2013
DOI: 10.1161/circheartfailure.112.000381
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Is There a Rationale for Antiplatelet Therapy in Acute Heart Failure?

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Cited by 5 publications
(5 citation statements)
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“…Given that ischemic heart disease is a leading cause of HF, we hypothesized that the 17% relative reduction in MI risk among vorapaxar‐treated trial participants would translate to a lower risk of subsequent HHF 11,22 . Moreover, heightened platelet activity leading to chronic coronary microthrombosis has been implicated as a mechanism of HF progression 23 . The observation that vorapaxar did not reduce HHF risk suggests either that follow‐up duration was insufficient or that the majority of HHF events were precipitated by events other than intercurrent MI.…”
Section: Discussionmentioning
confidence: 99%
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“…Given that ischemic heart disease is a leading cause of HF, we hypothesized that the 17% relative reduction in MI risk among vorapaxar‐treated trial participants would translate to a lower risk of subsequent HHF 11,22 . Moreover, heightened platelet activity leading to chronic coronary microthrombosis has been implicated as a mechanism of HF progression 23 . The observation that vorapaxar did not reduce HHF risk suggests either that follow‐up duration was insufficient or that the majority of HHF events were precipitated by events other than intercurrent MI.…”
Section: Discussionmentioning
confidence: 99%
“…11,22 Moreover, heightened platelet activity leading to chronic coronary microthrombosis has been implicated as a mechanism of HF progression. 23 The observation that vorapaxar did not reduce HHF risk suggests either that follow-up duration was insufficient or that the majority of HHF events were precipitated by events other than intercurrent MI. not exclude a possible benefit, particularly in higher-risk patients followed for a longer period of time.…”
Section: Effect Of Antiplatelet Therapy On Risk Of Hospitalization Fo...mentioning
confidence: 99%
“…Results from basic and clinical studies have demonstrated that acute heart failure would lead to increase angiotensin II levels, sympathetic overdrive, reduce nitric oxide bioavailability, and elevate inflammation cytokines. 33 All these alterations, via yet-to-be established mechanisms, contribute to platelet activation in acute heart failure. 33 In our study, in HPR patients defined by PAG levels, an increased incidence of anterior MI, as well as a decrease in LVEF ( P = .056; Table 1), was observed.…”
Section: Discussionmentioning
confidence: 99%
“…33 All these alterations, via yet-to-be established mechanisms, contribute to platelet activation in acute heart failure. 33 In our study, in HPR patients defined by PAG levels, an increased incidence of anterior MI, as well as a decrease in LVEF ( P = .056; Table 1), was observed. These characteristics are in agreement with the findings that patients with acute heart failure are more likely to present with activated state of platelets.…”
Section: Discussionmentioning
confidence: 99%
“…The activation of neurohormonal, inflammatory, and thrombotic pathways ( 20 - 22 ) has been found to be associated with enhanced platelet reactivity in patients with AHF ( 14 , 23 - 26 ). MPV has emerged as a relatively reliable marker of inflammation in patients with various diseases ( 27 , 28 ), with high MPV associated with low-grade inflammation.…”
Section: Discussionmentioning
confidence: 99%