Clinical characteristics and outcomes in acute myocardial infarction patients with versus without any cardiovascular risk factors

Abstract

Background/Aims Although cardiovascular (CV) risk factors are well established, some patients experience acute myocardial infarction (AMI) even without any risk factors. Methods We analyzed total 11,390 patients (63.6 ± 12.6 years old, 8,401 males) with AMI enrolled in Korea Acute Myocardial Infarction Registry-National Institute of Health from November, 2011 to December, 2015. Patients were divided into two groups according to the presence of any CV risk factors (group I, without risk factors, n = 1,420 [12.5%]; group II, with risk factors, n = 9,970 [87.5%]). In-hospital outcomes were defined as in-hospital mortality and complications. One-year clinical outcomes were defined as the composite of major adverse cardiac events (MACE). Results Group I was older (67.3 ± 11.6 years old vs. 63.0 ± 12.7 years old, p < 0.001) and had higher prevalence of female gender (36.2% vs. 24.8%, p < 0.001) than the group II. Group I experienced less previous history of angina pectoris (7.0% vs. 9.4%, p = 0.003) and the previous history of cerebrovascular accidents (3.4% vs. 6.9%, p < 0.001). In-hospital mortality (2.6% vs. 3.0%, p = 0.450) and complications (20.6% vs. 20.0%, p = 0.647) were no differences between the groups. And 1 year clinical outcomes (5.7% vs. 5.1%, p = 0.337) were no differences between the groups. In multivariate logistic regression analysis, serum creatinine level (hazard ratio, 1.35; 95% confidence interval, 1.05 to 1.75; p = 0.021) were independent predictors of 1 year MACE in patients without any CV risk factors. Conclusions Elderly female patients were prone to develop AMI even without any modifiable CV risk factors. We suggest that more intensive care is needed in AMI patients without any CV risk factors who have high serum creatinine levels.

Inhibition of SphK1/S1P Signaling Pathway Alleviates Fibrosis and Inflammation of Rat Myocardium after Myocardial Infarction

“…MI is one of the primary causes of human death and the pathophysiological mechanism of myocardial injury after MI has been a hot research topic in the field of cardiovascular disease [ 1 ]. Several pathophysiological mechanisms explain the occurrence and development of myocardial injury after myocardial infarction.…”

“…Myocardial infarction (MI) is caused by acute coronary occlusion and leads to myocardial injury in the corresponding blood supply area [ 1 ]. Acute MI still frequently leads to heart failure and contributes to cardiovascular morbidity and mortality.…”

Number of standard modifiable risk factors and mortality in patients with first-presentation ST-segment elevation myocardial infarction: insights from China Acute Myocardial Infarction registry

“…However, data documenting the clinical outcomes of patients without any SMuRFs are still limited and the underlying mechanisms for the increased mortality rate among this group of patients are not clear. Moreover, current evidence is predominantly from highly developed countries, where patients can homogeneously receive high-quality emergency medical service and standardized evidence-based clinical management [ 7 – 14 ], whereas, in China, a large proportion of patients might experience long pre-hospital delays and suboptimal medical care, especially in those low-level hospitals and remote areas [ 15 ]. A recent study even reported that the rate of reperfusion eligibility decreased among patients with STEMI from 2011 to 2015 in China, which was majorly driven by the increased prevalence of long pre-hospital delay [ 16 ].…”

PCSK9 promotes the secretion of pro-inflammatory cytokines by macrophages to aggravate H/R-induced cardiomyocyte injury via activating NF-κB signalling

“…Myocardial ischaemia has become one of the most common causes of death and disability in modern society (Berliner et al 2018). Clinical ischaemic heart disease is frequently accompanied by angina pectoris and myocardial infarction (Choi et al 2019). A recent study demonstrated that myocardial ischaemia contributed to myocardial necrosis as well as cardiomyocyte apoptosis (Ran et al 2015).…”