scholarly journals Ventricular Remodeling in Aortic Sclerosis

2020 ◽  
Vol 17 (4) ◽  
pp. 21-33
Author(s):  
Elena Mihaela Mihu ◽  
Alexandru Cristian Nechita ◽  
Costel Sorin Stamate ◽  
Rodica Lucia Avram ◽  
Laura Logofătu Cârstocea ◽  
...  

AbstractBackground and aims. Aortic sclerosis associates an increased risk of cardiovascular morbidity and mortality. Recent studies suggest that aortic sclerosis is able to produce ventricular remodeling through inflammatory, non-hemodynamic mechanisms. Our study aims to evaluate the correlation between ventricular remodeling and aortic sclerosis severity.Method. 68 patients with aortic sclerosis without other signifficant associated valvulopathies were examined clinically, biologically and echocardiographic. In 20 patients, we quantiffied the severity of aortic valve calciffication using the backscatter ecographic technique, in parasternal long and short axis view. Backscatter values obtained at the valvular level were calibrated to the blood and pericardium backscatter values.Results. In the 68 patients group, transvalvular aortic velocity correlates with left ventricular mass (p =0.031), which in turn incline to augment with increasing calciffication severity assessed by backscatter. Calciffication severity assessed by backscatter corellates with transvalvular aortic velocity in parasternal long axis view (p =0.039 for blood calibrated backscatter, p =0.029 for pericardium calibrated backscatter), and tends to augment with increasing transvalvular aortic velocity in parasternal short axis view. Patients with normal ventricular geometry incline to have lower aortic transvalvular velocities and a lower degree of calciffication (evaluated by backscatter) compared to patients with ventricular remodeling.Conclusions. Aortic sclerosis is not benign, and may lead, in time, to left ventricular remodeling. With the progression of valvular calciffications in aortic sclerosis patients, the prevalence of ventricular remodeling tends to increase.

2002 ◽  
Vol 12 (1) ◽  
pp. 37-43 ◽  
Author(s):  
Hiroyuki Nagasawa ◽  
Yoshio Arakaki

We assessed the thickness of the normal left ventricular wall according to gender by performing twodimensional echocardiography in children. While a few studies have evaluated left ventricular wall thicknesses in children using two-dimensional echocardiography, there is little information related to the influence of gender throughout childhood. We evaluated 251 patients (128 males and 123 females) with innocent murmurs but without congenital heart anomalies, or coronary artery lesions or arrhythmias, as determined by repeated echocardiographic, and electrocardiographic examinations. Intra-ventricular septal thicknesses at end-diastole and end-systole, and left ventricular posterior thicknesses at end-diastole and end-systole were determined in the parasternal short-axis view. Significant gender differences were observed in the thickness of all four measurements. There was a linear relationship between the thickness of the left ventricular wall and height. Height was the most appropriate and practical index for assessing the thickness of the wall of the left ventricle in children.


2006 ◽  
Vol 291 (5) ◽  
pp. H2021-H2025 ◽  
Author(s):  
Marc A. Pfeffer ◽  
Edward D. Frohlich

The expanding clinical indications for the use of angiotensin-converting enzyme (ACE) inhibitors during the past three decades to reduce cardiovascular morbidity and mortality across a broad spectrum of cardiovascular diseases have been the consequence of impressively productive interchanges between basic science and clinical medicine. In some areas, the initial discovery from animal investigations produced the hypotheses that were confirmed and expanded in patients with specific disease processes. In the development of ACE inhibitors, there are also important examples where an unexpected discovery from clinical trials spurred a host of laboratory investigations that uncovered novel mechanisms to underpin the clinical observations. Although developed as an antihypertensive agent, these effective interchanges, termed “translational research,” have collectively produced convincing data to demonstrate that ACE inhibitors can and should be used to slow progression of renal disease, prevent and treat heart failure, attenuate adverse left ventricular remodeling after myocardial infarction and improve prognosis, reduce atherosclerotic complications in patients with coronary artery disease, and, even more recently, reduce the incidence of Type II diabetes.


2017 ◽  
Vol 4 (4) ◽  
pp. 167-172
Author(s):  
T. Ashcheulova ◽  
O. Honchar ◽  
V. Smyrnova ◽  
N. Gerasimchuk ◽  
S. Ivanchenko

Left ventricular remodeling is one of the earliest complications of hypertension that has been proven to be an independent predictor of cardiovascular morbidity and mortality. In this article, the development of approaches to understanding its mechanics and prognostic value are briefly reviewed, with additional focus on patients with obesity and type 2 diabetes mellitus as frequent comorbid pathologies that significantly modify the typical morphological changes of the heart in hypertension. The main intacardiac mechanisms of decrease of left ventricular function constituing the direct pathophysiological and pathomorphological base for development of chronic heart failure are presented.KeyWords:  hypertension, left ventricle, remodeling, dysfunction, chronic heart failure. РЕМОДЕЛЮВАННЯ ЛІВОГО ШЛУНОЧКА У ХВОРИХ НА ГІПЕРТОНІЧНУ ХВОРОБУ:  ЕВОЛЮЦІЯ УЯВЛЕНЬАщеулова Т.В., Гончарь О.В., Смирнова В.І., Герасимчук Н.М., Іванченко С.В.Ремоделювання лівого шлуночка є одним із найранніших ускладнень гіпертонічної хвороби та має доведену незалежну цінність в якості предиктора серцево-судинної захворюваності та смертності. У статті наведено короткий історичний огляд розвитку уявлень про механізми та прогностичну цінність різних варіантів ремоделювання лівого шлуночка з додатковим фокусом на пацієнтах із супутнім ожирінням та цукровим діабетом 2 типу як частими коморбідним станами, що у значній мірі модифікують типові морфологічні зміни серця при артеріальній гіпертензії. Висвітлено основні інтракардіальні механізми порушення функціональної спроможності лівого шлуночка, що становлять безпосереднє патофізіологічне та патоморфологічне підгрунтя розвитку синдрому хронічної серцевої недостатності при гіпертонічній хворобі.Ключові слова: артеріальна гіпертензія, лівий шлуночок, ремоделювання, дисфункція, хронічна серцева недостатність. РЕМОДЕЛИРОВАНИЕ ЛЕВОГО ЖЕЛУДОЧКА У БОЛЬНЫХ ГИПЕРТОНИЧЕСКОЙ БОЛЕЗНЬЮ: ЭВОЛЮЦИЯ ПРЕДСТАВЛЕНИЙАщеулова Т.В., Гончарь А.В., Смирнова В.И., Герасимчук Н.Н., Иванченко С.В.Ремоделирование левого желудочка является одним из наиболее ранних осложнений гипертонической болезни и имеет доказанную независимую ценность в качестве предиктора сердечно-сосудистой заболеваемости и смертности. В статье приведен краткий исторический обзор развития представлений о механизмах и прогностической ценности разных вариантов ремоделирования левого желудочка с дополнительным фокусом на пациентах с сопутствующим ожирением и сахарным диабетом 2 типа как частыми коморбидным состояниями, в значительной степени модифицирующими типичные морфологические изменения сердца при артериальной гипертензии. Освещены основные интракардиальные механизмы нарушения функциональной состоятельности левого желудочка, что представляющие собой непосредственное патофизиологическое и патоморфологическое основание развития синдрома хронической сердечной недостаточности при гипертонической болезни.Ключевые слова: артериальная гипертензия, левый желудочек, ремоделирования, дисфункция, хроническая сердечная недостаточность.


Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Jan Stritzke ◽  
Marcello R Markus ◽  
Wolfgang Lieb ◽  
Andreas Luchner ◽  
Angela Döring ◽  
...  

Background: Obesity is related to left ventricular (LV) hypertrophy and diastolic dysfunction. However it remains unclear if changes in life style resulting in loss of body weight also have beneficial effects on left ventricular remodeling. In this study we evaluated the effects of weight loss on left ventricular geometry and function during ten years of follow-up. Methods: Subjects (n=1005, aged 25 to 74 years) who originated from a gender and age stratified random sample of German residents of the Augsburg area were examined by standardized echocardiography at baseline and again after ten years. The associations between weight loss and long-term changes of left ventricular end-diastolic diameter (LVEDD), wall thickness (WT), left ventricular mass (LVM), and left atrial diameter (LA) were assessed. Mean relative changes and odds ratios were computed by statistical models adjusting for gender, age, body height, systolic blood pressure and body weight at baseline. Results: After ten years of follow-up 305 individuals presented with a loss of body weight (−3.5+/−3.4kg on average). Whereas 700 subjects presented with an increase of body weight (+5.4+/−4.7kg). Ageing related changes in LV geometry were significantly different in the two groups. Specifically, individuals with weight loss displayed a favorable geometry with relative changes of WT (+5.9% [CI-95% 4.3, 7.5] vs. + 8.1% [7.0, 9.2], p=0.024), LVEDD (−0.6% [−1.5, 0.2] vs. 30.8% [0.2, 1.4], p=0.008), LVM (+6.5% [4.3, 8.8] vs. +11.9% [10.4, 13.5], p<0.001) and LA (−0.9% [−2.1, 0.2] vs. +2.5% [1.7, 3.3], p<0.001), as compared to individuals with weight gain. Moreover, the risk for incident left ventricular hypertrophy (OR 2.5 [1.5– 4.3], p=0.001) and incident diastolic dysfunction (OR 1.9 [1.1–3.4], p=0.023) was significantly higher in individuals presenting with an increase in body weight. Conclusions: As compared to weight gain, weight loss is associated with a significant deceleration of left ventricular remodeling during ageing of the heart. Nevertheless, even in the weight loss group there was no regression in left ventricular mass detectable. Consequently, early interventions especially in young obese individuals are essential for prevention of premature onset of cardiac remodeling.


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