China
Africa
Explore chapters and articles related to this topic
Cardiac Hypertrophy, Heart Failure and Cardiomyopathy
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Restrictive ventricular physiology can also be caused by endocardial pathology (fibrosis, fibroelastosis and thrombosis) that impairs diastolic function (seeTable 5.7). These disorders can be subclassified according to the presence of eosinophilia into endomyocardial diseases with hypereosinophilia [now grouped under hypereosinophilic syndromes (HES)] and endomyocardial disease without hypereosinophilia (e.g. endomyocardial fibrosis (EMF). Parasitic infection, drugs such as methysergide, and inflammatory and nutritional factors have been implicated in acquired forms of EMF.
Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Hypertrophic cardiomyopathy often causes death in younger athletes. It can cause unexplained syncope and never be diagnosed during life. Symptoms between ages 20 and 40 are usually due to exertion but can be varied. They include chest pain that usually resembles typical angina, dyspnea, palpitations, and syncope. Systolic function is adequate, so fatigue is uncommon. Most symptoms come from abnormal diastolic function. Syncope may occur after exertion due to either worsening outflow obstruction with increased contractility, or due to atrial or ventricular arrhythmias. Syncope indicates a higher risk of sudden death. The BP and heart rate are often normal. Increased venous pressure seldom causes any manifestations. With the obstructive type of hypertrophic cardiomyopathy, there is an audible systolic ejection-type murmur that does not radiate out to the neck. It is most easily heard at the left sternal edge, in the third or fourth intercostal space. At the apex, a mitral regurgitation murmur may be heard, because of distortion of the mitral apparatus. The LV outflow ejection murmur may be increased by a Valsalva maneuver. This reduces venous return as well as LV diastolic volume.
Pressure–Volume Loop of the Left Ventricle
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Normal diastolic function of the ventricle is dependent on ventricular diastolic compliance, distensibility and relaxation. Extrinsic and intrinsic factors affect ventricular diastolic function. Examination of the ventricular diastolic pressure–volume diagrams can differentiate the diastolic dysfunction caused by altered ventricular compliance, distensibility and relaxation (Figure 26.8).
Echocardiographic findings in subjects with an amyloidogenic apolipoprotein A1 pathogenic variant
Published in Amyloid, 2023
Daniela Tomasoni, Alberto Aimo, Marianna Adamo, Matilde Nardi, Carlo Mario Lombardi, Valentina Regazzoni, Maria Grazia De Angelis, Iacopo Fabiani, Giampaolo Merlini, Roberta Mussinelli, Laura Obici, Giorgia Panichella, Giuseppe Vergaro, Claudio Passino, Francesco Scolari, Stefano Perlini, Michele Emdin, Marco Metra
As reported in Table 1, median LV ejection fraction (LVEF) was 60% (55–66), and only 2% of patients had LVEF <50%. Diastolic function was generally preserved, with a median E/e’ ratio of 7 (6–10). A minority of subjects (2%) displayed a restrictive filling pattern. Overall, patients did not show a prominent LV hypertrophy, with a median interventricular septal thickness of 11 mm (9–12), a posterior wall thickness of 9 mm (8–11), and a LV mass index of 92 g/m2 (74–111). GLS (−19% [−21 to −17]), and the mass to strain ratio (10.0 [6.8–12.1]) were within normal limits. A ‘granular sparkling’ appearance of the interventricular septum (19%) was the most frequent echocardiographic red flag of CA, followed by pericardial effusion (11%), apical sparing pattern (10%) and thickened atrioventricular valves (8%) (Figure 1). Right ventricular (RV) function was preserved, with a borderline RV free wall thickness (6 mm [5–8]).
Sex-specific cardiac and vascular responses to hypertension in Chinese populations without overt cardiovascular diseases
Published in Postgraduate Medicine, 2021
Zhiming Li, Jingguang Liu, Jian Shen, Yumin Chen, Lizhen He, Menghao Li, Xiongwei Xie
Prior studies have shown that the effects of BP lowering on cardiac structure and function might vary by the type of antihypertensive medications. For example, a meta-analysis of randomized comparative studies showed that among the commonly used antihypertensive medications, renin-angiotensin system inhibitor (RASi) had the greatest effect on improving LVH while beta-blocker had the least efficacy [40]. Notably, in the current study, two thirds of patients in both groups were treated with RASi and calcium channel blocker, respectively. In addition, the use of beta-blocker, which might reduce e’ and thus resulting in E/e’ ratio, were also comparable between women and men. Interestingly and importantly, one randomized control trial has shown that among hypertensive patients with coexistent diastolic dysfunction, after 38 weeks’ treatment, BP lowering was associated with diastolic function improvement irrespective of the type of antihypertensive medications [41]. In the current study, systolic, and diastolic BP levels were also comparable by sex. These findings collectively indicate a sex-specific cardiac response to hypertension.
Matrix metalloproteinase-12 cleaved fragment of titin as a predictor of functional capacity in patients with heart failure and preserved ejection fraction
Published in Scandinavian Cardiovascular Journal, 2021
Patricia Palau, Alexander Lynge Reese-Petersen, Eloy Domínguez, Jose María Ramón, Laura López, Anna Mollar, Francisco Javier Chorro, Juan Sanchis, Julio Núñez
Normal myocardial diastolic function describes the capacity of the heart to fill adequately and at normal pressure during diastole. Myocardial diastolic function is determined by processes occurring at the level of the extracellular matrix and the cardiomyocyte sarcomere [15]. Titin is an elastic myofilament protein found in cardiac sarcomere that is the dominant regulator of passive myocardial tension and an essential determinant of diastolic function [1,2]. There are two main isoforms of titin coexpressed in sarcomeres: a shorter, firmer N2B-titin (3.0 MDa) and longer, more elastic N2BA isoform (3.2–3.7 MDa) [15]. Post-transcriptional and translational titin modifications have been postulated to determine cardiomyocyte stiffness found in HFpEF. At the transcriptional level, titin changes from its more elastic isoform N2BA toward its firmer isoform N2B have been postulated to be linked to a higher risk of HFpEF [16]. However, in an in vivo study with 70 ischemic patients, Zile et al. [4] did not find differences in the N2BA/N2B ratio between HFpEF and control patients.