China
Africa
Explore chapters and articles related to this topic
Atrial Flutter
Published in Andrea Natale, Oussama M. Wazni, Kalyanam Shivkumar, Francis E. Marchlinski, Handbook of Cardiac Electrophysiology, 2020
Ayman A. Hussein, Oussama M. Wazni
Acutely, patients often complain of shortness of breath, palpitations, diaphoresis, chest discomfort, dizziness, and weakness. Patients may also complain of polyuria, which occurs as a result of increased atrial pressure from rapidly contracting atria against a closed AV valve, and the subsequent release of atrial natriuretic factor (ANF). AFL may also present as exercise-induced fatigue or worsening heart failure. Patients tend to be more symptomatic when the ventricular response rate is rapid and/or when they present with episodes of both AF and AFL. On physical examination, the peripheral pulse is generally rapid and regular (less often irregular); cannon “a” waves may be observed, and S1 is of variable intensity.8
Gustatory Mechanisms of a Specific Appetite
Published in Robert H. Cagan, Neural Mechanisms in Taste, 2020
Sodium is the principal electrolyte of the extracellular fluid. The level of sodium in body fluids plays a crucial role in defining the electrochemical status of the intracellular and extracellular fluids. As such, sodium is essential for such processes as nerve cell function, blood volume and blood pressure maintenance, acid-base balance, and muscle contraction.3 Because of its importance to normal bodily processes, sodium levels are tightly regulated, primarily by the interplay of the kidneys and adrenal glands through hormonal signals. Physiochemical changes associated with sodium deficiency trigger activation of the renal-renin and blood-angiotensin system to promote the production and release of aldosterone from the adrenal gland. Aldosterone inhibits sodium loss through urination, perspiration, and salivation. Excess sodium, on the other hand, suppresses the renin-angiotensin system, thereby permitting sodium loss. In addition, a new hormonal factor was recently identified that may play an important role in promoting the excretion of excess sodium.4–6 In response to blood volume expansion, the atrial stretch receptors of the heart release atrial natriuretic factor, which, by its direct action on the kidney, promotes sodium excretion and inhibits aldosterone and renin secretion.
Summation of Basic Endocrine Data
Published in George H. Gass, Harold M. Kaplan, Handbook of Endocrinology, 2020
Although there may be other cardiac hormones, the atrial natriuretic factor (ANF) is the one most completely defined. The ANF is located in cells in both the right and left cardiac atria but chiefly in the right atrium. It is produced within the myocardial cells. The ANF, in contributing to blood volume control, acts as a set of stretch receptors in the atrial muscles.
Clinicopathological features of clinically undiagnosed sporadic transthyretin cardiac amyloidosis: a forensic autopsy-based series
Published in Amyloid, 2021
Shojiro Ichimata, Yukiko Hata, Keiichi Hirono, Yoshiaki Yamaguchi, Naoki Nishida
Besides left heart failure (HF) that typically appears in advanced-phase patients, ATTR amyloidosis might be associated with atrial arrhythmia, especially atrial fibrillation (AF) [5–8]. Compared to patients with immunoglobulin light chain-derived amyloidosis and hereditary ATTR amyloidosis, more patients with sporadic ATTR amyloidosis present with AF at the first evaluation [9,10]. Thus, AF may be one of the major early symptoms of sporadic ATTR amyloidosis. In addition, sporadic ATTR amyloidosis may exhibit a characteristic atrial deposition pattern that is not observed in other types of amyloidosis at an early stage. Conversely, atrial natriuretic factor (AANF)-related amyloidosis is a type of isolated atrial amyloidosis, which is associated with localised amyloid deposition [11–14]. However, the frequency of AANF deposition increases with aging, and reports have indicated that it also causes disturbances for atrial conduction, thereby increasing the risk of AF [13,14]. Nonetheless, no studies have fully elucidated whether these two amyloid deposits are associated with atrial arrhythmia, possibly because direct amyloid infiltration in the specialised conduction tissue does not account for the majority of these disturbances [15], making it challenging to arrive at definite conclusions. Moreover, ‘senile’ amyloid deposits might be associated with other amyloid depositions when several conditions are favourable [16]. We hypothesised that both ATTR and AANF deposits are associated with the clinicopathological features of the same or related health condition because these deposits are age-related and they frequently affect the heart.
Targeting calcium-mediated inter-organellar crosstalk in cardiac diseases
Published in Expert Opinion on Therapeutic Targets, 2022
Mohit M. Hulsurkar, Satadru K. Lahiri, Jason Karch, Meng C. Wang, Xander H.T. Wehrens
One of the challenges in targeting multiple channels together is to maintain the target and organ specificity. Since proteins like IP3R, VDAC, MCU, and lysosomal ion channels are ubiquitous, it will be challenging to maintain organ specificity while targeting them. Unintended inhibition of these channels in other organs might lead to undesired side-effects that need to be assessed carefully. A potential solution to maintaining target and organ specificity is to use sophisticated gene alteration approaches. We have recently achieved atrial-specific gene delivery using an adeno associated viral (AAV) vector containing a modified atrial natriuretic factor (ANF) promoter (REF 202). Similarly, other studies have achieved cardiac specific gene delivery and alteration using similar approaches (REF 203). ([202,203] These strategies could lead to specific targeting of a group of proteins in cardiac or even atrial specific way. Another strategy to achieve cardiac-directed effectiveness could be to target other channels along with RyR2 inhibitors. Since RyR2 is expressed only in the cardiomyocytes, a combinatorial therapeutic strategy using RyR2 inhibitors would make it more directed toward the heart than other organs and achieve relatively less side-effects. Please note that RyR2 expressed in the central nervous system would not be targeted assuming these drugs do not cross the blood-brain barrier. New advances in CRISPR-mediated genome editing [204–206] and gene delivery systems including capsid-engineered adeno-associated viruses [207], exosomes [208], naked DNA [209,210] and nanoparticles [211,212] mediated delivery may pave the way for organ-specific permanent gene alterations within the near future.
New and emerging cardiovascular and antihypertensive drugs
Published in Expert Opinion on Drug Safety, 2020
Steven G. Chrysant, George S. Chrysant
Sacubitril/valsartan is a single drug with dual action. It exerts its beneficial cardiovascular and BP lowering effects through its dual inhibition of RAS with valsartan and neprilysin with sacubitril. Neprilysin is an important catabolizing agent of the natriuretic peptides (NPs), which possess significant diuretic, natriuretic, and vasodilating effects [23–25]. The NPs are endogenous hormones released from the heart in response to wall stretching from pressure and volume overload and exert their beneficial cardiovascular and antihypertensive effects through plasma volume contraction and peripheral vasodilation. Since the original discovery of the atrial natriuretic factor by De Bold et al. [25], three natriuretic peptides have been discovered, the atrial natriuretic peptide (ANP), the beta natriuretic peptide (BNP), and the central natriuretic peptide (CNP). The ANP and BNP are circulatory peptides and help patients with HF and hypertension through their natriuretic, diuretic, and vasodilatory effects mediated by generation of (cGMP) cyclic guanosine monophoshate [23–25]. The CNP is not a circulatory peptide and is mainly localized in the central nervous system and not involved in the cardiovascular hemodynamics [26,27]. Unfortunately, the action of sacubitril/valsartan is associated with some desirable and some undesirable adverse effects [28]. Neprilysin is known to catabolize several peptide hormones, such as adrenomedulin, Ang II, bradykinin, endothelin, glucagon-like peptide-1 (GLP-1), NPs, neurotensin, oxytocin, substance P, and most importantly, amyloid β peptide. Therefore, the net effect of sacubitril/valsartan on its cardiovascular and BP effects will be a balance between the actions of valsartan on RAS and sacubitril on NEP.