Prognostic effect of inappropriately high left ventricular mass in asymptomatic severe aortic stenosis

Cioffi, Giovanni; Faggiano, Pompilio; Vizzardi, Enrico; Tarantini, Luigi; Cramariuc, Dana; Gerdts, Eva; Simone, Giovanni de

doi:10.1136/hrt.2010.192997

Cited by 267 publications

(216 citation statements)

References 35 publications

Supporting

Mentioning

197

Contrasting

Unclassified

Order By: Relevance

“…Nevertheless, patients with advanced CKD and ESRD represent a population that is at high risk for rapid progression of AS 20, 99, 100, 101. LVH, reduced LVEF, and PH are all linked to a higher risk of adverse events in patients with AS and are highly prevalent in patients with advanced CKD and ESRD 113, 114, 115, 116. With these considerations in mind, it may be reasonable to correct severe asymptomatic AS prior to renal transplantation with SAVR or TAVR.…”

Section: Valvular Disease In Patients With Esrdmentioning

confidence: 99%

Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Bhatti

Galougahi

Paz

et al. 2016

JAHA

View full text Add to dashboard Cite

Section: Valvular Disease In Patients With Esrdmentioning

confidence: 99%

Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Bhatti

Galougahi

Paz

et al. 2016

JAHA

View full text Add to dashboard Cite

“…19 Severe LVH is found in 17% of symptomatic patients with mild to moderate AS 20 and in 67% of those with asymptomatic severe AS. 21 The increased LV afterload produced by AS results in a structural hypertrophic adaptation that is generally concentric, characterized by wall thickening with normal LV cavity dimensions. 22 Systolic performance at rest is normal or mildly increased and diastolic dysfunction is present.…”

Section: Primary Lvhmentioning

confidence: 99%

From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

119

View full text Add to dashboard Cite

Left ventricular hypertrophy (LVH) is growth in left ventricular mass caused by increased cardiomyocyte size. LVH can be a physiological adaptation to strenuous physical exercise, as in athletes, or it can be a pathological condition, which is either genetic or secondary to LV overload. Physiological LVH is usually benign and regresses upon reduction/cessation of physical activity. Pathological LVH is a compensatory phenomenon, which eventually may become maladaptive and evolve towards progressive LV dysfunction and heart failure (HF). Both interstitial and replacement fibrosis play a major role in the progressive decompensation of the hypertrophied LV. Coronary microvascular dysfunction (CMD) and myocardial ischemia, which have been demonstrated in most forms of pathological LVH, have an important pathogenetic role in the formation of replacement fibrosis and both contribute to the evolution towards LV dysfunction and HF. Noninvasive imaging allows detection of myocardial fibrosis and CMD, thus providing unique information for the stratification of patients with LVH. DCM is generally caused by viral/bacterial myocarditis, exposure to cardiotoxic substances or is a manifestation of a systemic disease. Before cell death and fibrotic repair occur, multiple factors contribute to contractile dysfunction, including abnormalities in sarcolemmal integrity, energy production, calcium handling and force transmission. 10 Both systolic and diastolic dysfunction worsen with time and EF is progressively reduced, with symptoms and signs of HF. Secondary LVHCardiomyocyte hypertrophy is the primary mechanism by which the heart counteracts a protracted increase in stress (or load) on the ventricular wall. 11 According to Laplace's law, 12 wall stress is directly related to LV cavity size and intracavitary pressure and inversely related to wall thickness. Thus, wall thickening will counteract, at least in part, the increased stress and oxygen demand caused by pressure or volume overload, although, in the long run, this compensatory mechanism may become maladaptive. On the other hand, several other nonhemodynamic factors, including activation of the adrenergic and renin-angiotensin-aldosterone (RAAS) systems, release of growth factors and cytokines, contribute to the development of LVH. 13,14 Pressure Overload In most cases, pressure overload manifests as arterial hypertension (AH) or aortic stenosis (AS).Hypertensive Heart The most common condition associated with an increase in cardiac afterload and wall stress is AH. 15 Approximately 20-60% of patients with uncomplicated AH have evidence of increased LVM on echocardiography. 16 LVM can increase from wall thickening, chamber dilatation or both. Wall thickening occurs more commonly in response to pressure overload whereas chamber dilation occurs more commonly in response to volume overload. Although LV wall thickness is more closely related to systemic diastolic blood pressure (concentric hypertrophy), reflecting pure pressure load caused by increased systemic vascular resistance...

show abstract

“…This view, accepted for the past 40 years 3 and perhaps counterintuitively expected to mitigate the effects of LV pressure overload on cardiovascular morbidity and mortality, has begun to be challenged by new clinical data, suggesting that moderate or severe LVH may be associated with adverse outcomes in AS 4,5 and that inappropriately increased LV mass, found in 17% of patients with mild to moderate AS 6 and in 67% of patients with asymptomatic severe AS, was associated with a 4.5-fold increased risk of cardiovascular events. 7 Conversely, the absence of hypertrophy in one third of the patients with severe AS seems to have no adverse effects on systolic function or survival. 8,9 Experimental studies in genetically modified animal models are consistent with clinical observations.…”

Section: See Article By Gerdts Et Almentioning

confidence: 99%

Left Ventricular Hypertrophy in Asymptomatic Nonsevere Aortic Stenosis

Barasch

Reichek

2015

Circ: Cardiovascular Imaging

View full text Add to dashboard Cite

Barasch and Reichek Left Ventricular Hypertrophy in Aortic StenosisEffects of Rosuvastatin (ASTRONOMER) trial, which examined patients with mild to moderate AS and a mean age of 50 years, progression of LVH occurred only in those without LVH at baseline. 17 The older population enrolled in SEAS study and some differences in the baseline characteristics may explain this discrepancy. Asymmetrical septal hypertrophy present in 22% of patients enrolled in SEAS was not discussed. Efforts to refine evaluation of LV remodeling patterns using cardiac magnetic resonance have included proposals to distinguish asymmetrical septal remodeling and hypertrophy, 11 mixed hypertrophy, physiological hypertrophy, eccentric remodeling, 18 and dilated hypertrophy (concentric and eccentric).19 Indeterminate hypertrophy, which together with dilated hypertrophy has been proposed as an eccentric hypertrophic pattern, is reportedly associated with the lowest risk for adverse outcomes when compared with other remodeling patterns. Perhaps in this study, the impact of LV mass index on outcome variables was independent of concentricity because of predominance of eccentric hypertrophy of dilated subtype, which in the Dallas Heart Study was associated with an 8-fold increase in incidence of heart failure and cardiovascular death compared with the non-LVH group (16.7% versus 2%, respectively). 19In addition to hypertension, the presence of mild to moderate AS contributed to variations in LV geometry in SEAS. Despite similar AS severity by valve area, the LVH group had other echocardiographic variables suggestive of greater stenosis severity compared with the normal LV geometry group: higher transvalvular gradients and lower energy loss index. The latter takes into account the ascending aortic area at the sinotubular junction, and if aortic valve area was similar, the ascending aorta had to be smaller in the LVH than in the non-LVH group. Therefore, the higher prevalence of aortic regurgitation in patients with LVH was probably unrelated to ascending aortic dilatation. Considering the known limitations of echocardiographic aortic valve area calculation, especially measurement of the LV outflow tract area, and the known discrepancies between different echocardiographic indices reflecting AS severity, one cannot completely exclude a higher severity of AS in the LVH group. The association of elevated LV mass index with adverse outcomes in SEAS might be related to the presence of LVH itself, given known correlates including changes in myocardial matrix with increased collagen deposition and extracellular volume, increased coronary vascular resistance and reduced myocardial perfusion reserve, subclinical LV systolic dysfunction expressed as reduced systolic strain, altered diastolic filling, and increased risk of ventricular arrhythmias. Other contributors may include aortic valve calcification, which was shown to be associated with a 50% higher risk of cardiovascular events in the Multi-Ethnic Study of Atherosclerosis (MESA), 20 subclinical coronary...

show abstract

Prognostic effect of inappropriately high left ventricular mass in asymptomatic severe aortic stenosis

Abstract: iLVM is common in patients with asymptomatic severe AS and is associated with an increased rate of cardiovascular events independent of other prognostic covariates.

Cited by 267 publications

References 35 publications

Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

Diagnosis and Management of Cardiovascular Disease in Advanced and End‐Stage Renal Disease

From Left Ventricular Hypertrophy to Dysfunction and Failure

Left Ventricular Hypertrophy in Asymptomatic Nonsevere Aortic Stenosis

Contact Info

Product

Resources

About