Cold stimulation has been linked to acute myocardial infarction and other cardiovascular diseases. Residents in the frigid zones, such Heilongjiang Province, experience a higher incidence of adverse cardiovascular events during winter, posing a significant health threat and increasing the overall medical burden. Cold stimulation serves as an detrimental stressor, inducing inflammation in the body. Therefore, understanding the role of inflammatory responses induced by cold stimulation in the occurrence and development of cardiovascular diseases is of paramount importance. Given the impact of cold on inflammation in cardiovascular diseases and the expanding array of anti-inflammatory methods for the treatment of cardiovascular diseases, delving into the inflammatory responses mediated by can significantly complement cardiovascular disease management. This review explorest the synergistic relationship between cold stimulation and inflammation induction, elucidating how this interplay influences the occurrence and progression of cardiovascular diseases.

  Objective  Present study aimed to explore the effects of intermittent cold-exposure (ICE) on culprit plaque morphology in patients with STsegment elevation myocardial infarction (STEMI) in frigid zone.  Methods  Totally 848 STEMI patients with plaque rupture (N = 637) or plaque erosion (N = 211) were enrolled consecutively according to optical coherence tomography imaging. Data on the changes of outdoor air temperature corresponding to 24 solar terms were collected. Patients were divided into different groups according to 24 solar terms and the number of days with indoor central heating. Imaging data were measured and analyzed qualitatively and quantitatively. Statistical analysis was conducted to elucidate the possible association of the STEMI patients of different groups with plaque morphology of culprit vessel with alterations of ambient temperature.  Results  The incidence of both plaque rupture and plaque erosion presented trough in summer. The incidence of plaque rupture reached a peak value in early winter when outdoor air temperature dropped below 0℃ and declined with supply of central heating. Persistent cold exposure in early winter was positively and significantly associated with plaque rupture. The incidence of plaque erosion presented a peak in severe winter with outdoor air temperature dropping below -20℃ and steady supply of central heating. ICE in severe winter was positively and significantly associated with plaque with intact intima, especially in aged male or current smoking patients. The positive correlation of cold exposure with lipid size in culprit plaque in winter weakened with central heating.  Conclusion  ICE resulted from switching staying in between outdoor cold environment and indoor warm temperature with central heating in severe winter changed culprit plaque morphology in STEMI. Plaque rupture decreased whereas plaque erosion increased impacted by ICE. The effect of ICE on the transformation of plaque morphology might be explained by reduced lipid deposition.