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The Cardiovascular System and its Disorders
Published in Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss, Understanding Medical Terms, 2020
Walter F. Stanaszek, Mary J. Stanaszek, Robert J. Holt, Steven Strauss
The impulses from the right atrium gather at the atrioventricular node, which conducts them toward the right ventricle. Contraction in the ventricles begins in the interventricular septum, which shortens with the contraction. The impulse then stimulates contraction in the apex (which is formed from the tip of the left ventricle), moves up and around the heart in a wringing action, and terminates near the atrioventricular groove where the blood is leaving the ventricles.
Congenital Heart Disease in Pregnancy
Published in Afshan B. Hameed, Diana S. Wolfe, Cardio-Obstetrics, 2020
The incidence of ventricular septal defects (VSDs) varies widely in the literature, as many patients are asymptomatic, and many small defects close spontaneously but are among the most common forms of CHD in childhood. Approximately 10,000–11,000 isolated VSDs are diagnosed in infants in the United States annually [7,8]. Ventricular septal defects are divided into four types, based on their location within the interventricular septum: Perimembranous VSDs account for 80%Muscular VSDs account for 50%–10%Inlet VSDs account for 5%Supracristal VSDs account for 5%–7%
Cardiovascular system
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
Left anterior oblique (Figs 9.4d, e): the X-ray tube is rotated towards the right side of the patient until it is angled at 35–40° to the median sagittal plane. The FPD is positioned adjacent to the left anterior chest wall. In this projection the posterior wall of the ventricle, the interventricular septum and the aortic outflow tract are demonstrated. A bi-plane angiographic set will enable these two images to be acquired simultaneously, with a single injection of contrast medium.
Heart of lymphoma: a case report
Published in Acta Cardiologica, 2023
Annemie Jacobs, Thomas Gevaert, Wim Volders, Dieter De Cleen, Katrien Van Kolen, Frank Cools, Steven Hellemans
On gastroscopic review, several small erosions in the corpus and antrum were noted, as well as linear bulboduodenal ulcers, which could be responsible for the anaemia. Also, thoracocentesis from the unilateral pleural effusion was executed, and it showed benign, inflammatory findings on analysis. On transthoracic echocardiography, a mass (dd thrombus) near the tricuspid valve, and on the right sight of the right atrium was detected. Signs of right ventricular failure were noticed (pulmonary hypertension, flattening of the interventricular septum and D-shaping of the left ventricle). Empirical treatment with anticoagulation was started, although an intermediate dose was chosen due to the severe anaemia. Given the suspicion of pulmonary embolism, an additional CT thorax was prosecuted and revealed a limited amount of pericardial effusion, in the presence of a new mediastinal tumour with invasion of the right atrium and ventricle (Figure 2(A,B)).
Calanus oil attenuates isoproterenol-induced cardiac hypertrophy by regulating myocardial remodeling and oxidative stress
Published in Ultrastructural Pathology, 2023
Shrook Y. Abdellatif, Nagui H. Fares, Samar H. Elsharkawy, Yomna I. Mahmoud
Cardiac hypertrophy (CH) is an adaptive and compensatory response of the heart to preserve cardiac function during persistent increased workload. During this response, the cardiomyocytes change their shape, increase in size, and remodel the extracellular matrix (ECM),1 which leads to the hallmarks of cardiac hypertrophy: thickening of the interventricular septum and concentric left ventricular hypertrophy.2 However, sustained concentric hypertrophy constitutes a risk factor of heart failure and sudden death.1 Treatment strategies for heart failure commonly include diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and β-blockers; however, mortality rates remain high. Current CH pharmacotherapies such as diuretics, angiotensin converting enzyme inhibitors, angiotensin II receptor blockers and β-blockers, significantly delay the onset of heart failure, but they have many adverse effects,3 and limited success to restore the quality of life,4 and mortality rates remain high.3 Hence, there is a pressing need to explore novel strategies and therapeutic interventions to prevent ECM remodeling and CH symptoms, with lower side effects.
Assessment of salusin alpha and salusin beta levels in patients with newly diagnosed dipper and non-dipper hypertension
Published in Clinical and Experimental Hypertension, 2021
Seref Alpsoy, Burcin Dogan, Demet Ozkaramanli Gur, Aydin Akyüz, Çiğdem Fidan, Savas Guzel, Berna Ozkoyuncu
The patients’ echocardiography was performed by an experienced cardiologist blinded to the patient’s clinical and laboratory data, using Vivid S5 (General Electric Healthcare, USA) system with a 2.5–3.5 MHz transducer. All patients underwent an echocardiographic examination at the left side decubitus position. Echocardiography revealed interventricular septum (IVS) and posterior wall (PW) thicknesses. Left ventricular mass was calculated with the Devereux formula (14). LVMI was calculated by dividing the left ventricular mass by body surface area. To determine LV diastolic function, pulsed wave Doppler at mitral inflow measured early (E) and late (A) diastolic waves. With tissue Doppler examination, early (E’) and late (A’) waves from the septal and lateral mitral annulus were recorded. All measurements were repeated at least three times and were averaged. Pulsed wave Doppler mitral E/A ratio, tissue Doppler septal E ‘/A’, lateral E ‘/A’, mitral E/septal E’ and mitral E/lateral E’ were used to evaluate diastolic functions.