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Pathophysiology of Heart Failure with Reduced Ejection Fraction
Published in Andreas P. Kalogeropoulos, Hal A. Skopicki, Javed Butler, Heart Failure, 2023
Jacob Cao, John O'Sullivan, Sean Lal
Excitation contraction coupling refers to the coordinated process that starts when the action potential arrives at the sarcolemmal membrane and ends with sarcomere contraction and relaxation (Figure 3.4). Calcium plays a pivotal role in this entire process. Upon activation of the voltage-gated L-type calcium channels on the T tubules by the action potential, there is an initial small inward current of calcium. This small current acts on the closely apposed ryanodine receptors 2 and triggers a large release of calcium from the sarcoplasmic reticulum (calcium-induced calcium release). The cytosolic calcium subsequently binds to the cardiac troponin C. This induces conformational changes of the contractile proteins, leading to cross-bridge formation and sarcomeric contraction. The peak cytosolic calcium concentration is a major determinant of contractility. Relaxation occurs when the calcium is transported from the cytosol to either the sarcoplasmic reticulum via the SERCA-2a transporter (major mechanism) or out of the cells via the sodium-calcium exchanger (minor mechanism).
Gastrointestinal Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Gareth Davies, Chris Black, Keeley Fairbrass
The gut has an intrinsic neural network (enteric nervous system) coordinating gastrointestinal (GI) motility and secretions independent of central nervous control. In addition, the GI tract receives autonomic efferents throughout its length. Parasympathetic supply causes increased contractility and reduced sphincter tone; sympathetic effects are the opposite. The vagus nerve provides the main parasympathetic supply. Although it is best known for its efferent role in stimulating gastric acid output, 90% of vagal fibres are afferent (sensory). The autonomic nervous system provides stimuli for gastric and pancreatic secretion; however, hormonal stimuli are more important (see Table 10.1).
The patient with acute cardiovascular problems
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Contractility refers to the ability of the myocardium to contract. Healthy myocardium will contract effectively according to how much stretch the volume in the ventricle is exerting on the ventricular myocardium. As with an elastic band, if the myocardium becomes overstretched, it may not spring back so effectively, and so a damaged or failing heart, one with decreased contractility, may not have the capacity to contract so strongly. This is discussed in more detail later when considering heart failure. Factors that affect contractility are summarised in Table 6.1.
The current and future status of inotropes in heart failure management
Published in Expert Review of Cardiovascular Therapy, 2023
Angelos Arfaras-Melainis, Ioannis Ventoulis, Effie Polyzogopoulou, Antonios Boultadakis, John Parissis
Levosimendan works by sensitizing troponin C to the already existing levels of intracellular Ca2+, thereby increasing contractility. Since its mechanism does not result in increased intracellular Ca2+ ions, it is less proarrhythmic and less disruptive to myocardial relaxation and oxygen consumption/demand balance compared to the other commonly used inotropes. It also activates adenosine triphosphate (ATP)-ATP-sensitive potassium channels on vascular smooth muscle cells, leading to peripheral vasodilation. Notably, at higher doses, levosimendan demonstrates similar properties to PDE inhibitors [50,51]. In addition to the inotropic and vasodilatory net result of levosimendan, it has also been documented that this agent protects cardiac, neural, hepatic and renal cells from oxidative stress, most likely as a result of its effect on ATP-sensitive potassium channels in mitochondria [52]. An additional unique feature of levosimendan, contrary to the more traditional inotropes, is that its effect is prolonged for a few days after the discontinuation of its infusion, owing to the fact that its active metabolite OR-1896 has a half-life close to 80 h [53]. Of note, in patients with renal impairment, the half-life of OR-1896 can be increased significantly, which may result in a further prolongation of the agent’s effect by up to 1.5 fold [54].
Subarachnoidal hemorrhage related cardiomyopathy: an overview of Tako-Tsubo cardiomyopathy and related cardiac syndromes
Published in Expert Review of Cardiovascular Therapy, 2022
Susan Deenen, Dharmanand Ramnarain, Sjaak Pouwels
Heart failure including TTS is a well-recognized complication of neurologic diseases. In normal physiology, the parasympathetic and sympathetic nervous systems have an important role in the regulation of cardiac function [5,15]. The nervus vagus mediates the parasympathetic stimulation of the heart and leads to decreased heart rate, atrioventricular (AV) conduction, and ventricular excitability. Sympathetic stimulation leads to increased heart rate, AV conduction, and ventricular excitability and contractility. Also, the higher cerebral structures such as the frontal cortex, insula, amygdala, cingulate, hypothalamus, and periaqueductal gray matter influence cardiac function [5]. Furthermore, the hypothalamic–pituitary–adrenal axis (neuroendocrine system) influences the cardiac system by creating a stress response and thereby releasing cortisol and catecholamines. Catecholamines influence adrenergic receptors (ARs), leading to increased heart rate, contraction, and changes in blood pressure [5]. How these pathways can be disrupted by neurological injury and thereby cause cardiac dysfunction is a complex process, and many theories are mentioned. However, most recent studies describe an important role for catecholamines [5,9,12,13]. This theory is generally believed to explain the pathophysiology of cardiac dysfunction in SAH patients. SAH can cause mild-to-severe cardiac dysfunction in the form of ECG changes, arrhythmias, LV dysfunction, and release of cardiac biomarkers. In SAH patients with elevated catecholamine levels, it is also described that cardiac enzymes are elevated [1,2,5,12,13].
Specific FSTL1 polymorphism may determine the risk of cardiomyopathy in patients with acromegaly
Published in Acta Cardiologica, 2022
Suleyman Nahit Sendur, Tuncay Hazirolan, Busra Aydin, Incilay Lay, Mehmet Alikasifoglu, Tomris Erbas
It has been shown that GH and IGF-1 receptors are expressed in several parts of the cardiovascular system including cardiomyocytes [4]. GH exerts its effects on heart either directly by itself or indirectly by IGF-1. When exposure to high GH, myocardial fibres enlarge [5]. Increased IGF-1 receptor activation in cardiomyocytes leads to overexpression of muscle-specific proteins and ultimately hypertrophy [6]. Moreover, IGF-1 but not GH enhances myocardial contractility [7,8]. At advanced stages, interstitial collagen deposition, myofibrillar derangement, apoptosis and lympho-mononuclear infiltration accompany myocardial hypertrophy [9,10]. Ultimately, the configuration of heart changes. On a clinical basis, if left untreated, the typical cardiovascular complication of acromegaly is a cardiomyopathy characterised by three stages (acromegalic cardiomyopathy). In the first stage, both ventricles become enlarged. With increased myocardial contractility, systolic output increases. Therefore, heart functions in a hyperkinetic state. In the second stage, myocardial growth progresses further, interstitial fibrosis occurs and causes disruption of the diastolic filling and leads to diastolic dysfunction. In the last stage, the systolic function of the heart begins to deteriorate and eventually, congestive heart failure develops [11–13].