ventricular dilation
Recently Published Documents


TOTAL DOCUMENTS

308
(FIVE YEARS 51)

H-INDEX

41
(FIVE YEARS 4)

2021 ◽  
Author(s):  
Ravi Shah ◽  
Babken Asatryan ◽  
Ghaith Sharaf Dabbagh ◽  
Nay Aung ◽  
Mohammed Y Khanji ◽  
...  

Background: There is a paucity of data regarding the phenotype of dilated cardiomyopathy (DCM) gene variants in the general population. We aimed to determine the frequency and penetrance of DCM-associated putative pathogenic gene variants in a general, adult population, with a focus on the expression of clinical and subclinical phenotype, including structural, functional and arrhythmic disease features. Methods: UK Biobank participants who had undergone whole exome sequencing (WES), ECG and cardiovascular magnetic resonance (CMR) imaging were selected for study. Three different variant calling strategies (one primary and two secondary) were used to identify subjects with putative pathogenic variants in 44 DCM genes. The observed phenotype was graded to either 1) DCM (clinical or CMR diagnosis); 2) early DCM features, including arrhythmia and/or conduction disease, isolated ventricular dilation, and hypokinetic non-dilated cardiomyopathy; or 3) phenotype-negative. Results: Among 18,665 individuals included in the study, 1,463 (7.8%) subjects possessed ≥1 putative pathogenic variant in 44 DCM genes by the main variant calling strategy. A clinical diagnosis of DCM was present in 0.34% and early DCM features in 5.7% of individuals with putative pathogenic variants. ECG and CMR analysis revealed evidence of subclinical DCM in an additional 1.6% and early DCM features in 15.9% of individuals with putative pathogenic variants. Arrhythmias and/or conduction disease (15.2%) were the most common early DCM features, followed by hypokinetic non-dilated cardiomyopathy (4%). The combined clinical/subclinical penetrance was ≤30% with all three variant filtering strategies. Clinical DCM was slightly more prevalent among participants with putative pathogenic variants in definitive/strong evidence genes, as compared to those with variants in moderate/limited evidence genes. Conclusions: In the UK Biobank, approximately 1/6 of adults with putative pathogenic variants in DCM genes exhibited a subclinical phenotype based on ECG and/or CMR, most commonly manifesting with arrhythmias in the absence of substantial ventricular dilation/dysfunction.


Author(s):  
Grace Y. Lai ◽  
William Chu Kwan ◽  
Karolina Piorkowska ◽  
Matthias W. Wagner ◽  
Pouya Jamshidi ◽  
...  

OBJECTIVE While intraventricular hemorrhage (IVH) is associated with posthemorrhagic ventricular dilation (PHVD), not all infants affected by high-grade IVH develop PHVD. The authors aimed to determine clot-associated predictors of PHVD in a porcine model by varying the amount and rate of direct intraventricular injection of whole autologous blood. METHODS Seven 1-week-old piglets underwent craniectomy and injection of autologous blood into the right lateral ventricle. They survived for a maximum of 28 days. MRI was performed prior to injection, immediately postoperatively, and every 7 days thereafter. T1-weighted, T2-weighted, and susceptibility-weighted imaging (SWI) sequences were used to segment ventricular and clot volumes. Spearman correlations were used to determine the relationship between blood and clot volumes and ventricular volumes over time. RESULTS The maximum ventricular volume was up to 12 times that of baseline. One animal developed acute hydrocephalus on day 4. All other animals survived until planned endpoints. The interaction between volume of blood injected and duration of injection was significantly associated with clot volume on the postoperative scan (p = 0.003) but not the amount of blood injected alone (p = 0.38). Initial postoperative and day 7 clot volumes, but not volume of blood injected, were correlated with maximum (p = 0.007 and 0.014) and terminal (p = 0.014 and 0.036) ventricular volumes. Initial postoperative ventricular volume was correlated with maximum and terminal ventricular volume (p = 0.007 and p = 0.014). CONCLUSIONS Initial postoperative, maximum, and terminal ventricular dilations were associated with the amount of clot formed, rather than the amount of blood injected. This supports the hypothesis that PHVD is determined by clot burden rather than the presence of blood products and allows further testing of early clot lysis to minimize PHVD risk.


2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
T Miranda Aquino ◽  
J M Pereira-Forcado ◽  
B Ordonez-Salazar ◽  
G Dominguez-Trejo ◽  
A Rangel-Guerra ◽  
...  

Abstract Background Coronavirus disease 2019 is a systemic entity, where cardiac involvement has been described. The echocardiogram is a diagnostic tool that describes myocardial damage with good certainty. Objectives Determine which echocardiographic parameters are predictors of mortality. Analyze if there is a difference in clinical, laboratory and echocardiographic variables in terms of patients who died versus those who survived. Investigate the cut-off point of the echocardiographic parameters that is best associated with mortality. Methods Prospective, analytical, comparative study. Patients admitted to the hospital with Coronavirus 2019 infection. Clinical, laboratory and echocardiographic variables will be assessed. The association with three-month mortality of the different variables will be determined. We used ROC-curves for the best cut-off associated with mortality. The association with three-month mortality was analized using Cox regression, unadjusted analysis of the variables was performed, as well as adjusted analysis for age and gender. Results 84 patients were included, a mortality of 29% was documented. Significant differences were found in the left atrial volumen index, the E/e', the proportion of dilatation of the right ventricle and diastolic dysfunction. Tricuspid annulus anterior systolic excursion (TAPSE), pulmonary artery acceleration time (PAA), tricuspid regurgitation velocity (TRV), pulmonary artery systolic pressure (PASP), left ventricular longitudinal strain (LVGLS), of the left atrium (LAGLS) and the right ventricular free wall longitudinal strain (RVFWLS). Right ventricular dilation, right ventricular shortening fraction, TAPSE, PASP, TRV, LVGLS, LAGLS, and RVFWLS were associated with mortality. Conclusion Right ventricular dilation, right ventricular shortening fraction, TAPSE, PASP, TRV, LVGLS, LAGLS, and RVFWLS are the echocardiographic parameters that were associated with three-month mortality. FUNDunding Acknowledgement Type of funding sources: None. Table 2


Author(s):  
Timothy N. Audam ◽  
Caitlin M. Howard ◽  
Lauren F. Garrett ◽  
Yi Wei Zheng ◽  
James A. Bradley ◽  
...  

Coenzyme A (CoA) is an essential co-factor required for intermediary metabolism. Perturbations in homeostasis of CoA have been implicated in various pathologies; however, whether CoA homeostasis is changed and the extent to which CoA levels contribute to ventricular function and remodeling during pressure overload has not been explored. In this study, we sought to assess changes in CoA biosynthetic pathway during pressure overload and determine the impact of limiting CoA on cardiac function. We limited cardiac CoA levels by deleting the rate limiting enzyme in CoA biosynthesis, Pank1. We found that constitutive, cardiomyocyte-specific Pank1 deletion (cmPank1-/-) significantly reduced PANK1 mRNA, PANK1 protein, and CoA levels compared to Pank1 sufficient littermates (cmPank1+/+) but exerted no obvious deleterious impact on the mice at baseline. We then subjected both groups of mice to pressure overload-induced heart failure. Interestingly, there was more ventricular dilation in cmPank1-/- during pressure overload. To explore potential mechanisms contributing to this phenotype, we performed transcriptomic profiling, which suggested a role for Pank1 in regulating fibrotic and metabolic processes during pressure overload. Indeed, Pank1 deletion exacerbated cardiac fibrosis following pressure overload. Because we were interested in the possibility of early metabolic impacts in response to pressure overload, we performed untargeted metabolomics, which indicated significant changes to metabolites involved in fatty acid and ketone metabolism, among other pathways. Collectively, our study underscores the role of elevated CoA levels in supporting fatty acid and ketone body oxidation, which may be more important than CoA-driven, enzyme-independent acetylation in the failing heart.


Author(s):  
Arushi Dhar ◽  
Tung Ming Leung ◽  
Abena Appiah-Kubi ◽  
Dorota Gruber ◽  
Banu Aygun ◽  
...  

Cardiac abnormalities such as left ventricular hypertrophy, 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 on hydroxyurea therapy is lacking. In this retrospective study, we aim 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 on hydroxyurea. Twenty-five (41.6%) of the patients on hydroxyurea had been treated for less than 1 year; these patients had a significantly greater prevalence of left ventricular dilation compared to those who had been on treatment for more than 1 year. Serial echocardiograms were then analyzed on patients receiving hydroxyurea. Left ventricular dilation and hypertrophy improved significantly with hydroxyurea treatment. Additionally, 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 this patient cohort for a longer duration.


2021 ◽  
Vol 5 (2) ◽  
Author(s):  
Mohsin Shad ◽  
Faisal Sheraz Shah ◽  
Muhammad Zulqarnain ◽  
Muhammad Usman ◽  
Zulqarnain Haider ◽  
...  

Cardiac hypertrophy is the major pathway by which neurohormonal and mechanical stimuli act upon cardiomyocytes which gives the response to these stimuli. It leads to heart failure and ventricular dilation which is the main root of mortality in the western world. Many molecular targets are controlling cardiac hypertrophy development which may influence the growth factors signaling, cytokine release and gene expression. Through clinical trials on different models, recent research shows that cardiac hypertrophy might be inhibited or reversed. These findings have developed a vast drive to recognize specific and novel regulators of cardiac hypertrophy. Many molecular targets and signaling modulators have been studied in this review that induce the hypertrophic response which may involve MAPK pathway, oxidative stress, calcineurin, Cardiac angiogenesis, serum protein concentration, microRNA, and periodontitis. For the treatment of cardiac hypertrophy, the scientific knowledge of these signaling pathways and factors may be translated into potential nutritional and molecular therapies for the betterment of this diseases. The current and previous knowledge of molecular markers can be compiled in this review for the treatment of the molecular pathogenesis of cardiac hypertrophy.


2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Kang Peng ◽  
Sravanthi Koduri ◽  
Fan Xia ◽  
Feng Gao ◽  
Ya Hua ◽  
...  

Abstract Background Thrombin has been implicated in playing a role in hydrocephalus development following intraventricular hemorrhage (IVH). However, the mechanisms underlying the sex differences to the detrimental effects of thrombin post-IVH remain elusive. Method Three-month old male and female Sprague-Dawley rats underwent unilateral intracerebroventricular (ICV) injections of 3U or 5U thrombin, or saline, to examine differences in thrombin-induced hydrocephalus and white matter injury. Mortality, and lateral ventricle volume and white matter injury were measured on magnetic resonance imaging evaluation at 24 h post-injection. In addition, male rats were pretreated with 17-β estradiol (E2, 5 mg/kg) or vehicle at 24 and 2 h prior to ICV injection of 3U thrombin. All rats were euthanized at 24 h post-injection for histology and immunohistochemistry. Results ICV injection of 5U thrombin caused 100 and 0% mortality in female and male rats, respectively. 3U of thrombin resulted in significant ventricular dilation and white matter damage at 24 h in both male and female rats, but both were worse in females (p < 0.05). Furthermore, neutrophil infiltration into choroid plexus and periventricular white matter was enhanced in female rats and may play a critical role in the sex difference in brain injury. Pre-treating male rats with E2, increased thrombin (3U)-induced hydrocephalus, periventricular white matter injury and neutrophil infiltration into the choroid plexus and white matter. Conclusions ICV thrombin injection induced more severe ventricular dilation and white matter damage in female rats compared to males. Estrogen appears to contribute to this difference which may involve greater neutrophil infiltration in females. Understanding sex differences in thrombin-induced brain injury may shed light on future interventions for hemorrhagic stroke.


2021 ◽  
Vol 17 ◽  
Author(s):  
Diane Xavier de Ávila ◽  
Humberto Villacorta ◽  
Wolney de Andrade Martins ◽  
Evandro Tinoco Mesquita

Introduction: The knowledge on high-output cardiac failure (HOCF) has greatly improved in the last two decades. One of the advances was the identification of a new phenotype of HOCF, characterized by absence of ventricular dilation, already associated with liver disease, arteriovenous fistulas (AVF), lung disease, myelodysplastic syndromes, and obesity. However, it has been noted that any aetiology can present with one of the two phenotypes, depending on the evolution. Objective: To describe, through an integrative review, the physiopathology and aetiologies of HOCF and to discuss phenotypes associated with this condition. Methods: Revisions, guidelines, case-controls, cohort studies and clinical studies were searched in MEDLINE and LILACS, using the connectives in the "cardiac output, high" database [MeSH Terms] OR "high cardiac output" [All Fields]. Discussion: Two distinct phenotypes are currently described in the HOCF, regardless of the aetiology: 1) one with enlarged cardiac chambers; and 2) with normal heart chambers. The mechanisms related to HOCF are vasodilation, arteriovenous shunts that cause increased microvascular density, reduced systemic vascular resistance (RSVR), and high metabolism. These mechanisms lead to activation of the renin-angiotensin-aldosterone system, sodium and water retention, activation of neprilysin, of the sodium-glucose-2 transporter, which promote interstitial fibrosis, ventricular remodeling and a consequent increase in cardiac output >8L/min. Conclusion: Many aetiologies of HOCF have been described and some of them are potentially curable. Prompt recognition of this condition and proper treatment may lead to better outcomes.


Sign in / Sign up

Export Citation Format

Share Document