Clinical Impact of Left Ventricular Hypertrophy and Implications for Regression

Artham, Surya M.; Lavie, Carl J.; Milani, Richard V.; Patel, Dharmendrakumar A.; Verma, Anil; Ventura, Héctor O.

doi:10.1016/j.pcad.2009.05.002

Cited by 149 publications

(127 citation statements)

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“…[1][2][3][4][5] These structural changes in the left ventricle also lead to functional impairment, notably impaired LV filling, thereby facilitating the development of diastolic dysfunction 6 and ultimately leading to left atrial (LA) enlargement (LAE). 7 The left atrium is directly exposed to LV pressure during diastole through the open mitral valve, and therefore any morphologic changes in the left atrium are largely determined by the same factors that influence diastolic LV filling.…”

confidence: 99%

Left Atrial Volume Index Predictive of Mortality Independent of Left Ventricular Geometry in a Large Clinical Cohort With Preserved Ejection Fraction

Patel¹,

Lavie²,

Milani³

et al. 2011

Mayo Clinic Proceedings

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Objective: To determine the effect on mortality of the left atrial volume index (LAVI) and left ventricular (LV) geometry (normal, concentric remodeling, eccentric hypertrophy, and concentric hypertrophy). ReSultS: Progressive increases in LAVI and mortality were noted with abnormal LV geometry. Similarly, abnormal LV geometry and mortality were significantly higher in patients with increased LAVI.In patients who died vs surviving patients, the LAVI ± SD was significantly higher (33.0±14.8 vs 28.1±10.8 mL/m 2 ; P<.001) and abnormal LV geometry was significantly more prevalent (62% vs 44%; P<.001). Compared with those with a normal LAVI, patients with a severe LAVI had a 42% increased risk of mortality. In patients with normal LV geometry or concentric remodeling, a severe LAVI was a significant independent predictor of mortality, with an increased risk of 28% and 46%, respectively. Similarly, in patients with eccentric hypertrophy and concentric hypertrophy, the mortality risk in patients with a severe LAVI was twice that of patients with a normal LAVI. Comparison of area under the curve (0.565 [without LAVI] vs 0.596 [with LAVI]; P<.001] and predictive models with and without LAVI for mortality prediction were significant, indicating increased mortality prediction by the addition of LAVI to other independent predictors. cONcluSiON: The LAVI significantly predicts mortality risk, independent of LV geometry, and adds to the overall mortality prediction in a large cohort of patients with preserved systolic function. Mayo Clin © 2011 Mayo Foundation for Medical Education and ResearchL eft ventricular (LV) geometry, as an expression of the structural adaptation to an increased cardiovascular (CV) risk factor burden, is a well-known predictor of CV morbidity and mortality. [1][2][3][4][5] These structural changes in the left ventricle also lead to functional impairment, notably impaired LV filling, thereby facilitating the development of diastolic dysfunction 6 and ultimately leading to left atrial (LA) enlargement (LAE). 7 The left atrium is directly exposed to LV pressure during diastole through the open mitral valve, and therefore any morphologic changes in the left atrium are largely determined by the same factors that influence diastolic LV filling.8 Recent studies have shown that LA volume increases with the severity of diastolic dysfunction and may express long-term exposure to abnormal LV filling pressures, providing a more sensitive and stable morphophysiologic expression of LV diastolic dysfunction. 9Current evidence strongly suggests that LA size, as assessed by echocardiography, is strongly associated with mortality.7,10-12 However, it is still unknown whether LAE predicts mortality independent of LV geometry and also whether it provides additional prognostic information to that of other predictors of mortality in a large cohort of patients with preserved systolic function.To address this gap in the literature, we conducted a study of a large clinical cohort of 36,561 patients with preserved LV ejection ...

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confidence: 99%

Left Atrial Volume Index Predictive of Mortality Independent of Left Ventricular Geometry in a Large Clinical Cohort With Preserved Ejection Fraction

Patel¹,

Lavie²,

Milani³

et al. 2011

Mayo Clinic Proceedings

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“…Regardless its etiology, cardiac hypertrophy is associated with increased incidence of potentially life-threatening ventricular arrhythmias (Artham et al, 2009) and is one of the strongest risk factors for sudden cardiac death (Haider et al, 1998). The mechanisms of arrhythmias in eccentric hypertrophy due to volume overload are known less than in cardiac hypertrophy due to pressure overload or chronic myocardial infarction.…”

mentioning

confidence: 99%

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

Beneš

Melenovský

Škaroupková

et al. 2010

The Anatomical Record

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Chronic volume overload leads to cardiac hypertrophy and later to heart failure (HF), which are both associated with increased risk of cardiac arrhythmias. The goal of this study was to describe changes in myocardial morphology and to characterize arrhythmogenic substrate in rat model of developing HF due to volume overload. An arteriovenous fistula (AVF) was created in male Wistar rats between the inferior vena cava and abdominal aorta using needle technique. Myocardial morphology, tissue fibrosis, and connexin43 distribution, localization and phosphorylation were examined using confocal microscopy and Western blotting in the stage of compensated hypertrophy (11 weeks), and decompensated HF (21 weeks). Heart to body weight (BW) ratio was 89% and 133% higher in AVF rats at 11 and 21 weeks, respectively. At 21 weeks but not 11 weeks, AVF rats had pulmonary congestion (increased lung to BW ratio) indicating presence of decompensated HF. The myocytes in left ventricular midmyocardium were significantly thicker (þ8% and þ45%) and longer (þ88% and þ97%). Despite extensive hypertrophy, there was no excessive fibrosis in the AVF ventricles. Distribution and localization of connexin43 were similar between groups, but its phosphorylation was significantly lower in AVF hearts at 21st week, but not 11th week, suggesting that HF,

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“…41 In a double-blind crossover study, T. arjuna extract was orally administered at a dose of 500 mg 8-hourly, versus placebo for 2 weeks, to 18 healthy, normotensive, nondiabetic, normolipidemic, chronic cigarette smokers with no family history of CVD. 42 T. arjuna was shown to reverse smoking-related endothelial dysfunction as measured by both endothelium-dependent and endothelium-independent, flow-mediated dilation of the brachial artery. There was no smoking interruption during the intervention, in order to remove any beneficial effect from smoking cessation that could confound the study results.…”

Section: Arjuna (Terminalia Arjuna)mentioning

confidence: 96%

The potential role of herbal medicines in the treatment of chronic stable angina pectoris: a review of key herbs, and as illustration, exploration of the Chinese herbal medicine approach

O’Brien

Vitetta²

2012

BTAT

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Herbal medicines have been used for centuries within different cultures to treat cardiovascular disease, including stable angina pectoris. However, the use of herbs varies within traditions of natural medicine, and how they are understood to work in systems such as Chinese medicine, for example, is vastly different from the pharmaceutical model that seeks to reduce herbs to their active constituents. This review first discusses, individually, key herbs used within Western, Indian, and Chinese herbalism to treat stable angina pectoris and their main active constituents and pharmacological actions. The second part of the paper then specifically explores how angina is treated traditionally with Chinese herbal medicine, a unique approach to the understanding of health and illness underpinned by philosophies and theories that describe the physiological functioning and pathological changes in the body in terms very different from those of biomedicine. A foundational account of the guiding theories of Chinese medicine is followed by a description of the cardiovascular system and the etiology and pathogenesis of angina from the Chinese medical perspective. This forms the basis for understanding the rationale for construction of Chinese herbal medicinal formulae for treating angina pectoris. The scientific evidence of the efficacy of some Chinese herbal formulae is discussed.

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Clinical Impact of Left Ventricular Hypertrophy and Implications for Regression

Cited by 149 publications

References 100 publications

Left Atrial Volume Index Predictive of Mortality Independent of Left Ventricular Geometry in a Large Clinical Cohort With Preserved Ejection Fraction

Left Atrial Volume Index Predictive of Mortality Independent of Left Ventricular Geometry in a Large Clinical Cohort With Preserved Ejection Fraction

Myocardial Morphological Characteristics and Proarrhythmic Substrate in the Rat Model of Heart Failure Due to Chronic Volume Overload

The potential role of herbal medicines in the treatment of chronic stable angina pectoris: a review of key herbs, and as illustration, exploration of the Chinese herbal medicine approach

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