ResearchPad - heart-failure https://www.researchpad.co Default RSS Feed en-us © 2020 Newgen KnowledgeWorks <![CDATA[Circulating plasma concentrations of angiotensin-converting enzyme 2 in men and women with heart failure and effects of renin–angiotensin–aldosterone inhibitors]]> https://www.researchpad.co/article/elastic_article_12417 The current pandemic coronavirus SARS-CoV-2 infects a wide age group but predominantly elderly individuals, especially men and those with cardiovascular disease. Recent reports suggest an association with use of renin–angiotensin–aldosterone system (RAAS) inhibitors. Angiotensin-converting enzyme 2 (ACE2) is a functional receptor for coronaviruses. Higher ACE2 concentrations might lead to increased vulnerability to SARS-CoV-2 in patients on RAAS inhibitors.Methods and resultsWe measured ACE2 concentrations in 1485 men and 537 women with heart failure (index cohort). Results were validated in 1123 men and 575 women (validation cohort).The median age was 69 years for men and 75 years for women. The strongest predictor of elevated concentrations of ACE2 in both cohorts was male sex (estimate = 0.26, P < 0.001; and 0.19, P < 0.001, respectively). In the index cohort, use of ACE inhibitors, angiotensin receptor blockers (ARBs), or mineralocorticoid receptor antagonists (MRAs) was not an independent predictor of plasma ACE2. In the validation cohort, ACE inhibitor (estimate = –0.17, P = 0.002) and ARB use (estimate = –0.15, P = 0.03) were independent predictors of lower plasma ACE2, while use of an MRA (estimate = 0.11, P = 0.04) was an independent predictor of higher plasma ACE2 concentrations.ConclusionIn two independent cohorts of patients with heart failure, plasma concentrations of ACE2 were higher in men than in women, but use of neither an ACE inhibitor nor an ARB was associated with higher plasma ACE2 concentrations. These data might explain the higher incidence and fatality rate of COVID-19 in men, but do not support previous reports suggesting that ACE inhibitors or ARBs increase the vulnerability for COVID-19 through increased plasma ACE2 concentrations. ]]> <![CDATA[MitraClip<sup>®</sup> as bridging strategy for heart transplantation in Chagas cardiomyopathy: a case report]]> https://www.researchpad.co/article/elastic_article_10223 Patients with end-stage heart failure, suffering from severe pulmonary hypertension (PH) and elevated pulmonary vascular resistance, are not eligible for heart transplant due to high mortality risk and primary graft dysfunction. Severe PH may be favoured by functional severe mitral regurgitation, which is present in many cardiopathies like end-stage Chagasic cardiomyopathy.Case summaryWe present a case of a young man with end-stage heart failure secondary to Chagas cardiomyopathy with severe functional mitral regurgitation (FMR) and severe PH. The patient received percutaneous correction with MitraClip® system reducing PH and making him a suitable candidate for heart transplant.DiscussionIn patients with advanced heart failure, FMR, and severe PH, optimal treatment according to current guide lines is recommended. MitraClip® therapy appears to be safe and effective for control of severe PH as a bridge measure for cardiac transplantation. ]]> <![CDATA[Long-term Outcome of Pulmonary Vein Isolation Versus Amiodarone Therapy in Patients with Coexistent Persistent AF and Congestive Heart Failure]]> https://www.researchpad.co/article/N82af611f-ef65-4e29-b44f-6f02ecd6d4a9 Although pharmacological rhythm control of AF in patients with heart failure with reduced ejection fraction (HFrEF) does not seem to provide any benefit over rate control, catheter ablation of AF has been shown to improve clinical outcomes. These results can be explained with higher success rates of catheter ablation in restoring and maintaining sinus rhythm compared with antiarrhythmic drugs. In addition, pharmacotherapy is not void of side-effects, which are thought to offset its potential antiarrhythmic benefits. Therefore, efforts should be made towards optimisation of ablation techniques for AF in patients with HFrEF.

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<![CDATA[Asymptomatic Left Ventricle Systolic Dysfunction]]> https://www.researchpad.co/article/Na50cd32d-233b-4933-9bea-963a8b862395 Heart failure is a common debilitating illness, associated with significant morbidity and mortality, rehospitalisation and societal costs. Current guidelines and position statements emphasise the management of patients with overt symptomatic disease, but the increasing prevalence of congestive heart failure underscores the need to identify and manage patients with early left ventricular dysfunction prior to symptom onset. Asymptomatic left ventricular systolic dysfunction (ALVSD), classified as stage B heart failure, is defined as depressed left ventricular systolic function in the absence of clinical heart failure. Early initiation of therapies in patients with presumed ALVSD has been shown to lead to better outcomes. In this article, the authors clarify issues surrounding the definition and natural history of ALVSD, outline clinical tools that may be of value in identifying patients with ALVSD and highlight potential opportunities for future investigations to better address aspects of our understanding of this complex syndrome.

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<![CDATA[Heart Failure Treatment by Device]]> https://www.researchpad.co/article/N4092ce6f-ef0a-4213-ba3d-5028a913919b <![CDATA[MEF2C Silencing Attenuates Load-Induced Left Ventricular Hypertrophy by Modulating mTOR/S6K Pathway in Mice]]> https://www.researchpad.co/article/5989daeaab0ee8fa60bbee3f

Background

The activation of the members of the myocyte enhancer factor-2 family (MEF2A, B, C and D) of transcription factors promotes cardiac hypertrophy and failure. However, the role of its individual components in the pathogenesis of cardiac hypertrophy remains unclear.

Methodology/Principal Findings

In this study, we investigated whether MEF2C plays a role in mediating the left ventricular hypertrophy by pressure overload in mice. The knockdown of myocardial MEF2C induced by specific small interfering RNA (siRNA) has been shown to attenuate hypertrophy, interstitial fibrosis and the rise of ANP levels in aortic banded mice. We detected that the depletion of MEF2C also results in lowered levels of both PGC-1α and mitochondrial DNA in the overloaded left ventricle, associated with enhanced AMP:ATP ratio. Additionally, MEF2C depletion was accompanied by defective activation of S6K in response to pressure overload. Treatment with the amino acid leucine stimulated S6K and suppressed the attenuation of left ventricular hypertrophy and fibrosis in the aforementioned aortic banded mice.

Conclusion/Significance

These findings represent new evidences that MEF2C depletion attenuates the hypertrophic responses to mechanical stress and highlight the potential of MEF2C to be a target for new therapies to cardiac hypertrophy and failure.

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<![CDATA[Long-term outcomes after extracorporeal membrane oxygenation in patients with dialysis-requiring acute kidney injury: A cohort study]]> https://www.researchpad.co/article/5c92b361d5eed0c4843a3f31

Background

Acute kidney injury (AKI) is a common complication of extracorporeal membrane oxygenation (ECMO) treatment. The aim of this study was to elucidate the long-term outcomes of adult patients with AKI who receive ECMO.

Materials and methods

The study analyzed encrypted datasets from Taiwan’s National Health Insurance Research Database. The data of 3251 patients who received first-time ECMO treatment between January 1, 2003, and December 31, 2013, were analyzed. Characteristics and outcomes were compared between patients who required dialysis for AKI (D-AKI) and those who did not in order to evaluate the impact of D-AKI on long-term mortality and major adverse kidney events.

Results

Of the 3251 patients, 54.1% had D-AKI. Compared with the patients without D-AKI, those with D-AKI had higher rates of all-cause mortality (52.3% vs. 33.3%; adjusted hazard ratio [aHR] 1.82, 95% confidence interval [CI] 1.53–2.17), chronic kidney disease (13.7% vs. 8.1%; adjusted subdistribution HR [aSHR] 1.66, 95% CI 1.16–2.38), and end-stage renal disease (5.2% vs. 0.5%; aSHR 14.28, 95% CI 4.67–43.62). The long-term mortality of patients who survived more than 90 days after discharge was 22.0% (153/695), 32.3% (91/282), and 50.0% (10/20) in the patients without D-AKI, with recovery D-AKI, and with nonrecovery D-AKI who required long-term dialysis, respectively, demonstrating a significant trend (Pfor trend <0.001).

Conclusion

AKI is associated with an increased risk of long-term mortality and major adverse kidney events in adult patients who receive ECMO.

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<![CDATA[Influence of the tubular network on the characteristics of calcium transients in cardiac myocytes]]> https://www.researchpad.co/article/N7f446290-780e-4486-a1de-95187c6060a1

Transverse and axial tubules (TATS) are an essential ingredient of the excitation-contraction machinery that allow the effective coupling of L-type Calcium Channels (LCC) and ryanodine receptors (RyR2). They form a regular network in ventricular cells, while their presence in atrial myocytes is variable regionally and among animal species We have studied the effect of variations in the TAT network using a bidomain computational model of an atrial myocyte with variable density of tubules. At each z-line the t-tubule length is obtained from an exponential distribution, with a given mean penetration length. This gives rise to a distribution of t-tubules in the cell that is characterized by the fractional area (F.A.) occupied by the t-tubules. To obtain consistent results, we average over different realizations of the same mean penetration length. To this, in some simulations we add the effect of a network of axial tubules. Then we study global properties of calcium signaling, as well as regional heterogeneities and local properties of sparks and RyR2 openings. In agreement with recent experiments in detubulated ventricular and atrial cells, we find that detubulation reduces the calcium transient and synchronization in release. However, it does not affect sarcoplasmic reticulum (SR) load, so the decrease in SR calcium release is due to regional differences in Ca2+ release, that is restricted to the cell periphery in detubulated cells. Despite the decrease in release, the release gain is larger in detubulated cells, due to recruitment of orphaned RyR2s, i.e, those that are not confronting a cluster of LCCs. This probably provides a safeguard mechanism, allowing physiological values to be maintained upon small changes in the t-tubule density. Finally, we do not find any relevant change in spark properties between tubulated and detubulated cells, suggesting that the differences found in experiments could be due to differential properties of the RyR2s in the membrane and in the t-tubules, not incorporated in the present model. This work will help understand the effect of detubulation, that has been shown to occur in disease conditions such as heart failure (HF) in ventricular cells, or atrial fibrillation (AF) in atrial cells.

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<![CDATA[Predicting 30-day hospital readmissions using artificial neural networks with medical code embedding]]> https://www.researchpad.co/article/N1f40719a-4631-45e6-bedb-5cf8a42ecf53

Reducing unplanned readmissions is a major focus of current hospital quality efforts. In order to avoid unfair penalization, administrators and policymakers use prediction models to adjust for the performance of hospitals from healthcare claims data. Regression-based models are a commonly utilized method for such risk-standardization across hospitals; however, these models often suffer in accuracy. In this study we, compare four prediction models for unplanned patient readmission for patients hospitalized with acute myocardial infarction (AMI), congestive health failure (HF), and pneumonia (PNA) within the Nationwide Readmissions Database in 2014. We evaluated hierarchical logistic regression and compared its performance with gradient boosting and two models that utilize artificial neural networks. We show that unsupervised Global Vector for Word Representations embedding representations of administrative claims data combined with artificial neural network classification models improves prediction of 30-day readmission. Our best models increased the AUC for prediction of 30-day readmissions from 0.68 to 0.72 for AMI, 0.60 to 0.64 for HF, and 0.63 to 0.68 for PNA compared to hierarchical logistic regression. Furthermore, risk-standardized hospital readmission rates calculated from our artificial neural network model that employed embeddings led to reclassification of approximately 10% of hospitals across categories of hospital performance. This finding suggests that prediction models that incorporate new methods classify hospitals differently than traditional regression-based approaches and that their role in assessing hospital performance warrants further investigation.

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<![CDATA[Temporary Mechanical Circulatory Support in Acute Heart Failure]]> https://www.researchpad.co/article/N380ece30-d5e5-4b1f-9a62-ee366bd9fe35

Cardiogenic shock (CS) is a challenging syndrome, associated with significant morbidity and mortality. Although pharmacological therapies are successful and can successfully control this acute cardiac illness, some patients remain refractory to drugs. Therefore, a more aggressive treatment strategy is needed. Temporary mechanical circulatory support (TCS) can be used to stabilise patients with decompensated heart failure. In the last two decades, the increased use of TCS has led to several kinds of devices becoming available. However, indications for TCS and device selection are part of a complex process. It is necessary to evaluate the severity of CS, any early and prompt haemodynamic resuscitation, prior TCS, specific patient risk factors, technical limitations and adequacy of resources and training, as well as an assessment of whether care would be futile. This article examines options for commonly used TCS devices, including intra-aortic balloon pumps, a pulsatile percutaneous ventricular assist device (the iVAC), veno-arterial extra-corporeal membrane oxygenation and Impella (Abiomed) and TandemHeart (LivaNova) percutaneous ventricular assist device.

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<![CDATA[Cardiovascular magnetic resonance T2* mapping for the assessment of cardiovascular events in hypertrophic cardiomyopathy]]> https://www.researchpad.co/article/N130a8ca4-b130-4403-8ec0-d453357afc95

Background

Hypertrophic cardiomyopathy (HCM) is associated with an increased risk of adverse cardiac events. Beyond classic risk factors, relative myocardial ischaemia and succeeding myocardial alterations, which can be detected using either contrast agents or parametric mapping in cardiovascular magnetic resonance (CMR) imaging, have shown an impact on outcome in HCM. CMR may help to risk stratify using parametric T2* mapping. Therefore, the aim of the present study was to evaluate the association of T2* values or fibrosis with cardiovascular events in HCM.

Methods

The relationship between T2* with supraventricular, ventricular arrhythmia or heart failure was retrospectively assessed in 91 patients with HCM referred for CMR on a 1.5T MR imaging system. Fibrosis as a reference was added to the model. Patients were subdivided into groups according to T2* value quartiles.

Results

47 patients experienced an event of ventricular arrhythmia, 25 of atrial fibrillation/flutter and 17 of heart failure. T2*≤28.7 ms yielded no association with ventricular events in the whole HCM cohort. T2* of non-obstructive HCM showed a significant association with ventricular events in univariate analysis, but not in multivariate analysis. For the combined endpoint of arrhythmic events, there was already an association for the whole HCM cohort, but again only in univariate analyses. Fibrosis stayed the strongest predictor in all analyses. There was no association for T2* and fibrosis with heart failure.

Conclusions

Decreased T2* values by CMR only provide a small association with arrhythmic events in HCM, especially in non-obstructive HCM. No information is added for heart failure.

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<![CDATA[Iron deficiency in 78 805 people admitted with heart failure across England: a retrospective cohort study]]> https://www.researchpad.co/article/Ncc934d4c-82a1-4e8b-aa26-9f0a20c6b6bb

Objectives

Iron deficiency (ID), with or without anaemia (IDA), is an important comorbidity in people with chronic heart failure (HF), but the prevalence and significance in those admitted with HF is uncertain. We assessed the prevalence of ID or IDA in adults (age ≥21 years) hospitalised with a primary diagnosis of HF, and examined key metrics associated with these secondary diagnoses.

Methods

A retrospective cohort study of Hospital Episode Statistics describing all adults admitted to National Health Service (NHS) hospitals across England from April 2015 through March 2016 with primary diagnostic discharge coding as HF, with or without subsidiary coding for ID/IDA.

Results

78 805 adults were admitted to 177 NHS hospitals with primary coding as HF: 26 530 (33.7%) with secondary coding for ID/IDA, and 52 275 (66.3%) without. Proportionately more patients coded ID/IDA were admitted as emergencies (94.8% vs 87.6%; p<0.0001). Tending to be older and female, they required a longer length of stay (15.8 vs 12.2 days; p<0.0001), with higher per capita costs (£3623 vs £2918; p<0.0001), the cumulative excess expenditure being £21.5 million. HF-related (8.2% vs 5.2%; p<0.0001) and all-cause readmission rates (25.8% vs 17.7%; p<0.05) at ≤30 days were greater in those with ID/IDA against those without, and they manifested a small but statistically significant increased inpatient mortality (13.5% v 12.9%; p=0.009).

Conclusions

For adults admitted to hospitals in England, principally with acute HF, ID/IDA are significant comorbidities and associated with adverse outcomes, both for affected individuals, and the health economy.

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<![CDATA[A Score to differentiate Takotsubo syndrome from non-ST-elevation myocardial nfarction in women at the bedside]]> https://www.researchpad.co/article/N69cc84e4-34de-474f-940f-7e38a14ff069

Objective

A score to distinguish Takotsubo syndrome (TS) from acute coronary syndrome would be useful to facilitate appropriate patient investigation and management. This study sought to derive and validate a simple score using demographic, clinical and ECG data to distinguish women with non-ST elevation myocardial infarction (NSTEMI) from NSTE-TS.

Methods

The derivation cohort consisted of women with NSTE-TS (n=100) and NSTEMI (n=100). Logistic regression was used to derive the score using ECG values available on the postacute ward round on day 1 post-hospital admission. The score was then temporally validated in subsequent consecutive patients with NSTE-TS (n=40) and NSTEMI (n=70).

Results

The five variables in the score and their relative weights were: T-wave inversion in ≥6 leads (+3), recent stress (+2), diabetes (−1), prior cardiovascular disease (−2) and ST-depression in any lead (−3). When calculated using ECG values obtained at admission, discrimination between conditions was very good (area under the curve (AUC) 0.87 95% CI 0.83 to 0.92). The optimal score cut-point of ≥1 to predict NSTE-TS had 73% sensitivity and 90% specificity. When applied to the validation cohort at admission, AUC was 0.82 (95% CI 0.75 to 0.90) and positive and negative predictive values were 78% and 81%, respectively. On day 1 post-admission, AUC was 0.92 (95% CI 0.87 to 0.97), with positive and negative predictive values of 77% and 91%, respectively.

Conclusion

This NSTE-TS score is easy to use and may prove useful in clinical practice to distinguish women with NSTE-TS from NSTEMI. Further validation in external cohorts is needed.

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<![CDATA[Cardiomyopathy associated with Ceutzfeld–Jakob disease: a diagnosis of exclusion: a case report]]> https://www.researchpad.co/article/N43105d69-42dd-4687-90f5-5e94739d77e6

Abstract

Background

Creutzfeldt–Jakob disease (CJD), the most common prion disease in humans, is primarily known for its adverse neurological impact and inevitable mortality. Data regarding myocardial involvement in CJD are scarce.

Case summary

A 54-year-old female patient, presented with progressive effort dyspnoea, was diagnosed with unexplained non-ischaemic cardiomyopathy. An extensive cardiac work-up including cardiac magnetic resonance imaging (MRI) did not reveal any underlying aetiology. Simultaneously, the patient developed involuntary limb movements and progressive cognitive decline. Thalamic high-signal abnormalities on diffusion-weighted images were apparent on brain MRI. Based on these findings, she was subsequently referred to a neurology department, where she suddenly died the day after her admission. Brain autopsy demonstrated spongiform encephalopathy. A genetic analysis performed to her son revealed a mutation in the PRNP gene; all of these were consistent with CJD.

Discussion

This case describes the clinical association of CJD and cardiomyopathy and the diagnosis prion-induced cardiomyopathy by exclusion. It is not inconceivable that the coexistence of these two clinical entities may be related to genetic expression and contemporaneously deposition of infectious prions in myocardial muscle and brain tissue. Awareness of this possible association could be of important public-safety concern, and merits further collaborative cardiac-neurological work-up to elucidate this phenotype among patients with unexplained cardiomyopathy with neurological symptoms that resemble CJD.

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<![CDATA[Percutaneous closure of an iatrogenic aorto-right atrial fistula of the sinus of Valsalva through total arm approach: a case report]]> https://www.researchpad.co/article/Nf139d408-1292-42eb-9420-7c84dae0335a

Abstract

Background 

Creation of an iatrogenic aorto-right atrial fistula is a rare but clinically relevant complication of cardiac surgery. Transfemoral percutaneous closure is an attractive alternative to surgical repair, but there are no reports about transcatheter repair using a complete arm access.

Case summary 

We present the case of a 44-year-old woman with heart failure (NewYork Heart Association Class III) due to a longstanding iatrogenic fistula from the non-coronary aortic cusp to the right atrium (RA) with aorta to RA shunting and severe tricuspid regurgitation (TR) caused by mitral valve replacement 15 years ago. The patient was successfully treated by percutaneous closure with an Amplatzer Vascular Plug II using complete brachial access. Following the procedure right heart chambers and TR decreased and symptoms resolved.

Discussion 

To the best of our knowledge this is the first report of percutaneous repair of an aorto-right atrial fistula using total arm accesses (radial artery and basilic vein). In appropriately selected patients, this approach is an attractive alternative to femoral access.

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<![CDATA[Myocardial Effects of Aldosterone Antagonism in Heart Failure With Preserved Ejection Fraction]]> https://www.researchpad.co/article/N0616016d-89c7-445d-823b-a868aca552d7

Background

Spironolactone may have prognostic benefit in selected patients with heart failure with preserved ejection fraction. This study assessed the myocardial tissue effects of spironolactone in heart failure with preserved ejection fraction.

Methods and Results

A 1:1 randomized controlled study of 6 months of spironolactone versus control in heart failure with preserved ejection fraction. The primary outcome was change in myocardial extracellular volume fraction by cardiovascular magnetic resonance as a surrogate of diffuse fibrosis. Of 55 randomized patients, 40 (20 women; age, 75.2±5.9 years) completed follow‐up (19 treatment, 21 control). A significant change in extracellular volume over the study period was not seen (treatment, 28.7±3.7% versus 27.7±3.4% [P=0.14]; controls, 27.6±3.4% versus 28.3±4.4% [P=0.14]); however, the rate of extracellular volume expansion was decreased by spironolactone (−1.0±2.4% versus 0.8±2.2%). Indexed left ventricular mass decreased with treatment (104.4±26.6 versus 94.0±20.6 g/m2; P=0.001) but not in controls (101.4±29.4 versus 104.0±32.8 g/m2; P=0.111). Extracellular mass decreased by 13.8% (15.1±4.8 versus 13.0±3.4 g/m2; P=0.003), and cellular mass decreased by 8.3% (37.6±10.0 versus 34.3±7.9 g/m2; P=0.001) with spironolactone, but was static in controls.

Conclusions

Spironolactone did not lead to significant change in extracellular volume. However, spironolactone did decrease rate of extracellular expansion, with a decrease in the mass of both cellular and extracellular myocardial compartments. These data point to the mechanism of action of spironolactone in heart failure with preserved ejection fraction, including a direct tissue effect with a reduction in rate of myocardial fibrosis.

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<![CDATA[Clinical and Biomarker Predictors of Expanded Heart Failure Outcomes in Patients With Type 2 Diabetes Mellitus After a Recent Acute Coronary Syndrome: Insights From the EXAMINE Trial]]> https://www.researchpad.co/article/N67e59dc3-c801-4b1a-b074-ec3b95467da5

Background

Improved heart failure (HF) risk stratification after a recent acute coronary syndrome may identify those who can benefit from therapies that reduce HF risk. We aimed to identify clinical and biomarker predictors for expanded HF outcomes in patients with type 2 diabetes mellitus after recent acute coronary syndrome.

Methods and Results

The EXAMINE (Examination of Cardiovascular Outcomes with Alogliptin versus Standard of Care) trial was a multicenter, non‐inferiority, double‐masked, placebo‐controlled study which randomized 5380 patients with type 2 diabetes mellitus after recent acute coronary syndrome to alogliptin or placebo. Baseline biomarkers were measured in 5154 patients: NT‐proBNP (N‐terminal pro‐B‐type natriuretic peptide), high‐sensitivity troponin I, adiponectin, growth‐differentiation‐factor‐15, and galectin‐3. Our primary outcome was cardiovascular) death, HF hospitalization, elevated NT‐proBNP during follow‐up, or loop diuretics initiation. The association between clinical variables, biomarkers, and outcomes were assessed using Cox regression models. In the study population, the median age was 61.0 years, 67.7% were men, and 28.0% had baseline HF (median follow‐up was 18 months). In multivariable analyses, NT‐proBNP had the strongest association with the primary outcome (per log2, hazard ratio 1.24; Wald χ2 67.4; P<0.0001) followed by a prior HF history (hazard ratio 1.42; Wald χ2 20.8; P<0.0001). A model with clinical variables and biomarkers allowed for risk prediction for expanded HF outcomes (C‐statistic=0.72). Discrimination results were similar for cardiovascular death or HF hospitalization.

Conclusions

Among patients with type 2 diabetes mellitus after recent acute coronary syndrome, the use biomarkers such as N‐terminal pro‐B‐type natriuretic peptide and clinical variables enables risk stratification for expanded HF outcomes.

Clinical Trial Registration

URL: https://www.clinicaltrials.gov/. Unique identifier: NCT00968708.

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<![CDATA[Prognostic Significance of Serum Cholinesterase Level in Patients With Acute Decompensated Heart Failure With Preserved Ejection Fraction: Insights From the PURSUIT‐HFpEF Registry]]> https://www.researchpad.co/article/Nc6de7bc5-ce52-454d-a82a-90457f279a76

Background

Malnutrition is one of the most important comorbidities in patients with heart failure with preserved ejection fraction. We recently reported the prognostic significance of serum cholinesterase level and superior predictive power of cholinesterase level to other objective nutritional indices such as the controlling nutritional status score, prognostic nutritional index, and geriatric nutritional risk index in patients with acute decompensated heart failure. The aim of this study was to clarify the prognostic role of cholinesterase in patients with heart failure with preserved ejection fraction/acute decompensated heart failure and investigate incremental cholinesterase value.

Methods and Results

We prospectively studied 274 consecutive patients from the PURSUIT‐HFpEF (Prospective Multicenter Observational Study of Patients with Heart Failure With Preserved Ejection Fraction) study. During a follow‐up period of 1.2±0.6 years, 56 patients reached the composite end points (cardiovascular death and readmission for worsening heart failure). In the multivariable Cox analysis, cholinesterase level was significantly associated with the composite end points after adjustment for major confounders. A Kaplan–Meier analysis revealed that patients with low cholinesterase levels (stratified by tertile) had significantly greater risk of reaching the composite end points than those with middle or high cholinesterase levels (P=0.0025). Cholinesterase level showed the best C‐statistics (0.703) for prediction of the composite end points among the objective nutritional indices. C‐statistics of the Meta‐Analysis Global Group in Chronic Heart Failure (MAGGIC) risk score for prediction of the composite end points were improved when cholinesterase level was added (C‐statistics, from 0.601 to 0.705; P=0.0408).

Conclusions

Cholinesterase was a useful prognostic marker for prediction of adverse outcome in patients with heart failure with preserved ejection fraction/acute decompensated heart failure.

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<![CDATA[Gender Differences in Risk Factors Associated With Pulmonary Artery Systolic Pressure, Heart Failure, and Mortality in Blacks: Jackson Heart Study]]> https://www.researchpad.co/article/N22c26270-b67e-486b-93d1-617a266ddb39

Background

Pulmonary hypertension is prevalent in black individuals, especially women. Elevated pulmonary artery systolic pressure (PASP) is associated with significant morbidity and mortality.

Methods and Results

We developed linear and proportional hazards models to examine potential gender‐related differences in risk factors for elevated PASP (estimated by transthoracic echocardiography) and PASP‐associated clinical outcomes (incident heart failure admissions and mortality) in JHS (Jackson Heart Study) participants. JHS is a prospective observational cohort study of heart disease in blacks from the Jackson, Mississippi, metropolitan area. The study cohort included participants with measurable transtricuspid gradients (n=3286) at the time of first/baseline examination, 2000–2004. The median age (interquartile range) of patients at baseline was 57.8 years (18.6 years) with 67.5% being women. The median PASP at baseline was higher in women (men: 26 mm Hg [interquartile range 8], women: 27 mm Hg [interquartile range 9]. In multivariate linear regression analyses with PASP, significant gender interactions were noted for age, chronic lung disease, pulse pressure, and obstructive spirometry. In exploratory analyses stratified by gender, body mass index, and obstructive and restrictive spirometry patterns were associated with PASP in women, and chronic lung disease was associated with PASP in men. Age and pulse pressure had stronger associations with PASP in women compared with men. There was a significant interaction between gender and PASP for heart failure admissions but not mortality.

Conclusions

Specific cardiopulmonary risk factors are associated with elevated PASP in women and men. Women with elevated PASP have a higher risk of incident heart failure admissions. Future research is needed to understand associated gender‐specific mechanisms that can help identify targeted prevention and management strategies for patients with elevated PASP.

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<![CDATA[Significant cardiac disease complicating Graves’ disease in previously healthy young adults]]> https://www.researchpad.co/article/N799f442a-dba1-4542-ab7b-3253ae1ef914

Summary

Graves’ disease is associated with tachydysrythmia, cardiac ischaemia and cardiomyopathy – all uncommon in young adults without previous cardiac disease. We present three young individuals who developed cardiac complications after periods of uncontrolled Graves’ disease. Subject 1: A 34-year-old female had severe thyrotoxic symptoms for weeks. Investigations showed fT4: 98.4 (11–25 pmol/L), fT3: 46.9 (3.1–6.8 pmol/L), TSH <0.01 (0.27–4.2 mU/L) and thyrotrophin receptor antibody (TRAb): 34.8 (<0.9 U//l). She had appropriate treatment but several weeks later she became breathless despite improving thyroid function. Echocardiography showed a pericardial effusion of 2.9 cm. She responded well to steroids and NSAIDs but developed active severe Graves’ orbitopathy after early total thyroidectomy. Subject 2: A 28-year-old male developed thyrotoxic symptoms (fT4: 38 pmol/L, fT3: 13.9 pmol/L, TSH <0.01 (for over 6 months) and TRAb: 9.3 U/L). One month after starting carbimazole, he developed acute heart failure (HF) due to severe dilated cardiomyopathy – EF 10–15%. He partially recovered after treatment – EF 28% and had early radioiodine treatment. Subject 3: A 42-year-old woman who had been thyrotoxic for several months (fT4: 54.3; fT3 >46.1; TSH <0.01; TRAb: 4.5) developed atrial fibrillation (AF) and heart failure. Echocardiography showed cardiomegaly – EF 29%. She maintains sinus rhythm following early total thyroidectomy (EF 50%). Significant cardiac complications may occur in previously fit young adults, who have had uncontrolled Graves’ disease for weeks to months. Cardiac function recovers in the majority, but early definitive treatment should be discussed to avoid Graves’ disease relapse and further cardiac decompensation.

Learning points:

  • Cardiac complications of Graves’ disease are uncommon in young adults without previous cardiac disease.

  • These complications may however occur if Graves’ disease had been poorly controlled for several weeks or months prior to presentation.

  • Persistent symptoms after adequate control should alert clinicians to the possibility of cardiac disease.

  • Specific treatment of Graves’ disease and appropriate cardiac intervention results in complete recovery in the majority and carries a good prognosis.

  • Early definitive treatment should be offered to them to prevent cardiac decompensation at times of further relapse.

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