Cardiac Hypertrophy: An Introduction to Molecular and Cellular Basis

Samak, Mostafa; Fatullayev, Javid; Sabashnikov, Anton; Zeriouh, Mohamed; Schmack, Bastian; Farag, Mina; Popov, Aron‐Frederik; Dohmen, Pascal M.; Choi, Yeong‐Hoon; Wahlers, Thorsten; Weymann, Alexander

doi:10.12659/msmbr.900437

Cited by 171 publications

(124 citation statements)

References 42 publications

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“…Pathological cardiac hypertrophy is known to be caused by humoral activation, mechanical stress, transcription switch to fetal gene program and is linked to cardiac fibrosis. 50,51 These changes are also induced in Tgaq*44 mice via constitutive cardiomyocytespecific, postnatal activation of the Gaq pathway, which mimics the effects of neurohormonal activation in cardiomyocytes. 23 Subsequently, at different time points, but before development of end-stage HF, other signs of pathological cardiac hypertrophy occur and progress.…”

Section: Discussionmentioning

confidence: 95%

“…Therefore, slowly progressing pathology in Tgαq*44 mice uniquely enables the study of VCI development before development of advanced, end‐stage HF in the absence of preexisting vascular risk factors. Pathological cardiac hypertrophy is known to be caused by humoral activation, mechanical stress, transcription switch to fetal gene program and is linked to cardiac fibrosis . These changes are also induced in Tgαq*44 mice via constitutive cardiomyocyte‐specific, postnatal activation of the Gαq pathway, which mimics the effects of neurohormonal activation in cardiomyocytes .…”

Section: Discussionmentioning

confidence: 99%

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Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Adamski

Sternak

Mohaissen

et al. 2018

JAHA

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BackgroundAlthough advanced heart failure (HF) is a clinically documented risk factor for vascular cognitive impairment, the occurrence and pathomechanisms of vascular cognitive impairment in early stages of HF are equivocal. Here, we characterize vascular cognitive impairment in the early stages of HF development and assess whether cerebral hypoperfusion or prothrombotic conditions are involved.Methods and ResultsTgαq*44 mice with slowly developing isolated HF triggered by cardiomyocyte‐specific overexpression of G‐αq*44 protein were studied before the end‐stage HF, at the ages of 3, 6, and 10 months: before left ventricle dysfunction; at the stage of early left ventricle diastolic dysfunction (with preserved ejection fraction); and left ventricle diastolic/systolic dysfunction, respectively. In 6‐ to 10‐month‐old but not in 3‐month‐old Tgαq*44 mice, behavioral and cognitive impairment was identified with compromised blood‐brain barrier permeability, most significantly in brain cortex, that was associated with myelin sheet loss and changes in astrocytes and microglia. Brain endothelial cells displayed increased E‐selectin immunoreactivity, which was accompanied by increased amyloid‐β1‐42 accumulation in piriform cortex and increased cortical oxidative stress (8‐OHdG immunoreactivity). Resting cerebral blood flow measured by magnetic resonance imaging in vivo was preserved, but ex vivo NO‐dependent cortical arteriole flow regulation was impaired. Platelet hyperreactivity was present in 3‐ to 10‐month‐old Tgαq*44 mice, but it was not associated with increased platelet‐dependent thrombogenicity.ConclusionsWe report for the first time that vascular cognitive impairment is already present in the early stage of HF development, even before left ventricle systolic dysfunction. The underlying pathomechanism, independent of brain hypoperfusion, involves preceding platelet hyperreactivity and brain endothelium inflammatory activation.

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Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Adamski

Sternak

Mohaissen

et al. 2018

JAHA

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“…Applied to cardiology, the term comprises numerous pathophysiological conditions in which, in response to different stimuli, a cardiac enlargement occurs . The enlargement of the myocardium is an adaptive and compensatory mechanism to overcome increased demands of cardiac work and reduce ventricular wall tension . Cardiac hypertrophy can be classified as physiological, a mild and reversible condition accompanied by increased heart functionality, or pathological, characterized by a decrease in heart functionality .…”

Section: Introduction To Cardiac Hypertrophymentioning

confidence: 99%

“…The former is found in the heart of athletes . In the latter, the myocardium pump function is compromised, leading to the development of heart failure (HF) …”

Section: Introduction To Cardiac Hypertrophymentioning

confidence: 99%

Immunotherapy for cardiovascular disease

Martini

Stirparo

Kallikourdis

2017

Journal of Leukocyte Biology

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Heart failure (HF), the final stage of pathological cardiac hypertrophy, is a major cause of hospitalization and mortality. The role of inflammation in the pathogenesis of HF has been extensively studied, with great emphasis on proinflammatory cytokines. Yet, clinical trials targeting these cytokines failed to become a credible therapeutic strategy for HF. More recent studies are increasingly highlighting an active role for T cells in the progression of HF pathology. As a result, a number of novel immunotherapy strategies are emerging for the treatment of HF and other cardiovascular diseases, via the targeting of adaptive immunity. Here we provide an overview of the background, details, and expected outcomes of these attempts.

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“…LVH affects ventricular repolarization[17–19] and increases the risk of ventricular arrhythmias. LVH[20], fibrosis[21], and inflammation[22] are well-known mechanisms of the development of an abnormal electrophysiological substrate, associated with high risk of life-threatening ventricular arrhythmias as an underlying cause of SCD. The beneficial effect of BP reduction on CVD risk is well-known[23; 24].…”

mentioning

confidence: 99%

Risk stratification of sudden cardiac death in hypertension

Tereshchenko

Soliman

Davis

et al. 2017

Journal of Electrocardiology

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In the United States, up to 450,000 people per year die suddenly; an average of 1 sudden death every 70 seconds. Strategies for preventing sudden cardiac death are urgently needed. Systemic arterial hypertension is a major risk factor for sudden cardiac death and the increasing burden of hypertension is a worldwide problem. The lifetime risk of sudden cardiac death at 30 years of age is higher by 30% in individuals with hypertension. Each 20/10 mm Hg increase in systolic/diastolic blood pressure, is associated with a 20% additional increase in sudden cardiac death risk. Theoretically, antihypertensive treatment should be an effective strategy for sudden cardiac death prevention. However, a recent meta-analysis of 15 randomized controlled trials showed that antihypertensive treatment does not reduce the incidence of sudden cardiac death. This manuscript reviews ECG predictors of sudden cardiac death and the importance of risk stratification for appropriate management of hypertension.

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Cardiac Hypertrophy: An Introduction to Molecular and Cellular Basis

Cited by 171 publications

References 42 publications

Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Vascular Cognitive Impairment Linked to Brain Endothelium Inflammation in Early Stages of Heart Failure in Mice

Immunotherapy for cardiovascular disease

Risk stratification of sudden cardiac death in hypertension

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