Takotsubo syndrome (stress-induced cardiomyopathy) in the practice of a nurse

2021 ◽  
pp. 62-65
Author(s):  
Polina Denisovna Samokhvalova ◽  
Nikita Dmitrievich Matveev ◽  
Vsevolod Vladimirovich Skvortsov
Keyword(s):  
Coronary Arteries ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Reliable Information ◽  
Left Ventricular Myocardium ◽  
Takotsubo Syndrome ◽  
Diastolic Functions

Stress-induced cardiomyopathy is a disease that entails a transient violation of the systolic and diastolic functions of the left ventricular myocardium with subsequent enlargement of the heart chambers, akinesia of the apical and middle segments and normo- or hyperkinesia of the basal segments in the absence of pronounced hemodynamic stenosis of the coronary arteries. To date, there is no reliable information about the pathogenesis, methods of therapy and possible prognosis of this disease, so there is a need for further research.

scholarly journals A RARE COMBINATION OF NONCOMPACT MYOCARDIUM AND CORONARY DILATATION WITH TYPE 1 NEUROFIBROMATOSIS

2018 ◽  
Vol 2 (5) ◽  
pp. 159-162
Author(s):  
Олеся Ефремова ◽  
Olesya Efremova ◽  
Людмила Брегель ◽  
Lyudmila Bregel ◽  
Владимир Субботин ◽  
...  
Keyword(s):  
Left Ventricle ◽  
Coronary Arteries ◽  
Cognitive Disorders ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vascular Pathology ◽  
Left Ventricular Myocardium ◽  
Rare Combination ◽  
Type 1 Neurofibromatosis

The article describes the observation of a child with a very rare combination of noncompact left ventricular myocardium and coronary dilatation in type 1 neurofibromatosis (NF 1). The first of these complications, undifferentiated cardio- myopathy, also known as noncompact myocardium, is not described in combination with NF 1 in available literature, although cases of hypertrophic cardiomyopathy in patients with NF 1 have been previously reported. Dilatation of the coronary arteries also refers to infrequent manifestations of vascular pathology against the background of neurofibro- matosis, and the combination of all three signs (NF 1, noncompact myocardium and coronary dilatation) has not yet been reported by other authors. When examining the patient, we found the characteristic signs of NF 1 (foci of “coffee” pigmentation on the skin, multiple nevuses, fibroids of the forearm, cognitive disorders), electrocardiogram features of left ventricular hypertrophy, negative T-tooth and ST-segment displacement 1 mm below the isoline in Leads V4-6, in echocardiography - pronounced trabecularity, thinning of the compact myocardium layer and a “spongy myocardium” in the region of the left ventricle apex, dilatation of the coronary arteries. With magnetic resonance imaging, signs of noncompact myocardium of the left ventricle were found, with selective coronary angiography - slowing of the coronary blood flow. The patient receives the permanent treatment for heart failure and aspirin, his condition remains stable for 4 years of follow-up

Polar Presentation of Coronary Angiography and Thallium-201 Single Photon Emission Computed Tomography

1989 ◽  
Vol 30 (6) ◽  
pp. 561-574 ◽  
Author(s):  
B. Svane ◽  
D. Bone ◽  
A. Holmgren ◽  
C. Landou
Keyword(s):  
Coronary Angiography ◽  
Coronary Arteries ◽  
Single Photon ◽  
Photon Emission ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Thallium 201 ◽  
Left Ventricular Myocardium ◽  
Emission Computed Tomography ◽  
Perfusion Defects

Individual results of coronary angiography were compared with tomographic myocardial scintigraphy (SPECT) in 99 patients. Coronary angiography findings were transferred to polar maps. Borders between arteries were assigned angles in a coordinate system constructed as a compass-rose. Areas perfused by different arteries were described by sectors. Findings were visually compared with the perfusion defects in a polar presentation of thallium-201 SPECT also described by angles. The mean values and SD for the angles representing arterial borders and perfusion defects were presented. The left ventricular myocardium was perfused by 3 coronary arteries in 92/99 patients. Dominant left artery was present in 7/99 patients; 79 perfusion defects were related to 118 arterial sectors 84 per cent had totally or partially matched stenotic arteries. Inter-individual differences in distribution of coronary arteries influence the localization of perfusion defects in myocardial SPECT and can be estimated with this polar presentation method.

scholarly journals Effects of Telmisartan on Myocardial Protein Profiles in Hypertensive Rats

2021 ◽  
Vol 34 (3) ◽  
pp. 299-299
Author(s):  
Yu Feng ◽  
Man-li Zhou ◽  
Jian-zhang Wang ◽  
Jia-qi Zhang ◽  
Shu-le Qian ◽  
...  
Keyword(s):  
Heat Shock ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Sterile Water ◽  
Protein Profiles ◽  
Related Protein ◽  
Hypertensive Rats ◽  
Treatment Groups ◽  
Proteasome 26S

Abstract Background To investigate the effects of telmisartan on the protein profiles of the left ventricular myocardium in spontaneously hypertensive rats (SHR). Methods Sixteen SHR were randomly divided into control and telmisartan treatment groups. Rats were treated with sterile water (10 ml/kg) or telmisartan (4.33 mg/kg) by gavage for 12 weeks. Wistar-Kyoto (WKY) rats treated with sterile water (10 ml/kg) as controls. At the end of 12 weeks of control or telmisartan treatment, rats were sacrificed, and hearts were collected for protein preparations, isotope labeling, and mass spectrometric analysis. Results In total, there were 23 differentially expressed proteins in the left ventricular myocardium between control and telmisartan treatment groups in SHR. Compared with the telmisartan group, the upregulated proteins in the SHR were dual-specificity mitogen-activated protein kinase kinase 3-like, transgelin, and haptoglobin subtype 2. The downregulated proteins in the SHR were as follows: von Willebrand factor (fragment), kininogen 1, small ribonucleoprotein-related protein, fibrinogen beta chain, protein mass 3 (fragment), proteasome 26s, heat shock protein 27-related protein 1, tenascin X, fibronectin subtype 2, transferrin receptor protein, platelets 1, cathepsin L1, complement factor B, isoform CRA_b, fibrinogen isomer, immunoglobulin heavy chain (γ polypeptide), and α 1 antiprotease. Conclusions Telmisartan differentially regulates myocardial protein expression in hypertensive rats including heat shock protein 27, fibrinogen, fibronectin, proteasome 26s and transgelin, as well as proteins in biochemical, metabolic, and signal transduction pathways. These changes in protein expression may contribute to the antihypertrophic effects of telmisartan in hypertension.

scholarly journals Remodeling of t-system and proteins underlying excitation-contraction coupling in aging versus failing human heart

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Yankun Lyu ◽  
Vipin K. Verma ◽  
Younjee Lee ◽  
Iosif Taleb ◽  
Rachit Badolia ◽  
...  
Keyword(s):  
Heart Function ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Excitation Contraction Coupling ◽  
Transverse Tubular System ◽  
Contraction Coupling ◽  
Senescent Phenotype ◽  
Cellular Microstructure ◽  
T System

AbstractIt is well established that the aging heart progressively remodels towards a senescent phenotype, but alterations of cellular microstructure and their differences to chronic heart failure (HF) associated remodeling remain ill-defined. Here, we show that the transverse tubular system (t-system) and proteins underlying excitation-contraction coupling in cardiomyocytes are characteristically remodeled with age. We shed light on mechanisms of this remodeling and identified similarities and differences to chronic HF. Using left ventricular myocardium from donors and HF patients with ages between 19 and 75 years, we established a library of 3D reconstructions of the t-system as well as ryanodine receptor (RyR) and junctophilin 2 (JPH2) clusters. Aging was characterized by t-system alterations and sarcolemmal dissociation of RyR clusters. This remodeling was less pronounced than in HF and accompanied by major alterations of JPH2 arrangement. Our study indicates that targeting sarcolemmal association of JPH2 might ameliorate age-associated deficiencies of heart function.

scholarly journals Myxomatous Mitral Valve Disease with Mitral Valve Prolapse and Mitral Annular Disjunction: Clinical and Functional Significance of the Coincidence

2021 ◽  
Vol 8 (2) ◽  
pp. 9
Author(s):  
Nina C. Wunderlich ◽  
Siew Yen Ho ◽  
Nir Flint ◽  
Robert J. Siegel
Keyword(s):  
Mitral Valve ◽  
Mitral Valve Disease ◽  
Morphological Changes ◽  
Morphological Characteristics ◽  
Mitral Annulus ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Valve Disease ◽  
Left Ventricular Myocardium ◽  
Basal Portion

The morphological changes that occur in myxomatous mitral valve disease (MMVD) involve various components, ultimately leading to the impairment of mitral valve (MV) function. In this context, intrinsic mitral annular abnormalities are increasingly recognized, such as a mitral annular disjunction (MAD), a specific anatomical abnormality whereby there is a distinct separation between the mitral annulus and the left atrial wall and the basal portion of the posterolateral left ventricular myocardium. In recent years, several studies have suggested that MAD contributes to myxomatous degeneration of the mitral leaflets, and there is growing evidence that MAD is associated with ventricular arrhythmias and sudden cardiac death. In this review, the morphological characteristics of MAD and imaging tools for diagnosis will be described, and the clinical and functional aspects of the coincidence of MAD and myxomatous MVP will be discussed.

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