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The Journal of Thoracic and... May 2022
Topics: Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Ventricular Function, Left; Ventricular Remodeling
PubMed: 32981706
DOI: 10.1016/j.jtcvs.2020.09.002 -
Open Heart Jan 2021To phenotype patients referred to a tertiary centre for the exploration of a left ventricular hypertrophy (LVH) starting from 12 mm of left ventricular wall thickness...
AIMS
To phenotype patients referred to a tertiary centre for the exploration of a left ventricular hypertrophy (LVH) starting from 12 mm of left ventricular wall thickness (LVWT).
METHODS AND RESULTS
Consecutive patients referred for aetiological workup of LVH, beginning at 12 mm of LVWT were retrospectively included in this tertiary single-centred observational study. Patients presenting with severe aortic stenosis were excluded. Aetiological workup was reviewed for each subject and aetiologies were adjudicated by expert consensus.Among 591 patients referred for LVH aetiological workup, 41% had a maximal LVWT below 15 mm. LVH aetiologies were led by cardiac amyloidosis (CA, 34.3%), followed by sarcomeric hypertrophic cardiomyopathy (S-HCM, 32.1%), hypertensive cardiomyopathy (21.7%), unknown aetiology (7.6%) and other (4.2%), including Anderson-Fabry's disease (1.7%). CA and S-HCM affected over 50% of patients with mild LVH (12-14 mm); the prevalence of these aetiologies rose with LVH severity. Among patients with Anderson-Fabry's disease, 4 (40%) had a maximal LVWT <15 mm.
CONCLUSIONS
Mild LVH (ie, 12-14 mm) conceals multiple aetiologies that can lead to specific treatment, cascade family screening and specific follow-up. Overall, CA is nowadays the leading cause of LVH in tertiary centers.
Topics: Aged; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Magnetic Resonance Imaging, Cine; Male; Middle Aged; Retrospective Studies; Tertiary Care Centers; Ventricular Function, Left
PubMed: 33441470
DOI: 10.1136/openhrt-2020-001462 -
Echocardiography (Mount Kisco, N.Y.) Sep 2018Left ventricular hypertrophy (LVH) may reflect a wide variety of physiologic and pathologic conditions. Thus, it can be misleading to consider all LVH to be homogenous...
Refined 4-group classification of left ventricular hypertrophy based on ventricular concentricity and volume dilatation outlines distinct noninvasive hemodynamic profiles in a large contemporary echocardiographic population.
BACKGROUND
Left ventricular hypertrophy (LVH) may reflect a wide variety of physiologic and pathologic conditions. Thus, it can be misleading to consider all LVH to be homogenous or similar. Refined 4-group classification of LVH based on ventricular concentricity and dilatation may be identified. To determine whether the 4-group classification of LVH identified distinct phenotypes, we compared their association with various noninvasive markers of cardiac stress.
METHODS
Cohort of unselected adult outpatients referred to a seven tertiary care echocardiographic laboratory for any indication in a 2-week period. We evaluated the LV geometric patterns using validated echocardiographic indexation methods and partition values.
RESULTS
Standard echocardiography was performed in 1137 consecutive subjects, and LVH was found in 42%. The newly proposed 4-group classification of LVH was applicable in 88% of patients. The most common pattern resulted in concentric LVH (19%). The worst functional and hemodynamic profile was associated with eccentric LVH and those with mixed LVH had a higher prevalence of reduced EF than those with concentric LVH (P < .001 for all).
CONCLUSIONS
The new 4-group classification of LVH system showed distinct differences in cardiac function and noninvasive hemodynamics allowing clinicians to distinguish different LV hemodynamic stress adaptations in patients with LVH.
Topics: Aged; Cross-Sectional Studies; Echocardiography; Female; Heart Ventricles; Hemodynamics; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged; Reproducibility of Results; Severity of Illness Index
PubMed: 29797430
DOI: 10.1111/echo.14031 -
European Biophysics Journal : EBJ Jul 2020Mathematical action potential (AP) modeling is a well-established but still-developing area of research to better understand physiological and pathological processes. In...
Mathematical action potential (AP) modeling is a well-established but still-developing area of research to better understand physiological and pathological processes. In particular, changes in AP mechanisms in the isoproterenol (ISO) -induced hypertrophic heart model are incompletely understood. Here we present a mathematical model of the rat AP based on recordings from rat ventricular myocytes. In our model, for the first time, all channel kinetics are defined with a single type of function that is simple and easy to apply. The model AP and channels dynamics are consistent with the APs recorded from rats for both Control (absence of ISO) and ISO-treated cases. Our mathematical model helps us to understand the reason for the prolongation in AP duration after ISO application while ISO treatment helps us to validate our mathematical model. We reveal that the smaller density and the slower gating kinetics of the transient K current help explain the prolonged AP duration after ISO treatment and the increasing amplitude of the rapid and the slow inward rectifier currents also contribute to this prolongation alongside the flux in Ca currents. ISO induced an increase in the density of the Na current that can explain the faster upstroke. We believe that AP dynamics from rat ventricular myocytes can be reproduced very well with this mathematical model and that it provides a powerful tool for improved insights into the underlying dynamics of clinically important AP properties such as ISO application.
Topics: Action Potentials; Animals; Cardiomegaly; Heart Ventricles; Ion Channels; Isoproterenol; Kinetics; Male; Models, Cardiovascular; Rats; Rats, Wistar
PubMed: 32462262
DOI: 10.1007/s00249-020-01439-8 -
The Annals of Pharmacotherapy Jun 1993To discuss the effects of angiotensin-converting enzyme (ACE) inhibitors on ventricular remodeling and survival after acute myocardial infarction (AMI). An overview is... (Review)
Review
OBJECTIVE
To discuss the effects of angiotensin-converting enzyme (ACE) inhibitors on ventricular remodeling and survival after acute myocardial infarction (AMI). An overview is provided of the pathophysiologic changes produced by AMI and the ventricular remodeling process. ACE inhibitors have been studied for their use in the prevention of ventricular remodeling and reduction in postinfarction mortality. Trials in humans and animals are reviewed, including study methods, results, and limitations.
DATA SOURCES
MEDLINE searches identified applicable literature, including experimental trials and review articles.
STUDY SELECTION
All clinical trials of ACE inhibitors following AMI were reviewed.
DATA EXTRACTION
Morbidity and mortality data evaluating the effect of postinfarction ventricular remodeling are rare. At the time of publication, all available clinical trials studying the effects of ACE inhibitors on postinfarction ventricular remodeling were included, regardless of whether morbidity and mortality were assessed. Data from the Survival and Ventricular Enlargement (SAVE) and Cooperative New Scandinavian Enalapril Survival Study II (CONSENSUS II) trials include almost 10,000 patients. Data were extracted by two independent observers. Data quality and validity were assessed based on sample size, stratification of study population, and statistical power of the studies.
DATA SYNTHESIS
ACE inhibitors may prevent the deleterious consequences of AMI, including ventricular remodeling and neurohumoral activation. Ventricular hypertrophy begins acutely following infarction, an early physiologic response to myocardial injury. Hemodynamic benefits from the initial phase of left ventricular hypertrophy include increased ventricular working capacity, normalized systolic wall stress, and maintenance of stroke volume. Although acute dilatation may delay hemodynamic deterioration for six to eight months, it also results in reduced coronary reserve, decreased ventricular compliance, and altered myocardial contractility. With chronic dilatation, the beneficial effects reach a plateau, stroke volume decreases, contractility is reduced, and cardiac failure may ensue. Ventricular hypertrophy is associated with worsened prognosis following infarction and may be the most important single determinant of late prognosis. Ventricular hypertrophy contributes to postinfarction heart failure, angina, and sudden death. Clinical trials show a beneficial effect of the ACE inhibitor captopril on the prevention of left ventricular dysfunction. Although captopril therapy significantly improved survival and myocardial function following AMI in the SAVE trial, these results cannot be generalized to all patient subpopulations. The CONSENSUS II trial demonstrated a decreased survival rate when enalapril was administered within 24 hours of AMI, indicating that timing of therapy may be an important consideration. Captopril therapy may positively affect outcome when initiated 3-16 days following infarction in patients with ejection fractions below 40 percent and who have no signs of ischemia or heart failure. Based on the CONSENSUS II results, enalapril therapy immediately following AMI cannot be recommended.
CONCLUSIONS
Clinical trials have demonstrated that ACE inhibitors can limit ventricular hypertrophy following AMI, resulting in clinical benefit and improved survival. These effects may be secondary to modulation of neurohumoral activation or the antiischemic effect of ACE inhibitors, which may also reduce the incidence of reinfarction. Early intervention with ACE inhibitors (within 3-16 days of infarction) can slow the progression of cardiovascular disease and improve the survival rate.
Topics: Angiotensin-Converting Enzyme Inhibitors; Animals; Clinical Trials as Topic; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Hypertrophy, Right Ventricular; Myocardial Infarction; Prognosis
PubMed: 8329800
DOI: 10.1177/106002809302700617 -
Journal of the American College of... Dec 1995This study sought to achieve an understanding of the true structural heterogeneity of hypertrophic cardiomyopathy.
Phenotypic spectrum and patterns of left ventricular hypertrophy in hypertrophic cardiomyopathy: morphologic observations and significance as assessed by two-dimensional echocardiography in 600 patients.
OBJECTIVES
This study sought to achieve an understanding of the true structural heterogeneity of hypertrophic cardiomyopathy.
BACKGROUND
The diversity and clinical significance of the morphologic expression of hypertrophic cardiomyopathy have not been fully defined within this broad disease spectrum.
METHODS
Patterns of left ventricular hypertrophy were characterized by two-dimensional echocardiography in a large study cohort of 600 patients (7 to 79 years old, mean age 45; 393 [66%] men) consecutively studied at two referral centers.
RESULTS
Left ventricular wall thickness was 15 to 52 mm (mean [+/- SD] 22.3 +/- 5). A multitude of patterns of asymmetric left ventricular hypertrophy were identified, with the most common showing diffuse involvement of substantial portions of both ventricular septum and free wall. Of 16 possible patterns of left ventricular hypertrophy, 12 (78%) were identified among the 600 patients. Hypertrophy most commonly involved two left ventricular segments (228 patients [38%]) or three or more segments (202 patients [34%]), but was also localized to one segment in a substantial number of patients (170 [28%]). The anterior portion of the ventricular septum was the region of the left ventricle that most frequently showed thickening (573 patients [96%]), and was also the predominant site of hypertrophy in most patients (492 patients [83%]). Patterns of wall thickening that were either concentric (i.e., symmetric) or confined to the apex were particularly uncommon (in 1% each).
CONCLUSIONS
1) In hypertrophic cardiomyopathy, the distribution of left ventricular hypertrophy is characteristically asymmetric and particularly heterogeneous, encompassing most possible patterns of wall thickening, from extensive and diffuse to mild and segmental, and with no single morphologic expression considered typical or classic. 2) A greater extent of left ventricular hypertrophy was associated with younger age and more marked mitral valve systolic anterior motion and outflow obstruction but showed no relation to either magnitude of symptoms or gender.
Topics: Adolescent; Adult; Aged; Cardiomyopathy, Hypertrophic; Child; Echocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Middle Aged
PubMed: 7594106
DOI: 10.1016/0735-1097(95)00390-8 -
Journal of the American College of... Mar 1986To determine the prevalence and correlates of echocardiographic left ventricular hypertrophy among subjects in a general population, we studied 621 employed subjects....
To determine the prevalence and correlates of echocardiographic left ventricular hypertrophy among subjects in a general population, we studied 621 employed subjects. Patients with uncomplicated essential hypertension in a worksite-based treatment program included 145 with borderline hypertension and 316 with sustained hypertension by World Health Organization criteria. Normotensive subjects were randomly selected from members of the same unions. M-mode echocardiographic left ventricular dimensions were used to calculate left ventricular mass and other indexes of left ventricular anatomy. The specificity of 13 echocardiographic criteria of left ventricular hypertrophy was determined in normotensive individuals, and the prevalence of left ventricular hypertrophy by each criterion was assessed in patients with borderline or sustained essential hypertension. The results suggest that the most suitable reference standard for detection of left ventricular hypertrophy in a heterogeneous urban population utilizes sex-specific cutoff values for left ventricular mass index of 110 g/m2 or greater for women and 134 g/m2 or greater for men. With 97% specificity, the prevalence of left ventricular hypertrophy by these criteria is approximately 12% among patients with borderline hypertension and 20% among patients with relatively mild, uncomplicated sustained essential hypertension. Wall thickness measurements performed slightly less well. At similar levels of blood pressure, black patients were more likely than white patients to exhibit concentric left ventricular hypertrophy, especially among borderline hypertensive patients. Left ventricular hypertrophy occurred in patients with sustained hypertension who also exhibited increased cardiac output, strongly associated with low plasma renin activity.
Topics: Adult; Cardiomegaly; Echocardiography; Female; Heart Ventricles; Humans; Hypertension; Male; Middle Aged; Occupational Diseases; Risk
PubMed: 2936789
DOI: 10.1016/s0735-1097(86)80476-4 -
ESC Heart Failure Feb 2019In hypertrophy and heart failure, the proarrhythmic persistent Na current (I ) is enhanced. We aimed to investigate the electrophysiological role of neuronal sodium...
AIMS
In hypertrophy and heart failure, the proarrhythmic persistent Na current (I ) is enhanced. We aimed to investigate the electrophysiological role of neuronal sodium channel Na 1.8 in human hypertrophied myocardium.
METHODS AND RESULTS
Myocardial tissue of 24 patients suffering from symptomatic severe aortic stenosis and concomitant significant afterload-induced hypertrophy with preserved ejection fraction was used and compared with 12 healthy controls. We performed quantitative real-time PCR and western blot and detected a significant up-regulation of Na 1.8 mRNA (2.34-fold) and protein expression (1.96-fold) in human hypertrophied myocardium compared with healthy hearts. Interestingly, Na 1.5 protein expression was significantly reduced in parallel (0.60-fold). Using whole-cell patch-clamp technique, we found that the prominent I was significantly reduced after addition of novel Na 1.8-specific blockers either A-803467 (30 nM) or PF-01247324 (1 μM) in human hypertrophic cardiomyocytes. This clearly demonstrates the relevant contribution of Na 1.8 to this proarrhythmic current. We observed a significant action potential duration shortening and performed confocal microscopy, demonstrating a 50% decrease in proarrhythmic diastolic sarcoplasmic reticulum (SR)-Ca leak and SR-Ca spark frequency after exposure to both Na 1.8 inhibitors.
CONCLUSIONS
We show for the first time that the neuronal sodium channel Na 1.8 is up-regulated on mRNA and protein level in the human hypertrophied myocardium. Furthermore, inhibition of Na 1.8 reduced augmented I , abbreviated the action potential duration, and decreased the SR-Ca leak. The findings of our study suggest that Na 1.8 could be a promising antiarrhythmic therapeutic target and merits further investigation.
Topics: Action Potentials; Aged; Blotting, Western; Diastole; Female; Gene Expression Regulation; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Myocytes, Cardiac; NAV1.8 Voltage-Gated Sodium Channel; Patch-Clamp Techniques; RNA; Real-Time Polymerase Chain Reaction; Sarcoplasmic Reticulum
PubMed: 30378291
DOI: 10.1002/ehf2.12378 -
British Heart Journal Nov 1977To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by...
To assess the adaptation of the left ventricle to a chronic pressure overload we used echocardiography to study 18 patients with left ventricular hypertrophy caused by systemic arterial hypertension. Increased values for either posterior wall or interventricular septal thickness or both confirmed the presence of left ventricular hypertrophy in all patients and an increase in the average wall thickness to radius ratio was consistent with the development of concentric hypertrophy. No patient had clinical evidence of ischaemic heart disease. Ejection phase indices of left ventricular performance (mean Vcf, fractional per cent of shortening, normalised posterior wall velocity, and ejection fraction) were within the normal range in the basal state in 16 of the 18 patients. The hypothesis is advanced that patients with concentric left ventricular hypertrophy resulting from systemic arterial hypertension usually have normal left ventricular performance in the basal state because values for wall stress remain within the normal range. We conclude that the hypertrophic response to a chronic increase in systemic arterial pressure does not per se result in depression of the basal inotropic state of the left ventricle.
Topics: Adult; Aged; Cardiomegaly; Echocardiography; Female; Heart Ventricles; Humans; Hypertension; Male; Middle Aged; Myocardial Contraction; Stress, Mechanical
PubMed: 145228
DOI: 10.1136/hrt.39.11.1239 -
International Journal of Sports Medicine Mar 2014Time-tested data indicate that ECG diagnosis of left ventricular hypertrophy in young athletes is challenging due to low sensitivity of the commonly used criteria. We...
Time-tested data indicate that ECG diagnosis of left ventricular hypertrophy in young athletes is challenging due to low sensitivity of the commonly used criteria. We sought to establish whether adult ECG criteria can be appropriate to make diagnosis of both common and uncommon patterns of left ventricular hypertrophy in young trained athletes. A total of 122 athletes, ages 16.2±3.8 years, training at least 5 h per week, were studied with Sokolow-Lyon voltage, Romhilt-Estes, Cornell voltage, Cornell Product, Perugia and Framingham scores. Garson Criteria were also investigated in athletes under 16. Participants were divided into 2 groups based on the presence (group-A, n=56) or absence (group-B, n=66) of at least one positive ECG score. Test performance was calculated with respect to accurate echocardiographic diagnosis of left ventricular hypertrophy. There were no inter-group differences regarding physical characteristics and training burden. 9 athletes from group-A (16%) and 2 from group-B (3%) were found to have left ventricular hypertrophy, likely to be pathological in 2 cases from group-A. Criteria gathering both QRS voltages and ST-T anomalies, like Perugia-score, best identified this subgroup and should be preferred to those based on QRS voltage analysis alone.
Topics: Diagnosis, Differential; Electrocardiography; Female; Heart Ventricles; Humans; Hypertrophy, Left Ventricular; Male; Physical Conditioning, Human; Sensitivity and Specificity; Sports; Ultrasonography; Ventricular Function
PubMed: 23900896
DOI: 10.1055/s-0033-1345180