Study on left atrial contractile performance. Participation of Frank-Starling mechanism.

Yamaguchi, Masato; Arakawa, Michio; Tanaka, Tsutomu; Takaya, Tomofumi; Nagano, Toshihiko; Hirakawa, Senri

doi:10.1253/jcj.51.1001

Cited by 54 publications

(28 citation statements)

References 18 publications

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“…At the same time the associated development of tension in the LA wall increases pressure within the cavity, thus establishing an atrioventricular pressure gradient and flow. LA systolic function is governed by the same factors that govern LV systolic function, namely: (1) the pre-contraction fibre length, defining according to the Frank-Starling mechanism the maximum developed force [27,28]; (2) the afterload, becoming a major determinant of LA ejection when the LA preload reaches its limit (afterload mismatch) [29]; (3) the autonomic nervous system, which exhibits a positive inotropic effect via catecholamine release activating the b1-and b2-adrenoreceptors and a negative inotropic effect via the muscarinic receptors [30] and (4) the renin-angiotensin system via angiotensin I and angiotensin II, which exert positive inotropic effects mediated by the AT1 receptor [31].…”

Section: Active (Systolic) Emptyingmentioning

confidence: 99%

Left atrial remodelling contributes to the progression of asymptomatic left ventricular systolic dysfunction to chronic symptomatic heart failure

et al. 2007

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Systolic heart failure (HF) is a progressive disorder that often begins with asymptomatic left ventricular (LV) systolic dysfunction and culminates in symptoms from fluid overload and poor end-organ perfusion. The progression to symptomatic HF is accompanied by marked activation of neurohormonal and cytokine systems, as well as a series of adaptive LV anatomical and functional changes, collectively referred to as LV remodelling. However, the mechanisms underlying symptom appearance have not been delineated and the weight of experimental and clinical evidence suggests that the development of symptomatic HF occurs independently of the haemodynamic status of the patient. The left atrium is a muscular chamber strategically located between the left ventricle and the pulmonary circulation with important mechanical function (modulation of LV filling), which is closely coupled with its endocrine (atrial natriuretic peptide synthesis and secretion) and regulatory (contribution to the control of sympathetic activity and vasopressin release) functions. In this narrative review we provide evidence supporting the concept that left atrial dilation and systolic dysfunction (left atrial remodelling) contributes to the progression of asymptomatic LV dysfunction to chronic symptomatic systolic HF as it is a prerequisite for the development of the pulmonary congestion and marked neuronhormoral activity that characterize the symptomatic state.

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Section: Active (Systolic) Emptyingmentioning

confidence: 99%

Left atrial remodelling contributes to the progression of asymptomatic left ventricular systolic dysfunction to chronic symptomatic heart failure

et al. 2007

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“…In the current study the conduit contribution to LV filling remained unchanged. LA contracts in a manner similar to the Frank -Starling mechanism [16]. Thus, LA volume before atrial contraction, which corresponds to the preload of left atrium, has a certain relation with LA stroke volume.…”

Section: Discussionmentioning

confidence: 94%

The effect of pulmonary hypertension on left atrial mechanical functions in chronic obstructive lung disease

Açıkel

Yılmaz

Gürlertop

et al. 2004

International Journal of Cardiology

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“…Experimental and clinical studies have demonstrated that LA systolic function is affected by (1) the precontraction fiber length, defining the maximum developed force according to the Frank Starling mechanism; [22][23][24] (2) the afterload, becoming a major determinant of LA ejection when the LA preload reaches its limit; 25 (3) the autonomic nervous system, which exhibits a positive inotropic effect via catecholamine release and a negative inotropic effect via the muscarinic receptors; and (4) the rennin-angiotensin system, which exerts a positive inotropic effect via the AT1 receptors. 26,27 The mechanism of atrial systolic dysfunction in cardiac amyloidosis is incompletely understood, although amyloid infiltration of the atrial myocardium may result in a reduction in chamber contractility; 5 however, other mechanisms may also be implicated.…”

Section: Discussionmentioning

confidence: 99%

Left atrial systolic function in primary and familial amyloidosis: Assessment from left atrial volume change

Moyssakis

Triposkiadis

Pantazopoulos

et al. 2004

Clinical Cardiology

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Summary:The severity of left ventricular involvement may differ between primary (PA) and familial amyloidosis (FA). This study examined whether differences in left atrial (LA) systolic function are also present. Twenty-eight patients (18 men, 10 women, aged 59 ± 12 years) with PA, 17 (11 men, 6 women, aged 40 ± 11 years) with FA, and 25 normal controls (18 men, 7 women, aged 56 ± 14 years) underwent transthoracic M-mode, two-dimensional, and Doppler echocardiography. Left atrial volumes were determined at mitral valve (MV) opening (maximal, Vmax), electrocardiographic P wave (onset of atrial systole, Vp), and MV closure (minimal, Vmin) from the apical two-and four-chamber views using the biplane area-length method. Left atrial systolic function was assessed with the LA active emptying volume (ACTEV) = Vp-Vmin and fraction (ACTEF) = ACTEV/Vp. The E/A ratio was increased (1.34 ± 0.93 vs. 0.89 ± 0.3), whereas deceleration time was decreased (168.1 ± 33.7 vs. 196.2 ± 34.2 ms) in PA compared with FA (p<0.05). Vmax and Vp were similar in PA and FA and greater than in the controls (46.6 ± 14 vs. 40 ± 11.4 vs. 27.1 ± 6.3 cm 3 /m 2 , p < 0.01, and 33.4 ± 11.6 vs. 29.7 ± 10.8 vs. 16.8 ± 3.8 cm 3 /m 2 , p < 0.01, respectively). The ACTEV was lower in PA and in the controls than in FA (6.7 ± 2 vs. 6.2 ± 2.2 vs. 8.5 ± 3.3, respectively, p < 0.05). The ACTEF was lower in PA than in FA and both were lower than those in the controls (20 ± 5% vs. 28 ± 7% vs. 36 ± 11%, respectively, p < 0.01). Despite a similar increase in LA volume, LA systolic dysfunction is more pronounced in PA than in FA. This is most likely due to the restrictive left ventricular physiology possibly associated with depressed LA contractility in the former.

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Study on left atrial contractile performance. Participation of Frank-Starling mechanism.

Cited by 54 publications

References 18 publications

Left atrial remodelling contributes to the progression of asymptomatic left ventricular systolic dysfunction to chronic symptomatic heart failure

Left atrial remodelling contributes to the progression of asymptomatic left ventricular systolic dysfunction to chronic symptomatic heart failure

The effect of pulmonary hypertension on left atrial mechanical functions in chronic obstructive lung disease

Left atrial systolic function in primary and familial amyloidosis: Assessment from left atrial volume change

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