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Heart Failure/Congestive Heart Failure
Published in Charles Theisler, Adjuvant Medical Care, 2023
In left-sided heart failure, the left ventricle is too weak or stiff to properly circulate blood. As a result, fluid backs up in the pulmonary veins carrying blood away from the lungs back to the heart. The increased pressure forces fluid out of the veins and into the lungs’ air sacs. This causes difficulty breathing (dyspnea) and shortness of breath, especially when lying flat. Shortness of breath is the main symptom of left-sided heart failure.
The Patient with Ischemic Heart Failure
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Konstantinos Aznaouridis, Constantina Masoura, Charalambos Vlachopoulos
Remodeling of the left ventricle is an adaptive structural process secondary to acute or chronic ischemic or non-ischemic insults (i.e., valvular regurgitations). In early stages, remodeling is associated with thinning of the wall and dilation of the ventricle, whereas, in later stages, remodeling is due to irreversible fibrosis and scarring of the myocardium. In general, remodeling due to coronary disease is mostly secondary to necrosis and presence of scar tissue following an acute myocardial infarction. However, even hibernated, predominantly non-necrotic myocardium with minimal scar due to chronic obstructive coronary artery disease may also lead to LV remodeling. From a clinical point of view, it is crucial to identify the patients with predominantly hibernating myocardium, and the patients who have scarred myocardium. In patients with heart failure and hibernated, viable myocardium due to coronary artery disease, it is expected that their symptoms and overall prognoses improve after appropriate revascularization.6–9 On the other hand, patients with heart failure and scarred, non-viable myocardium are mainly treated with heart failure medications and devices (biventricular pacemakers and/or implantable cardioverter defibrillators [ICDs]). Therefore, the presence and the extent of viability is important in the management of patients with ischemic heart failure. Several imaging modalities have been developed to detect hibernated/viable myocardium and are briefly described herein.
Coupling of the Left Ventricle with the Systemic Circulation
Published in Wilmer W Nichols, Michael F O'Rourke, Elazer R Edelman, Charalambos Vlachopoulos, McDonald's Blood Flow in Arteries, 2022
The function of the left ventricle is to pump blood, so that the tissues of the body may be perfused with nutrients according to their need. Whereas blood flow through the tissues is continuous, or nearly so, the heart’s output is intermittent. The arterial system links the left ventricle to the capillary circulation (Figure 12.1) and thus subserves two functions: first, as a low-resistance conduit and second, as a cushion (or buffer) to flow pulsations at its input (O'Rourke, 1982a, 1982b, 2009a; Taylor, 1967, 1969, 1973). Efficiency of the arterial system is apparent in the tiny mean pressure gradient (normally 1.0 to 3.0 mmHg) over a meter or more between central and peripheral arteries (Pauca et al., 1992) and in the relatively small amount of extra energy (normally around 10 percent of total external work) dissipated in the arterial tree on account of flow pulsations (O'Rourke, 1968; Nichols et al., 1977a; Kelly and Fitchett, 1992) (see Chapter 11). However, both conduit and cushioning functions can be affected by disease—the former by narrowing (and atrophy) of small arteries and arterioles (Laragh and Brenner, 1995) and the latter predominantly by stiffening of the aorta and elastic arteries (Chirinos et al., 2019).
Features of Turner syndrome in patients managed at the adult endocrinology clinic, Steve Biko Academic Hospital
Published in Journal of Endocrinology, Metabolism and Diabetes of South Africa, 2023
Cardiovascular disease is a major cause of morbidity and mortality in Turner syndrome patients. It has been shown to reduce their life expectancy by approximately 10 years. The prevalence of cardiac malformations was 23%, and as high as 56% in some studies. The karyotype most involved is 45,X.10,11 The congenital abnormalities described are mostly left heart obstructive lesions. The most common lesions identified were bicuspid aortic valve (12.5–30%), coarctation of the aorta (6.9–11%) and aortic valve disease (3.2%). Frequently acquired cardiac conditions of the left side of the heart include atherosclerotic heart disease, hypertension, left ventricle hypertrophy, left atria hypertrophy and aortic aneurysm with or without aortic rupture.10–12 Aortic dissection may occur at any age. The incidence is increased 100-fold in patients with Turner syndrome. Bicuspid aortic valve is an independent risk factor for aortic aneurysm and rupture.13 Our population had an incidence of cardiovascular disease similar to that reported in other studies with equal distribution between classic Turner syndrome and mosaic Turner syndrome.
Current and emerging pharmacotherapy for the management of hypertrophic cardiomyopathy
Published in Expert Opinion on Pharmacotherapy, 2023
Akiva Rosenzveig, Neil Garg, Shiavax J. Rao, Amreen K. Kanwal, Arjun Kanwal, Wilbert S. Aronow, Matthew W. Martinez
Current pharmacologic management of HCM includes symptomatic and therapeutic approaches to mitigate the myriad of complications caused by HCM. Left ventricular hypertrophy with or without obstruction, dysfunctional myocytes, diastolic and systolic dysfunction, arrhythmias, and ischemia causing dyspnea, chest pain, syncope, and death are some of the clinical features present in HCM patients [12,13]. Current evidence-based clinical practice guidelines suggest the use of nonselective beta blockers as well as cardio-selective agents, such as non-dihydropyridine calcium receptor antagonists and disopyramide [13] for relief of symptoms. However, reducing the pathological effects and adverse outcomes of this disease state requires reversal of the HCM-associated LVOTO present in almost 70% patients [13]. This pathophysiology is correlated with anatomical and functional abnormalities primarily caused by the hypertrophy and hypercontractility of the left ventricle [14]. The LVOTO is defined by continuous wave (CW) Doppler echocardiography with an LVOT pressure gradient over 30 mmHg [13]. LVOTO is a primary driver of disability as well as the main predictor for unfavorable outcomes, such as heart failure [14]. Thus, LVOTO reduction is the primary target for pharmacologic agents, such as beta blockers, non-dihydropyridine calcium receptor antagonists, and class 1a antiarrhythmics namely, disopyramide.
The non-invasive echocardiographic assessment of right ventricular myocardial work in a healthy population
Published in Acta Cardiologica, 2023
Jian Wu, Xinyi Huang, Kunhui Huang, Qiumei Gao, Xu Chen, Yuan Tian, Yiruo Tang, Biqin Lin, Maolong Su
For decades, the importance of the right ventricle in clinical work and research on cardiovascular disease was neglected compared to that of the left ventricle. However, with increasing evidence that right ventricular (RV) dysfunction is closely related to the treatment and prognosis of diseases (e.g. acute myocardial infarction, heart failure, pulmonary hypertension [PH], after cardiac surgery and congenital heart disease), the right ventricle has received increasing attention from clinical and scientific researchers [1]. The most frequently used methods to analyse RV function are measuring the tricuspid annular plane systolic excursion (TAPSE), RV fractional area change (RV FAC) and myocardial tissue Doppler velocities (S’) [2–4]. However, TAPSE, RV FAC and S’ do not consider RV afterload. Because afterload has a major effect on the thin-walled right ventricle, ignoring the influence of afterload will make the parameters incapable of being used to accurately evaluate RV function [5]. Recently, RV longitudinal strain, as a superior method of RV function evaluation, is still an afterload-dependent parameter [6,7].