Search

Key Points Cardiac abnormalities in children and young adults with sickle cell anemia are common.Timely initiation of treatment with hydroxyurea may lead to reverse cardiac remodeling and improvement in these cardiac abnormalities., Visual Abstract, Cardiac abnormalities such as left ventricular hypertrophy, left ventricular dilation, and pulmonary hypertension in sickle cell anemia have been previously described. Hydroxyurea, a disease-modifying therapy for sickle cell anemia, has been used for several decades. Longitudinal assessment of echocardiographic abnormalities in children and young adults with sickle cell anemia receiving hydroxyurea therapy is lacking. The goal of this retrospective study was to determine the prevalence of echocardiographic abnormalities in children and young adults with sickle cell anemia and to examine the effects of hydroxyurea on reverse cardiac remodeling. We reviewed the records of patients with sickle cell anemia who underwent routine cardiac screening at Cohen Children’s Medical Center between 2010 and 2017, followed by retrospective longitudinal analysis of echocardiograms performed on patients receiving treatment with hydroxyurea. Data on a total of 100 patients with sickle cell anemia were analyzed; 60 (60%) were being treated with hydroxyurea. Twenty-five (41.6%) of the patients on hydroxyurea had been treated for 1 year. Serial echocardiograms of patients receiving hydroxyurea were then analyzed. Left ventricular dilation and hypertrophy improved significantly with hydroxyurea treatment. In addition, the left ventricular volume and mass correlated negatively with duration of treatment with hydroxyurea. Our study provides evidence that prolonged hydroxyurea therapy may lead to reverse cardiac remodeling. Future studies should attempt to follow up this patient cohort for a longer duration.

Increased left ventricular dilation and reduced systolic function are consistently associated with a poor prognosis and worse clinical outcomes. In this review, we discuss the pathophysiological me...

MitraClip implantation has become the standard transcatheter mitral valve repair (TMVR) technique for severe mitral regurgitation (MR). However, approximately one third of patients have poor outcomes, with MR recurrence at follow-up. The aim of this study was to investigate whether quantitative analysis of mitral valve (MV) geometry on three-dimensional (3D) echocardiography can identify geometric parameters associated with the recurrence of severe functional MR (FMR) versus organic MR (OMR) at 6-month follow-up after TMVR using the MitraClip.Sixty-one patients with severe FMR (n = 45) or OMR (n = 16) who underwent transesophageal 3D echocardiography before and 6 months after TMVR were retrospectively analyzed. MV geometry was quantified using 3D echocardiography software. Vena contracta area (VCA) at 6-month follow-up was used to define two outcome groups: patients with good results with VCA 0.6 cmMR recurrence was found in 34% of all study patients (21 of 61). In patients with FMR, significant differences between MR 0.6 and MR ≥ 0.6 were found at baseline for tenting index (1.13 vs 1.23, P = .004), tenting volume (2.8 vs 4.0 ml, P = .04), indexed left ventricular (LV) end-diastolic volume (68.0 vs 99.9 ml/mMR recurrence after TMVR in patients with FMR is associated with advanced LV dilation and MV tenting before TMVR, which provides clinical implications for a point of no return beyond which progressive LV dilation with MV geometry dilation and tethering cannot be effectively prevented by TMVR. In contrast, no significant determinants of MR recurrence and progressive MV annular dilation could be identified in patients with OMR.

Dilated cardiomyopathy (DCM) is a major cause of heart failure and cardiovascular mortality. In the past 20 years, there has been an overwhelming focus on developing therapeutics that target common downstream disease pathways thought to be involved in all forms of heart failure independent of the initial etiology. While this strategy is effective at the population level, individual responses vary tremendously and only approximately one third of patients receive benefit from modern heart failure treatments. In this perspective, we propose that DCM should be considered as a collection of diseases with a common phenotype of left ventricular dilation and systolic dysfunction rather than a single disease entity, and that mechanism-based classification of disease subtypes will revolutionize our understanding and clinical approach towards DCM. We discuss how these efforts are central to realizing the potential of precision medicine and how they are empowered by the development of new tools that allow investigators to strategically employ genomic and transcriptomic information. Finally, we outline an investigational strategy to (1) define DCM at the patient level, (2) develop new tools to model and mechanistically dissect subtypes of human heart failure, and (3) harness these insights for the development of precision therapeutics.

Administration of active growth differentiation factor 11 (GDF11) to aged mice can reduce cardiac hypertrophy, and low serum levels of GDF11 measured together with the related protein, myostatin (also known as GDF8), predict future morbidity and mortality in coronary heart patients. Using mice with a loxP-flanked (“floxed”) allele of Gdf11 and Myh6-driven expression of Cre recombinase to delete Gdf11 in cardiomyocytes, we tested the hypothesis that cardiac-specific Gdf11 deficiency might lead to cardiac hypertrophy in young adulthood. We observed that targeted deletion of Gdf11 in cardiomyocytes does not cause cardiac hypertrophy but rather leads to left ventricular dilation when compared with control mice carrying only the Myh6-cre or Gdf11-floxed alleles, suggesting a possible etiology for dilated cardiomyopathy. However, the mechanism underlying this finding remains unclear because of multiple confounding effects associated with the selected model. First, whole heart Gdf11 expression did not decrease in Myh6-cre; Gdf11-floxed mice, possibly because of upregulation of Gdf11 in noncardiomyocytes in the heart. Second, we observed Cre-associated toxicity, with lower body weights and increased global fibrosis, in Cre-only control male mice compared with flox-only controls, making it challenging to infer which changes in Myh6-cre;Gdf11-floxed mice were the result of Cre toxicity versus deletion of Gdf11. Third, we observed differential expression of cre mRNA in Cre-only controls compared with the cardiomyocyte-specific knockout mice, also making comparison between these two groups difficult. Thus, targeted Gdf11 deletion in cardiomyocytes may lead to left ventricular dilation without hypertrophy, but alternative animal models are necessary to understand the mechanism for these findings. NEW & NOTEWORTHY We observed that targeted deletion of growth differentiation factor 11 in cardiomyocytes does not cause cardiac hypertrophy but rather leads to left ventricular dilation compared with control mice carrying only the Myh6-cre or growth differentiation factor 11-floxed alleles. However, the mechanism underlying this finding remains unclear because of multiple confounding effects associated with the selected mouse model.

Several left ventricular geometric patterns have been described both in healthy and pathologic hearts. Left ventricular mass, wall thickness, and the ratio of wall thickness to radius are important measures to characterize the spectrum of left ventricular geometry. For clinicians, an increase in left ventricular mass is the hallmark of left ventricular hypertrophy. Although pathologic hypertrophy initially can be compensatory, eventually it may become maladaptive and evolve toward progressive left ventricular dysfunction and heart failure. In particular, patients who show left ventricular dilation and hypertrophy in association with a low relative wall thickness are likely to carry the highest risk.

Dilated cardiomyopathy (DCM) is the most prevalent cardiomyopathy, typified by left ventricular dilation and systolic dysfunction. Many patients with DCM have altered thyroid status, especially lower levels of free triiodothyronine (T3) and elevated levels of thyroid-stimulating hormone. Moreover, growing evidence indicates that even subtle changes in thyroid status (especially low T3) are linked with a worse long-term prognosis and a higher risk of mortality. Notably, recent discoveries have shown that not only local myocardial thyroid hormones (THs) bioavailability could be diminished due to impaired expression of the activating deiodinase, but virtually all genes involved in TH biosynthesis are also expressed in the myocardium of DCM patients. Importantly, some studies have suggested beneficial effects of TH therapy in patients suffering from DCM. Our aim was to discuss new insights into the association between TH status and prognosis in DCM, abnormal expression of genes involved in the myocardial synthesis of TH in DCM, and the potential for TH use in the future treatment of DCM.

In asymptomatic severe aortic (AR) and mitral regurgitation (MR), left ventricular (LV) dimension criteria were established to guide timing of valve replacement to prevent irreversible LV dysfunction. Given both lesions are primary LV volume overload ''leaks'', it might be expected that both lesions would induce similar impact on the LV and result in equivalent dimension criteria for intervention. However, the dimension-based intervention criteria for AR versus MR (developed through natural history studies), differ markedly. The pathophysiological foundations for such discordance have neither been fully elucidated nor emphasized. This case-based treatise compares the two regurgitant lesions with respect to: (a) ''total regurgitant circuits''; (b) ''driving pressures'' resulting in LV volume overload from each respective ''leak''; and (c) volume and afterload wall stresses imposed on the LV.Key points The ''total circuits'' of volume overload differ: The AR circuit includes the LV and systemic vasculature, whereas MR includes the LV ejecting into the left atrium/pulmonary veins and systemic circulation. The ''driving pressure'' of regurgitation and afterload are high with AR and low with MR. Differing ''total circuits'' and ''driving pressures'' impose disparate wall stresses upon the LV. Parallel and serial sarcomere replication occurs in AR, while only serial replication occurs in MR. It therefore follows that for regurgitation of similar severities, AR results in greater LV dilation at the point of irreversible myocardial dysfunction compared to MR. These considerations may explain, at least in part, the disparate dimension criteria employed for valve intervention for severe AR vs MR.

Introduction: Guideline directed medical therapy (GDMT) can result in improvement in left ventricular (LV) size and function following heart failure with reduced ejection fraction (HFrEF) diagnosis. Some therapies, such as device based interventions, are thus delayed in hopes of achieving recovery. We report remodeling and clinical outcomes in a large, consecutive series of patients presenting with a severely dilated and dysfunctional LV following 3-6 months of initial GDMT. Hypothesis: Patients with HFrEF and LVEDD ≥ 6.5cm at initial diagnosis will have a low likelihood of myocardial recovery in 3-9 months and a high burden of associated morbidity and mortality. Methods: Patients were retrospectively identified by a database search of echocardiogram studies obtained at Emory Healthcare hospitals between 2008-2018. Chart review was done to select patients’ with a new diagnosis of HFrEF and LVEDD ≥ 6.5 cm. Myocardial recovery was defined as LVEF > 35% at a follow-up echocardiogram done at least 3 months after initial study. Primary endpoint for Kaplan-Meier survival analysis was freedom from composite of death, enrollment in hospice, left ventricular assist device, or cardiac transplantation. Results: 339 patients with a median follow-up of 3.4 years were identified. The mean age was 49.0 ± 14.9 year and 68 (20.1%) were female. The mean LVEF at diagnosis was 16.9 ± 7.9% with a mean LVEDD of 7.0 ± 0.4 cm. Median time to repeat echocardiogram was 6.0 months. LVEF at follow-up was 18.3 ± 8.8% with a mean LVEDD of 6.9 ± 0.6 cm. Only 8 (2.5%) patients had myocardial recovery. 1- and 5-year primary event survival was 82.4% and 55.4% respectively. The median event free time was 5.9 years. Conclusions: Patients with de novo diagnosis of HFrEF and moderate or severe left ventricular enlargement have very low rates of myocardial recovery. Low survival estimate at 5 years suggests a potential benefit for early consideration of advanced therapies and device based therapies in this cohort.

Background: The N-Terminal of pro-B-type natriuretic peptide (NT-proBNP) is a potent biomarker for heart failure (HF), reflecting left ventricular dilation and stress. The association among obesity, HF, and NT-proBNP is complex, with paradoxically lower levels of NT-proBNP in obese individuals, despite their elevated HF risk. Furthermore, a few studies have reported decreased HF risk, but also increases in NT-proBNP, after weight loss via bariatric surgery. However, studies have not simultaneously evaluated changes in NT-proBNP and cardiac function after bariatric surgery. Hypothesis: There will be discordance between improvements in cardiac filling pressures (as reflected by E/e’) and increases in NT-proBNP with weight loss following bariatric surgery. Methods: We conducted a single-center analysis of participants in the BARI-Heart Study who underwent bariatric surgery and attended study visits 3-6 months and 2 weeks before surgery, and 6 and 12 months after surgery. We examined pre- and post-surgery changes in NT-proBNP and in echocardiographic measures of cardiac function. We also assessed the correlation between NT-pro-BNP and E/e’, at 2 weeks pre- and 6 months post-surgery. Results: Among 71 BARI-Heart participants (mean age 45 years, 74% female, 87% white, mean BMI 47.0 kg/m 2 ), there were no significant pre-surgery changes in BMI, NT-proBNP, or E/e’. By 6-12 months, there were marked reductions in BMI and significant increases in NT-proBNP, but decreases in E/e’ ( Figure ). Changes from surgery to the 6 month visit in NT-proBNP and E/e’ were associated (r=0.295; p=0.02). There was a tendency towards stronger correlations between NT-proBNP and E/e’ post- (r= 0.436; p Conclusions: Weight loss is associated with increases in NT-proBNP despite reduced LV filling pressures, suggesting a non-cardiac etiology underlying increases in NT-proBNP after weight loss. The interpretation of NT-proBNP for cardiac dysfunction may change with decreasing adiposity.

A 35-year-old woman was referred to our hospital for the management of acutely decompensated heart failure due to peripartum cardiomyopathy (PPCM). Generally, cardiac examinations are performed after the manifestation of heart failure in patients with PPCM. Thus, reports of serial cardiac examinations before the onset of PPCM are scarce. In this case, we were able to document the serial echocardiographic findings before the onset of life-threatening PPCM. We found that the left ventricular systolic function was preserved at 35 weeks of gestation but declined acutely after delivery at 38 weeks. Although speculative, these findings suggest that left ventricular dilation might precede the onset of PPCM.

Surgical mitral valve annuloplasty has been a cornerstone of surgical mitral valve repair since first described over 50 years ago by Carpentier ([1][1]). In patients without excessive leaflet tethering or left ventricular dilation, mitral ring annuloplasty can effectively correct secondary mitral

Athletic physical conditioning results in changes in cardiac anatomy and function that make it challenging to distinguish normal physiological changes from a pathological process in athletes with left ventricular (LV) dilation or a reduced ejection fraction. Millar and colleagues1 propose an approach for identifying athletes with dilated cardiomyopathy (DCM) based on sequential evaluation using N-terminal pro-brain natriuretic peptide (NT-proBNP) measurement, resting ECG, ambulatory ECG monitoring, exercise echocardiography and cardiac magnetic resonance (CMR) imaging. In 25 male athletes with LV dilation and an ejection fraction 11% compared with baseline on exercise echocardiography had the highest sensitivity, with a high specificity, for prediction of DCM. (figure 1) Figure 1 The figure demonstrates the utility of the stepwise clinical algorithm for differentiating between physiological adaptation and morphologically mild DCM in apparently healthy individuals with LV dilatation and LVEF

PURPOSE This study aimed to analyze left ventricular (LV) remodeling in patients with LV dilation using three-dimensional (3D) echocardiography, and to compare geometry and systolic function between patients with dilated cardiomyopathy (DCM) and with mitral regurgitation (MR) but similar LV dimension. METHODS Cross-sectional study of 60 DCM and 60 MR patients with LV end diastolic diameter (LVEDD) > 35 mm/m2 , and of 60 healthy control volunteers. RESULTS Despite a similar LVEDD, DCM patients showed a significantly higher 3D sphericity index (3D-SI) than MR patients, whereas 3D ejection fraction (3D-EF) was significantly lower (P

Background Changes in the plasma adenosine concentration and the effects on left ventricular (LV) function and remodeling in patients with acute myocardial infarction (AMI) remain unclear. Methods and Results: In 58 patients with AMI and 14 subjects without cardiac disease (controls), we measured the plasma adenosine concentration by LC-MS/MS. Blood samples were taken from the antecubital vein on days 0, 1, 7, and 14 after AMI, and from the controls on admission. Cardiac echocardiography was performed in the acute (within 7 days) and chronic (6 months) phases of AMI. There were no significant differences in the plasma adenosine concentrations among days 0 (211.5±150.2 nmol/L), 1 (192.7±141.3 nmol/L), 7 (218.8±154.1 nmol/L), and the controls (136.0±50.9 nmol/L). The plasma adenosine concentration increased significantly on day 14 (321.1±195.4 nmol/L) after AMI as compared with days 0, 1 and 7. AMI patients with a greater increase in the plasma adenosine concentration in the subacute phase showed an attenuation of LV dilation in the chronic phase. The plasma adenosine concentration in the acute phase did not affect the LV ejection fraction in the chronic phase. Conclusions The plasma adenosine concentration significantly increased 14 days after AMI, which may contribute to attenuation of LV dilation in the chronic phase.

Background— Surgery for severe mitral regurgitation is indicated if symptoms or left ventricular dilation or dysfunction occur. However, prognosis is already reduced by this stage, and earlier surgery on asymptomatic patients has been advocated if valve repair is likely, but identifying suitable patients for early surgery is difficult. Quantifying the regurgitation may help, but evidence for its link with outcome is limited. Cardiovascular magnetic resonance (CMR) can accurately quantify mitral regurgitation, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred nine asymptomatic patients with echocardiographic moderate or severe mitral regurgitation had baseline CMR scans and were followed up for up to 8 years (mean, 2.5±1.9 years). CMR quantification accurately identified patients who progressed to symptoms or other indications for surgery: 91% of subjects with regurgitant volume ≤55 mL survived to 5 years without surgery compared with only 21% with regurgitant volume >55 mL ( P 40%. CMR-derived end-diastolic volume index showed a weaker association with outcome (proportions surviving without surgery at 5 years, 90% for left ventricular end-diastolic volume index 2 versus 48% for ≥100 mL/m 2 ) and added little to the discriminatory power of regurgitant fraction/volume alone. Conclusions— CMR quantification of mitral regurgitation was associated with the development of symptoms or other indications for surgery and showed better discriminatory ability than the reference-standard CMR-derived ventricular volumes. CMR may be able to identify appropriate patients for early surgery, with the potential to change clinical practice, although the clinical benefits of early surgery require confirmation in a clinical trial.

Aim The aim of this work was to determine whether ethanol-associated myocardial apoptosis and cardiac dilation are related to myocardial telomere shortening in rats. Methods and Results Sprague-Dawley (SD) rats received either drinking water with (ethanol: n = 19) or without (control: n = 19) 5% (v/v) ethanol ad libitum, for 4 months. Left ventricular (LV) dimensions and function (echocardiography and isolated perfused heart preparations), cardiomyocyte apoptosis (terminal deoxynucleotide transferase–mediated dUTP nick-end labeling), and leukocyte and myocardial telomere length (real-time polymerase chain reaction) were determined at the end of the study. Ethanol administration resulted in a marked increase in cardiomyocyte apoptosis (ethanol 0.85 ± 0.13% vs control 0.36 ± 0.06%; P = .0021) and LV dilation (LV end-diastolic diameter: ethanol 8.20 ± 0.14 mm vs control 7.56 ± 0.11 mm [ P = .0014]; volume intercept at 0 mm Hg (V 0 ) of the LV end-diastolic pressure-volume relationship: ethanol 0.40 ± 0.03 mL vs control 0.31 ± 0.02 mL [ P = .020]). However, there were no changes in systolic chamber function as indexed by LV endocardial fractional shortening or the slope of the LV systolic pressure-volume relationship (end systolic elastance). The percentage of myocardial apoptosis was correlated with the degree of LV dilation (% apoptosis vs LV EDD: r = 0.39; n = 38; P = .021; vs V 0 : r = 0.44; n = 19; P = .046). No differences in leukocyte or cardiac telomere length were noted between the ethanol and control groups. Furthermore, cardiac telomere length was not associated with indexes of LV dilation (LVEDD and V 0 ) or cardiomyocyte apoptosis. Conclusions Chronic ethanol-associated myocardial apoptosis and adverse remodeling occurs independently from changes in cardiac telomere length. Telomere shortening may not be a critical mechanism responsible for cardiomyocyte apoptosis and adverse cardiac remodeling.

Aortic valve disease imposes significant challenges upon the circulatory system during exercise. However, during the pediatric years, left ventricular dilation and the decline in systemic vascular resistance that accompanies exercise tend to effectively mitigate the effects of aortic regurgitation. Similarly, in pediatric patients with less than severe aortic stenosis, compensatory hypertrophy often mitigates the hemodynamic impact of the stenosis. Hence the exercise function of most pediatric patients with aortic valve disease is usually remarkably well preserved. Exercise testing can help identify the subset of patients in whom the compensatory mechanisms are no longer effective.

Reduction of left ventricular (LV) dilation (RD) beyond the first year after ST-segment-elevation myocardial infarction (STEMI) is unknown. We investigated its potential occurrence in comparison with stationary (SD) and progressive (PD) dilation.Perfusion gated SPECT features at 1 and 3 years were evaluated in 168 3-year survivors of a first anterior STEMI. Comparisons were made among patients with RD (≥15% reduction of LV end-systolic volume [LVESV]), SD (15% reduction or increase), and PD (≥15% increase). There were 35 patients with RD (21%), 84 with SD (50%), and 49 with PD (29%). At 1 year, ejection fraction, wall motion and perfusion scores, and LV volumes were similar. In RD patients, the fall in LVESV, nearly 22%, was apparent in those with frank (51 mL; P.001) or little/moderate LV dilation at 1 year (LVESV ≤51 mL; P = .002) and was associated with increased ejection fraction (P values .008 and .009, respectively). In the 3 groups, however, LVESV changes were unrelated to 1-year LV volumes, ejection fraction, or contractility score.At 3 years following anterior STEMI there is reduction of LV dilation in about 21% of patients associated with increases in ejection fraction in those with or without clearly dilated ventricles at 1year. These findings add to the complexity of LV remodeling and possibly suggest very late changes in infarct size.

A questionnaire based study was carried on 50 patients suffering from uremic cardiomyopathy. The patients were selected randomly at Mayo hospital and Sheikh Zaid hospital, Lahore. The aims and objectives of the study were to identify the occurrence and management of uremic cardiomyopathy. Uremic cardiomyopathy is the condition of left ventricular hypertrophy, left ventricular dilatation or LV systolic dysfunction and it is reported to be a leading cause of premature cardiovascular mortality in patients with end-stage renal disease the medication given was beta blockers and ca-channel blockers. Dialysis is an alternative medical treatment option for many people living without functioning kidneys. Frequent hemodialysis is associated with less dialysis-induced hypotension and myocardial stunning compared with conventional hemodialysis. Dialysis patients often require multiple pharmacotherapies and complicated drug regimens to manage their conditions. They have increased risk of drug adverse events and drug complications. Key words: Left ventricular hypertrophy; Left ventricular dilation; end-stage renal disease; chronic kidney disease A questionnaire based study was carried on 50 patients suffering from uremic cardiomyopathy. The patients were selected randomly at Mayo hospital and Sheikh Zaid hospital, Lahore. The aims and objectives of the study were to identify the occurrence and management of uremic cardiomyopathy. Uremic cardiomyopathy is the condition of left ventricular hypertrophy, left ventricular dilatation or LV systolic dysfunction and it is reported to be a leading cause of premature cardiovascular mortality in patients with end-stage renal disease the medication given was beta blockers and ca-channel blockers. Dialysis is an alternative medical treatment option for many people living without functioning kidneys. Frequent hemodialysis is associated with less dialysis-induced hypotension and myocardial stunning compared with conventional hemodialysis. Dialysis patients often require multiple pharmacotherapies and complicated drug regimens to manage their conditions. They have increased risk of drug adverse events and drug complications. Key words: Left ventricular hypertrophy; Left ventricular dilation; end-stage renal disease; chronic kidney disease

Measuring and grading left ventricular (LV) size is essential for diagnostic, treatment, and prognostic purposes. Guidelines for quantifying LV size exist for pediatric and adult patients via M-mode measurements, but no data exist determining how well they agree with one another. The goal of this study was to determine the agreement between pediatric echocardiographic readers (PER), pediatric guidelines, and adult guidelines in assessing LV dilation. A retrospective review of all noncongenital echocardiograms from 9/2002 to 11/2015 that had a left ventricular end-diastolic diameter (LVEDD) >5.8 cm for males and >5.2 cm for females was performed. LV size was graded as normal (Z-score ≤ 2), mild (2

Right ventricular apical pacing may cause or worsen mitral regurgitation (MR). Potential mechanisms for this adverse sequelae include intraventricular dyssynchrony, altered papillary muscle function, pacing-induced cardiomyopathy with left ventricular dilation, and annular dilation. In contrast, biventricular (BiV) pacing may improve MR presumably by opposing the negative effects. Whether or not left ventricular lead location is important in treating mitral regurgitation in patients with pacemakers is unknown.We report a case of severe MR and left ventricular (LV) systolic failure in a patient with right ventricular pacing. Multiple potential etiologies for the worsening valve function were noted, and a stepwise iterative optimizing scheme that included basal lateral LV pacing improved mitral valve function and ameliorated heart failure symptoms.

Previous studies documented the common occurrence of transitory cyanosis and echocardiographic aortic insufficiency in mature commercial broiler breeder roosters. During further investigations, we observed a high prevalence of hearts exhibiting extensive dilation of the left ventricle chamber compatible with dilated left ventricular cardiomyopathy present in both cyanotic and normal subpopulations. We conducted quantitative studies focused on documentation of cardiac ventricle parameters by using simple gross morphometric methods performed on formalin-fixed hearts obtained from both clinically normal roosters and those exhibiting variable transitory cyanosis, echocardiographic aortic insufficiency, or both. A high prevalence of often dramatic left ventricular dilation reflected in enlarged left ventricular chamber areas and elevated left ventricle-to-total ventricle area ratios was morphometrically documented. However, no statistically significant differences in the occurrence of ventricular abnormalities were observed between normal and cyanotic roosters. Age-associated changes were also demonstrated by comparative morphometric studies on hearts from normal market-age broilers (average age of 7 wk) and those of mature roosters (average age of 42 wk). Elevation in both left and right ventricular weight-to-total heart weight ratios dramatically increased with aging. In addition, values (average ± SD) for the left ventricle chamber area-to-total ventricle area ratios increased from 3.2 ± 2.0% in broilers up to 10.0 ± 8.8% in roosters. None of the normal broilers studied demonstrated left ventricular volume ratios above 10%, whereas 33% of the roosters had left ventricular volume ratios above 10%, including 13% with ratios of 20% or higher. However, the left ventricle wall area-to-body weight ratios were much closer for the two age groups (0.85 ± 0.18 cm(2)/kg in broilers and 0.79 ± 0.13 cm(2)/kg in roosters). Also, the standard right ventricle-to-total ventricle weight ratio (RV/TV) went from 0.18 ± 0.04 in broilers to 0.25 ± 0.12 in roosters, whereas the left ventricle-to-total ventricle weight ratios were similar for the two age groups (0.74 ± 0.12 and 0.75 ± 0.08 in broilers and roosters, respectively). Our results for RV/TV in normal broilers were similar to the reported values for normal market-age broilers. In contrast, 36% of the roosters had RV/TV above values reported for broilers considered reflective of right ventricular hypertrophy due to pulmonary hypertension, whereas 4% had values above the reported threshold for broilers dying with ascites (ratios greater than 0.0249 and 0.299, respectively). However, ascites was not observed for any of the roosters. Although essentially all cardiac morphometric parameters demonstrated statistically significant correlations with the age-class group comparisons, significance could not be documented for comparisons between cardiomorphometrics and the subjective occurrences of transitory cyanosis or echocardiographic aortic insufficiency.

Background— Current indications for surgery in patients with significant aortic regurgitation (AR) focus on symptoms and left ventricular dilation/dysfunction. However, prognosis is already reduced by this stage, and earlier identification of patients for surgery could be beneficial. Quantifying the regurgitation may help, but there are limited data on its link with outcome. Cardiovascular magnetic resonance (CMR) can accurately quantify AR, and we examined whether this was associated with the future need for surgery. Methods and Results— One hundred thirteen patients with echocardiographic moderate or severe AR were monitored for up to 9 years (mean 2.6±2.1 years) following a CMR scan, and the progression to symptoms or other indications for surgery was monitored. AR quantification identified outcome with high accuracy: 85% of the 39 subjects with regurgitant fraction >33% progressed to surgery (mostly within 3 years) in comparison with 8% of 74 subjects with regurgitant fraction ≤33% ( P P 246 mL had good, although lower, discriminatory ability (area under the curve 0.88), but the combination of this measure with regurgitant fraction provided the best discriminatory power. Conclusions— High degrees of CMR-quantified AR were associated with the development of symptoms or other indications for surgery. Quantifying AR showed slightly better discriminatory ability than “gold standard” CMR ventricular volume assessment. This could provide a new paradigm for the timing of surgical intervention but requires confirmation in a clinical trial.

Congest Heart Fail. ****;**:**–**. ©2012 Wiley Periodicals, Inc. The aim of this study was to evaluate whether small left ventricular (LV) volumes increase the negative prognostic impact of a restrictive filling pattern (RFP) and that of mitral regurgitation (MR) in patients with nonischemic heart failure (HF). The Meta-analysis Research Group in Echocardiography (MeRGE) is a meta-analysis that collated individual patient data from several prospective echocardiography outcome studies. This analysis was restricted to 10 studies and 601 patients with nonischemic HF. The role of MR was tested in a subgroup of 252 patients. A total of 106 deaths occurred during a median follow-up of 32 months. At multivariate analysis, RFP (hazard ratio [HR], 4.16; 95% confidence interval [CI], 1.54–11.23; P=.005) and New York Heart Association class III or IV (HR, 2.15; 95% CI, 1.33–3.47; P=.001) were the independent predictors of poor prognosis, and there was no statistically significant interaction between LV dilation and RFP. Moderate/severe MR was associated with poorer outcome in the group of patients with normal volumes, whereas it was not a significant predictor of mortality in patients with any degree of LV dilation. In patients with nonischemic HF, RFP is the most important indicator of poor prognosis, irrespective of the degree of LV dilation. Normal LV volumes increase the negative prognostic impact of moderate to severe MR.

Objective. A dilated aortic root is a common finding in children and adults with some forms of congenital heart defects. No data exist on root dilation in truncus arteriosus. We sought to delineate root dimensions across a population of patients with truncus arteriosus. Design. We performed a single-center retrospective review of all patients with truncus arteriosus. Demographic information, clinical history, and most recent echocardiographic data were evaluated. Results. We identified 76 patients whose most recent study was at a median age of 5.4 years (range 0–32.7 years). Mean truncal root z-score was 5.1 ± 2.3. All but three patients had truncal root z-scores greater than or equal to 2. Truncal root z-scores remained stable with increasing body surface area and age. There were no cases of dissection or rupture. Six patients underwent truncal root surgery, typically for indications of root dilation with significant truncal valve insufficiency and left ventricular dilation. Conclusions. In conclusion, mean truncal root z-score was 5, and all but three patients had truncal root z-scores greater than or equal to 2. Although repeat surgical intervention was rare and major complications related to root dilation did not occur in our cohort, further studies with longitudinal follow-up into adulthood are needed.

Dr. Levelt and colleagues [(1)][1] present an interesting hypothesis linking diabetes to cardiac remodeling through cardiolipotoxicity. Whether vildagliptin reverses cardiolipotoxicity and whether this would lead to left ventricular dilation without a change in left ventricular mass or ejection

Currently, the preferred treatment of persistent ST-segment elevation acute myocardial infarction is primary angioplasty. After successful primary angioplasty, up to 30% of patients develop left ventricular dilation and heart failure, as a result of incomplete microvascular reperfusion. The pathophysiology of the microvascular dysfunction in the setting of primary angioplasty is complex and not completely known. Distal embolization of necrotic and thrombotic material acts as a mayor factor. No treatment has so far demonstrated proven efficacy in this scenario. However, several prophylactic measures have been identified. Among them, the rheolytic trombectomy offers interesting benefits both in surrogate and clinical outcome variables.

Whether cardiac ventricles can acutely dilate during septic myocardial dysfunction.A prospective echocardiographic study was performed to assess changes of left ventricular dimensions over time in patients with septic shock.A 20-bed surgical intensive care unit of Pitié-Salpêtrière university hospital in Paris.Forty-five patients were studied over the first 10 days of septic shock.None.Left ventricular end-diastolic area (LVEDA), fractional area change (FAC), velocity time integral of the aortic flow, echocardiographic indices of left ventricular relaxation, and cardiac troponin I (cTnI) were measured at day 1, 2, 3, 4, 7, and 10. Three groups were defined: 29 patients without increased cTnI and cardiac impairment (group 1), eight patients with increased cTnI and left systolic ventricular dysfunction (group 2), and eight patients with increased cTnI and isolated impairment of left ventricular relaxation (group 3). At day 1, LVEDA was significantly higher in group 2 (13 +/- 3 cm/m, p0.05) compared with groups 1 (10 +/- 2 cm/m) and 3 (11 +/- 2 cm/m). LVEDA did not change in groups 1 and 3. In group 2, LVEDA and FAC returned within 10 days to values observed in groups 1 and 2. A significant correlation was found between aortic velocity time integral and LVDEA (r =.78, p = 0.022) and FAC (r =.89, p = 0.003) only in group 2.Acute and reversible left ventricular dilation accompanies septic shock-induced systolic left ventricular dysfunction. When septic myocardial abnormalities are limited to reversible impairment of left ventricular relaxation, left ventricular dimensions remain unchanged.

Objective The aim of this study was to prospectively investigate the long-term cardiovascular and pulmonary hemodynamic effects of surgical shunt for treatment of portal hypertension (PH) due to Schistosomiasis mansoni. Location The University of São Paulo Medical School, Brazil; Public Practice. Methods Hemodynamic evaluation was performed with transesophageal Doppler and contrast-enhanced echocardiography (ECHO) on twenty-eight participants with schistosomal portal hypertension. Participants were divided into two groups according to the surgical procedure used to treat their schistosomal portal hypertension within the last two years: group 1—distal splenorenal shunt (DSRS, n = 13) and group 2—esophagogastric devascularization and splenectomy (EGDS, n = 15). Results The cardiac output (5.08 ± 0.91 L/min) and systolic volume (60.1 ± 5.6 ml) were increased (p = 0.001) in the DSRS group. DSRS participants had a significant increase (p < 0.0001) in their left ventricular end-systolic and end-diastolic diameters as well as in their left ventricular end-diastolic and end-systolic volumes (p < 0.001) compared with the preoperative period. No statistically significant difference was found in the patients who underwent EGDS. ECHO revealed intrapulmonary vasodilatation (IPV) in 18 participants (64%), 9 DSRS and 9 EGDS (p > 0.05). Conclusions The late increase in the cardiac output, stroke volume and left ventricular diameters demonstrated left ventricular dilatation after a distal splenorenal shunt. ECHO revealed a greater prevalence for IPV in patients with schistosomiasis than has previously been described in patients with PH from liver cirrhosis.

The definition of an abnormal transient ischemic dilation (TID) ratio may be different according to stress type, type of isotope, and imaging protocols. The aim of this study was to derive the normal threshold and assessment of the TID ratio via 2-day dipyridamole stress/rest technetium 99m sestamibi myocardial perfusion single photon emission computed tomography (MPS).We performed 2-day dipyridamole stress/rest Tc-99m sestamibi MPS in 665 patients. The TID ratio was calculated automatically with the Emory Cardiac Toolbox. The upper limit of normal (1.19) for the TID ratio was derived from 131 patients with a low (5%) likelihood of coronary artery disease as mean + 2 SDs. Patients with complete or partial reversible defects or multivessel-type or left anterior descending artery (LAD) territory perfusion abnormalities had higher TID ratios than the other patients. These patients had a higher frequency of an abnormal TID ratio (1.19) as well. Binary logistic regression analysis showed that ischemia and LAD territory perfusion abnormality were independent predictors of an abnormal TID ratio.The threshold for an abnormal TID ratio via 2-day post-dipyridamole stress/rest Tc-99m sestamibi MPS was greater than 1.19. By use of this protocol, TID is not uncommon and it is related to a greater amount of ischemic burden as well as multivessel-type or LAD territory perfusion abnormality.

ABSTRACT Increased cardiothoracic ratio noted on chest radiographs often prompts concern and further evaluation with additional imaging. This study pools available data assessing the utility of cardiothoracic ratio in predicting left ventricular dilation. A systematic review of the literature was conducted to identify studies comparing cardiothoracic ratio by chest x-ray to left ventricular dilation by echocardiography. Electronic databases were used to identify studies which were then assessed for quality and bias, with those with adequate quality and minimal bias ultimately being included in the pooled analysis. The pooled data were used to determine the sensitivity, specificity, positive predictive value and negative predictive value of cardiomegaly in predicting left ventricular dilation. A total of six studies consisting of 466 patients were included in this analysis. Cardiothoracic ratio had 83.3% sensitivity, 45.4% specificity, 43.5% positive predictive value and 82.7% negative predictive value. When a secondary analysis was conducted with a pediatric study excluded, a total of five studies consisting of 371 patients were included. Cardiothoracic ratio had 86.2% sensitivity, 25.2% specificity, 42.5% positive predictive value and 74.0% negative predictive value. Cardiothoracic ratio as determined by chest radiograph is sensitive but not specific for identifying left ventricular dilation. Cardiothoracic ratio also has a strong negative predictive value for identifying left ventricular dilation.

31-year-old male with no past medical history apart from high blood pressure noted by GP one week prior to admission presented with a three-week history of a flu-like illness and symptoms of heart failure with severe global left ventricular dilation and dysfunction on Transthoracic Echocardiography (TTE). Two weeks following admission he complained of left arm pain and CT upper limb confirmed embolic occlusion of the left brachial artery and incidental severe coarctation of the proximal descending aorta after the origin of the left subclavian artery. Follow-up TTE suggested the presence of coarctation of the aorta on a suprasternal view which was not performed at the time of his first TTE. His heart failure and blood pressure responded very well to medical therapy and he has been referred for surgical correction of his aortic coarctation.

The purpose of this study was to determine the effects of exercise training on LV geometry and LV diastolic function in a rat model of MI.One month after MI induced by ligation of the left anterior descending artery (N = 45) or sham operation (N = 26), rats were randomized to either a sedentary or exercise group. Exercise consisted of treadmill running at 24 m.min-1, 1 h.d-1, 5 d.wk-1, for 3 wk. Passive LV pressure volume relationships were established with an isolated, red-cell-perfused Langendorff preparation. Infarct size was determined histologically and categorized as small (30% of LV) or large (or =30% of LV).LV end-diastolic pressure-volume relationships were shifted rightward with increasing infarct size (P0.05). Exercise training further shifted the LV end-diastolic pressure-volume relationships rightward in sham, small MI and large MI (P0.05). Peak LV developed pressure was comparable in sedentary and exercised-trained hearts in sham, small MI, and large MI. LV diameter and septal wall thickness were greatest in large MI (P0.05). Exercise-trained hearts showed a tendency for a greater LV diameter and septal wall thickness in sham, small MI, and large MI. Scar thinning was most notable in large MI (P0.05).Moderate-intensity treadmill running induces myocardial remodeling and a rightward shift in the LV end-diastolic pressure-volume relationship after MI, an adaptation similar to what is observed with exercise training in sham hearts without MI.