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The Heartbreak of Wheat-Related Disorders
Published in Stephen T. Sinatra, Mark C. Houston, Nutritional and Integrative Strategies in Cardiovascular Medicine, 2022
The large diversity of inflammatory triggers further addresses the need for a tailored characterization of inflammation enabling differentiation of inflammation and subsequent target-specific strategies.11 As you will see, the potential complications of a WRD are startling. For example, untreated CD children had larger left ventricle end diastolic dimension, reduced left ventricular ejection fraction (<55%), and a higher (>0.6) myocardial performance index as compared to controls. Re-evaluation after one year with good dietary compliance showed changes in isovolumic relaxation time and deceleration time, reflecting improved cardiac diastolic function. GFD-compliant patients had lower myocardial performance index (MPI) than non-compliant patients, reflecting improvement in load-independent echocardiographic parameters.12
Cardiac Damage from Left Ventricular Hypertrophy to Heart Failure
Published in Giuseppe Mancia, Guido Grassi, Konstantinos P. Tsioufis, Anna F. Dominiczak, Enrico Agabiti Rosei, Manual of Hypertension of the European Society of Hypertension, 2019
Enrico Agabiti Rosei, Maria Lorenza Muiesan, Cesare Cuspidi
Myocardial relaxation reflects the time course and extent of cross-bridge dissociation after systolic contraction. The load imposed on the muscle, the rapid reduction of cytosolic calcium to baseline levels and alterations in sensitivity of myofilaments to calcium may profoundly modify myocardial relaxation. Myocardial relaxation alterations may be related to the down-regulation and reductions in protein levels of sarcoplasmic reticulum pumps ATP-dependent, influencing the time course of calcium transient and the frequency-force response. In addition, the increase of beta-myosin ATP-ase activity and the changes in troponin subunit isoform expression and phosphorylation represent other molecular adaptations affecting myocardial relaxation. The increase of isovolumic relaxation time due to a slower and delayed relaxation is frequently observed in hypertensive patients. Invasive techniques with cardiac catheterization and simultaneous pressure and volume measurements represent the gold standard to assess left ventricular diastolic function, with measurement of the rate of left ventricular relaxation, and the rate and timing of diastolic filling as well as myocardial stiffness; however, these techniques are clearly unpractical for routine diagnostic evaluation, which is relevant in the large population of hypertensive patients (80).
Clinical features of mitral stenosis
Published in Neeraj Parakh, Ravi S. Math, Vivek Chaturvedi, Mitral Stenosis, 2018
The A2-OS interval is the time lapsed from the time the aortic valve closes to the opening of the mitral valve. In the cardiac cycle, this represents the isovolumic relaxation time as both the valves are in a closed position during this interval. A2 represents the closure of the aortic valve, which occurs a short time after the crossover of the LV and aortic pressure due to the hang-out interval. The hang-out interval is short on the left side because of the high-impedance characteristics of the systemic circulation as compared to the pulmonary circulation. The LV pressure can be considerably lower than the pressure in the aorta at the time of aortic valve closure if the hang-out interval on the left side is prolonged as in aortic stenosis. The mitral valve opens at the crossover of the LV and LA pressure. Thus, the A2-OS interval does not represent exactly the time taken for the LV pressure, at the LV-aorta pressure crossover, to drop below the LA pressure as A2 occurs a short time after the pressure crosses over due to the hang-out interval. (A2-OS interval = LV-AO pressure crossover to LV-LA pressure crossover time – left-sided hangout interval.)
Triglyceride glucose index reflects the unfavorable changes of left ventricular diastolic functions and structure in uncomplicated newly diagnosed hypertensive patients
Published in Clinical and Experimental Hypertension, 2022
Sara Cetin Sanlialp, Musa Sanlialp, Gokay Nar, Aydan Malcok
The guideline of the American Society of Echocardiography and the European Society of Cardiovascular Imaging (ASE/EACVI) was primarily considered in the evaluation of diastolic function (24). Left atrial (LA) volume was calculated using the area-length method formulated as 0.85 × 4-chamber area × 2-chamber area/common length at ventricular end systole and divided by BSA to get LA volume index (LAVi). In pulsed-wave (PW) Doppler, 1–2 sample volumes were placed between the tips of mitral valve during diastole in the apical 4-chamber imagings to assess the LV inflow velocities described as the peak velocity of early diastolic filling (E wave), the peak velocity of atrial filling (A wave) at end-expiration, and E/A ratio was calculated. Maximal tricuspid regurgitation velocity (TRV) was assessed by continuous wave (CW) Doppler from multiple views because of its variability depending on the angle. E wave deceleration time (EDT) and isovolumic relaxation time (IVRT) were also recorded as another diastolic parameters. Subsequently, the pulse-wave tissue Doppler (TDI) echocardiography was performed and sample volume was placed at the lateral site of the mitral annulus in the apical 4-chamber views. From these imagings, early diastolic velocity (e’) was measured and E/e’ ratio was calculated. At least three consecutive cardiac cycles were examinated for all Doppler ultrasound data and avaraged.
A single exposure to eucalyptus smoke sensitizes rats to the postprandial cardiovascular effects of a high carbohydrate oral load
Published in Inhalation Toxicology, 2020
Brandi L. Martin, Leslie C. Thompson, Yong Ho Kim, Samantha J. Snow, Mette C. Schladweiler, Pamela Phillips, Molly Harmon, Charly King, Judy Richards, Ingrid George, Najwa Haykal-Coates, M. Ian Gilmour, Urmila P. Kodavanti, Mehdi S. Hazari, Aimen K. Farraj
Echocardiography data analyses were also performed while blinded to identities of exposure groups using Vevo® LAB software (FujiFilm VisualSonics Inc., Toronto, Canada). Two beats between breaths from each of the three cine loops were collected. This yielded a total of six beats analyzed per animal. We analyzed data collected via pulsed wave Doppler of transmitral flow for isovolumic contraction time (IVCT), aortic ejection time (AET), and isovolumic relaxation time (IVRT). The Tei index of myocardial performance was calculated with the following equation: (IVCT + IVRT)/AET. Long-axis M-mode loops were used to determine stroke volume (SV), cardiac output (CO), ejection fraction (EF), fractional shortening, end diastolic volume (EDV), and end systolic volume (ESV). SMA loops were used to calculate blood flow, and data were normalized as a percent of CO to compare across subject and experimental groups.
An update on the conquests and perspectives of cardio-oncology in the field of tumor angiogenesis-targeting TKI-based therapy
Published in Expert Opinion on Drug Safety, 2019
Antonio Galvano, Aurelia Guarini, Federica Iacono, Marta Castiglia, Sergio Rizzo, Luigi Tarantini, Stefania Gori, Giuseppina Novo, Viviana Bazan, Antonio Russo
Sunitinib is a small TKI molecule. Its mechanism is based on regulating both tumor cell proliferation and tumor angiogenesis, including VEGFRs1-3, PDGFR, ckit, FMS like Tyrosin Kinase 3(FLT3), CSF receptor. Among these mechanisms, new activities, related to this small molecule, have been discovered. Recently, Huang YX et al., demonstrated that Sunitinib induced downregulation of its targets, such as VEGF, PDGF, and c- Kit in multiple -drug-resistant nasopharyngeal carcinoma cell line CNE2/DDP and Hepatoma cell line HepG2. They also discovered that Sunitinib also induced apoptosis and DNA damage in cell line CNE2/DDP and Hep G2. CNE2/DDP and HepG2 cells sunitinib-treated in coculture experiments were able to improve the activity and cytotoxicity of NK cells. Quantitative polymerase chain reaction results showed that sunitinib upregulated NKG2DLs, apoptotic genes, DNA damage repair genes, and nuclear factor (NF)-κβ family genes [30]. In a report, Takeshi Wada et al. showed that Sunitinib was able to decrease the amplitude of maximum down-stroke velocity of the left ventricular pressure. Moreover, Sunitinib did prolong the isovolumic relaxation time and increased the left ventricular end-diastolic pressure according to dosage without affecting the other cardiohemodynamic and electrophysiological parameters. They also showed that sunitinib significantly elevated cardiac troponin I level for 30–60 min after the high dose without altering the other biomarkers [31].