1991
DOI: 10.1016/0002-9149(91)90494-6
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Left atrial afterload mismatch in hypertrophic cardiomyopathy

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Cited by 40 publications
(35 citation statements)
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“…As it had been shown in previous studies [3,4], the present study found that, compared with controls, patients with HCM showed increased LA volumes and decreased LA systolic function (emptying fraction). As with LA dyssynchrony, it was currently observed that the derived indexes were increased throughout the cardiac cycle in the patients.…”
Section: Present Observationssupporting
confidence: 89%
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“…As it had been shown in previous studies [3,4], the present study found that, compared with controls, patients with HCM showed increased LA volumes and decreased LA systolic function (emptying fraction). As with LA dyssynchrony, it was currently observed that the derived indexes were increased throughout the cardiac cycle in the patients.…”
Section: Present Observationssupporting
confidence: 89%
“…Since the heart rate, mitral flow, and annular velocity profiles were similar between the subgroups of patients, it is reasonable to assume that LA in relation to LV myocardial involvement may contribute to the development of LA dyssynchrony. This hypothesis is further supported by previous studies demonstrating a positive correlation between LA size and LV wall thickness [3,4,22] and a higher degree of cell damage and fibrotic change in the thicker ventricular wall [23]. Moreover, it was recently reported in a study of 2-dimensional speckle tracking that patients with HCM had more severe LV dyssynchrony than those with hypertensive heart disease [24].…”
Section: Present Observationssupporting
confidence: 77%
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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%