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Outpatient Management of Stable Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Leah Reid, Jonathan Murrow, Kent Nilsson, Catherine Marti
Angiotensin-converting enzyme inhibitors (ACEI) are well established in HF therapy, with overwhelming evidence in symptomatic and asymptomatic HFrEF (left ventricular EF<40%).15–17 ACEIs interfere with the renin angiotensin system, inhibiting the enzyme that is responsible for converting angiotensin I to angiotensin II (Figure 10.2). Because of inhibition of kininase II, ACEIs may also lead to the upregulation of bradykinin, further enhancing effects of angiotensin suppression. These agents have been shown to reduce mortality, reduce hospitalization for HF, result in left ventricular remodeling, and improve quality of life.18 As such, the ACC/AHA HF Guidelines have given the use of ACEI a class I, LOE: A recommendation.1
Cardiac Hypertrophy, Heart Failure and Cardiomyopathy
Published in Mary N. Sheppard, Practical Cardiovascular Pathology, 2022
Different mutations in many of the same genes that have been associated with DCM also cause familial HCM. Individuals affected by DCM-causing sarcomeric mutations have ventricular dilatation and contractile dysfunction in the absence of preceding myocardial hypertrophy. This implies that distinct pathways lead to the two phenotypes. Functional studies of HCM mutant sarcomeric proteins have shown that they are likely to cause increased activation (e.g., increased Ca2+ sensitivity or higher unloaded shortening speed) compared with wild type. In contrast, studies of DCM mutations in thin filament regulatory proteins using cardiac troponin T, α-tropomyosin and cardiac troponin C mutants have shown that these cause the opposite effect, a decrease in Ca2+ sensitivity and maximum ATPase activity, indicating a fundamentally different effect at the level of the sarcomere. How these different alterations lead to distinct ventricular remodelling patterns is unclear.
Natural History of Hypertrophic Cardiomyopathy
Published in Srilakshmi M. Adhyapak, V. Rao Parachuri, Hypertrophic Cardiomyopathy, 2020
In adults, left ventricular remodeling results from progressive left ventricular wall thinning and cavity dilatation. These changes in wall thickness are also associated with a progressive increase in left ventricular cavity dimension, though absolute left ventricular dilatation is rare. Marked wall thinning, relative cavity dilatation, and systolic dysfunction have been reported in about 10% of patients with HCM and moderate-to-severe symptoms [6]. Therefore, this malignant morphological evolution with extensive left ventricular remodeling occurs in a significant minority of patients with symptoms. At necropsy, the hearts of patients with wall thinning and cavity dilatation show diffuse left ventricular scarring, usually of both the septum and the left ventricular free wall. The mechanisms responsible for myocardial scarring and wall thinning in HCM have not been established. It is likely, however, that chronic ischemia plays an important part in scarring. Several studies have shown myocardial ischemia in HCM [7–9]. Ischemia could be caused by inadequate capillary density relative to the increased myocardial mass. In addition, abnormal intramyocardial arterioles with thickened walls and an apparently narrowed lumen have been described in HCM [10] and may contribute to myocardial ischemia.
Updates in the management of congenital heart disease in adult patients
Published in Expert Review of Cardiovascular Therapy, 2022
Danielle Massarella, Rafael Alonso-Gonzalez
The role of device therapy in combatting maladaptive ventricular remodeling has yet to be elucidated in the adult congenital heart failure population, though it has been identified as a major evidence gap which warrants further investigation [8,82]. Well recognized parametric indications for cardiac resynchronization therapy (CRT) in those with left ventricular dyssynchrony not related to an underlying congenital anomaly may not apply to the more heterogeneous congenital population. Those patients with a systemic left ventricle and pacing-induced cardiomyopathy likely represent the most analogous subset of the congenital population, and CRT upgrade should be considered as it may confer a similar benefit. Otherwise, CRT is typically considered in symptomatic congenital cardiac patients with QRS prolongation in the setting of systemic ventricular dilation and dysfunction, and this currently represents the most common indication for the application of this technology [71,91,92]. There is some evidence to suggest that, compared to propensity-matched controls, CRT improves transplant-free (as well as overall) survival in younger congenital patients with symptomatic systemic ventricular dysfunction [93]. However, efficacy and degree of reverse ventricular remodeling are variable across anatomic and pathophysiologic substrates [94]. Of note, lead implantation is more challenging in the congenital heart disease population, in whom systemic venous anomalies and post-operative anatomy may preclude conventional transvenous approaches [62,92,94,95].
Left Ventricular Volume Reduction and Reshaping as a Treatment Option for Heart Failure
Published in Structural Heart, 2020
Michael I. Brener, Nir Uriel, Daniel Burkhoff
Left ventricular remodeling is the process that describes progressive cavity dilation, distortion of the normal elliptical shape, and contractile dysfunction of the left ventricle (LV). LV remodeling is the hallmark of both ischemic and non-ischemic cardiomyopathies; although the nature of the initial insult differs (regional vs global; primary muscle loss vs primary muscle dysfunction), the ensuing process is similar. LV function deteriorates as the ventricle dilates in accordance with Laplace’s law, which states that ventricular pressure generation (LVP) is proportional to myocardial force generation per unit cross-sectional area of wall thickness (i.e., wall stress, σ) and wall thickness (h), but is inversely proportional to the radius of curvature of the LV cavity (r): LVP = 2·σ·h/r. This also means that for a given ventricular pressure, the myocardium is under greater stress as the heart dilates: σ = (LVP·r)/(2 h). Increased myocardial wall stress during systole results in myocyte hypertrophy (sarcomeres laid down in parallel), while increased stress during diastole results in myocyte elongation (sarcomeres laid down in series) which increases ventricular diastolic volume; both result in increased LV mass.1
Doses of renin-angiotensin system inhibitors but not beta-blockers predict outcome after ST-elevation myocardial infarction
Published in Acta Clinica Belgica, 2019
Pei-Yu Liu, Chien-Lin Chen, Min-Chien Yu, Yu-Lin Ko, Shun-Yi Hsu, Hsin-Hua Chou, Kuan-Hung Yeh, De‑Min Duan, Ming-Hsin Chen, Jeng-Feng Lin
There is little published information about dose-dependent effects of ACEI/ARB and beta-blockers on left ventricular remodeling in patients with AMI. Previous studies evaluating left ventricular remodeling were usually conducted in patients with heart failure. In patients with idiopathic dilated cardiomyopathy, high-dose ACEI or ARB was associated with significant reduction in LVEDVI, in contrast to their respective low-dose therapy [31]. The MOCHA trial revealed that beta-blocker treatment was associated with dose-related improvement of LVEF in patients with chronic heart failure. However, dose-related improvement of LVEF was more evident in the nonischemic group than the ischemic group [28]. In a recent study evaluating up-titrated treatment of beta-blocker in patients with heart failure, the reduction in left ventricular dimension was more prominent in the high-dose group. However, patients receiving PCI in the preceding 6 months were excluded from that study [32]. In our study, patients receiving high-dose ACEI/ARB had less increased in LVEDVI at 6 months, when compared with low-dose group. However, the difference was only modest and can be partly explained by higher baseline LVEF and lower peak creatine kinase level in the high-dose group. After multivariable adjustment, ACEI/ARB dose or beta-blocker dose was not an independent predictor of increase in LVEDVI. For further evaluating the effects of high-dose ACEI/ARB and beta-blocker on left ventricular remodeling after AMI, randomized trials may be needed to control other confounding factors, such as baseline LVEF and infarct size.