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  • American Physiological Society  (3)
  • English  (3)
  • 1
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 293, No. 3 ( 2007-09), p. H1987-H1996
    Abstract: In a vulnerable plaque (VP), rupture often occurs at a site of high stress within the cap. It is also known that vessels do not become free of stress when all external loads are removed. Previous studies have shown that such residual stress/strain (RS/S) tends to make the stress distribution more uniform throughout the media of a normal artery. However, the influence of RS/S on the wall stress distribution in pathological coronaries remains unclear. The aim of this study was to investigate the effects of RS/S on the biomechanical stability of VPs. RS/S patterns were studied ex vivo in six human vulnerable coronary plaque samples. Because the existence of RS/S can only be assessed by releasing it, the opening angle technique was the experimental approach used to study the geometrical opening configurations of the diseased arteries, producing an arterial wall in a near-zero stress state. Reciprocally, these opening geometries were used in finite element simulations to reconstruct the RS/S distributions in closed arteries. It was found that the RS/S 1) is not negligible, 2) dramatically affects the physiological peak stress amplitude in the thin fibrous cap, 3) spotlights some new high stress areas, and 4) could be a landmark of the lipid core's developmental process within a VP. This study demonstrates that plaque rupture is not to be viewed as a consequence of intravascular pressure alone, but rather of a subtle combination of external loading and intraplaque RS/S.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
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  • 2
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 295, No. 2 ( 2008-08), p. H717-H727
    Abstract: Fibrous cap thickness is often considered as diagnostic of the degree of plaque instability. Necrotic core area (Core area ) and the arterial remodeling index (Remod index ), on the other hand, are difficult to use as clinical morphological indexes: literature data show a wide dispersion of Core area thresholds above which plaque becomes unstable. Although histopathology shows a strong correlation between Core area and Remod index , it remains unclear how these interact and affect peak cap stress (Cap stress ), a known predictor of rupture. The aim of this study was to investigate the change in plaque vulnerability as a function of necrotic core size and plaque morphology. Cap stress value was calculated on 5,500 idealized atherosclerotic vessel models that had the original feature of mimicking the positive arterial remodeling process described by Glagov. Twenty-four nonruptured plaques acquired by intravascular ultrasound on patients were used to test the performance of the associated idealized morphological models. Taking advantage of the extensive simulations, we investigated the effects of anatomical plaque features on Cap stress . It was found that: 1) at the early stages of positive remodeling, lesions were more prone to rupture, which could explain the progression and growth of clinically silent plaques and 2) in addition to cap thickness, necrotic core thickness, rather than area, was critical in determining plaque stability. This study demonstrates that plaque instability is to be viewed not as a consequence of fibrous cap thickness alone but rather as a combination of cap thickness, necrotic core thickness, and the arterial remodeling index.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2008
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    Online Resource
    Online Resource
    American Physiological Society ; 1997
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 273, No. 6 ( 1997-12-01), p. H2804-H2810
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 273, No. 6 ( 1997-12-01), p. H2804-H2810
    Abstract: ATP-dependent potassium ([Formula: see text]) channels play a role in the infarct size-limiting effect of preconditioning in pigs. We previously demonstrated that preconditioning shortens monophasic action potential duration (MAPD) and accelerates the time to ventricular fibrillation (VF) during a prolonged ischemia in pigs. We sought to determine whether the mechanism of the reduced time to VF in preconditioned pigs is a consequence of[Formula: see text] channel activation. Pigs underwent 40 min of coronary occlusion and 2 h of reperfusion. Before this, animals received either no intervention (control), 10 min of ischemia and 10 min of reperfusion (preconditioned), or an intravenous infusion of nicorandil, a [Formula: see text] channel opener. Additional control, preconditioned, and nicorandil-treated pigs were pretreated by glibenclamide, an antagonist of[Formula: see text] channels. Because 1) the[Formula: see text] channel activator nicorandil did not produce shorter time to VF, 2) the[Formula: see text] channel inhibitor glibenclamide did not block the acceleration of VF by preconditioning, and 3) there was no relationship between time to VF and infarct size or MAPD, the major conclusion is that reduced time to VF in preconditioned animals is not a consequence of [Formula: see text] channel activation.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    RVK:
    Language: English
    Publisher: American Physiological Society
    Publication Date: 1997
    detail.hit.zdb_id: 1477308-9
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
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