Left Heart Failure Research Articles

#201 Bedside lung ultrasound and bioimpedance spectroscopy for assessment of volume status in chronic kidney disease patients on hemodialysis

Abstract Background and Aims Fluid balance is important in patients with chronic kidney disease undergoing hemodialysis (HD). Majority of HD treatment incorporate a prescription for fluid removal targeted to patient's dry weight. Overestimation of dry weight causes hypertension, left ventricular hypertrophy and heart failure, while underestimation is responsible for chronic dehydration leading to the risk of hypotension. Both complications have a significant impact on the overall morbidity and mortality. Dry weight of the patient is usually assessed by using clinical parameters (edema, BP, JVP etc.), Biochemical parameters (BNP, ANP), Bioimpedance Spectroscopy (BIS) or IVC diameter and collapsibility on ultrasound (VCI index). The use of chest ultrasound to detect lung water has recently received growing attention in clinical research. Ultrasonographic lung comets (counting B-lines artifact) evaluate extravascular lung water and hence is considered as a useful tool to evaluate the hydration status of hemodialysis patients. This study aims to compare the efficacy of body fluid volume status and lung water assessment by clinical methods, Ultrasound chest and Bioimpedance Spectroscopy in chronic kidney disease patients on hemodialysis. Method A cross-sectional study was conducted over a period of 6 months. Dry weight of the patient was assessed by the attending nephrologist based on clinical criteria such as: weight, blood pressure, presence of edema or vascular congestion. A Longitudinal Ultrasound scan of the chest was performed using MicroMaxx Ultrasound System with patient in supine position from second to fourth intercostal space of left hemi-thorax and second to fifth intercostal space of right hemi-thorax along parasternal, midclavicular, anterior axillary and midaxillary lines of each side in a total of 28 sectors. B-lines were defined as hyperechogenic linear artifact emerging from the pleural line, up to the bottom of the screen. Pre and Post dialysis comet score was determined by calculating the total B-lines in each sector. Bioimpedance spectroscopy using Bodystat QuadScan 4000 was performed. Pre and post dialysis total body water (TBW), intracellular water (ICW), extracellular water (ECW) and residual fluid overload (ECW pre HD- ECW post HD) were recorded. Results We conducted 100 assessments on 34 patients presenting to the hospital for maintenance hemodialysis. The mean age of the study population was 54.3 + 11 years with a sex ratio (M/F) of 6:1. Mean systolic blood pressure was 141.1 + 19 mmHg and diastolic blood pressure was 83 + 9.3 mmHg with 3 episodes of intradialytic hypotension. The mean dry weight was 59.8 + 10 Kg and weight gain by clinical assessment was 2.1 + 1.5 Kg. Comet score assessed by ultrasound chest had a mean of 4.54 + 2.53 before dialysis and 1.73 ± 1.36 after dialysis. Residual fluid overload on Bio impedance spectroscopy was 1.11 ± 0.85 litre. The residual fluid overload on Bio impedance spectroscopy and lung ultrasound comet score after dialysis had a significant correlation (p value <0.0001). Of the 100 assessments, 40% had fluid overload after dialysis on Bio impedance and 35% had lung congestion on ultrasound chest even after achieving euvolemia according to the dry weight assessed clinically. Conclusion Lung comets on ultrasound chest and residual volume on bio impedance spectroscopy may precede the development of clinical sign and symptoms in a patient. Therefore, these methods are superior to clinical volume status assessment in chronic kidney disease patients on hemodialysis.

Comparison of the stage-dependent mitochondrial changes in response to pressure overload between the diseased right and left ventricle in the rat.

The right ventricle (RV) differs developmentally, anatomically and functionally from the left ventricle (LV). Therefore, characteristics of LV adaptation to chronic pressure overload cannot easily be extrapolated to the RV. Mitochondrial abnormalities are considered a crucial contributor in heart failure (HF), but have never been compared directly between RV and LV tissues and cardiomyocytes. To identify ventricle-specific mitochondrial molecular and functional signatures, we established rat models with two slowly developing disease stages (compensated and decompensated) in response to pulmonary artery banding (PAB) or ascending aortic banding (AOB). Genome-wide transcriptomic and proteomic analyses were used to identify differentially expressed mitochondrial genes and proteins and were accompanied by a detailed characterization of mitochondrial function and morphology. Two clearly distinguishable disease stages, which culminated in a comparable systolic impairment of the respective ventricle, were observed. Mitochondrial respiration was similarly impaired at the decompensated stage, while respiratory chain activity or mitochondrial biogenesis were more severely deteriorated in the failing LV. Bioinformatics analyses of the RNA-seq. and proteomic data sets identified specifically deregulated mitochondrial components and pathways. Although the top regulated mitochondrial genes and proteins differed between the RV and LV, the overall changes in tissue and cardiomyocyte gene expression were highly similar. In conclusion, mitochondrial dysfuntion contributes to disease progression in right and left heart failure. Ventricle-specific differences in mitochondrial gene and protein expression are mostly related to the extent of observed changes, suggesting that despite developmental, anatomical and functional differences mitochondrial adaptations to chronic pressure overload are comparable in both ventricles.

The Clinical Outcome of Cardiac Rehabilitation in Coronary Artery Disease Patients with Regard to the Presence of Left Ventricular Systolic Dysfunction.

Background: Despite the use of advanced treatment techniques, coronary artery disease (CAD) still remains the main cause of left ventricular (LV) dysfunction and heart failure. Participation in cardiac rehabilitation (CR) programs can lead to a number of beneficial effects, but some patients do not demonstrate the expected improvement. The aim of this study is to evaluate the impact of CR on changes in exercise capacity with regard to the presence of LV dysfunction. Methods: A group of 428 patients with CAD were consecutively admitted to an outpatient comprehensive cardiac rehabilitation program comprising 24 exercise sessions of interval training on cycle ergometers, three times a week for 45 min, and a health education. The patients were compared in two subgroups, i.e., with LV systolic dysfunction (LVEF < 50%, n = 175) and LVEF ≥ 50% (n = 253). Results: In the LVEF < 50% group, the exercise capacity improved by 1 ± 0.78 MET (median 1.15 MET), and 0.86 ± 0.77 MET (median 1.08 MET) in the LVEF ≥ 50% group. Women with LVEF < 50% demonstrated a significant increase in exercise capacity by 1.2 MET, while those with LVEF ≥ 50% did not display any such increase. All men, regardless of LVEF, exhibited a similar improvement in exercise capacity greater than 1 MET. Conclusions: An outpatient eight-week cardiac rehabilitation program based on 45 min aerobic interval training sessions three times a week appears less effective for women with CAD and EF ≥ 50%. In this group, the proposed training intervention is insufficient in improving exercise capacity to an extent that could indicate a reduction in mortality risk.

“SEEK, AND YOU WILL FIND” - IMPLICATIONS OF PULMONARY HYPERTENSION DIAGNOSIS AND TREATMENT OF PATIENT WITH CHRONIC OBSTRUCTIVE PULMONARY DISEASE AND LEFT HEART FAILURE

Objective: The case report presents a patient with multimorbidity. A diagnosis of pulmonary hypertension was made during multiple hospitalizations due to bad compliance. The objective of this case report is to describe the difficulties involved in diagnosing pulmonary hypertension in a patient with chronic obstructive pulmonary disease and left heart failure. Design and method: Case report of patient with pulmonary hypertension, chronic obstructive pulmonary disease, left heart failure and multiple comorbidities. Observation of the patient's health condition during many hospitalizations led to further diagnosis of pulmonary hypertension and forced the modification of current treatment. Results: Patient went through many hospitalizations because of bad compliance to chronic obstructive pulmonary disease and left heart failure pharmacotherapy. The patient was hospitalized in our ward for chest pain. He also presented combination of nonspecific symptoms such as dyspnoea (including resting dyspnoea), exercise intolerance and peripheral oedema. Chest x-ray showed signs of pneumonia. Therefore, the diagnosis of pulmonary hypertension was not made during the first hospitalisations. Echocardiography was planned to exclude chronic coronary syndrome. It revealed patent ductus arteriosus, right ventriculum and pulmonary trunk dilation, tricuspid regurgitation and high probability of pulmonary hypertension (mean pulmonary artery pressure 46,5mmHg), without regional cardiac wall dysfunction. The next hospitalization was scheduled, during which cardiac catheterization was performed (pulmonary capillary wedge pressure 14,5 mmHg) and precapillary pulmonary hypertension was confirmed. After many consultations, excluding other causes, such as thromboembolic changes, chronic obstructive pulmonary disease was considered the most likely cause of precapillary pulmonary hypertension. Treatment of basal diseases has been modified, off-label treatment with sildenafil was started, and then due to ineffective treatment (deterioration of the patient's condition resulted in a transition from WHO functional class II to III) the patient was qualified for the bosentan clinical drug treatment program. Conclusions: Diagnosis of pulmonary hypertension can be difficult when symptoms of diseases from other systems are overlapping. This case shows the necessity of watchful observation of patients with multimorbidity, but also difficulties in maintaining good medical compliance. Pulmonary hypertension is still a rare diagnosis, but we should stay alerted about it.

CD8 T cells exert a critical role in the transition from left heart failure to lung remodeling and right ventricular hypertrophy

Chronic left ventricular (LV) failure or heart failure (HF) often progress to pulmonary remodeling and right ventricular (RV) hypertrophy even with optimal medical care. Cytotoxic CD8+ T cells play an important role in modulating virus infection and tissue injury by producing proinflammatory cytokines and cytolysis of the infected or injured cells. However, the role of CD8+ T cells in heart failure (HF)-induced lung remodeling and RV hypertrophy is unknown. To determine the role of CD8 T cells in modulating HF progression under preexisting HF conditions, wild type mice with existing LV failure produced by transverse aortic constriction (TAC) were randomized to depletion of cytotoxic CD8+ T cells, regulatory T cells (Tregs), or both by using specific blocking antibodies. The cardiac function, lung inflammation, fibrosis, vascular remodeling, and right ventricular remodeling were determined. As anticipated, LV failure caused lung inflammation and activation of pulmonary CD4+ T cells and CD8+ T cells. Interestingly, depletion of CD8+ T cells dramatically attenuated the increase of lung weight, lung inflammation, lung vascular remodeling, and RV hypertrophy in mice with existing LV failure. LV failure was associated with an increased ratio of activated T cells to Tregs, and Treg depletion exacerbated lung inflammation and the progression of LV failure. Treg depletion also exacerbated the lung CD4+ and CD8+ T cell infiltration, and the percentage of effector memory T cells (Tem) in HF mice. Depletion of CD8+ T cells was suffcient to rescued HF mice from the exacerbated lung inflammation and the progression of LV failure that was caused by Treg depletion. These findings demonstrate that CD8+ T cells play a critical role in promoting the transition from LV failure to lung remodeling and RV hypertrophy. NIH funding. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Ventilatory Variability Is Increased at Rest in Pulmonary Arterial Hypertension

Ventilatory instability is associated with adverse outcomes in left heart failure, with periodic breathing during awake, rest, sleep and exercise (exercise oscillatory ventilation) associated with increased mortality. Increased peripheral and central chemoreflex sensitivities and impairment of cardiac output have been implicated as causative mechanisms of ventilatory instability in heart failure. As these factors are also present in pulmonary arterial hypertension (PAH), we tested the hypothesis that variability of breath-by-breath ventilation at rest would be increased in PAH compared with healthy controls. In fourteen patients with PAH (9 female, age 48.4±12.8 years, mean ± SD) and 14 healthy participants (9 female, age 49.4±14.2 years) breath-by-breath measurement of tidal volume and breathing frequency was undertaken with a pneumotachometer connected via a mouthpiece with nose-clip for 10 minutes while they rested awake and supine. Ventilatory (V̇E) variability was assessed using root mean square of successive differences (RMSSD), standard deviation (SD), average real variability (ARV, i.e., sum of absolute differences in successive observations), coeffcient of variation (CoV), as well as Poincaré analysis and compared between PAH and healthy controls (Student’s t-test). Correlations between measures of ventilatory variability and pulmonary hemodynamic characteristics, exercise capacity and function were assessed with Pearson’s correlation coeffcient. Resting V̇E was higher in PAH compared to healthy controls (14.3±1.1 and 12.1±0.5 L·min−1 respectively; p=0.009). Measures of variability for V̇E were increased in PAH compared to healthy controls. More specifically, RMSSD (3.59±1.36 vs. 2.48±0.87 L·min−1, p=0.017), SD (2.92±1.14 vs. 1.98±0.53 L·min−1, p=0.012), ARV (2.47±0.97 vs. 1.67±0.60 L·min−1, p=0.016), Poincaré SD1 (short-term variability, p=0.020) and SD2 (long-term variability, p=0.028) were increased in PAH compared to healthy controls, respectively. No correlations were found between measures of ventilatory variability and pulmonary hemodynamics (mean pulmonary artery pressure, pulmonary vascular resistance, and cardiac output), six-minute walk distance or WHO functional class. In summary, resting ventilatory variability is increased in PAH and not associated with haemodynamic factors and exercise capacity. Whether such raised ventilatory variability in PAH is related to increased chemoreflex sensitivity requires exploration. This study received funding support from the Greenlane Research and Educational Fund (21/01/4153), Health Research Council of New Zealand (19/687), and the Sidney Taylor Trust. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Aerobic Exercise Training Attenuates Differences between Black and White Adults in Left Ventricular-Vascular Coupling and Wasted Pressure Effort

Background: Black adults have a higher risk for left-ventricular hypertrophy and heart failure, when compared to white adults. This stems, in part, from their frequent potential alterations in ventricular-vascular coupling indexed by the arterial (Ea) to ventricular elastance (Ev) ratio and heightened wasted pressure effort (Ew). Exercise training preserves ventricular-vascular coupling and attenuates Ew, but whether this applies to black adults is unknown. Purpose: We hypothesized that aerobic training would attenuate reported racial differences in both left ventricular-vascular coupling and Ew. Methods: Fifty-four young adults [blacks= 24 (14 females); whites= 30 (15 females), aged: 19-35 years] completed an 8-week aerobic training intervention (3 times/wk, 65-85% peak oxygen uptake). Pre-and post-training systolic function and ventricular-vascular coupling were assessed via echocardiography. The Ew was estimated from pulse contour analysis. Pre-and-post-training changes were examined with linear mixed models. Results: Pre-training, blacks had higher Ev (difference (d) = 0.49, 95% CI: 0.14 to 0.84 mmHg/ml, p=0.007) and Ew (d= 1130, 95% CI: 477 to 1784 dyne cm−2 s, p&lt;0.001). After training, both groups exhibited similar reductions in Ea (d= -0.22, 95% CI: -0.32 to -0.13 mmHg/ml, p&lt;0.001). In white, but not black adults, Ev increased (dwhite= 0.30, 95% CI: 0.04 to 0.56 mmHg/ml , p=0.027) and Ea/Ev was reduced (dwhite= -0.21, 95% CI: -0.29 to -0.12 mmHg/ml, p&lt;0.001). Conversely, black but not white adults exhibited reductions in Ew after training (dblack= -699, 95% CI: -1209 to -189 dyne cm−2 s, p=0.008). Systolic function markers (i.e., race-independent increases in ejection fraction) supported ventricular-vascular coupling results. Controlling for cardiorespiratory fitness, and body mass index attenuated training-induced changes in Ev and Ew, while controlling for sex did no change results. Conclusions: In black adults, Ew was reduced following 8 weeks of aerobic training, while Ea was reduced in both black and white adults. Although ventricular-vascular coupling was only altered in white adults, there was no difference between white and black adults in coupling or its components following training. Despite not controlling for social determinants of health shown to partly explain biological racial disparities, our data suggests a positive effect of aerobic training on risk factors associated with the development of left ventricular hypertrophy and heart failure in black adults. This study was funded by the National Instituteof Health (NHLBI 1R01HL093249-01A1 awarded to Bo Fernhall). This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

Pulmonary Hypertension in Sickle Cell Disease: Novel Findings of Gene Polymorphisms Related to Pathophysiology.

Pulmonary hypertension (PH) is a progressive and potentially fatal complication of sickle cell disease (SCD), affecting 6-10% of adult SCD patients. Various mechanisms and theories have been evaluated to explain the pathophysiology of this disease. However, questions remain, particularly regarding the clinical heterogeneity of the disease in terms of symptoms, complications, and survival. Beyond the classical mechanisms that have been thoroughly investigated and include hemolysis, nitric oxide availability, endothelial disorders, thrombosis, and left heart failure, attention is currently focused on the potential role of genes involved in such processes. Potential candidate genes are investigated through next-generation sequencing, with the transforming growth factor-beta (TGF-β) pathway being the initial target. This field of research may also provide novel targets for pharmacologic agents in the future, as is already the case with idiopathic PH. The collection and processing of data and samples from multiple centers can yield reliable results that will allow a better understanding of SCD-related PH as a part of the disease's clinical spectrum. This review attempts to capture the most recent findings of studies on gene polymorphisms that have been associated with PH in SCD patients.

Right ventricular dysfunction in chronic heart failure: clinical laboratory and echocardiographic characteristics. (the RIVED-CHF registry).

Right ventricular dysfunction (RVD) and pulmonary hypertension have been recognized as two important prognostic features in patients with left side heart failure. Current literature does not distinguish between right heart failure (RHF) and RVD, and the two terms are used indiscriminately to describe pulmonary hypertension and RVD as well as clinical sign of RHF. Therefore, the right ventricle (RV) adaptation across the whole spectrum of left ventricular ejection fraction (LVEF) values has been poorly investigated. This is a multicenter observational prospective study endorsed by the Italian Society of Cardiology aiming to analyze the concordance between the signs and symptoms of RHF and echocardiographic features of RVD. The protocol will assess patients affected by chronic heart failure in stable condition regardless of the LVEF threshold by clinical, laboratory, and detailed echocardiographic study. During the follow-up period, patients will be observed by direct check-up visit and/or virtual visits every 6 months for a mean period of 3 years. All clinical laboratory and echocardiographic data will be recorded in a web platform system accessible for all centers included in the study. The main study goals are: to investigate the concordance and discordance between clinical signs of RHF and RVD measured by ultrasonographic examination; to evaluate prognostic impact (in terms of cardiovascular mortality and heart failure hospitalization) of RVD and RHF during a mean follow-up period of 3 years; to investigate the prevalence of different right ventricular maladaptation (isolated right ventricular dilatation, isolated pulmonary hypertension, combined pattern) and the related prognostic impact. With this protocol, we would investigate the three main RVD patterns according to heart failure types and stages; we would clarify different RVD and pulmonary hypertension severity according to the heart failure types. Additionally, by a serial multiparametric analysis of RV, we would provide a better definition of RVD stage and how much is it related with clinical signs of RHF (ClinicalTrials.gov Identifier: NCT06002321).

Mavacamten: A Review of a Novel Therapeutic Approach for Hypertrophic Cardiomyopathy.

Hypertrophic Cardiomyopathy (HCM) is a heart disease that can cause left ventricular hypertrophy, arrhythmias, heart failure, and sudden cardiac death. Currently, pharmacological treatment is limited and ineffective. Mavacamten (CamzyosTM) is a cardiac myosin inhibitor developed as a therapeutic option to reduce myocardial contractility and restoration of myocardial function. The Food and Drug Administration (FDA) approved the use of Mavacamten in 2022 for HCM symptoms. Clinical studies have proven that Mavacamten can reduce Left Ventricular Outflow Tract (LVOT) involvement, cardiac hypercontraction, and hypertrophy. This review provides an overview of HCM, its pathophysiology, current treatments, synthesis of Mavacamten, and the clinical trials of Mavacamten.

A roadmap for therapeutic discovery in pulmonary hypertension associated with left heart failure. A scientific statement of the Heart Failure Association (HFA) of the ESC and the ESC Working Group on Pulmonary Circulation & Right Ventricular Function.

Pulmonary hypertension (PH) associated with left heart failure (LHF) (PH-LHF) is one of the most common causes of PH. It directly contributes to symptoms and reduced functional capacity and negatively affects right heart function, ultimately leading to a poor prognosis. There are no specific treatments for PH-LHF, despite the high number of drugs tested so far. This scientific document addresses the main knowledge gaps in PH-LHF with emphasis on pathophysiology and clinical trials. Key identified issues include better understanding of the role of pulmonary venous versus arteriolar remodelling, multidimensional phenotyping to recognize patient subgroups positioned to respond to different therapies, and conduct of rigorous pre-clinical studies combining small and large animal models. Advancements in these areas are expected to better inform the design of clinical trials and extend treatment options beyond those effective in pulmonary arterial hypertension. Enrichment strategies, endpoint assessments, and thorough haemodynamic studies, both at rest and during exercise, are proposed to play primary roles to optimize early-stage development of candidate therapies for PH-LHF.

Comparative analysis of the clinical features of nonvalvular atrial fibrillation among Tibetan, Han, and Hui patients in Qinghai Province, China

BackgroundGlobal nonvalvular AF rises, impacting health severely. In Qinghai, China's diverse setting, studying AF among varied ethnic groups is crucial ObjectivesThe purpose of this study was to compares cardiac features in AF among Tibetan, Han, and Hui patients to develop tailored prevention and treatment strategies for this region, the goal was to enhance the understanding of AF and provide an empirical basis for developing prevention and treatment strategies specific to this region MethodsThis study included a total of 3445 Tibetan, Han, and Hui patients diagnosed with nonvalvular atrial fibrillation and treated at the Qinghai Cardiovascular and Cerebrovascular Specialist Hospital, China, between January 2019 and January 2021. We analyzed the differences in cardiac structure, comorbidities, and other influencing factors among the different ethnic groups ResultsWe found significant differences in gender, age, smoking history, lone atrial fibrillation, left heart failure, dilated cardiomyopathy, and diabetes between Tibetan, Han, and Hui patients (P < 0.05). Tibetan, Han, and Hui patients also differed with regard to left ventricular end-diastolic volume, left ventricular ejection fraction, fractional shortening, NT-proBNP, glycated hemoglobin, red blood cell distribution width, platelet count, platelet hematocrit, platelet distribution width, homocysteine (Hcy), C-reactive protein, and superoxide dismutase (SOD) (P < 0.05) ConclusionOur study revealed variations in comorbidities, cardiac structure, and blood indexes among Tibetan, Han, and Hui AF patients, highlighting distinct patterns in complications and biomarker levels across ethnic groups.

Atrial Septal Defect, Pulmonary Arterial Hypertension, and Diastolic Left Heart Failure: When 3 Players Come into the Game.

Atrial Septal Defect, Pulmonary Arterial Hypertension, and Diastolic Left Heart Failure: When 3 Players Come into the Game.

Implementation of the Care Bundle for the Management of Chronic Obstructive Pulmonary Disease with/without Heart Failure.

Chronic obstructive pulmonary disease (COPD) is often part of a more complex cardiopulmonary disease, especially in older patients. The differential diagnosis of the acute exacerbation of COPD and/or heart failure (HF) in emergency settings is challenging due to their frequent coexistence and symptom overlap. Both conditions have a detrimental impact on each other's prognosis, leading to increased mortality rates. The timely diagnosis and treatment of COPD and coexisting factors like left ventricular overload or HF in inpatient and outpatient care can improve prognosis, quality of life, and long-term outcomes, helping to avoid exacerbations and hospitalization, which increase future exacerbation risk. This work aims to address existing gaps, providing management recommendations for COPD with/without HF, particularly when both conditions coexist. During virtual meetings, a panel of experts (the authors) discussed and reached a consensus on the differential and paired diagnosis of COPD and HF, providing suggestions for risk stratification, accurate diagnosis, and appropriate therapy for inpatients and outpatients. They emphasize that when COPD and HF are concomitant, both conditions should receive adequate treatment and that recommended HF treatments are not contraindicated in COPD and have favorable effects. Accurate diagnosis and therapy is crucial for effective treatment, reducing hospital readmissions and associated costs. The management considerations discussed in this study can potentially be extended to address other cardiopulmonary challenges frequently encountered by COPD patients.

Subclinical myocardial damage after anthracycline chemotherapy in Japanese patients with breast cancer

BackgroundData on the incidence, timing, and severity of myocardial damage after anthracycline-based chemotherapy (AC) in Japanese patients with breast cancer are limited. MethodWe evaluated cancer therapy-related cardiac dysfunction (CTRCD) in Japanese women with breast cancer (n = 51) after the first AC according to the definitions of the 2022 European Society of Cardiology onco-cardiology guideline, including assessment of high-sensitivity troponin I (TnI) and B-type natriuretic peptide (BNP) levels. ResultsCTRCD was detected in 67 % of the patients (3.9 %, 7.8 %, 9.8 %, 43 %, 37 %, 22 %, 20 %, and 9.8 % of patients at 1 week and 1, 2, 3, 6, 9, 12, and 15 months post-AC, respectively) without significant left ventricular ejection fraction reduction (<50 %) and heart failure. Elevated TnI levels (>26 pg/mL) were found in 43 % of patients, and elevated BNP levels (≥35 pg/mL) were observed in 22 % of patients during the follow-up period. ConclusionsApproximately two-thirds of the Japanese patients in this study experienced CTRCD, which was frequently observed at 3 or 6 months post-AC. However, all patients with CTRCD were diagnosed with mild asymptomatic CTRCD. Although, these patients were diagnosed with mild asymptomatic CTRCD, careful long-term follow-up will be required.

Complications of left bundle branch area pacing compared with biventricular pacing in candidates for resynchronization therapy: Results of a propensity score–matched analysis from a multicenter registry

BackgroundCardiac resynchronization therapy (CRT) with biventricular pacing (BVP) is a well-established therapy in patients with reduced left ventricular ejection fraction, heart failure, and left bundle branch block. Left bundle branch area pacing (LBBAP) has recently been shown to be a feasible and effective alternative to BVP. Comparative data on the risk of complications between LBBAP and BVP among patients undergoing CRT are lacking. ObjectiveThe aim of this study was to compare the long-term risk of procedure-related complications between LBBAP and BVP in a cohort of patients undergoing CRT. MethodsThis prospective, multicenter, observational study enrolled 668 consecutive patients (mean age 71.2 ± 10.0 years; 52.2% male; 59.4% with New York Heart Association class III-IV heart failure symptoms) with left ventricular ejection fraction 33.4% ± 4.3% who underwent BVP (n = 561) or LBBAP (n = 107) for a class I or II indication for CRT. Propensity score matching for baseline characteristics yielded 93 matched pairs. The rate and nature of intraprocedural and long-term post-procedural complications occurring during follow-up were prospectively collected and compared between the 2 groups. ResultsDuring a mean follow-up of 18 months, procedure-related complications were observed in 16 patients: 12 in BVP (12.9%) and 4 in LBBAP (4.3%) (P = .036). Compared with patients who underwent LBBAP, those who underwent BVP showed a lower complication-free survival (P = .032). In multivariate analysis, BVP resulted an independent predictive factor associated with a higher risk of complications (hazard ratio 3.234; P = .042). Complications related to the coronary sinus lead were most frequently observed in patients who underwent BVP (50.0% of all complications). ConclusionLBBAP was associated with a lower long-term risk of device-related complications compared with BVP in patients with an indication for CRT.

Mechanism of Qili Qiangxin Capsule for Heart Failure Based on miR133a-Endoplasmic Reticulum Stress.

To investigate the pharmacological mechanism of Qili Qiangxin Capsule (QLQX) improvement of heart failure (HF) based on miR133a-endoplasmic reticulum stress (ERS) pathway. A left coronary artery ligation-induced HF after myocardial infarction model was used in this study. Rats were randomly assigned to the sham group, the model group, the QLQX group [0.32 g/(kg·d)], and the captopril group [2.25 mg/(kg·d)], 15 rats per group, followed by 4 weeks of medication. Cardiac function such as left ventricular ejection fraction (EF), fractional shortening (FS), left ventricular systolic pressure (LVSP), left ventricular end diastolic pressure (LVEDP), the maximal rate of increase of left ventricular pressure (+dp/dt max), and the maximal rate of decrease of left ventricular pressure (-dp/dt max) were monitored by echocardiography and hemodynamics. Hematoxylin and eosin (HE) and Masson stainings were used to visualize pathological changes in myocardial tissue. The mRNA expression of miR133a, glucose-regulated protein78 (GRP78), inositol-requiring enzyme 1 (IRE1), activating transcription factor 6 (ATF6), X-box binding protein1 (XBP1), C/EBP homologous protein (CHOP) and Caspase 12 were detected by RT-PCR. The protein expression of GRP78, p-IRE1/IRE1 ratio, cleaved-ATF6, XBP1-s (the spliced form of XBP1), CHOP and Caspase 12 were detected by Western blot. TdT-mediated dUTP nick-end labeling (TUNEL) staining was used to detect the rate of apoptosis. QLQX significantly improved cardiac function as evidenced by increased EF, FS, LVSP, +dp/dt max, -dp/dt max, and decreased LVEDP (P<0.05, P<0.01). HE staining showed that QLQX ameliorated cardiac pathologic damage to some extent. Masson staining indicated that QLQX significantly reduced collagen volume fraction in myocardial tissue (P<0.01). Results from RT-PCR and Western blot showed that QLQX significantly increased the expression of miR133a and inhibited the mRNA expressions of GRP78, IRE1, ATF6 and XBP1, as well as decreased the protein expressions of GRP78, cleaved-ATF6 and XBP1-s and decreased p-IRE1/IRE1 ratio (P<0.05, P<0.01). Further studies showed that QLQX significantly reduced the expression of CHOP and Caspase12, resulting in a significant reduction in apoptosis rate (P<0.05, P<0.01). The pharmacological mechanism of QLQX in improving HF is partly attributed to its regulatory effect on the miR133a-IRE1/XBP1 pathway.

Guyton perspective in managing peripartum cardiomyopathy patient with pulmonary edema: a case report

BackgroundPeripartum cardiomyopathy (PPCM) is a potentially life-threatening pregnancy-related condition characterized by left ventricular dysfunction and heart failure, typically occurring in the peripartum period. Individuals with a history of preeclampsia and hypertension are particularly prone to developing PPCM. Recent research suggests that the condition may be triggered by vascular dysfunction influenced by maternal hormones in the late stages of gestation. The onset of left heart failure results in decreased cardiac output, leading to insufficient perfusion, which in turn, contributes to pulmonary edema and exacerbates tissue hypoxia. This cardiovascular response activates the neurohumoral system, causing peripheral vasoconstriction and elevating both mean capillary filling pressure (MCFP) and central venous pressure (CVP). Early administration of furosemide reduces volume overload due to negative cumulative fluid balance gaining and vasodilation, which increases the velocity of intravascular refilling and causes interstitial edema to resolve. This will decrease interstitial fluid pressure, resulting in decreased mechanical compression to systemic capillary and systemic vein pressure, thus decreasing MCFP and CVP subsequently. Reduced CVP also contributes to increased venous return by decreasing the gradient pressure between MCFP and CVP, resulting in increased cardiac output (CO) and improved tissue oxygenation.CaseA 33-year-old Asian woman, para 3 at full term pregnancy, admitted to the intensive care unit (ICU) after c-section and tubectomy due to shortness of breath and palpitation. Based on history taking, physical examination and echocardiography the patient fulfilled the criteria of PPCM which was also complicated by pulmonary edema. Despite impending respiratory failure, the patient rejected intubation and continuous positive airway pressure (CPAP), and was given oxygen supplementation through nasal cannula. Furosemide was given rapidly continued by maintenance dose and CVP was monitored. Antihypertensive drug, anticoagulants, and bromocriptine were also administered. After achieving negative cumulative fluid balance the patient’s symptoms resolved and was discharged one week later.ConclusionThere is a correlation between negative cumulative fluid balance and reduced central venous pressure after early furosemide therapy. Suspicion for PPCM should not be lowered in the presence of preeclampsia, it could delay appropriate treatment and increase the mortality.

Long-Term Outcomes of Cardiac Resynchronization Therapy in Patients With Repaired Tetralogy of Fallot: A Multicenter Study.

A growing number of patients with tetralogy of Fallot develop left ventricular systolic dysfunction and heart failure, in addition to right ventricular dysfunction. Although cardiac resynchronization therapy (CRT) is an established treatment option, the effect of CRT in this population is still not well defined. This study aimed to investigate the early and late efficacy, survival, and safety of CRT in patients with tetralogy of Fallot. Data were analyzed from an observational, retrospective, multicenter cohort, initiated jointly by the Pediatric and Congenital Electrophysiology Society and the International Society of Adult Congenital Heart Disease. Twelve centers contributed baseline and longitudinal data, including vital status, left ventricular ejection fraction (LVEF), QRS duration, and NYHA functional class. Outcomes were analyzed at early (3 months), intermediate (1 year), and late follow-up (≥2 years) after CRT implantation. A total of 44 patients (40.3±19.2 years) with tetralogy of Fallot and CRT were enrolled. Twenty-nine (65.9%) patients had right ventricular pacing before CRT upgrade. The left ventricular ejection fraction improved from 32% [24%-44%] at baseline to 42% [32%-50%] at early follow-up (P<0.001) and remained improved from baseline thereafter (P≤0.002). The QRS duration decreased from 180 [160-205] ms at baseline to 152 [133-182] ms at early follow-up (P<0.001) and remained decreased at intermediate and late follow-up (P≤0.001). Patients with upgraded CRT had consistent improvement in left ventricular ejection fraction and QRS duration at each time point (P≤0.004). Patients had a significantly improved New York Heart Association functional class after CRT implantation at each time point compared with baseline (P≤0.002). The transplant-free survival rates at 3, 5, and 8 years after CRT implantation were 85%, 79%, and 73%. In patients with tetralogy of Fallot treated with CRT consistent improvement in QRS duration, left ventricular ejection fraction, New York Heart Association functional class, and reasonable long-term survival were observed. The findings from this multicenter study support the consideration of CRT in this unique population.

Pectoral muscle mass is not a robust prognostic factor for survival after left ventricular assist device (LVAD) implantation

BackgroundLeft ventricular assist devices (LVAD) are an established treatment for end-stage left ventricular heart failure. Parameters are needed to identify the most appropriate patients for LVADs. This study aimed to evaluate pectoral muscle mass and density as prognostic parameters.MethodsThis single-center study included all patients with LVAD implantation between January 2010 and October 2017 and a preoperative chest CT scan. Pectoral muscle mass was assessed using the Pectoralis Muscle Index (PMI, surface area indexed to height, cm2/m2) and pectoral muscle density by Hounsfield Units (HU). Overall mortality was analyzed with Kaplan–Meier survival analysis and 1-year and 3-year mortality with receiver operating characteristic (ROC) curves and Cox regression models.Results57 patients (89.5% male, mean age 57.8 years) were included. 64.9% of patients had end-stage left ventricular failure due to ischemic heart disease and 35.1% due to dilated cardiomyopathy. 49.2% of patients had preoperative INTERMACS profile of 1 or 2 and 33.3% received mechanical circulatory support prior to LVAD implantation. Total mean PMI was 4.7 cm2/m2 (± 1.6), overall HU of the major pectoral muscle was 39.0 (± 14.9) and of the minor pectoral muscle 37.1 (± 16.6). Mean follow-up was 2.8 years (± 0.2). Mortality rates were 37.5% at 1 year and 48.0% at 3 years. Neither PMI nor HU were significantly associated with overall mortality at 1-year or 3-year.ConclusionsThe results of our study do not confirm the association between higher pectoral muscle mass and better survival after LVAD implantation previously described in the literature.