scholarly journals CASE STUDY EXEMPLAR OF DETECTING SEVERE DIASTOLIC DYSFUNCTION USING BALLISTOCARDIOGRAM

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S88-S89
Author(s):  
Laurel A Despins ◽  
Giovanna Guidoboni ◽  
Marjorie Skubic ◽  
Lorenzo Sala ◽  
Moein Enayati ◽  
...  

Abstract The specific aim of this case study was to describe how monitoring ballistocardiogram (BCG) waveforms can detect early heart failure (HF) changes. HF significantly impairs quality of life and is the principal cause for hospital readmissions in older adults. HF prevalence in American adults aged 65 years and older is expected to increase over 70% by 2030. Detecting worsening HF is challenging. Invasive arterial waveforms display blood pressure changes with each heartbeat; BCG waveforms display repetitive body motions resulting from ejection of blood into the great vessels. BCG waveforms change as cardiac function changes. Currently, BCG signals can be captured non-invasively using sensors placed under a bed mattress and provide heart and respiratory rates. We have developed a new way to analyze the BCG waveform using an innovative closed-loop physiological model of the cardiovascular system. The subject, a 94-year old female with hypertension, presented to her physician with symptoms associated with a new diagnosis of acute mixed congestive HF. Mean heart and respiratory rate trends obtained from her bed sensor in the prior two months did not indicate HF. We simulated cardiac cycles using normal cardiac function data, mildly impaired diastolic function data, and the subject’s echocardiography data. The results demonstrated BCG waveform changes that correlated with decreasing cardiac output related to worsening diastolic function. New methods for clinically interpreting BCG waveforms present a significant opportunity for improving early HF detection and improving outcomes. Working on a clinical problem from an engineering perspective merges two disciplines, creating a new methodology.

2017 ◽  
Vol 121 (suppl_1) ◽  
Author(s):  
Adolfo G Mauro ◽  
Donatas Kraskauskas ◽  
Bassem M Mohammed ◽  
Bernard J Fisher ◽  
Eleonora Mezzaroma ◽  
...  

Introduction: L-gulonolactone oxidase (Gulo) is the rate limiting enzyme for Vitamin C (VitC) biosynthesis. Humans rely on dietary VitC for collagen synthesis, extracellular matrix formation, and tissue regeneration. VitC deficiency is an unrecognized condition and its role in cardiac homeostasis and post-acute myocardial infarction (AMI) remodeling is unknown. Hypothesis: Low levels of VitC impair cardiac function and tissue repair following AMI. Methods: Adult male Gulo -/- knockout mice (C57BL6 background, N=8) and control C57BL (N=8), which are able to synthesize VitC were used. VitC deficiency was maintained supplying low levels of VitC (30mg/l) to Gulo -/- mice in drinking water. Mice underwent M-mode and Doppler echocardiography to measure left ventricular (LV) diameters and wall thicknesses, fractional shortening (FS), E and A waves, E/A ratio, isovolumetric relaxation time (IRT) and myocardial performance index (MPI). Experimental AMI was induced by coronary artery ligation for 7 days. An additional group of Gulo -/- were mice supplemented with physiological levels of VitC (330 mg/l) and underwent AMI. Results: VitC deficient Gulo -/- mice exhibited significantly reduced LV wall thicknesses, reduced FS, and impaired diastolic function, measured as significantly reduced E/A ratio and longer IRT (Panel A, B & C). Following AMI, 100% (8/8) of deficient Gulo -/- mice died within 5 days. Supplementation with physiological levels of VitC significantly improved survival after AMI (Panel D). Conclusion: VitC deficiency impairs systolic and diastolic function. Moreover, VitC is critical for the post-AMI survival.


2021 ◽  
Vol 129 (Suppl_1) ◽  
Author(s):  
Monique Williams ◽  
Camila Iansen Irion ◽  
Jose Manuel Condor Capcha ◽  
Guerline Lambert ◽  
Grace Seo ◽  
...  

Background: Hyperlipidemia is a major risk factor for CVD. Patients with HF with preserved ejection fraction (HFpEF) have more myocardial lipid accumulation than patients with reduced EF (HFrEF). RNASeq data from cardiac biopsies showed downregulation of the gene for lipoprotein lipase (LPL) that degrades triglycerides, in HFpEF patients compared to healthy and HFrEF controls. Poloxamer-407 (p407) induces hyperlipidemia by blocking LPL and subsequent increase in plasma triglycerides and low-density lipoprotein (LDL) cholesterol. We hypothesized that mice treated with p407 and cardiac LDL-Receptor (LDLR) over-expression (OE) develop hyperlipidemia, myocardial lipid accumulation, and diastolic dysfunction resulting in HFpEF and arrhythmias. Methods: Baseline cardiac function was assessed by echo for male and female C57Bl6 mice (n=9) for 2 groups: 4wk biweekly i.p. p407-injections with (n=4) or without (n=3) single i.v. injection with AAV9-cTnT-LDLR. Cardiac function was assessed by echocardiography at 3 and 4 wks. Blood Pressure (BP) and Whole Body Plethysmography (WBP) were assessed during wk4. Ttest was used for statistics. PR and ORO staining and telemetry were performed at wk4. Results: At wk3, P407 and LDLR OE led to alterations in diastolic function (increased IVCT, IVRT, MV E/E’, MPI, and NFT) and increased LV wall thickness, p<0.05. At wk4, there was pulmonary hypertension (increased mean pulmonary arterial pressure, decreased pulmonary acceleration time p <.05).Histology showed excessive myocardial lipids and fibrosis, and telemetry showed incidents of second-degree and higher-degree AV block. The group injected solely with p407 show e d alterations in diastolic function (increased IVCT, IVRT, NFT, LVMPI, LVMPI NFT p<.05 ) and decreased EDV, ESV, EDLVM, ESLVM, p<.05 at wk4. All groups had preserved %EF and no abnormalities in BP or WBP. Conclusions: P407 and cardiac LDLR OE induce a drastic decline in cardiac diastolic function over a shorter period of time compared to p407 alone. Diastolic dysfunction was observed in wk3 followed by pulmonary hypertension, arrhythmia, myocardial lipid accumulation and fibrosis in wk4. This new model may allow for more rapid investigations of cardiac abnormalities seen in HFpEF patients.


2021 ◽  
Vol 38 (03) ◽  
pp. 273-279
Author(s):  
Nitin Katariya ◽  
Amit K. Mathur

AbstractBiliary strictures can be a challenging clinical problem to manage and often have unclear etiologies, including benign and malignant causes. Left untreated, these problems can lead to significant morbidity and mortality linked to their underlying diagnosis. The approach to adult patients with biliary strictures requires a multidisciplinary team involving surgeons, interventional endoscopists, and interventional radiologists for diagnosis, symptom relief, palliation, as well as potential curative management. From a surgeon's perspective, there are many ways to classify and approach these strictures. It is of paramount importance to start with an excellent understanding of the patient's prior surgical history. In approaching a patient with a new diagnosis of biliary stricture, it is also critical to understand its etiology relatively quickly, as 70% are malignant in the adult population. Concurrently, one must clearly define the location and extent of the stricture: intrahepatic, hilar, or distal extrahepatic bile duct, as well as whether it is a singular lesion or multifocal phenotypes. This information provides a path forward in clinical decision-making regarding durability and efficacy of therapy, which is typically aimed at decompression and/or surgical resection to prevent cholangitis, sepsis, and progressive hepatic insufficiency.


2018 ◽  
Vol 2 (1) ◽  
Author(s):  
Brent Walker

Readmission penalties on hospitals hit a new high in 2016, increasing by a fifth over 2015 numbers to $528 million. Yet, according to data from the Centers for Medicare & Medicaid Services (CMS), the 30-day readmission rate is on the decline. Since the Hospital Readmission Reduction Program (HRRP) began in 2010, preventable readmissions have dropped by 8% nationally.1 So why will hospitals lose out on more than half a billion dollars in CMS reimbursements next year? Changes in how the rehospitalization rate is calculated influenced the jump in penalties. But that is not the only factor influencing 30-day readmissions. Patient engagement efforts often fall short, too.


2014 ◽  
Vol 63 (12) ◽  
pp. A1081
Author(s):  
Payal Kohli ◽  
Beth Cohen ◽  
Rakesh Mishra ◽  
Mathilda Regan ◽  
Nelson Schiller

2019 ◽  
Vol 29 (10) ◽  
pp. 1264-1267 ◽  
Author(s):  
Muhammad Mohsin ◽  
Saleem Sadqani ◽  
Kamran Younus ◽  
Zahra Hoodbhoy ◽  
Salima Ashiqali ◽  
...  

AbstractObjective:The purpose of this study was to assess fetal cardiac function in normal fetuses (control group) compared to those who are exposed to gestational diabetes mellitus using different echocardiographic measurements, and to explore the application of left atrial shortening fraction in determination of fetal diastolic function with gestational diabetes mellitus.Methods:A total of 50 women with gestational diabetes and 50 women with a healthy pregnancy were included in the study. Fetal echocardiography was performed and structural as well as functional fetal cardiac parameters were measured. Data were compared between with or without fetal myocardial hypertrophy and the control group.Results:In the study group, out of 50 fetuses of gestational diabetic mothers, 18 had myocardial hypertrophy and 32 had normal septal thickness. Gestational age at time of examination did not differ significantly between the control and gestational diabetes group (p = 0.55). Mitral E/A ratio was lower in gestational diabetes group as compared to the control (p < 0.001). Isovolumetric relaxation and contraction times and myocardial performance index were greater in fetuses of gestational diabetic mothers (p < 0.001). In fetuses of gestational diabetic mothers with myocardial hypertrophy, left atrial shortening fraction was lower as compared to those without myocardial hypertrophy and those of the control group (p < 0.001).Conclusions:The results of this study suggest that fetuses of gestational diabetic mothers have altered cardiac function even in the absence of septal hypertrophy, and that left atrial shortening fraction can be used as a reliable alternate parameter in the assessment of fetal diastolic function.


1999 ◽  
Vol 122 (2) ◽  
pp. 109-117 ◽  
Author(s):  
Jack D. Lemmon ◽  
Ajit P. Yoganathan

Aided by advancements in computer speed and modeling techniques, computational modeling of cardiac function has continued to develop over the past twenty years. The goal of the current study was to develop a computational model that provides blood–tissue interaction under physiologic flow conditions, and apply it to a thin-walled model of the left heart. To accomplish this goal, the Immersed Boundary Method was used to study the interaction of the tissue and blood in response to fluid forces and changes in tissue pathophysiology. The fluid mass and momentum conservation equations were solved using Patankar’s Semi-Implicit Method for Pressure Linked Equations (SIMPLE). A left heart model was developed to examine diastolic function, and consisted of the left ventricle, left atrium, and pulmonary flow. The input functions for the model included the pulmonary driving pressure and time-dependent relationship for changes in chamber tissue properties during the simulation. The results obtained from the left heart model were compared to clinically observed diastolic flow conditions for validation. The inflow velocities through the mitral valve corresponded with clinical values (E-wave=74.4 cm/s, A-wave=43 cm/s, and E/A=1.73). The pressure traces for the atrium and ventricle, and the appearance of the ventricular flow fields throughout filling, agreed with those observed in the heart. In addition, the atrial flow fields could be observed in this model and showed the conduit and pump functions that current theory suggests. The ability to examine atrial function in the present model is something not described previously in computational simulations of cardiac function. [S0148-0731(00)01302-9]


1996 ◽  
Vol 85 (5) ◽  
pp. 1063-1075 ◽  
Author(s):  
Stefan G. De Hert ◽  
Inez E. Rodrigus ◽  
Luc R. Haenen ◽  
Peter A. De Mulder ◽  
Thierry C. Gillebert

Background Impairment of left ventricular function after cardiopulmonary bypass (CPB) is well recognized, but little is known about the time course of recovery of cardiac function early after separation from CPB. Therefore, recovery of left ventricular function was evaluated early after separation from CPB in patients undergoing coronary artery surgery. The authors tried to determine whether this recovery might be attributed to autoregulation of function by preload. Methods Left ventricular pressure was measured with fluid-filled catheters. Data were digitally recorded during increased pressure induced by elevating the legs. Transgastric short-axis echocardiographic views of the left ventricle were simultaneously recorded on videotape. Systolic function was evaluated with the slope (Ees, mmHg/ml) of the systolic pressure-volume relation. Diastolic function was evaluated with the chamber stiffness constant (Kc, ml-1) of the diastolic pressure-volume relation. Cardiac function was assessed before CPB, after termination of CPB, and 5, 10, and 15 min later. Two different separation procedures from CPB were compared: in protocol 1, left ventricular function was documented during the standard procedure (n = 24); in protocol 2, the heart was optimally filled 10 min before separation from CPB (n = 12). Results In protocol 1, Ees was 2.88 +/- 0.21 mmHg/ml (mean +/- SEM) and Kc was 0.012 +/- 0.001 ml-1 before CPB. Within 10 min after separation from CPB, Ees increased from 1.10 +/- 0.32 to 2.92 +/- 0.34 (P = 0.001) and Kc decreased from 0.022 +/- 0.002 to 0.011 +/- 0.001 (P = 0.001). The parameters remained stable thereafter. In protocol 2, Ees was 2.92 +/- 0.51 mmHg/ ml and Kc was 0.011 +/- 0.002 ml-1 before CPB. Depression of systolic and diastolic function was not observed in these patients. At time 0, Ees was 2.46 +/- 0.16 and Kc was 0.012 +/- 0.002. These values remained stable throughout the entire observation period. Conclusions Significant functional recovery was observed early after separation from CPB, which was suggestive of time-dependent changes in both systolic and diastolic left ventricular function induced by preload restoration.


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