Background: peripheral arterial disease (PAD) is identified late in diabetic patients because, in the majority of cases, it is associated with diabetic peripheral neuropathy, resulting in little or no symptoms, or symptoms that are completely neglected. Methods: In this study were enrolled all patients over 18 years of age, with diabetes mellitus type II for more than a year with poor glycemic control, diagnosed with diabetic polyneuropathy admitted to the Diabetology Department, Emergency County Hospital of Targu Mures, Romania between January 2020 and March 2023. We divided the patients into two groups, based on the presence or absence of subclinical atherosclerosis in the lower limb, named “SA” and “non-SA”. Results: Patients in the SA group were older (p = 0.01) and had a higher incidence of IHD (p = 0.03), history of MI (p = 0.02), and diabetic nephropathy (p = 0.01). Moreover, patients with subclinical atherosclerosis had a higher BMI (p < 0.0001) and a longer duration of diabetes (p < 0.0001). Among all patients, the systemic inflammatory markers, MLR (r = 0.331, p < 0.001), NLR (r = 0.517, p < 0.001), PLR (r = 0.296, p < 0.001), SII (r = 0.413, p < 0.001), as well as BMI (r = 0.241, p < 0.001) and HbA1C (r = 0.489, p < 0.001), demonstrated a strong positive correlation with the diabetes duration. The multivariate logistic regression analysis showed that older patients (OR: 2.58, p < 0.001), the male gender (OR: 2.30, p = 0.006), a higher baseline levels of BMI (OR: 7.71, p < 0.001), and the duration of diabetes (OR: 8.65, p < 0.001) are predictors of subclinical atherosclerosis in DN patients. Additionally, the high baseline levels of all systemic inflammatory markers (for all: p < 0.001) and poor diabetes management (OR: 10.4, p < 0.001 for HbA1C; OR: 10.78, p < 0.001 for admission glucose) are independent predictors of SA. Conclusions: the inflammatory markers, NLR, MLR, PLR, and SII, being cheap and easy to collect in routine medical practice from the standard blood tests, could be an important step in predicting vascular outcomes in diabetic patients and the disease’s progression, playing a key role in follow-up visits in type-2 diabetic patients and PAD patients.

Background/Objectives: In recent decades, the advantages of minimizing surgical trauma have led to the development of minimally invasive surgical procedures. While the benefits often outweigh the risks, several challenges are encountered that are not present in conventional surgical approaches. Unilateral pulmonary edema (UPE) after mitral interventions performed through a right-sided approach is a rare but potentially life-threatening event. Methods: We present the case of a 49-year-old patient who underwent endoscopic mitral valve repair. Immediately following ICU admission, the patient’s oxygen saturation suddenly dropped, and serous discharge was exteriorized from the endotracheal tube, with a thoracic X-ray revealing right-sided unilateral pulmonary edema. Results: The therapeutical course was complex. The patient developed hemodynamic instability, leading to cardiac arrest, which required cardiopulmonary resuscitation and the initiation of peripheral veno-arterial extracorporeal membrane oxygenation (VA-ECMO). The endotracheal cannula was replaced with a right-sided double-lumen cannula, and the patient was placed on two ventilators operating independently. The patient was weaned off extracorporeal membrane oxygenation (ECMO) on the fifth day and extubated on the sixth postoperative day. Conclusions: We successfully treated this patient using ECMO and independent lung ventilation. Several cases have been described in the literature, but the pathogenesis and risk factors of UPE remain unclear. Management depends on the severity of UPE, but a deeper understanding of its underlying mechanisms could provide cardiac surgeons with enhanced strategies for preventing UPE and implementing timely interventions.

Background: Totally endoscopic techniques have become increasingly popular in cardiac surgery, with minimally invasive mitral valve repair emerging as an effective alternative to median sternotomy. This approach could be particularly advantageous for patients with Noonan syndrome, who often present with structural thoracic anomalies and other comorbidities like bleeding disorders. Endoscopic mitral valve surgery is rapidly establishing itself as the new standard of care for mitral valve operations, demonstrating both safety and efficacy. Noonan syndrome is an autosomal-dominant multisystem disorder with variable expression and is the second most common syndromic cause of congenital heart disease, surpassed only by Down syndrome. A wide spectrum of cardiovascular phenotypes is associated with Noonan syndrome, including pulmonary valve stenosis (often with dysplastic valves), hypertrophic cardiomyopathy, secundum atrial septal defect and mitral valve abnormalities. Methods: Given the limited data in the literature regarding the experience of other centers with endoscopic mitral surgery in patients with this condition, we aim to present the case of a 46-year-old male with a known diagnosis of Noonan syndrome who presented to a cardiologist with a 6-month history of dyspnea and fatigue. Transthoracic echocardiography revealed severe mitral regurgitation. Following multidisciplinary discussions within the Heart Team and after obtaining informed consent from the patient and his family, the decision was made to proceed with totally endoscopic mitral valve repair. Results: The patient experienced an uneventful postoperative course and was discharged 8 days after the procedure. In this case, endoscopic surgery was essential for successfully repairing the mitral valve. Structural abnormalities, such as chest wall deformities causing heart malrotation and atypical positioning, significantly impaired visualization. Conclusions: The endoscopic approach provided superior access to the mitral valve, enabling precise and effective repair. Additionally, it offered benefits such as improved esthetic outcomes, faster recovery, and a reduced risk of exacerbating thoracic deformities due to improper sternal bone healing.

Plantar fibromatosis (or Ledderhose’s disease) is a rare benign condition, difficult to treat, defined by gradual-growing nodules in the central medial part of the plantar fascia, with the possibility of sclerosis and shrinkage of the entire fascia or, rarely, contractures of the toes. From a histopathological point of view, it is linked to Dupuytren’s contracture of the hand and Peyronie’s disease of the penis, being part of a large group of fibromatoses, based on a proliferation of collagen and fibroblasts. Its etiology is still not fully understood, even though it has been associated with trauma, diabetes mellitus, use of anticonvulsants, frozen shoulder, alcohol consumption, and liver disease. Typically, ultrasound confirms the diagnosis, and magnetic resonance imaging is used for more aggressive and advanced types. Several conservative treatment techniques, such as steroid injections, verapamil, imatinib, radiation therapy, extracorporeal shock wave therapy, tamoxifen, sorafenib, mitomycin C, and collagenase, have been documented. When non-operative care fails, surgical measures may be considered, even though recurrence is expected. We attempted to provide a better understanding of this disease by covering all of the important aspects: its history, clinical and radiologic findings, diagnosis, pathophysiology features, conservative and surgical treatment, recurrence rate, and prognosis.

This study aimed to investigate the impact of long-term survival on cardiac serum biomarkers such as natriuretic peptides (mid-regional pro-atrial natriuretic peptide [MR-proANP], B-type natriuretic peptide [BNP], N-terminal prohormone BNP [NT-proBNP]), soluble ST2 (sST2), galectin-3 and mid-regional pro-adrenomedullin (MR-proAMD). Consecutive patients hospitalized in a tertiary center, undergoing echocardiographic and invasive left cardiac catheterization for diastolic dysfunction assessment were prospectively included in this study. Cardiac biomarkers were determined from pre-procedural peripheral venous blood samples. A total of 110 patients were included, with a median follow-up of 1.66 (1.23–2.16) years during which 16 (14.5%) patients died. A total of 45.4% (50) of patients had diastolic dysfunction. In the univariate Cox regression, long-term survival was predicted by BNP (p < 0.0001, HR = 0.39 [0.20–0.53]), NT-proBNP (p < 0.0001, HR = 0.40 [0.22–0.55]), MR-proANP (p = 0.001, HR = 0.30 [0.11–0.46]), sST2 (p < 0.0001, HR = 0.47 [0.30–0.60]), but not with MR-proAMD (p = 0.77) or galectin-3 (p = 0.76). In the final stepwise multivariable Cox regression non-invasive and invasive models, NT-proBNP and sST2 remained independent predictors of survival. Natriuretic peptides (BNP and NT-proBNP) and sST2 were predictors of long-term survival, while MR-proANP, MR-proADM and galectin-3 did not have predictive values. NT-proBNP and sST2 improved survival prediction in both a non-invasive scenario (including clinical, serum and echocardiographic parameters) and an invasive clinical scenario (including left heart catheterization parameters). The sST2 pathway could provide a target for therapeutic intervention.

Background: Mitral valve prolapse is a common valvular heart disorder, usually associated with a benign prognosis in the absence of significant mitral regurgitation. However, a subset of patients is at increased risk for complex ventricular arrhythmias and sudden cardiac death. Identifying these high-risk individuals remains a major clinical challenge. Case Summary: We present the case of a 71-year-old female patient with recurrent syncopal episodes, a strong family history of sudden cardiac death, and complex ventricular ectopy. Multimodality imaging revealed bileaflet mitral valve prolapse, severe mitral regurgitation, mitral annular disjunction, and the Pickelhaube sign, with no evidence of myocardial fibrosis on cardiac magnetic resonance imaging. The patient underwent minimally invasive mitral valve repair and received an implantable cardioverter-defibrillator for primary prevention of sudden cardiac death. Follow-up revealed significant reverse cardiac remodeling, marked reduction in arrhythmic burden, and restoration of mitral valve function. Family screening identified mitral annular disjunction in both of her daughters, who were asymptomatic and without arrhythmias. Discussion: Mitral annular disjunction has emerged as a potentially arrhythmogenic substrate, especially in patients with familial clustering, raising the possibility of a genetic predisposition. Risk stratification remains difficult, as no individual clinical, electrocardiographic, or imaging marker has demonstrated consistent predictive value. Surgical correction of mitral valve prolapse with associated mitral annular disjunction may lead to a reduction in arrhythmic risk and promote favorable structural remodeling. Conclusions: This case-based review emphasizes the importance of advanced imaging techniques in the identification and management of high-risk mitral valve prolapse phenotypes. Early surgical intervention and close arrhythmic surveillance may improve outcomes, although further research is necessary to define risk assessment tools and explore the genetic background of arrhythmogenic mitral valve disease.