Cardiac Components Research Articles

Photoplethysmographic imaging and analysis of pulsatile pressure wave in palmar artery at 10 wavelengths.

As a noncontact method, imaging photoplethysmography (iPPG) may provide a powerful tool to measure pulsatile pressure wave (PPW) in superficial arteries and extract biomarkers for monitoring of artery wall stiffness. We intend to develop a approach for extraction of the very weak cardiac component from iPPG data by identifying locations of strong PPW signals with optimized illumination wavelength and determining pulse wave velocity (PWV). Monochromatic in vivo iPPG datasets have been acquired from left hands to investigate various algorithms for retrieval of PPW signals, distribution maps and waveforms, and their dependence on arterial location and wavelength. A robust algorithm of pixelated independent component analysis (pICA) has been developed and combined with spatiotemporal filtering to retrieve PPW signals. Spatial distributions of PPW signals have been mapped in 10 wavelength bands from 445 to 940nm and waveforms were analyzed at multiple locations near the palmar artery tree. At the wavelength of 850nm selected for timing analysis, we determined PWV values from 12 healthy volunteers in a range of 0.5 to 5.8m/s across the hand region from wrist to midpalm and fingertip. These results demonstrate the potentials of the iPPG method based on pICA algorithm for translation into a monitoring tool to characterize wall stiffness of superficial artery by rapid and noncontact measurement of PWV and other biomarkers within 10s.

Abstract 13200: Loss of Cardiomyocyte β2 Spectrin Promotes Cardiac Dyad Dysfunction and Accelerated Heart Failure

Background: The cardiac dyad and associated calcium (Ca 2+ ) release units (CRUs) are integral for cardiac excitation-contraction (E-C) coupling. The cardiac dyad is a multicomponent complex composed of the transverse-tubules, junctional sarcoplasmic reticulum (jSR), and CRU-associated proteins. Proper E-C coupling requires Ca 2+ influx via long-lasting-L-type Ca 2+ channels (Cav1.2), which triggers Ca 2+ release from adjacent ryanodine receptor 2 (RyR2) located in jSR. βII-spectrin loss alters RyR2 localization, but its contribution to cardiac dyad organization and E-C coupling remains unclear. Hypothesis: We hypothesized that βII-spectrin is required for cardiac dyad organization and proper cardiomyocyte calcium signaling. Methods: Cardiomyocyte-specific βII-spectrin knockout (βII-cKO) and control mice (βII-flox) were generated and harvested for immunoblotting, qRT-PCR, and imaging by transmission electron microscopy (TEM). Mice hearts were also interrogated by echocardiography following transaortic constriction. Results: Cardiac dyad structure and CRU components are significantly altered in βII-cKO hearts. Ultrastructural analysis of βII-cKOhearts by TEM showed fragmented cardiac dyads, dilated jSR and reduced jSR contact with T-tubules. Quantitative RT-PCR showed increased expression of calsequestrin 1 and 2, decreased phospholambam, Ncx and Cacna1c (major Cav1.2 subunit), while Ryr2 , Jph2 , Serca2a are unchanged. Protein expression of NCX was decreased, while expression of CAV1.2, RYR2, CASQ2, and SERCA2A remained unchanged. Furthermore, pressure-induced overload of βII-cKO hearts promoted accelerated heart failure (HF). Conclusions: This is the first demonstration that the βII-spectrin cytoskeletal protein is critically important for maintaining the structural integrity of the cardiac dyad. βII-spectrin loss and the resulting alterations in CRU structure, genes, and protein composition promoting accelerated HF.

Hippo-Yap Signaling Maintains Sinoatrial Node Homeostasis.

The sinoatrial node (SAN) functions as the pacemaker of the heart, initiating rhythmic heartbeats. Despite its importance, the SAN is one of the most poorly understood cardiac entities because of its small size and complex composition and function. The Hippo signaling pathway is a molecular signaling pathway fundamental to heart development and regeneration. Although abnormalities of the Hippo pathway are associated with cardiac arrhythmias in human patients, the role of this pathway in the SAN is unknown. We investigated key regulators of the Hippo pathway in SAN pacemaker cells by conditionally inactivating the Hippo signaling kinases Lats1 and Lats2 using the tamoxifen-inducible, cardiac conduction system-specific Cre driver Hcn4CreERT2 with Lats1 and Lats2 conditional knockout alleles. In addition, the Hippo-signaling effectors Yap and Taz were conditionally inactivated in the SAN. To determine the function of Hippo signaling in the SAN and other cardiac conduction system components, we conducted a series of physiological and molecular experiments, including telemetry ECG recording, echocardiography, Masson Trichrome staining, calcium imaging, immunostaining, RNAscope, cleavage under targets and tagmentation sequencing using antibodies against Yap1 or H3K4me3, quantitative real-time polymerase chain reaction, and Western blotting. We also performed comprehensive bioinformatics analyses of various datasets. We found that Lats1/2 inactivation caused severe sinus node dysfunction. Compared with the controls, Lats1/2 conditional knockout mutants exhibited dysregulated calcium handling and increased fibrosis in the SAN, indicating that Lats1/2 function through both cell-autonomous and non-cell-autonomous mechanisms. It is notable that the Lats1/2 conditional knockout phenotype was rescued by genetic deletion of Yap and Taz in the cardiac conduction system. These rescued mice had normal sinus rhythm and reduced fibrosis of the SAN, indicating that Lats1/2 function through Yap and Taz. Cleavage Under Targets and Tagmentation sequencing data showed that Yap potentially regulates genes critical for calcium homeostasis such as Ryr2 and genes encoding paracrine factors important in intercellular communication and fibrosis induction such as Tgfb1 and Tgfb3. Consistent with this, Lats1/2 conditional knockout mutants had decreased Ryr2 expression and increased Tgfb1 and Tgfb3 expression compared with control mice. We reveal, for the first time to our knowledge, that the canonical Hippo-Yap pathway plays a pivotal role in maintaining SAN homeostasis.

Retrospective Analysis of the Treatment of Patients with Pain in Osteochondrosis of the Thoracic Spine

Summary. The purpose of this study was to identify signs of cardiac component in the development of chronic pain in osteochondrosis of the thoracic spine.
 Materials and Methods. Case histories of 434 patients with osteochondrosis of the thoracic spine who underwent examination and treatment in the SI “Institute of Traumatology and Orthopedics of NAMS of Ukraine” were retrospectively studied. Among them were 207 males and 227 females. The materials of inpatient and outpatient medical histories and consultative conclusions were processed. The place of residence, lifestyle of patients, the presence of concomitant pathology, duration of the disease, and the frequency of exacerbations per year were analyzed. Risk factors and complaints of patients with a careful emphasis on the nature of the pain syndrome were studied. The results of treatment were evaluated.
 Results. Males (47.7±2.4%) and females (52.3±2.3%) of working age (89.0%) suffered from thoracic osteochondrosis almost equally. The vast majority lived in cities (88.2%). Isolated thoracic osteochondrosis (43.3±0.3%) with the duration of the disease up to 1 year (72.3%) and the frequency of exacerbations once a year (54.4%) was the most common according to localization. The pain was mainly aching in nature with irradiation to the right half of the chest and right upper extremity (88.5%). The dependence of the pain syndrome on changes in body position and duration over time from one hour to several days was observed (92.1%). Risk factors for the development of the disease include hypodynamia (10.4%), obesity (5.5%), other comorbidities (4.6%), as well as genetic predisposition and bad habits (4.1% and 3%, respectively). In 90.0% of cases, the patients received drug treatment – nonsteroidal anti-inflammatory drugs (NSAIDs) and analgesics. 10.0% were treated with physiotherapy (52.7%), massage (97.2%), and therapeutic gymnastics (91.7%). 63.2% of patients were treated using a combination of medical and non-medical methods. According to the outcomes of treatment, a positive effect was noted in 87.5% of patients.
 Conclusions. Careful analysis of the negative outcomes indicates the presence in this category of patients probable concomitant cardiac pathology, which requires further study and examination.

Blind source separation of inspiration and expiration in respiratory sEMG signals

Objective. Surface electromyography (sEMG) is a noninvasive option for monitoring respiratory effort in ventilated patients. However, respiratory sEMG signals are affected by crosstalk and cardiac activity. This work addresses the blind source separation (BSS) of inspiratory and expiratory electrical activity in single- or two-channel recordings. The main contribution of the presented methodology is its applicability to the addressed muscles and the number of available channels. Approach. We propose a two-step procedure consisting of a single-channel cardiac artifact removal algorithm, followed by a single- or multi-channel BSS stage. First, cardiac components are removed in the wavelet domain. Subsequently, a nonnegative matrix factorization (NMF) algorithm is applied to the envelopes of the resulting wavelet bands. The NMF is initialized based on simultaneous standard pneumatic measurements of the ventilated patient. Main results. The proposed estimation scheme is applied to twelve clinical datasets and simulated sEMG signals of the respiratory system. The results on the clinical datasets are validated based on expert annotations using invasive pneumatic measurements. In the simulation, three measures evaluate the separation success: The distortion and the correlation to the known ground truth and the inspiratory-to-expiratory signal power ratio. We find an improvement across all SNRs, recruitment patterns, and channel configurations. Moreover, our results indicate that the initialization strategy replaces the manual matching of sources after the BSS. Significance. The proposed separation algorithm facilitates the interpretation of respiratory sEMG signals. In crosstalk affected measurements, the developed method may help clinicians distinguish between inspiratory effort and other muscle activities using only noninvasive measurements.

Central modulation of cardiac baroreflex moment-to-moment sensitivity during treadmill exercise in conscious cats.

It remains undetermined whether the cardiac component of the entire arterial baroreflex is blunted even at the onset of low‐intensity exercise. We sought to examine the moment‐to‐moment sensitivity of the cardiac baroreflex during walking at different speeds and the presumed mechanisms responsible for baroreflex modulation in conscious cats. Arterial baroreflex sensitivity for heart rate was estimated from the baroreflex ratio between changes in systolic arterial blood pressure and heart rate and from the slope of the baroreflex curve between the cardiovascular responses to brief occlusion of the abdominal aorta. Treadmill walking was performed for 1 min at three levels of speed (low: 20–30 m/min, moderate: 40 m/min, and high: 50–60 m/min) or for 3 min at the stepwise change of speed (low to high to low transition). Cardiac baroreflex sensitivity was blunted at the onset of walking, irrespective of speed. Thereafter, the blunted cardiac baroreflex sensitivity was restored around 15 s of walking at any speed, while the blunting occurred again at 45 s of high‐speed walking. The inhibition of cardiac baroreflex sensitivity also occurred (1) during the speed transition from low to high and (2) at 45 s of high‐speed exercise of the stepwise exercise. The blunted cardiac baroreflex sensitivity was restored immediately to the resting level during the speed transition from high to low, despite sustained pressor and tachycardiac responses. Therefore, moment‐to‐moment modulation of the cardiac baroreflex during exercise would occur in association with motor intention (i.e., exercise onset) and effort (i.e., treadmill speed).

Integrin α11β1 and syndecan-4 dual receptor ablation attenuate cardiac hypertrophy in the pressure overloaded heart.

Pathological myocardial hypertrophy in response to an increase in left ventricular (LV) afterload may ultimately lead to heart failure. Cell surface receptors bridge the interface between the cell and the extracellular matrix (ECM) in cardiac myocytes and cardiac fibroblasts and have been suggested to be important mediators of pathological myocardial hypertrophy. We identify for the first time that integrin α11 (α11) is preferentially upregulated among integrin β1 heterodimer-forming α-subunits in response to increased afterload induced by aortic banding (AB) in wild-type (WT) mice. Mice were anesthetized in a chamber with 4% isoflurane and 95% oxygen before being intubated and ventilated with 2.5% isoflurane and 97% oxygen. For pre- and postoperative analgesia, animals were administered 0.02-mL buprenorphine (0.3 mg/mL) subcutaneously. Surprisingly, mice lacking α11 develop myocardial hypertrophy following AB comparable to WT. In the mice lacking α11, we further show a compensatory increase in the expression of another mechanoreceptor, syndecan-4, following AB compared with WT AB mice, indicating that syndecan-4 compensated for lack of α11. Intriguingly, mice lacking mechanoreceptors α11 and syndecan-4 show ablated myocardial hypertrophy following AB compared with WT mice. Expression of the main cardiac collagen isoforms col1a2 and col3a1 was significantly reduced in AB mice lacking mechanoreceptors α11 and syndecan-4 compared with WT AB.NEW & NOTEWORTHY Despite their putative importance in stress sensing, the specific integrin α-subunit(s) involved in cardiac hypertrophy has not been identified. Here, we show that α11 and syndecan-4 are critical and interdependent mediators of the hypertrophic response to increased LV afterload. We demonstrate in cells lacking both receptors an interdependent reduction in cell attachment to the major cardiac extracellular matrix components, suggesting that their interplay represents an important mechanism for stress sensing in cardiac cells.

Telerehabilitation In Monitoring Treatment of Heart Disease Patients: Literature Review

Aims: Heart disease is a chronic disease that affects the patient's physical and psychological adaptation. Currently, cardiac rehabilitation focuses on delivering rehabilitation components remotely using technology via telerehabilitation. Objective: The purpose of this review is to identify the use of telerehabilitation in monitoring signs and symptoms of heart disease. Methods: Literature review method with four databases PubMed, Proquest, Ebsco, Cochrane Library, Taylor & Francis database, and identification of gray literature, spanning 2011-2021, and 24 articles were reviewed. Results: The results of the review show that cardiac rehabilitation components are provided through various tele media mobile phones, messenger applications (SMS, QQ, and WeChat), videoconferencing, online information (websites, emails), e-visit, and virtual reality (VR). Telerehabilitation is useful in monitoring exercise capacity, resting systolic blood pressure, blood pressure control, ECG monitoring media, monitoring of dysrhythmias (atrial fibrillation/AF), complaints of fatigue, monitoring of dyspnoea symptoms, hemoglobin and electrolyte levels. sodium and potassium), and depressive symptoms. Conclusions: Telerehabilitation can be an alternative for continuous care of patients in monitoring signs and symptoms of heart disease, both physical and psychological aspects.

Spatial distribution and network morphology of epicardial, endocardial, interstitial, and Purkinje cell-associated elastin fibers in porcine left ventricle.

Cardiac extracellular matrices (ECM) play crucial functional roles in cardiac biomechanics. Previous studies have mainly focused on collagen, the major structural ECM in heart wall. The role of elastin in cardiac mechanics, however, is poorly understood. In this study, we investigated the spatial distribution and microstructural morphologies of cardiac elastin in porcine left ventricles. We demonstrated that the epicardial elastin network had location- and depth-dependency, and the overall epicardial elastin fiber mapping showed certain correlation with the helical heart muscle fiber architecture. When compared to the epicardial layer, the endocardial layer was thicker and has a higher elastin-collagen ratio and a denser elastin fiber network; moreover, the endocardial elastin fibers were finer and more wavy than the epicardial elastin fibers, all suggesting various interface mechanics. The myocardial interstitial elastin fibers co-exist with the perimysial collagen to bind the cardiomyocyte bundles; some of the interstitial elastin fibers showed a locally aligned, hinge-like structure to connect the adjacent cardiomyocyte bundles. This collagen-elastin combination reflects an optimal design in which the collagen provides mechanical strength and elastin fibers facilitate recoiling during systole. Moreover, cardiac elastin fibers, along with collagen network, closely associated with the Purkinje cells, indicating that this ECM association could be essential in organizing cardiac Purkinje cells into “fibrous” and “branching” morphologies and serving as a protective feature when Purkinje fibers experience large deformations in vivo. In short, our observations provide a structural basis for future in-depth biomechanical investigations and biomimicking of this long-overlooked cardiac ECM component.

Evaluation of vasomotor dysfunction with a reduction of disease activity in patients with rheumatoid arthritis: a prospective study

Introduction. Endothelial dysfunction (ED) makes a significant contribution to the pathogenesis of rheumatoid arthritis (RA). However, changes of vasomotor function (VF) in patients with a reduction in disease activity have not been studied enough. Objective – to study VF changes in patients with RA and a reduce in disease activity, to clarify the role of RA serological profile and the presence of arterial hypertension (AH) in the formation of vasomotor dysfunction.Materials and methods. A total of 94 patients took part in the study (74 – the study group, 20 – the comparison group). The longitudinal study included 48 patients with 10 days interval between visits. RA activity reduced after prescribed anti-inflammatory therapy. All patients underwent laser Doppler flowmetry with functional tests (FT) to study VF. Also, the intensity of oxidative phosphorylation (IOP), levels of rheumatoid factor, antibodies to cyclic citrullinated peptide (ACCP) and antinuclear factor titer were assessed.Results. Correlations of ACCP with endothelial (EС), neurogenic (NС) and cardiac (CC) components of the amplitude-frequency spectrum were revealed. With a decrease in RA activity, an increase in CC and a decrease in the total tone of resistive vessels (TTRV) were observed. There was a tendency to improve the parameters of post-occlusive hyperemia (not statistically significant). The duration and area of the reaction after acetylcholine iontophoresis increased and IOP decreased. The presence of AH reduced EС and NС, worsened post-occlusive hyperemia, and was associated with the presence of factors for RA unfavourable course.Conclusion. The RA activity, the level of ACCP and the presence of AH make a significant contribution to the vasomotor dysfunction. At the same time, AH can be considered as a surrogate marker of an unfavourable course of RA. Endothelium-dependent regulation of blood flow, measured in FT, and IOP are closely related to disease activity. The reduce of RA activity was accompanied by a decrease in TTRV, confirming the leading role of the vasoconstriction in formation the ED pattern, the severity of ED will predominantly depend on the activity of the disease.

Review of Mechanisms and Treatment of Cancer-Induced Cardiac Cachexia.

Cancer cachexia is a multifactorial, paraneoplastic syndrome that impacts roughly half of all cancer patients. It can negatively impact patient quality of life and prognosis by causing physical impairment, reducing chemotherapy tolerance, and precluding them as surgical candidates. While there is substantial research on cancer-induced skeletal muscle cachexia, there are comparatively fewer studies and therapies regarding cardiac cachexia in the setting of malignancy. A literature review was performed using the PubMed database to identify original articles pertaining to cancer-induced cardiac cachexia, including its mechanisms and potential therapeutic modalities. Seventy studies were identified by two independent reviewers based on inclusion and exclusion criteria. While there are multiple studies addressing the pathophysiology of cardiac-induced cancer cachexia, there are no studies evaluating therapeutic options in the clinical setting. Many treatment modalities including nutrition, heart failure medication, cancer drugs, exercise, and gene therapy have been explored in in vitro and mice models with varying degrees of success. While these may be beneficial in cancer patients, further prospective studies specifically focusing on the assessment and treatment of the cardiac component of cachexia are needed.

Asymmetrical Septal Hypertrophy: A Rare Case of Respiratory Distress in an Infant of a Diabetic Mother

Cardiomyopathy is a disease that affects the myocardium and causes mechanical or electric dysfunction. Hypertrophic cardiomyopathy comprises various cardiac components such as thickening of ventricular walls, hypertrophy of interventricular septum thereby resulting in subaortic stenosis, systolic and/or diastolic dysfunction. This cardiac complication is a known but rare entity in infants of diabetic mothers wherein the clinical presentation ranges from being asymptomatic to respiratory distress to congestive cardiac failure. Incidence of Congenital Heart Disease in infants of Diabetic Mothers is 5% and the percentage of symptomatic HOCM babies is 12%. Here, we report a term neonate, born to a G2P2L2 mother with Gestational Diabetes Mellitus with poor glycemic control, presenting with respiratory distress manifesting as silent tachypnea at 24 hours of life, diagnosed as Asymmetrical Septal Hypertrophy on 2D-Echo, treated successfully with Propranolol and showed resolution of hypertrophy in follow-up echocardiography. In this condition, foetal hyperinsulinemia is responsible for an increase in synthesis and deposition of fat and glycogen in the myocardial cells which explains the cardiac hypertrophy. Due to increase in the thickness of the Interventricular Septum, there is Left Ventricular Hypertrophy and during systole, the systolic anterior motion of the anterior leaflet (SAM) of the aortic valve is elongated. Therefore, due to this obstruction of the orifice by the aortic valve, there is reversal of blood flow clinically manifesting as Silent Tachypnea. Symptomatic babies are treated with Oral Propranolol which acts by improving left ventricular outflow obstruction.

First experimental exploration of real-time cardiorespiratory motion management for future stereotactic arrhythmia radioablation treatments on the MR-linac

Objective. Stereotactic arrhythmia radioablation (STAR) is a novel, non-invasive treatment for refractory ventricular tachycardia (VT). The VT isthmus is subject to both respiratory and cardiac motion. Rapid cardiac motion presents a unique challenge. In this study, we provide first experimental evidence for real-time cardiorespiratory motion-mitigated MRI-guided STAR on the 1.5 T Unity MR-linac (Elekta AB, Stockholm, Sweden) aimed at simultaneously compensating cardiac and respiratory motions. Approach. A real-time cardiorespiratory motion-mitigated radiotherapy workflow was developed on the Unity MR-linac in research mode. A 15-beam intensity-modulated radiation therapy treatment plan (1 × 25 Gy) was created in Monaco v.5.40.01 (Elekta AB) for the Quasar MRI4D phantom (ModusQA, London, ON). A film dosimetry insert was moved by combining either artificial (cos4, 70 bpm, 10 mm peak-to-peak) or subject-derived (59 average bpm, 15.3 mm peak-to-peak) cardiac motion with respiratory (sin, 12 bpm, 20 mm peak-to-peak) motion. A balanced 2D cine MRI sequence (13 Hz, field-of-view = 400 × 207 mm2, resolution = 3 × 3 × 15 mm3) was developed to estimate cardiorespiratory motion. Cardiorespiratory motion was estimated by rigid registration and then deconvoluted into cardiac and respiratory components. For beam gating, the cardiac component was used, whereas the respiratory component was used for MLC-tracking. In-silico dose accumulation experiments were performed on three patient data sets to simulate the dosimetric effect of cardiac motion on VT targets. Main results. Experimentally, a duty cycle of 57% was achieved when simultaneously applying respiratory MLC-tracking and cardiac gating. Using film, excellent agreement was observed compared to a static reference delivery, resulting in a 1%/1 mm gamma pass rate of 99%. The end-to-end gating latency was 126 ms on the Unity MR-linac. Simulations showed that cardiac motion decreased the target's D98% dose between 0.1 and 1.3 Gy, with gating providing effective mitigation. Significance. Real-time MRI-guided cardiorespiratory motion management greatly reduces motion-induced dosimetric uncertainty and warrants further research and development for potential future use in STAR.

Deciphering Cell-Type-Specific Gene Expression Signatures of Cardiac Diseases Through Reconstruction of Bulk Transcriptomes.

Cardiac diseases compose a fatal disease category worldwide. Over the past decade, high-throughput transcriptome sequencing of bulk heart tissues has widened our understanding of the onset and progression of cardiac diseases. The recent rise of single-cell RNA sequencing (scRNA-seq) technology further enables deep explorations of their molecular mechanisms in a cell-type-specific manner. However, due to technical difficulties in performing scRNA-seq on heart tissues, there are still few scRNA-seq studies on cardiac diseases. In this study, we demonstrate that an effective alternative could be cell-type-specific computational reconstruction of bulk transcriptomes. An integrative bulk transcriptome dataset covering 110 samples from 12 studies was first constructed by re-analysis of raw sequencing data derived from the heart tissues of four common cardiac disease mouse models (myocardial infarction, dilated cardiomyopathy, hypertrophic cardiomyopathy, and arrhythmogenic right ventricular cardiomyopathy). Based on the single-cell reference covering four major cardiac component cell types and 22 immune cell subtypes, for each sample, the bulk transcriptome was reconstructed into cellular compositions and cell-type-specific expression profiles by CIBERSORTx. Variations in the estimated cell composition revealed elevated abundances of fibroblast and monocyte during myocardial infarction, which were further verified by our flow cytometry experiment. Moreover, through cell-type-specific differential gene expression and pathway enrichment analysis, we observed a series of signaling pathways that mapped to specific cell type in diseases, like MAPK and EGFR1 signaling pathways in fibroblasts in myocardial infarction. We also found an increased expression of several secretory proteins in monocytes which may serve as regulatory factors in cardiac fibrosis. Finally, a ligand–receptor analysis identified key cell types which may serve as hubs in cellular communication in cardiac diseases. Our results provide novel clues for the cell-type-specific signatures of cardiac diseases that would promote better understanding of their pathophysiological mechanisms.

Transition of a Community Outreach Program to Virtual Learning during the COVID-19 Pandemic

The COVID-19 pandemic curtailed nearly all in-person educational activities and forced institutions to transition to hybrid or full virtual learning via on-line venues. Our Division of Cardiac Anesthesia has participated in a community outreach initiative through the Youth Scholars Program since 2013. The cardiac anesthesia component has involved an in-person cadaveric dissection of porcine heart and lungs led by faculty anesthesiologists and fellows in adult cardiothoracic anesthesiology.

A systematic review, meta-analysis, and meta-regression of patient education for secondary prevention in patients with coronary heart disease: impact on psychological outcomes.

Patient education is a cardiac rehabilitation core component and is associated with improvements in self-management of patients with coronary heart disease (CHD). However, the efficacy of such interventions on psychosocial outcomes and relative impact of duration is less clear. This study aimed to assess the efficacy of patient education for secondary prevention related to behaviour change and risk factor modification on psychological outcomes in CHD patients. A systematic review and meta-analysis. PsycINFO, CINAHL, Embase, EmCare, MEDLINE, PubMed, and the Cochrane Central Register of Controlled Trials were searched from inception to February 2021. Randomized controlled trials (RCTs) evaluating patient education in CHD patients, or following myocardial infarction, or revascularization compared with usual care were identified. Outcomes included depression and anxiety at <6 and 6-12 months of follow-up. A total of 39 RCTs and 8748 participants were included. Patient education significantly improved participants' depressive symptoms at <6 (SMD -0.82) and 6-12 months (SMD -0.38) of follow-up and anxiety level at <6 (SMD -0.90), and 6-12 months (SMD -0.32) of follow-up. Patient education also reduced the risk for having clinical depression by 35% and anxiety by 60%. Longer patient education of ≥3 months, resulted in more improvement in depressive symptoms at 6-12 months (coefficient -0.210) compared to shorter duration. Patient education for secondary prevention reduces anxiety and depressive symptoms in CHD patients. Regardless of intensity, longer patient education improves depression more than short duration. More information is needed on the relative impact of other intervention components. PROSPERO (CRD42020200504).

Stroke Volume Estimation from Respiratory Inductive Plethysmography: Double Empirical Decomposition

In this study, we have developed a “double-empirical mode decomposition algorithm” to estimate cardiac stroke volume from respiratory inductive plethysmography (RIP) signals. The algorithm consists of first an ensemble empirical mode decomposition (EEMD) to extract the cardiorespiratory components. Then, it is followed by an empirical mode decomposition (EMD) to extract only the cardiac components. This double approach permits (a) solving problems of mixing between cardiac and respiratory components (mode and scale mixing), (b) cardiogenic oscillations extraction in the respiratory inductive plethysmography signal, and (c) subsequent estimation of stroke volume. The algorithm is applied to simulated and real RIP signals. The simulated signals are generated by a cardiorespiratory model previously published by the authors. The real signals are measured via a developed inductive vest. In the real case, the values of estimated stroke volumes are compared to the values obtained by thoracocardiographic filter-based method. In the simulated case, the values are compared to the simulated cardiac activity. The results of comparison through Bland and Altman indicate an error lying in the range ±10%. In contrast to thoracocardiography, the proposed method consists of a promising tool for continuous noninvasive adaptive cardiac monitoring that does not need adjusting parameters or cut-off based on ECG. Also, in comparison to echocardiography and impedance-based methods, it does not necessitate the presence of an expert and is not too sensitive to current penetration.

Recapitulating human cardio-pulmonary co-development using simultaneous multilineage differentiation of pluripotent stem cells.

The extensive crosstalk between the developing heart and lung is critical to their proper morphogenesis and maturation. However, there remains a lack of models that investigate the critical cardio-pulmonary mutual interaction during human embryogenesis. Here, we reported a novel stepwise strategy for directing the simultaneous induction of both mesoderm-derived cardiac and endoderm-derived lung epithelial lineages within a single differentiation of human-induced pluripotent stem cells (hiPSCs) via temporal specific tuning of WNT and nodal signaling in the absence of exogenous growth factors. Using 3D suspension culture, we established concentric cardio-pulmonary micro-Tissues (μTs), and expedited alveolar maturation in the presence of cardiac accompaniment. Upon withdrawal of WNT agonist, the cardiac and pulmonary components within each dual-lineage μT effectively segregated from each other with concurrent initiation of cardiac contraction. We expect that our multilineage differentiation model will offer an experimentally tractable system for investigating human cardio-pulmonary interaction and tissue boundary formation during embryogenesis.

Helicopter Emergency Medical Services Performed Extended Focused Assessment With Sonography: Training, Workflow, and Sustainable Quality

The extended focused assessment of trauma (EFAST) examination is an invaluable tool for the initial evaluation of the trauma patient. Miniaturization of ultrasound has enabled helicopter emergency medical services (HEMS) to use point-of-care ultrasound to care for trauma patients on scene. Our study demonstrated that HEMS crews accurately performed EFAST examinations after the implementation of a novel HEMS EFAST workflow, multifaceted training, and ongoing quality assurance. The HEMS crews’ overall sensitivity was 53%, and specificity was 98%. The obtained image quality was highest for the lung, cardiac, and right upper quadrant components of the EFAST. Our results suggest that with a structured multifaceted training program, user-friendly workflow, and ongoing quality assurance, HEMS crews can perform EFAST examinations safely and reliably in the field. This would allow HEMS crews to detect life-threatening, time-sensitive conditions such as a pneumothorax, pericardial effusion, and intraperitoneal hemorrhage. HEMS EFAST has the potential to triage certain trauma patients directly to the operating room or newly emerging hybrid suites, bypassing the emergency room and saving crucial time.

Post-exercise Hypotension in Patients With Coronary Artery Disease.

Background: Blood pressure (BP) and hemodynamic changes occurring in the recovery phase after a single bout of exercise have not been extensively studied in coronary artery patients, despite the potential clinical implications of reducing BP through exercise. This study aimed at investigating the hemodynamic and arterial baroreflex mechanisms possibly involved in post-exercise hypotension (PEH) in patients with coronary artery disease.Methods: In 42 normotensive coronary artery patients undergone a Cardiac Rehabilitation Program, we evaluated before and after their daily exercise training session: blood pressure (BP) and heart rate (HR). In a subgroup (n = 29), daily BP profile was also evaluated by ambulatory BP monitoring. In those patients showing PEH (n = 15), we evaluated: Cardiac Output (CO), Stroke Volume (SV), total peripheral resistances (TPR), forearm (FVR) and calf (CVR) vascular resistances, and spontaneous baroreflex sensitivity (BRS).Results: After exercise TPR was significantly reduced with a similar contribution from CVR and FVR, whereas CO and SV significantly increased. BRS showed a significant reduction mainly due to a BRS decrease in response to hypertensive stimuli. Systolic BP (SBP) was significantly reduced for 12 h after the end of a single exercise session.Conclusion: These findings indicate that in coronary artery patients, the recovery phase after exercise is characterized by PEH which is mediated mainly by a generalized peripheral vasodilation and appears to influence BP behavior throughout the daily life. Finally, the cardiac component of the arterial baroreflex seems to contribute indirectly to BP reduction occurring after exercise.