According to the literature, electrocardiographic signs of right ventricular hypertrophy have low sensitivity. The cause of this low sensitivity may be attributed to the original studies that were performed mostly in children with hypoplastic left ventricles or congenital heart abnormalities. In adulthood cases of normal or hypertrophic left ventricles, electrocardiographic right ventricular hypertrophy can only be detected during the late phase of ventricular depolarization. Two hundred four adult cardiac patients with complete noninvasive and invasive records were systematically studied by conventional and vectocardiographic methods. The terminal QRS (S wave) of the standard lead I has proved to be informative for detecting electrocardiographic signs in the presence of elevated right ventricular pressure. In cases of chronic right ventricular pressure overload (right ventricular hypertrophy) the terminal depolarization QRS vectors pointed posteriorly and to the right; therefore, a characteristic terminal S wave was represented in the standard lead I. If right and left ventricular hypertrophy were simultaneously present, the same resultant vectors pointed posteriorly and slightly to the left. In these cases, notching of the declining phase of the R wave was frequent, and a flatness of the terminal R wave portion was characteristic. The latter electrocardiographic sign has been called "simultaneous overloading of both ventricles" by the authors. The clinical utility of the new signs have also been proved by statistical methods.
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http://dx.doi.org/10.1016/s0022-0736(05)80106-2 | DOI Listing |
Proc Natl Acad Sci U S A
February 2025
Department of Physiology and Membrane Biology, University of California Davis, Davis, CA 95616.
The L-type Ca channel (Ca1.2) is essential for cardiac excitation-contraction coupling. To contribute to the inward Ca flux that drives Ca-induced-Ca-release, Ca1.
View Article and Find Full Text PDFRev Cardiovasc Med
January 2025
The First School of Clinical Medicine, Southern Medical University, 510000 Guangzhou, Guangdong, China.
Background: Given the close relationship between excessive cortisol secretion and obesity, as well as their intimate associations with cardiometabolic sequelae, this study aimed to evaluate whether elevated cortisol levels and obesity are independently and potentially interactively related to hypertension-mediated organ damage (HMOD) in patients with untreated hypertension.
Methods: A total of 936 untreated hypertensive patients were recruited. Body mass index (BMI), 24-hour urinary free cortisol (24 h UFC), and HMOD indicators, including left ventricular hypertrophy (LVH), carotid intima-media thickness (CIMT), and albuminuria, were assessed.
World J Cardiol
January 2025
Institute of Cardiovascular Diseases & Department of Cardiology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu 610072, Sichuan Province, China.
Hypertrophic cardiomyopathy (HCM) is an autosomal dominant inherited cardiomyopathy characterized by left ventricular hypertrophy. It is one of the chief causes of sudden cardiac death in younger people and athletes. Molecular-genetic studies have confirmed that the vast majority of HCM is caused by mutations in genes encoding sarcomere proteins.
View Article and Find Full Text PDFKidney Int
January 2025
Laboratório de Fisiopatologia Renal (LIM 16), Nephrology Department, Hospital das Clínicas da Faculdade de Medicina da Universidade de São Paulo (HCFMUSP), Universidade de São Paulo, São Paulo, Brazil. Electronic address:
In 2017, Kidney Disease: Improving Global Outcomes (KDIGO) published a Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Since then, new lines of evidence have been published related to evaluating disordered mineral metabolism and bone quality and turnover, identifying and inhibiting vascular calcification, targeting vitamin D levels, and regulating parathyroid hormone. For an in-depth consideration of the new insights, in October 2023, KDIGO held a Controversies Conference on CKD-MBD: Progress and Knowledge Gaps Toward Personalizing Care.
View Article and Find Full Text PDFInt J Mol Sci
January 2025
Institute for Biomedical Research and Innovation (IRIB), National Research Council (CNR), 90146 Palermo, Italy.
Anderson-Fabry (or Fabry) disease is a rare lysosomal storage disorder caused by a functional deficiency of the enzyme alpha-galactosidase A. The partial or total defect of this lysosomal enzyme, which is caused by variants in the gene, leads to the accumulation of glycosphingolipids, mainly globotriaosylceramide in the lysosomes of different cell types. The clinical presentation of Fabry disease is multisystemic and can vary depending on the specific genetic variants associated with the disease.
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