Background: Acute coronary syndrome (ACS) is a leading cause of death, with significant disparities in risk factors and outcomes. The relationship between periodontal disease (PD), periostin (PN), and cardiovascular disease is complex, with both conditions sharing inflammatory pathways and risk factors. This study investigates the link between PN serum levels and cardiovascular risk factors in patients with ACS and concomitant PD. Methods: This case–control study involved 92 patients with ACS and PD admitted to the County Emergency Clinical Hospital of Târgu Mureș, Romania. Patients were divided into low PN (LP) and high PN (HP) groups based on a median PN level of 30.63 ng/ml. Clinical data, lipid profiles, and biomarkers were compared between groups. Results: Patients in the LP group had significantly higher total HDL cholesterol and triglyceride levels, and significantly lower LDL cholesterol levels compared to the HP group. Linear regression analysis showed a positive correlation between serum PN and LDL cholesterol (p < 0.0001) and a negative correlation between PN and HDL cholesterol (p < 0.0001). There were no statistically significant differences in apolipoprotein B, serum uric acid, creatinine, or blood glucose levels between the groups. However, patients in the HP group had a significantly higher prevalence of ST-elevation myocardial infarction (p < 0.05). Conclusion: In patients with ACS and PD, PN levels correlate with lipid profiles, particularly LDL and HDL cholesterol, and are associated with the type of myocardial infarction. These findings suggest PN may play a role in the complex interplay between PD, ACS, and cardiovascular risk, warranting further research to clarify its potential as a biomarker.

Introduction: Kounis syndrome is a complex clinical entity at the intersection of acute coronary syndromes and allergic reactions. Case presentation: We report the case of a 55-year-old woman with hypertension, autoimmune thyroiditis, and recurrent allergic complaints who was admitted with ST-elevation myocardial infarction and found to have myocardial infarction with non-obstructive coronary arteries (MINOCA), likely due to coronary vasospasm. During hospitalization, she developed cutaneous symptoms and was subsequently diagnosed with chronic spontaneous urticaria. Retrospectively, the diagnosis of Kounis syndrome type I was established. Conclusions: Reporting cases with subtle or absent allergic manifestations is essential to improve diagnostic accuracy and guide appropriate management, particularly given the potential for recurrence.

We present the case of an 88-year-old patient with multiple cardiovascular comorbidities who, on the first day after transcatheter aortic valve implantation (TAVI), developed sudden severe pain in the right lower extremity. Urgent computed tomography angiography (CTA) of the abdominal aorta and lower limbs revealed a patent right common iliac artery with thrombotic occlusion of the external iliac and femoral arteries. A transfemoral thromboembolectomy using a Fogarty catheter was performed at the iliofemoral axis, supplemented by local endarterectomy and patch angioplasty. Over the following three weeks, two additional interventions were required to evacuate an inguinal hematoma and secure hemostasis at the patch level. Three months later, the patient returned to the emergency department with severe groin pain and active bleeding from the wound. CTA revealed a large infected pseudoaneurysm of the common femoral artery, measuring approximately 4 × 2.5 cm. Reconstruction of the neo-femoral artery was carried out using an autologous bifurcated great saphenous vein graft, combined with a proximal sartorius muscle flap. At six months, CTA demonstrated patent femoral arteries without thrombus or hematoma and complete tissue healing.

Hypertrophic cardiomyopathy (HCM) is a myocardial disease characterized by abnormal thickening of the ventricular myocardium. It is most commonly inherited as an autosomal dominant disorder caused by mutations in sarcomere or sarcomere-associated protein genes. We report the case of a 15-year-old female with HCM and a strong family history (mother, sister, and maternal grandfather). Despite this background, her diagnosis was made incidentally following the onset of cardiac symptoms. Genetic testing confirmed a pathogenic MYH7 mutation. Based on elevated risk scores (HCM-Risk Kids = 8.6%, Primacy Risk Score = 13.09), she was considered at high risk for sudden cardiac death and underwent implantation of an implantable cardioverter-defibrillator (ICD) for primary prophylaxis. This case highlights the importance of a comprehensive approach to pediatric and adolescent HCM, including family history, genetic testing of at-risk relatives, early diagnosis, and multidisciplinary management. It also emphasizes the urgent need for systematic family screening of first-degree relatives using echocardiography and electrocardiography. Although genetic testing confirmed the diagnosis in our patient, it could not be extended to relatives due to financial limitations. Expanding access to genetic screening at a national level should be a priority. Future research should focus on optimizing genetic testing protocols and improving quality-of-life interventions for young patients with HCM and ICDs. Hypertrophic cardiomyopathy (HCM) is a myocardial disease characterized by abnormal thickening of the ventricular myocardium. It is most commonly inherited as an autosomal dominant disorder caused by mutations in sarcomere or sarcomere-associated protein genes. We report the case of a 15-year-old female with HCM and a strong family history (mother, sister, and maternal grandfather). Despite this background, her diagnosis was made incidentally following the onset of cardiac symptoms. Genetic testing confirmed a pathogenic MYH7 mutation. Based on elevated risk scores (HCM-Risk Kids = 8.6%, Primacy Risk Score = 13.09), she was considered at high risk for sudden cardiac death and underwent implantation of an implantable cardioverter-defibrillator (ICD) for primary prophylaxis. This case highlights the importance of a comprehensive approach to pediatric and adolescent HCM, including family history, genetic testing of at-risk relatives, early diagnosis, and multidisciplinary management. It also emphasizes the urgent need for systematic family screening of first-degree relatives using echocardiography and electrocardiography. Although genetic testing confirmed the diagnosis in our patient, it could not be extended to relatives due to financial limitations. Expanding access to genetic screening at a national level should be a priority. Future research should focus on optimizing genetic testing protocols and improving quality-of-life interventions for young patients with HCM and ICDs.