Medical errors are a serious public health problem and the third-leading cause of death after heart disease and cancer. Every day, the health care professionals (HCPs) practice their skill and knowledge within excessively complex situations and meet unexpected patient outcomes. These unexpected complications and unintentional errors will always be a part of the medical system due to the universal nature of human fallibility and technology. While not all errors are life-threatening, they can significantly compromise a patient’s quality of life. However, the victims of medical error reach far beyond the patient. The second victim (SV), which defined for the first time by Albert Wu in his description of the impact of errors on HCPs by both personally and professionally, is a medical emergency equivalent to post-traumatic stress disorder. When the errors occur, it causes a domino effect including the four groups: the patient and family (first victim), the HCP [SV], the hospital reputation (third victim), and patients who are harmed subsequently (fourth victims). The rights of our patients to safe, reliable, and patient-centered care are critical and most important as a primary and utmost aim of medicine. However, we also have to take care of our own (SVs), especially when we have good people who mean to do well and then find themselves in an emotionally complex situation. There is a need to articulate to the public, politicians, and media how system failure leads to medical error even in hand of well-educated and competent HCPs are given an increasing clinical workload. Furthermore, despite several leading institutions in western countries have developed formal support programs that allow HCPs to cope with their emotional distress by obtaining timely support in an emphatic, confidential, non-judgmental environment, we need to raise awareness of this phenomenon and appropriate institutional responses both to harmed patients and their families and HCPs.
The platelet to lymphocyte ratio (PLR) has recently emerged as a potential inflammatory biomarker. Hence, we assessed the relationship between PLR and the extent/severity of coronary artery disease (CAD) using the Gensini score in association with the inflammatory marker C-reactive protein (CRP) in patients with stable CAD. Angiographic data of 1646 patients were analyzed in this cross-sectional study. Patients were categorized according to Gensini scores as no CAD (control), mild, and severe CAD groups. The PLR in the control group was significantly lower than those of mild and severe CAD groups. In multivariate logistic regression analysis, PLR was found to be an independent predictor of the presence of severe CAD (odds ratio: 1.043 [1.036-1.049], P < .001). Furthermore, there was a significant correlation between PLR and the severity of CAD (r = .370, P < .001) and CRP levels (r = .312, P < .001). In conclusion, PLR was independently and positively associated with the severity of coronary atherosclerosis. These results suggest that PLR is an easily available and cheap inflammatory indicator that can be used in predicting the severity of CAD.
Metabolic syndrome (MetS) as a cluster of several cardio-metabolic components is rapidly growing public-health problem worldwide and significantly associated with poor cardiovascular outcomes. Increased visceral adiposity activates the important pathways connecting low-grade chronic inflammation, oxidative stress and blood coagulation. Recently, platelet to lymphocyte ratio (PLR) has been evidenced as a novel indirect inflammatory marker. Therefore, for the first time, we aimed to investigate the association of PLR with both the presence and severity of MetS. In this cross-sectional study, a total of 1146 participants were enrolled (n = 539 with MetS and n = 607 without MetS). MetS was defined according to NCEP-ATP III criteria. MetS (+) group revealed significantly higher PLR and C-reactive protein (CRP) levels as compared to MetS (−) group (p < 0.05). There was a graded relationship between increasing number of MetS components and PLR (p < 0.05). Also, PLR was positively correlated with CRP level (r = 0.163, p < 0.001). In multivariate regression analysis, PLR [1.121 (1.113–1.135), p < 0.001], CRP [1.044 (1.029–1.060), p < 0.001], and age [1.030 (1.017–1.043), p < 0.001] were remained as independent predictors for the presence of MetS. In conclusion, our findings showed that increased PLR was significantly associated with both the presence and severity of MetS which was linked to systemic inflammation based on the correlation between PLR and CRP. As PLR is an easily available, simple and cheap indirect indicator of inflammation, it can be used in clinical practice as a predictor of MetS.
Diabetes mellitus (DM) is associated with more extensive coronary atherosclerosis and more vulnerable plaque phenotypes. However, DM should not be considered a homogeneous and purely binary entity in terms of risk assessment. We evaluated the impact of prediabetic status on coronary atherosclerosis burden in patients with first-time acute coronary syndrome (ACS) who underwent urgent coronary angiography. The patients were divided into DM, prediabetes, and control groups. The 3-vessel disease (TVD) rates and SYNTAX and Gensini scoring systems for defining atherosclerotic burden were compared. The study was conducted in 469 consecutive patients admitted with a diagnosis of ACS. Of these, 250 patients were admitted at the first occurrence of ACS undergoing diagnostic coronary angiography. SYNTAX and Gensini scores and TVD rates were higher in prediabetic patients than in nondiabetic patients (P = .004, P = .008, and P = .014, respectively), but similar in prediabetic and diabetic patients (P = .912, P = .773, and P = 1.000, respectively). Coronary atherosclerosis burden is more advanced in prediabetic patients than in nondiabetic patients and is comparable between prediabetic and diabetic patients at first presentation of ACS. Cardiologists should not miss the opportunity to diagnose prediabetes and DM when patients present with an ACS.