Left Ventricular Hypertrophy in Valvular Aortic Stenosis: Mechanisms and Clinical Implications

Rader, Florian; Sachdev, Esha; Arsanjani, Reza; Siegel, Robert J.

doi:10.1016/j.amjmed.2014.10.054

Cited by 79 publications

(57 citation statements)

References 86 publications

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“…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. 22 The natural history of AS is characterized, in most cases, by progressive LV dysfunction and HF, although it may be favorably changed by valve replacement, particularly in those patients with preserved EF before surgery.…”

Section: Primary Lvhmentioning

confidence: 99%

“…22 Systolic performance at rest is normal or mildly increased and diastolic dysfunction is present. 22 The natural history of AS is characterized, in most cases, by progressive LV dysfunction and HF, although it may be favorably changed by valve replacement, particularly in those patients with preserved EF before surgery. 23 Volume Overload In most cases of volume overload, the enlarged intracavitary volume contributes to the increased LV systolic pressure and afterload, leading to a combined pressure and volume overload and an eccentric pattern of hypertrophy.…”

Section: Primary Lvhmentioning

confidence: 99%

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From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

124

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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...

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Section: Primary Lvhmentioning

confidence: 99%

Section: Primary Lvhmentioning

confidence: 99%

From Left Ventricular Hypertrophy to Dysfunction and Failure

Lazzeroni

Rimoldi

Camici

2016

Circ J

124

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“…Currently, heart valve diseases are the most common life-threatening cardiovascular events in developed and developing countries [Bin Abdulhak et al, 2014;Rader et al, 2015], and cardiac valve replacement has established as a primary surgical treatment. The widely used valve substitutes are mechanical and bioprosthetic valves.…”

Section: Discussionmentioning

confidence: 99%

De-Endothelialized Aortic Homografts: A Promising Scaffold Material for Tissue-Engineered Heart Valves

Jing¹,

Wang²,

Chang³

2014

Cells Tissues Organs

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This study was designed to investigate the feasibility of de-endothelialized aortic homografts as a scaffold for tissue-engineered heart valves. Aortic homografts obtained from donor rabbits were treated either with collagenase to eliminate endotheliocytes or with the enzyme-detergent-nuclease method to remove all cell components. Then biomechanical properties of fresh, de-endothelialized and acellular homografts were investigated comparatively. The inflammation potential and immunogenicity were also assessed after allogenic transplantation. Expression of immune indices and inflammatory infiltration in de-endothelialized and acellular homografts were much weaker than in the controls, and no significant difference was observed between treated groups. However, heat shrinkage temperature, tensile strength and broken extension rate of acellular homografts decreased significantly compared to de-endothelialized ones. It is concluded that both de-endothelialization and thorough decellularization could reduce the immunogenicity and inflammation potential significantly, but the de-endothelialized scaffold retained better structural strength. The de-endothelialized aortic homograft might be a promising scaffold for tissue-engineered heart valves.

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“…Use of medications which improve the outcome of heart failure has no effect on survival in these patients [8,9]. Treated with medical therapy alone, 1-year-mortality 1 3 exceeds 50 % and 5-year-mortality approaches to 90 % [8,10].…”

Section: Introductionmentioning

confidence: 99%

Transcatheter aortic valve implantation in a cancer patient denied for surgical aortic valve replacement—a case report

Mrak

Ambrožič

Mušič

et al. 2016

Wien Klin Wochenschr

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Aortic valve replacement improves survival of cancer patients with symptomatic aortic stenosis. Transcatheter aortic valve replacement (TAVI) is a treatment option in inoperable patients and patients at high surgical risk. Symptoms should not be confused for the progression of the malignant disease. In patient selection emphasis should be made on their frailty and futility. Eligible patients must have a life expectancy of at least 1 year. Final decision has to be made by a multidisciplinary heart team. TAVI can reduce treatment risk and facilitate the oncologic treatment.

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Left Ventricular Hypertrophy in Valvular Aortic Stenosis: Mechanisms and Clinical Implications

Cited by 79 publications

References 86 publications

From Left Ventricular Hypertrophy to Dysfunction and Failure

From Left Ventricular Hypertrophy to Dysfunction and Failure

De-Endothelialized Aortic Homografts: A Promising Scaffold Material for Tissue-Engineered Heart Valves

Transcatheter aortic valve implantation in a cancer patient denied for surgical aortic valve replacement—a case report

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