Key result
Vascular inflammation, driven by a complex network of leukocytes, endothelial cells, platelets, and cholesterol, plays a central role in the pathogenesis of acute coronary syndromes.
This review highlights the complex role of vascular inflammation in the pathogenesis of acute coronary syndromes, emphasizing the need to address these mechanisms for better prevention and treatment.
Supports targeting vascular inflammation in ACS; leaves open optimal pathways and trials for clinical translation.
From the onset to the healing stage of acute coronary syndromes, an endless inflammation has been presented with complex, multiple cross-talk mechanisms at the molecular, cellular, and organ levels. Even though the early reperfusion treatment either by thrombolysis or percutaneous coronary intervention provides the excellent clinical benefits in patients with acute coronary syndromes, ischemia/ reperfusion injury may somewhat offset those great advantages. Inflammation, although potentially protective, has been deeply associated with those detrimental conditions. The hexagonal vascular inflammatory network which is composed of activated various leukocytes, vascular endothelial cells, vascular smooth muscle cells, platelets, excess reactive oxygen species, and cholesterol may contribute these vicious circles. To address these complex syndromes with more benefits regarding the prevention and treatment, this review comprehensively updates the pathogenesis of acute coronary syndromes from the view points of vascular inflammation.
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Makoto Suzuki (2012) conducted a review in Acute coronary syndromes. Vascular inflammation, driven by a complex network of leukocytes, endothelial cells, platelets, and cholesterol, plays a central role in the pathogenesis of acute coronary syndromes.
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