Acute Valvular Regurgitation

Stout, Karen; Verrier, Edward D.

doi:10.1161/circulationaha.108.782292

Cited by 145 publications

(84 citation statements)

References 38 publications

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“…The rapid equilibration of LA and LV pressures seen in acute MR can significantly diminish the murmur 10 . Accurate auscultation of a distressed patient in a noisy resuscitation room can be challenging, and the information gained from heart sounds may contribute little towards the diagnosis.…”

Section: Discussionmentioning

confidence: 99%

Three patients with signs of acute flail mitral leaflet seen on emergency department echo: a critical constellation within the focused cardiac exam

Bomann

Stephenson

Wallace

et al. 2014

Australas J Ultrason Med

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Acute flail mitral leaflet is a time‐sensitive, reversible cause of cardiogenic shock. Transthoracic echocardiography (echo) is increasingly becoming a vital tool for non‐cardiologist physicians who treat patients with undifferentiated chest pain and dyspnoea. The sonographic abnormalities seen in acute flail mitral leaflet are within the boundaries of a focused echo. Individually, these findings are non‐specific. As a constellation, however, they are highly suggestive of this disease process. We present a case series of three patients with acute flail mitral leaflet seen on emergency department echo along with a discussion of the findings and the disease itself.

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Section: Discussionmentioning

confidence: 99%

Three patients with signs of acute flail mitral leaflet seen on emergency department echo: a critical constellation within the focused cardiac exam

Bomann

Stephenson

Wallace

et al. 2014

Australas J Ultrason Med

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“…In acute AF, the widening of pulse pressure and other peripheral signals associated with chronic AF, are often absent. Moreover, the holodiastolic murmur of chronic AF is replaced by a protodiastolic murmur little audible in acute AF [1]. Patients often have dyspnea, hemodynamic instability and shock.…”

Section: Discussionmentioning

confidence: 99%

“…It is most often caused by bacterial endocarditis, aortic dissection or blunt chest trauma [1]. Another mechanism is the fenestration rupture of a valve, or the avulsion of the commissures of the aortic wall [2].…”

Section: Introductionmentioning

confidence: 99%

Insuficiência aórtica aguda por avulsão de comissura valvar aórtica

Cunha¹,

Santos²,

Atik³

et al. 2012

Rev Bras Cir Cardiovasc

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A 66-year-old male patient, prior hypertension, a history of orthopnea, palpitations and chest pain of sudden onset, which was diagnosed as spontaneous avulsion of aortic valve commissure and consequent aortic insufficiency progressing to acute left heart failure refractory to medical treatment. The patient underwent early surgical replacement of the aortic valve by a bioprosthesis, and presented satisfactory postoperative course. Currently, four years after the event, he is still in attendance in functional class I.Descriptors: Aortic valve insufficiency. Heart valve diseases. Cardiac surgical procedures. RBCCV 44205-1365

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“…Many lines of evidence indicate that concentric and eccentric hypertrophy differ not only in terms of phenotype but also in the intracellular signaling pathways that are involved 5,6 . Various studies investigated the molecular mechanism of hypertrophy, especially in concentric hypertrophy caused by PO 7,8 ; however, the molecular mechanism of eccentric hypertrophy has yet to be fully elucidated.Mitral and aortic regurgitation are typical pathophysiologies that cause VO, especially in the acute phase 9 . In those pathophysiologies, insufficient net forward output inevitably induces pulmonary congestion resulting from increased left ventricular end-diastolic pressure (LVEDP) and diastolic wall stress to…”

mentioning

confidence: 99%

“…Mitral and aortic regurgitation are typical pathophysiologies that cause VO, especially in the acute phase 9 . In those pathophysiologies, insufficient net forward output inevitably induces pulmonary congestion resulting from increased left ventricular end-diastolic pressure (LVEDP) and diastolic wall stress to…”

mentioning

confidence: 99%

The Akt-mTOR Axis is a Pivotal Regulator of Eccentric Hypertrophy during Volume Overload

Ikeda

Ide

Fujino

et al. 2015

Journal of Cardiac Failure

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The heart has two major modalities of hypertrophy in response to hemodynamic loads: concentric and eccentric hypertrophy caused by pressure and volume overload (VO), respectively. However, the molecular mechanism of eccentric hypertrophy remains poorly understood. Here we demonstrate that the Akt-mammalian target of rapamycin (mTOR) axis is a pivotal regulator of eccentric hypertrophy during VO. While mTOR in the heart was activated in a left ventricular end-diastolic pressure (LVEDP)-dependent manner, mTOR inhibition suppressed eccentric hypertrophy and induced cardiac atrophy even under VO. Notably, Akt was ubiquitinated and phosphorylated in response to VO, and blocking the recruitment of Akt to the membrane completely abolished mTOR activation. Various growth factors were upregulated during VO, suggesting that these might be involved in Akt-mTOR activation. Furthermore, the rate of eccentric hypertrophy progression was proportional to mTOR activity, which allowed accurate estimation of eccentric hypertrophy by time-integration of mTOR activity. These results suggested that the Akt-mTOR axis plays a pivotal role in eccentric hypertrophy, and mTOR activity quantitatively determines the rate of eccentric hypertrophy progression. As eccentric hypertrophy is an inherent system of the heart for regulating cardiac output and LVEDP, our findings provide a new mechanistic insight into the adaptive mechanism of the heart.The heart is a vital organ that maintains homeostasis in the body via blood circulation. To maintain blood circulation in the peripheral tissues, the heart is capable of remodeling in response to various stresses including hemodynamic load, neurohormones, oxidative stress, and cytokines [1][2][3] . Among those, mechanical loads are major inputs for the heart because the heart is incessantly subject to hemodynamic stresses. Given that mechanical load induces hypertrophy, mechanical stretching forces in systole and diastole in myocytes in vivo can be calculated as wall stresses in systole and diastole in accordance with Laplace's law. In 1975, Grossman et al. demonstrated that pressure overload (PO) increases systolic wall stress, resulting in concentric hypertrophy, which in turn normalizes systolic wall stress, and that volume overload (VO) increases diastolic wall stress, resulting in eccentric hypertrophy 1 . Based on this clinical observation, they proposed that the hypertrophic response was evoked by increased wall stress 1 . Currently, it is widely accepted that increased systolic and diastolic wall stresses lead to concentric and eccentric hypertrophy, respectively 4 . Many lines of evidence indicate that concentric and eccentric hypertrophy differ not only in terms of phenotype but also in the intracellular signaling pathways that are involved 5,6 . Various studies investigated the molecular mechanism of hypertrophy, especially in concentric hypertrophy caused by PO 7,8 ; however, the molecular mechanism of eccentric hypertrophy has yet to be fully elucidated.Mitral and aortic regurgitation are...

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Acute Valvular Regurgitation

Cited by 145 publications

References 38 publications

Three patients with signs of acute flail mitral leaflet seen on emergency department echo: a critical constellation within the focused cardiac exam

Three patients with signs of acute flail mitral leaflet seen on emergency department echo: a critical constellation within the focused cardiac exam

Insuficiência aórtica aguda por avulsão de comissura valvar aórtica

The Akt-mTOR Axis is a Pivotal Regulator of Eccentric Hypertrophy during Volume Overload

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