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Congestive Heart Failure
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Dilated cardiomyopathy occurs without other disorders that are able to cause the myocardium to be dilated. These include severe occlusive CAD, hypertension, and valvular heart disease. Sometimes, dilated cardiomyopathy starts with acute myocarditis (usually of viral origin). There is a latent phase of various lengths, then diffuse necrosis of the myocardial myocytes because of an autoimmune reaction to myocytes altered by the virus, and then, chronic fibrosis. The myocardium is dilated, thinner, and hypertrophied as a compensatory mechanism. This often results in functional tricuspid or mitral regurgitation as well as atrial dilation. Dilated cardiomyopathy affects both ventricles in most cases, less often affecting just the LV, and only rarely affecting just the RV. When chamber dilation and dysfunction progress, mural thrombi can form because of stasis of blood. The acute myocarditis and late chronic dilated phases are often complicated by cardiac tachyarrhythmias. Atrioventricular block may also develop. As the left atrium becomes dilated, atrial fibrillation often occurs.
Stroke and Transient Ischemic Attacks of the Brain and Eye
Published in Philip B. Gorelick, Fernando D. Testai, Graeme J. Hankey, Joanna M. Wardlaw, Hankey's Clinical Neurology, 2020
Intracardiac tumors include myxomas and valvular fibroelastomas. Myxomas are most frequently found in the left atrium. Some are familial. Tumor or associated thrombus may embolize to the brain, eye, and elsewhere. Myxomatous emboli may not only cause focal cerebral ischemia but also aneurysmal dilation at sites of earlier emboli. These mycotic aneurysms can rupture and cause intracranial hemorrhage. Brain metastases have also been described. Myxomas also can obstruct cardiac outflow and cause syncope. Frequently, there are associated constitutional symptoms, such as malaise, fatigue, weight loss, fever, rash, arthralgia, myalgia, anemia, raised erythrocyte sedimentation rate (ESR), and hypergammaglobulinemia.
Common Tips on Communication
Published in Justin C Konje, Complete Revision Guide for MRCOG Part 3, 2020
Your baby has an abnormality in its heart. Before I proceed to explain this to you, I would like to describe what a normal heart looks like. The heart is divided into two sides (left and right), separated by a wall with no gap or hole in it, and on each side, there are two compartments – an upper and lower compartments. The upper compartments are known as atria and receive blood. This is then passed to the lower compartments (known as ventricles), which then pump it out. The blood from the right ventricle goes to the lungs, where oxygen is added and carbon dioxide is removed. This blood comes back through the left atrium into the left ventricle, which then pumps it to the rest of the body, where the oxygen is used.
Management of congenitally corrected transposition from fetal diagnosis to adulthood
Published in Expert Review of Cardiovascular Therapy, 2023
Congenitally corrected transposition of the great arteries (ccTGA) is a complex congenital heart disease first described from an autopsy by a Bohemian pathologist working in Vienna, Karl von Rokitansky, in 1875 [1]. The anomaly is characterized by atrioventricular and ventriculo-arterial discordance [2]. Deoxygenated blood from the right atrium flows through the mitral valve into the morphological left ventricle, which gives rise to the pulmonary artery. Then, oxygenated blood flows into the left atrium that communicates with the morphological tricuspid valve and right ventricle, that is connected to the aorta. The aorta is located usually anterior and to the left. Consequently, the double discordance results in hemodynamic compensation, but the morphologically right ventricle works as systemic ventricle (systemic right ventricle, sRV). The most common anomalies are ventricular septal defect, pulmonary or subpulmonary stenosis, and systemic atrioventricular (morphological tricuspid) valve abnormalities [3] (Table 1). Additionally, cardiac malposition (dextrocardia or mesocardia) occurs in up to one-third of the patients. Associated malformations, especially the Ebstein-like anomaly of the systemic atrioventricular valve, have a significant impact on the clinical course of the disease. Conduction disturbances, including complete atrio-ventricular block, are another common cause of increased morbidity in ccTGA patients and might be the first manifestation of the disease.
Left atrial reservoir and pump function after catheter ablation with persistent atrial fibrillation: a two-dimensional speckle tracking imaging study
Published in Acta Cardiologica, 2023
Xiao-fang Zhong, Dong-sheng Liu, Ying-qi Zheng, Gui-juan Peng, Yuan-yuan Sheng, Li-xin Chen, Ying-ying Liu
It is well-known that the role of LA mechanical function is very important in cardiovascular disease. During sinus rhythm, the LA has three functions (reservoir, conduit and pump). The loss of effective LA active contraction and diastolic function of the LV during atrial fibrillation results in a decrease in the volume of blood filling the left ventricle, causing LV output to be reduced in late diastole. Furthermore, AF causes a rapid and irregular ventricular rate, resulting in damaging compliance and relaxation of the left ventricle, and increased diastolic filling pressure of the LA, LA serves as a reservoir for blood during ventricular systole. This all results in damage to the left atrial reservoir function the application of tissue doppler imaging (TDI) for the determination of strain and SR, which reflect left atrial myocardial deformation as an estimate of LA function, was affirmed by a previous study [10]. However, some shortcomings, such as angle dependency, limit the application of TDI. Tsai et al. [11] used speckle tracking echocardiography to assess LA function and found that LA function was impaired in paroxysmal AF. Our study also found that both regional and global reservoir functions were seriously damaged in PAF, and pump function disappeared. In 1999, researchers proposed that AF could cause left atrial enlargement [12], the increase in volume and pressure load of the left atrium would cause the LA to enlarge and left atrial enlargement was also confirmed in our study. Left atrium enlargement indicates heart remodelling associated with pathophysiologic processes.
The relationship between oxidative stress and autophagy and apoptosis in patients with paroxysmal atrial fibrillation
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2022
Halil Fedai, Ibrahim Halil Altiparmak, Mustafa Begenc Tascanov, Zulkif Tanriverdi, Asuman Bicer, Fatih Gungoren, Recep Demirbag, Ismail Koyuncu
Atrial fibrillation (AF) is the most common clinical arrhythmia, and early recognition is important in terms of preventing complications with treatment and preserving left atrium (LA) functions by keeping the rhythm in the sinus. Paroxysmal AF (PAF) is a type of AF in which sinus rhythm is achieved spontaneously or with medical interventions in less than 7 days [1]. Many studies have shown increased oxidative stress (OS) in patients with both AF and PAF subgroups. On the other hand, it has also been shown that remodeling develops in the LA in PAF patients and, accordingly, it expands and undergoes structural, electrical and even contractile changes [2,3]. The main pathophysiologic mechanisms of AF are structural and electrical remodeling of the atrial tissue result from atrial fibrosis, OS, inflammation, genetic factors, endothelial dysfunction, and behavioral factors including caffeine and alcohol consumptions, sedentary lifestyle e.g. [4,5].