF) 22±4%. The etiology was coronary artery disease (CAD) in 7 pts and dilated cardiomyopathy (DCM) in 8 pts. All the patients received cardiac resynchronisation therapy. An echocardiogram was performed within one week after implantation with biventricular pacing (CRT on) and without pacing (CRT off). The CPMA i.e. distance between coaptation point of mitral leaflets and mitral annulus, was measured from the apical 4-chamber view in midsystole and was evaluated with CRT on and CRT off. Echocardiographic indices such as LV end diastolic diameter (LVEDD), end systolic diameter (LVESD), ejection fraction (LVEF) and mitral annulus diameter (MAD) were also measured at CRT off and at CRT on. Results There was a non-significant increase in LVEF, and a non-significant decrease in LVEDD and LVESD with CRT on. CPMA decreased from 10.6±1.9mm at CRT off to 8.1±1.4 at CRT on and MAD decreased from 38.4±4.2 mm at CRT off to 37.7±3.7mm at CRT on (both p<0.05). Moreover the absolute change in CPMA was related to the LVEDD (r=0.74, p<0.05) and inversely related with the LVEF (r= −0.72, p<0.05). Conclusion In patients with severe LV systolic dysfunction and LV dilatation biventricular pacing led to an improvement in both CPMA and MAD. This finding underlines the acute effect of resynchronisation therapy in the mitral apparatus in heart failure patients.

Intracoronary adenovirus encoding adenylyl cyclase VI increases left ventricular function in heart failure.

We tested the hypothesis that intracoronary delivery of an adenovirus encoding adenylyl cyclase type VI (Ad.AC(VI)) would be associated with increased left ventricular (LV) function in pigs with congestive heart failure. Pigs (52+/-6 kg; n=16) underwent placement of pacemakers, LV pressure transducers, and left atrial and aortic catheters. Physiological and echocardiographic studies were obtained from conscious animals 13 days later, and pacing was initiated (220 bpm). Seven days later, measures of LV function were reduced, documenting severe LV dysfunction and dilation. Pigs then received intracoronary Ad.AC(VI) (1.4x10(12) vp; n=7) or saline (PBS; n=9) (randomized, blinded), with concomitant infusion of nitroprusside (50 microg/min, 6.4 minutes) to increase gene transfer. Pacing was continued for 14 days, and final studies were obtained. The a priori key end point was change in LV dP/dt during isoproterenol infusion (pre-Ad.AC(VI) value minus value after 21 days of pacing). Pigs receiving Ad.AC(VI) showed a smaller decrease in both LV +dP/dt (P=0.0014) and LV -dP/dt (P=0.0008). Serial echocardiography showed that Ad.AC(VI) treatment was associated with increased LV function and reduced LV dilation and that end-systolic wall stress was reduced. AC-stimulated cAMP production was increased 1.7-fold in LV samples from Ad.AC(VI)-treated pigs (P=0.006), and B-type natriuretic peptide was reduced (0.035). Gene transfer was confirmed by polymerase chain reaction. AC(VI) gene transfer increases LV function and attenuates deleterious LV remodeling in congestive heart failure.

Direct evidence for a beta 1-adrenergic receptor-directed autoimmune attack as a cause of idiopathic dilated cardiomyopathy.

Today, dilated cardiomyopathy (DCM) represents the main cause of severe heart failure and disability in younger adults and thus is a challenge for public health. About 30% of DCM cases are genetic in origin; however, the large majority of cases are sporadic, and a viral or immune pathogenesis is suspected. Following the established postulates for pathogenesis of autoimmune diseases, here we provide direct evidence that an autoimmune attack directed against the cardiac beta(1)-adrenergic receptor may play a causal role in DCM. First, we immunized inbred rats against the second extracellular beta(1)-receptor loop (beta(1)-EC(II); 100% sequence identity between human and rat) every month. All these rats developed first, receptor-stimulating anti-beta(1)-EC(II) Ab's and then, after 9 months, progressive severe left ventricular dilatation and dysfunction. Second, we transferred sera from anti-beta(1)-EC(II)-positive and Ab-negative animals every month to healthy rats of the same strain. Strikingly, all anti-beta(1)-EC(II)-transferred rats also developed a similar cardiomyopathic phenotype within a similar time frame, underlining the pathogenic potential of these receptor Ab's. As a consequence, beta(1)-adrenergic receptor-targeted autoimmune DCM should now be categorized with other known receptor Ab-mediated autoimmune diseases, such as Graves disease or myasthenia gravis. Although carried out in an experimental animal model, our findings should further encourage the development of therapeutic strategies that combat harmful anti-beta(1)-EC(II) in receptor Ab-positive DCM patients.

Doppler-derived mitral deceleration time as a strong prognostic marker of left ventricular remodeling and survival after acute myocardial infarction: Results of the GISSI-3 Echo substudy

ObjectivesThe goal of this study was to assess the impact of left ventricular (LV) diastolic filling on remodeling and survival after acute myocardial infarction (AMI). BackgroundLittle is known regarding the link between LV filling, its changes over time, and six-month remodeling and late survival in uncomplicated AMI. MethodsDoppler mitral profile, end-diastolic volume index (EDVi) and end-systolic volume index (ESVi), ejection fraction (EF), and wall motion abnormalities (%WMA) were evaluated in 571 patients from the GISSI-3 Echo substudy at baseline, pre-discharge, and six months after AMI. Patients with baseline early mitral deceleration time (DT) 130 ms were assigned to the restrictive group (n = 147), and those with DT >130 ms to the nonrestrictive group (n = 424). ResultsRestrictive group patients had greater baseline ESVi and %WMA and lower EF than nonrestrictive group, and six-month greater LV dilation (EDVi, ESVi: p < 0.001 for EDVi and ESVi), smaller decrease in %WMA decrease (p < 0.01), and larger EF impairment (p < 0.008). Among the restrictive group, patients (n = 56) with pre-discharge persistent restrictive filling (n = 56) showed six-month greater LV enlargement (p < 0.001) and EF impairment (p < 0.009) than those (n = 91) with reversible restrictive filling. Baseline %WMA and EDVi, together with pre-discharge persistent restrictive filling, predicted severe (>20%) LV dilation. Four-year survival was 93% in nonrestrictive patients versus 88% in the restrictive group (p < 0.06), and 93% in pre-discharge reversible restrictive versus 79% in persistent restrictive (p < 0.0003). The single best predictor of mortality, by Cox analysis, was pre-discharge persistent restrictive filling (chi-square 14.88). ConclusionsLeft ventricular dilation may occur even after uncomplicated AMI and may be paralleled by an improvement in LV filling. However, a baseline restrictive filling that persists at pre-discharge identifies more compromised patients at higher risk for six-month remodeling and four-year mortality.

Prevalence of QRS prolongation in a community hospital cohort of patients with heart failure and its relation to left ventricular systolic dysfunction

Adverse outcomes in heart failure occur more frequently with QRS prolongation. The results of our study have shown that 1/4 of community hospital patients with heart failure of sufficient severity leading to hospitalization have a QRS duration of ≥120 ms and that this degree of QRS prolongation is associated with substantially more severe left ventricular (LV) systolic dysfunction, LV dilation, and mitral regurgitation.

Transesophageal echocardiography of a new paravalvular echolucent area after aortic valve replacement

THIS CASE INVOLVES a 73-year-old man with severe aortic stenosis who was scheduled for aortic valve replacement. The patient had a 2-year history of exertional angina, occasional presyncopal episodes, shortness of breath on exertion, and orthopnea. He also had non-insulin-dependent diabetes mellitus and hyperlipidemia. His medications included atenolol, entrophen, and simvastatine. Preoperative transthoracic echocardiographic (TTE) assessment revealed severe aortic stenosis with an aortic valve area of 0.6 cm2 and a mean pressure gradient of 59 mmHg. Severe left ventricular dilatation with trivial mitral regurgitation and an ejection fraction of 35% were also noted. Coronary angiography was normal except for a 50% stenosis of the second diagonal artery.