The purpose of this investigation was to investigate whether there was an association between the Naples prognostic score and the development of acute kidney injury (AKI) in ST-elevation myocardial infarction (STEMI) patients following primary percutaneous coronary intervention (pPCI). The study comprised 2901 consecutive STEMI patients who had pPCI. For each patient, the Naples prognostic score was determined. To evaluate the predictive performance of the Naples score (which included either continuous and categorical variables), we developed a Nested model and a nested model combined with the Naples score. The Naples prognostic score was the most significant predictor of AKI occurrence after admission creatinine, age, and contrast volume. The continuous Naples prognostic score model provided the best prediction performance and discriminative ability. The C-index of the Nested and full models with continuous Naples prognostic score were significantly higher than that of the Nested model. The decision curve analysis found that the overall model had a higher full range of probability of clinical net benefit than the baseline model, with a 10% AKI likelihood. The present study found that the Naples prognostic score may be useful to predict the risk of AKI in STEMI patients undergoing pPCI.

Venous thromboembolism (VTE) is a common and potentially lethal disorder that manifests mainly as deep vein thrombosis (DVT) of the extremities or pulmonary embolism (PE) and occurs as a consequence of genetic and environmental risk factors. We aimed to assess the role of inherited thrombophilia as a causative or additive factor in the development of VTE. The study included 310 patients (female: 154; mean age: 52.3 ± 16.9 years) with a first episode of VTE and 289 age- and sex-matched healthy controls. All participants underwent screening for thrombophilia-associated polymorphisms including factor V Leiden (FVL), prothrombin G20210A (PTG), factor V H1299 R (factor V HR2), factor XIII V34 L, β-fibrinogen-455 G>A, plasminogen activator inhibitor-1 4G/5G, human platelet antigen-1 a/b, methylene tetrahydrofolate reductase (MTHFR) C677 T, MTHFR A1298C, angiotensin-converting enzyme I/D, apolipoprotein B R3500Q, and apolipoprotein E (Apo E). In addition, serum homocysteine (Hcy) levels were measured. In the patient group, 247 (80%) had isolated DVT, 43 (14%) had DVT plus PE, and 20 (6%) had isolated PE. The mean Hcy levels were similar in VTE subgroups and controls. Compared to controls, patients with isolated DVT, DVT plus PE, and isolated PE showed significantly higher frequencies for the following—heterozygous FVL mutation, isolated DVT (28.3%), DVT plus PE (44.2%), isolated PE (50%), controls (8.3%; P < .001); heterozygous PTG mutation, isolated DVT (11.3%), DVT plus PE (20.9%), isolated PE (25%), controls (5.9%; P < .01); Apo E 2/4, isolated DVT (9.7%), DVT plus PE (9.3%), isolated PE (5%), controls (1%; P < .01).The MTHFR A1298C mutation showed a significantly higher frequency in isolated patients with PE than in those with isolated DVT (P = .006) and in controls (P = .008). The frequencies of other genetic mutations or polymorphisms showed similar frequencies in all comparisons. In logistic regression analysis, heterozygous FVL mutation was the only independent predictor of VTE (odds ratio: 3.9, 95% confidence interval: 1.3-11.2; P = .012). Except than FVL, PTG, and Apo E 2/4 mutations, many of aforementioned thrombophilic factors known to be associated with VTE did not demonstrate any relationship with VTE. Heterozygous mutation of FVL was an independent predictor for VTE.

Congenital anomalies of the mitral valve apparatus are rare. Of such cases, congenital mitral stenosis, atresia, accessory valvular tissue, and cleft mitral valve are more common. Descriptions of unileaflet mitral valves (either partial or complete leaflet agenesis/hypoplasia) are extremely rare and largely limited to a few case reports. We report herein a 45-year-old nulliparous woman presenting to our outpatient clinic with chest discomfort and dyspnea on minimal exertion. Mitral valve with a single leaflet leading to a significant obstruction in left ventricular outflow was seen on transthoracic echocardiography and confirmed with transesophageal two- (2D) and three-dimensional (3D) echocardiography. Metoprolol was prescribed to relieve obstruction and symptoms.

To evaluate the association between angiotensin I-converting enzyme insertion/deletion (ACE I/D) gene polymorphism and retinal vein occlusion (RVO). A total of 80 patients with retinal vein occlusion who was admitted to the Eye Department of Kartal Training and Research Hospital between 2008 and 2011, and 80 subjects were enrolled in this retrospective case–control study. Patients who experienced RVO within one week to six months of study enrolment were included, and those with coronary artery diseases, prior myocardial infarction history and coagulation disturbances were excluded from the study. The diagnosis was made by ophthalmoscopic fundus examination and fluorescein angiography. The ACE gene I/D polymorphism was determined by polymerase chain reaction, and the ACE gene was classified into three types: I/I, I/D and D/D. In multivariate logistic regression analysis, ACE D/D genotype (p = 0.035), diabetes-mellitus (p = 0.019) and hypertension (p = 0.001) were found to be independent predictive factors for RVO. The results of the present study reveal that ACE D/D polymorphism is an independent predictive factor for RVO. However, one cannot definitely conclude that ACE gene polymorphism is a risk factor for retinal vein occlusion.

The concurrence of acute coronary syndrome with allergy or hypersensitivity as well as with anaphylactic or anaphylactoid reactions is increasingly encountered in daily clinical practice. There are several reports associating mast cell activation with acute cardiovascular events in adults. This was first described by Kounis as 'allergic angina syndrome',progressing to 'allergic myocardial infarction'. The main mechanism proposed is the vasospasm of coronary arteries. We present a case of a 28-year-old man who was admitted to our hospital with thoracic pain and dyspnoea. The symptoms recurred after simultaneous use of 1 g amoxicillin/clavulanic acid orally and 1 g ampicillin/sulbactam parenterally for tonsillitis the night before presentation and on the morning of admission.