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Revue Medicale Suisse May 2017Left ventricular hypertrophy is a common finding during echocardiography. A precise evaluation of the left ventricular wall thickness, ventricular mass and distribution...
Left ventricular hypertrophy is a common finding during echocardiography. A precise evaluation of the left ventricular wall thickness, ventricular mass and distribution of hypertrophy is crucial both for diagnostic workup, follow-up and for prognostic evaluation. The differential diagnosis of left ventricular hypertrophy includes hypertrophic cardiomyopathies, hypertrophy secondary to abnormal left ventricular filling conditions, hypertrophy linked to intense physical training and the isolated basal septal hypertrophy of the elderly. Amongst the tools at the disposition of the cardiologist, regional analysis of longitudinal strain appears promising in helping distinguish cardiac amyloidosis form other forms of hypertrophy.
Topics: Adult; Aged; Amyloidosis; Diagnosis, Differential; Echocardiography; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Prognosis
PubMed: 28639774
DOI: No ID Found -
Journal of Hypertension. Supplement :... Sep 1998Hemodynamic and non-hemodynamic factors contribute to the development of left ventricular hypertrophy (LVH). The presence of LVH is an important independent risk factor... (Comparative Study)
Comparative Study Review
Hemodynamic and non-hemodynamic factors contribute to the development of left ventricular hypertrophy (LVH). The presence of LVH is an important independent risk factor for total mortality and for cardiovascular morbidity and mortality. Direct cardiac effects of LVH include an increased risk of developing of congestive heart failure, an increased risk of arrhythmic events, and a reduced coronary flow reserve, promoting myocardial ischemic episodes. In addition, hypertension may promote the development of coronary artery atherosclerosis. The prognostic implications of LVH underscore the importance of diagnostic procedures. The electrocardiogram has a high specificity to identify patients with LVH but the sensitivity is fairly low. Echocardiography provides higher sensitivity and also gives important information, such as the pattern of left ventricular geometry, which is of prognostic importance, and the presence of diastolic dysfunction, which is an early abnormality in the evolution of hypertensive LVH. Reversal of LVH appears to improve prognosis. Reduction of blood pressure is one important component in the regression of LVH. Important quantitative differences exist between drug classes in the reversal of cardiac hypertrophy despite similar antihypertensive effects, suggesting other factors to be of importance in the regression of left ventricular mass. LVH is reduced more by angiotensin-converting enzyme inhibitors than by other antihypertensive drug classes, suggesting an effect on structural myocardial changes beyond that provided by the reduction of blood pressure. Recent data suggest that angiotensin II receptor antagonists (AIIRAs) have quantitatively similar effects on left ventricular mass as do angiotensin-converting enzyme inhibitors. A comparative trial of the AIIRA irbesartan and the beta-blocker atenolol demonstrated that despite similar reductions in blood pressure, the reductions attained in left ventricular mass with irbesartan were progressive and numerically greater than those attained with atenolol. Taken together, these findings provide circumstantial evidence for an important role of angiotensin II acting on angiotensin type 1 (AT1) receptors in the development or maintenance of cardiac hypertrophy. Confirmation of the favorable effects of angiotensin-converting enzyme inhibitors and AIIRAs on left ventricular mass in larger trials, including those assessing cardiovascular morbidity and mortality, will be of major importance in the future treatment of hypertension.
Topics: Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antihypertensive Agents; Female; Follow-Up Studies; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Male; Middle Aged; Randomized Controlled Trials as Topic; Ultrasonography
PubMed: 9855028
DOI: No ID Found -
Heart Failure Reviews Mar 2010Recent studies in various rodent models of pathologic ventricular hypertrophy report the re-expression of deiodinase type 3 (D3) in cardiomyocytes. D3 inactivates... (Review)
Review
Recent studies in various rodent models of pathologic ventricular hypertrophy report the re-expression of deiodinase type 3 (D3) in cardiomyocytes. D3 inactivates thyroid hormone (T3) and is mainly expressed in tissues during development. The stimulation of D3 activity in ventricular hypertrophy and subsequent heart failure is associated with severe impairment of cardiac T3 signaling. Hypoxia-induced signaling appears to drive D3 expression in the hypertrophic cardiomyocyte, but other signaling cascades implicated in hypertrophy are also capable of stimulating transcription of the DIO3 gene. Many cardiac genes are transcriptionally regulated by T3 and impairment of T3 signaling will not only reduce energy turnover, but also lead to changes in gene expression that contribute to contractile dysfunction in pathologic remodeling. Whether stimulation of D3 activity and the ensuing local T3-deficiency is an adaptive response of the stressed heart or part of the pathologic signaling network leading to heart failure, remains to be established.
Topics: Animals; Cardiomegaly; Heart Failure; Heart Ventricles; Humans; Iodide Peroxidase; Myocytes, Cardiac; Rats; Signal Transduction; Thyroid Hormones
PubMed: 19107595
DOI: 10.1007/s10741-008-9133-7 -
Nutrition, Metabolism, and... Oct 2013Obesity is characterized by the disproportionate growth of the components of body size, including adipose tissue and lean body mass. Left ventricular (LV) hypertrophy... (Review)
Review
Obesity is characterized by the disproportionate growth of the components of body size, including adipose tissue and lean body mass. Left ventricular (LV) hypertrophy often develops, due to the coexistence of hemodynamic (cardiac workload) and non-hemodynamic components (including body composition and activity of visceral fat). While the hypertrophy of cardiomyocytes is produced by the hemodynamic load, through sarcomeric replication, there is a parallel growth of non-muscular myocardial components, including interstitial fat infiltration and accumulation of triglycerides in the contractile elements, which are thought to influence LV geometric pattern. Thus, pure intervention on hemodynamic load is unlikely to result in effective reduction of LV hypertrophy in obese. We review pathophysiology and prevalence of LV hypertrophy in obesity, with specific attention to LV geometric abnormalities and relations with body size.
Topics: Body Size; Female; Heart Ventricles; Hemodynamics; Humans; Hypertrophy, Left Ventricular; Male; Models, Biological; Obesity; Prevalence; Sex Characteristics; Weight Loss
PubMed: 24095148
DOI: 10.1016/j.numecd.2013.06.012 -
Medical Science Monitor : International... 2001Pictures certainly are worth a thousand words in the case of the structure of the connective tissue skeleton of normal and diseased myocardium. This report reviews the... (Review)
Review
Pictures certainly are worth a thousand words in the case of the structure of the connective tissue skeleton of normal and diseased myocardium. This report reviews the connective tissue matrix of the normal human myocardial tissue and the pathological myocardial fibrosis in left ventricular hypertrophy due to chronic arterial hypertension in humans and in human chronic chagasic myocarditis. The myocardial connective tissue matrix was studied employing a cell-maceration method that removes the myocardial tissue non-fibrous elements, and leaves behind a non-collapsed matrix, thus allowing a better three-dimensional view. Such information extends our knowledge of the expression of interstitial myocardial fibrous tissue in normal hearts and in hypertensive left ventricular hypertrophy and chronic chagasic myocarditis. The progressive accumulation of interstitial collagen fibers in both chronic cardiac diseases may be expected to decrease myocardial compliance and disrupt synchronous contractions of the ventricles during systole, contributing to a spectrum of ventricular dysfunction that involve either the diastolic or systolic phase of the cardiac cycle or both. In hypertensive heart disease myocardial fibrosis can be also implicated in the genesis of ventricular dysrhythmias, possible causes of sudden death among chronic hypertensive patients. Regarding chronic chagasic myocarditis, myocardial fibrosis is probably implicated in the genesis of malignant ventricular tachyarrhythmias (ventricular tachycardia and ventricular fibrillation), major causes of sudden death among patients with chronic Chagas' heart disease. The collagen distribution could interfere on the electrical properties of the myocardium. Fibrosis can block the cardiac impulse that may recycle (re-entry) through an alternative route and could slow conduction. In addition, the thick collagenous septa encompassing muscle fiber bundles could interfere with lateral impulse conduction, which would favor re-entry. Moreover, the methodology used is a useful tool to study the spatial organization of the collagen fibrils of the myocardium under normal and pathological conditions.
Topics: Chagas Cardiomyopathy; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Microscopy, Electron, Scanning
PubMed: 11433216
DOI: No ID Found -
Biomedicine & Pharmacotherapy =... Jan 2021Maternal obesity induces adverse cardiac programming in offspring, and effective interventions are needed to prevent cardiovascular ill-health. Herein we hypothesized...
BACKGROUND
Maternal obesity induces adverse cardiac programming in offspring, and effective interventions are needed to prevent cardiovascular ill-health. Herein we hypothesized that exposure to maternal obesogenic diet-induced obesity in mice results in left ventricular remodelling and hypertrophy in early childhood, and that maternal N-acetylcysteine (NAC) treatment alleviates these effects in a sex-dependent manner.
METHODS AND RESULTS
The maternal obesity was induced in mice by the consumption of a Western diet accompanied by a 20 % sucrose solution. To determine the effect of NAC on the cardiac outcomes induced by maternal obesity, obese dams were continuously exposed to the obesogenic diet, with or without the oral NAC treatment during pregnancy. Left ventricular remodelling and hypertrophy occurred as early as 7 days after birth in the male offspring of obese dams (O-OB) compared with controls (O-CO). An over-expression of key genes and markers related to cardiac fibrosis accompanied by more disorganized myofibrils was observed in the hearts of neonatal male O-OB mice. When we next evaluated the level of oxidative stress in the hearts of neonatal mice, the activity of enzymatic antioxidants declined and expression of NOX enzyme complex was up-regulated in O-OB offspring hearts, but was normal in the offspring of NAC treated mice (O-OB/NAC). Maternal obesity also activated cardiac Akt and mammalian target of rapamycin (mTOR) signalling in offspring, and NAC treatment restored offspring cardiac Akt-mTOR signalling to normal irrespective of sex. NAC treatment did not prevent cardiomyocyte hypertrophy but did alleviate increased heart weight, interventricular septal thickness, and collagen content in male O-OB/NAC pups.
CONCLUSIONS
Collectively, our results indicated that NAC blunted cardiac fibrosis and related ventricular hypertrophy of male neonatal offspring in the setting of maternal obesity, potentially acting by reducing oxidative stress. The present study provides a basis for investigating the role of NAC in nutrition-related cardiac programming.
Topics: Acetylcysteine; Animal Nutritional Physiological Phenomena; Animals; Animals, Newborn; Antioxidants; Disease Models, Animal; Female; Fibrosis; Heart Ventricles; Hypertrophy, Left Ventricular; Male; Maternal Nutritional Physiological Phenomena; Mice, Inbred C57BL; Obesity, Maternal; Oxidative Stress; Pregnancy; Prenatal Exposure Delayed Effects; Sex Factors; Ventricular Function, Left; Ventricular Remodeling; Mice
PubMed: 33378994
DOI: 10.1016/j.biopha.2020.110989 -
The Journal of Surgical Research Nov 2019Before birth, the fetal right ventricle (RV) is the pump for the systemic circulation and is about as thick as the left ventricle (LV). After birth, the RV becomes the... (Review)
Review
BACKGROUND
Before birth, the fetal right ventricle (RV) is the pump for the systemic circulation and is about as thick as the left ventricle (LV). After birth, the RV becomes the pump for the lower pressure pulmonary circulation, and the RV chamber elongates without change in its wall thickness. We hypothesize that the fetal RV may be a model of compensated RV hypertrophy, and understanding this process may aid in discovering therapeutic strategies for RV failure.
METHODS
We performed a literature review and identified pertinent articles from 1980 to present.
RESULTS
The following topics were identified to be most pertinent in right ventricular involution: morphologic and histologic changes of the RV, cellular proliferation and terminal differentiation, the effect of stress on RV development, excitation contraction coupling and inotropic response change over time, and the amount of apoptosis through RV development.
CONCLUSIONS
The RV changes on multiple levels after its transition from systemic to pulmonary circulation. Although published literature has variable results due partly from differences between animal models, the literature shows a clear need for more research in the field.
Topics: Animals; Cell Proliferation; Heart Ventricles; Humans; Hypertrophy, Right Ventricular
PubMed: 31252349
DOI: 10.1016/j.jss.2019.05.048 -
Kardiologiia 2014In a review article reflects the leading role of combined treatment of blockers of the renin-angiotensin-aldosterone system and dihydropyridine calcium antagonists in... (Review)
Review
In a review article reflects the leading role of combined treatment of blockers of the renin-angiotensin-aldosterone system and dihydropyridine calcium antagonists in reducing left ventricular mass. The advantages of fixed combinations in the treatment of hypertensive patients, including those with left ventricular hypertrophy. The advantages of the low risk of side effects and high patient adherence to treatment using antagonists of angiotensin II receptor in comparison with other classes of antihypertensive drugs in selecting initial therapy, patients with hypertension, including the combination of drugs.
Topics: Antihypertensive Agents; Disease Management; Drug Combinations; Heart Ventricles; Humans; Hypertension; Hypertrophy, Left Ventricular; Patient Selection
PubMed: 25102754
DOI: 10.18565/cardio.2014.3.82-91 -
The American Journal of Cardiology Nov 1997Left ventricular wall thickness >1.3 cm, septal-to-posterior wall ratios > 1.5, diastolic left ventricular size >6.0 cm, and eccentric or concentric remodeling are rare...
Left ventricular wall thickness >1.3 cm, septal-to-posterior wall ratios > 1.5, diastolic left ventricular size >6.0 cm, and eccentric or concentric remodeling are rare in athletes. Values outside of these cutoffs in an athlete of any age probably represent a pathologic state.
Topics: Adult; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged; Sports
PubMed: 9388126
DOI: 10.1016/s0002-9149(97)00693-0 -
Journal of the American Heart... Sep 2015
Think Small and Examine the Constituents of Left Ventricular Hypertrophy and Heart Failure: Cardiomyocytes Versus Fibroblasts, Collagen, and Capillaries in the Interstitium.
Topics: Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging; Male; Ventricular Remodeling
PubMed: 26374296
DOI: 10.1161/JAHA.115.002491