Background: Increased level of high‐sensitivity C‐reactive protein (hs‐CRP) is associated with no‐reflow phenomenon. Therefore, even when timely coronary revascularization is performed through the primary percutaneous coronary intervention (pPCI), the process can induce reperfusion injury. Purpose: We evaluated the influence of hs‐CRP level on the no‐reflow phenomenon in patients with ST‐segment elevation myocardial infarction (STEMI). Methods: In this study, we included one hundred and eighty‐two consecutive patients with STEMI of onset < 12 h, who underwent pPCI. The levels of creatine kinase (CK), the MB fraction of creatine kinase (CK‐MB), troponin I, hs‐CRP, and other routine laboratory parameters were measured. Measurement of hs‐CRP was done on the day of admission by Cobas assay (particle‐enhanced immunoturbidimetric assay) on Cobas c501 (Roche). Thereafter, patients were divided in two groups according to the thrombolysis in myocardial infarction (TIMI) flow grade. Results: From a total of 182 STEMI patients who underwent pPCI, the median value of hs‐CRP of the patients with TIMI grade flow 3 (successful reperfusion) was 8.5 (0.4–268) and of the patients with no‐reflow phenomenon (unsuccessful reperfusion, TIMI flow grade ≤ 2) was 37.90 (1.8–271.20), p < 0.0001. Receiver operating characteristics (ROC) curve of hs‐CRP plots the true positive rate against the false positive rate at different cutoff points, AUC = 0.73 (95% CI, 0.64–0.81), and the cutoff value for the hs‐CRP was 18.0 mg/L, p = 0.0001. Conclusions: hs‐CRP may be associated with no‐reflow phenomenon in STEMI patients. The cutoff value for hs‐CRP may be used to identify patients at risk for reperfusion injury.

Ventricular septal defect (VSD) represents a severe complication that may manifest after a myocardial infarction (MI), typically occurring between 2 and 7 days later. Due to advancements in reperfusion management, the incidence of VSDs after MI has become very rare, occurring in approximately 0.2% of MIs. The current guidelines recommend urgent post-infarction VSD (PI-VSD) closure. We report a case of a patient with a VSD, which was diagnosed 2.5 years after MI. At the time of acute inferior MI, the patient was managed with primary percutaneous intervention in the culprit artery, and 1 month later coronary artery by-pass grafting (CABG) was completed. Twenty and thirty months after AMI patient presented with ventricular tachycardia (VT). Following the second VT episode patient was hospitalized for further examination. Echocardiography revealed the presence of VSD at the site of inferioseptal wall aneurysm. An ICD was implanted owing to recurrent malignant rhythm disorders. In conclusion, although the PI-VSD might have been overlooked and the patient missed the chance of concomitant CABG and VSD repair, this case has reached a 3-year survival, which appears to be the longest survival recorded in a medically treated patient with PI-VSD.

Objective: Long-standing diabetes mellitus is often associated with cardiovascular complications. We aimed to evaluate the presence, extent and composition of subclinical atherosclerotic plaques in coronary arteries by Computed Tomography in patients with newly diagnosed type 2 diabetes mellitus (NDT2DM), and to identify the predictors. Methods: In this study 101 consecutive patients with NDT2DM were included. Patients were categorized into five groups based on their Coronary Artery Calcium Score (CACS) ranging from 0, 0-10, 11-100, 101-400 to >400. All parameters were compared across these groups. Results: The average patient age was 54.4 ± 11.6 years and 48 (47.5%) were females. Eight (7.9%) patients had CACS 0, 6.9% CACS 1-10, 42.6% CACS 11-100, 22.8% CACS 101-400 and 19.8% had CACS >400. Multiple regression analysis for the general data identified weight ( p = .04) and systolic blood pressure ( p = .033) as independent predictors for CACS. Conclusions: Asymptomatic patients with NDT2DM in more than 90% of cases may present with calcified atherosclerotic plaques and this may be predicted by: patient weight and the level of systolic arterial pressure. Our study emphasizes the need for comprehensive care and early prevention of cardiovascular complications in individuals with NDT2DM.

Left ventricular (LV) thrombus is one of myocardial infarction (MI) complications and if the thrombus is mobile and protruding, there is a high risk of embolization. It is exceptionally rare that the presenting serious symptom of acute MI is severe leg pain. We report here a rare case of a 36-year-old Caucasian male patient with unrecognized MI complicated by LV thrombus. His initial visit to the physician was due to sudden onset of severe left leg pain as a consequence of thromboembolism. Medical examination revealed occluded left femoral commune artery and femoral superficial artery, subacute MI and apical LV thrombus, which were treated accordingly. On follow-up, 2 months after hospital discharge, patient affirmed that he has been walking for approximately 3 km every day, without leg cramps or angina. Early recognition of MI, even when presented with atypical symptoms in young individuals and its prompt treatment is important to improve survival, as well as to reduce thrombotic events. J Med Cases. 2016;7(5):184-186 doi: http://dx.doi.org/10.14740/jmc2480w

Background: Apelin-36 may be used to identify patients with ST-segment elevation myocardial infarction (STEMI) who are at risk for the no-reflow phenomenon. Patients presenting with STEMI were evaluated and stratified according to their apelin-36 levels. Methods: In this study, 161 patients presenting with STEMI within 12 hours of symptom onset and undergoing primary percutaneous coronary intervention (pPCI) were enrolled. Biochemical parameters, including apelin-36, troponin T, creatine kinase (CK), the MB fraction of creatine kinase (CK-MB), total cholesterol, triglycerides, and other routine laboratory parameters, were measured. Blood samples for apelin-36 measurement were collected prior to PCI, centrifuged to obtain serum, and preserved at -80⁰C until being assayed. Two-dimensional echocardiography was performed in all patients. Thereafter, patients were divided into two groups according to their level of Apelin-36. Results: Among the 161 consecutive STEMI patients, 115 (71.42%) had Apelin-36 levels ≤0.58ng/mL (group 1), whereas 46 (28.57%) had Apelin-36 levels > 0.58ng/mL (group 2). In total, 51 (31.67%) STEMI patients experienced no-reflow phenomenon after PCI: 29 (18.01%) patients with apelin-36 ≤ 0.58ng/mL and 22 (13.66%) with a value > 0.58ng/mL (p < 0.001). In terms of Gensini score, the mean value in group 1 was (70.29 (±28.76), while in group 2, it was 81.95 (±23.82) (p=0.004). Overall, a positive correlation between apelin-36 and Gensini score was observed in both groups using Kendall’s correlation analysis (group 1: Figure 2, p=0.05; group 2: Figure 2, p 0.58ng/mL had troponin T levels of 132.15 (9.4-5190.0) (p < 0.012). The receiver operating characteristics (ROC) curve of apelin-36 was used to plot the true positive rate against the false positive rate at different cut-off points, with AUC=0.67 (95% CI, 0.57-0.76), and the cut-off value for apelin-36 was 0.58ng/mL, with p=0.001. Conclusions: Significant associations were observed between apelin-36 and no-reflow phenomenon in patients with STEMI. An apelin-36 cut-off value of 0.58ng/mL, measured at admission, could be used to identify patients who were at increased risk of no-reflow phenomenon/reperfusion injury.