Acute kidney injury (AKI) after transcatheter aortic valve implantation (TAVI) is a frequent complication associated with adverse outcomes and mortality. Various scores have been developed to predict this complication in the coronary setting. However, none have ever been tested in a large TAVI population. This study aimed to evaluate the power of four different scores in predicting AKI after TAVI. Overall, 1535 consecutive TAVI patients from the observational multicentric "Magna Graecia" TAVI registry were included in the analysis. Of the study population, 235 (15.31%) developed AKI early. The Mehran, William Beaumont Hospital, CR₄EATME₃AD₃, and ACEF scores were calculated retrospectively. The patients who developed TAVI-related AKI had significantly higher absolute values of all risk scores than those who did not. The receiver-operating characteristic analysis also showed a significant correlation between these four scores and AKI, but without a significant difference among all of them (p value = 0.176). Nevertheless, based on their area under the curve values (≤0.604 for all), none had adequate diagnostic accuracy in predicting TAVI-related AKI. Importantly, multivariate analysis identified myocardial revascularization close to the TAVI procedure and implantation of self-expanding prostheses, as well as atrial fibrillation, low-osmolar contrast media administration, corrected contrast medium volume, and any transfusion (p value < 0.05 for all) as independent risk factors for AKI. Although high values of current AKI risk scores are significantly associated with the development of this complication, these are not sufficiently accurate. Further studies are needed so that a TAVI-dedicated AKI risk score may be created.

Arrhythmic risk stratification in patients with Lamin A/C gene (LMNA)-related cardiomyopathy influences clinical decisions. An implantable cardioverter defibrillator (ICD) should be considered in patients with an estimated 5-year risk of malignant ventricular arrhythmia (MVA) of ≥10%. The risk prediction score for MVA includes non-missense LMNA mutations, despite their role as an established risk factor for sudden cardiac death (SCD) has been questioned in several studies. The purpose of this study is to investigate cardiac features and find gene–phenotype correlations that would contribute to the evidence on the prognostic implications of non-missense vs. missense mutations in a cohort of LMNA mutant patients. An observational, prospective study was conducted in which 54 patients positive for a Lamin A/C mutation were enrolled, and 20 probands (37%) were included. The median age at first clinical manifestation was 41 (IQR 19) years. The median follow-up was 8 years (IQR 8). The type of LMNA gene mutation was distributed as follows: missense in 26 patients (48%), non-frameshift insertions in 16 (30%), frameshift deletions in 5 (9%), and nonsense in 7 (13%). Among the missense mutation carriers, two (8%) died and four (15%) were admitted onto the heart transplant list or underwent transplantation, with a major adverse cardiovascular event (MACE) rate of 35%. No statistically significant differences in MACE prevalence were identified according to the missense and non-missense mutation groups (p value = 0.847). Our data shift the spotlight on this considerable topic and could suggest that some missense mutations may deserve attention regarding SCD risk stratification in real-world clinical settings.

Background: Surgical mortality risk scores, even if not properly designed and rarely tested in the transcatheter aortic valve implantation (TAVI) setting, still guide the heart team in managing significant aortic stenosis. Methods: After splitting 1763 consecutive patients retrospectively based on their mortality risk thresholds, the composite endpoint early safety (ES) was adjudicated according to Valve Academic Research Consortium (VARC)-2 and -3 consensus documents. Results: ES incidence was higher if VARC-2 rather than VARC-3 defined. Despite only patients showing VARC-2 ES had significantly lower absolute values of all three main risk scores, these last still failed to foresee both VARC-2 and -3 ES in intermediate-risk patients. The receiver operating characteristic analysis also showed a significant correlation, but with poor diagnostic accuracy, among the three scores and only VARC-2 ES; moreover, the absence of VARC-2 ES and low-osmolar contrast media administration were identified as independent predictors of 1-year mortality and absence of VARC-3 ES, respectively. Finally, even a single complication included in the ES definition could significantly affect 1-year mortality. Conclusion: Currently, the most used mortality risk scores do not have adequate diagnostic accuracy in predicting ES after TAVI. The absence of VARC-2, instead of VARC-3, ES is an independent predictor of 1-year mortality.

Acute coronary syndrome (ACS) and stroke are interconnected conditions that often share risk factors such as atherosclerosis, thrombosis, and systemic inflammation. When these events occur simultaneously, they present unique diagnostic and therapeutic challenges. This review explores the pathophysiological mechanisms linking ACS and stroke, including common pathways like plaque instability, cardioembolism, and endothelial dysfunction, while highlighting the distinct features of ischemic and hemorrhagic strokes. The manuscript provides an overview of diagnostic strategies, emphasizing the role of biomarkers, advanced neuroimaging, and risk stratification tools in guiding acute management. Furthermore, the review delves into treatment approach, emphasizing the need to balance reperfusion therapies for ACS with thrombolysis or thrombectomy for ischemic stroke while carefully managing the challenges posed by anticoagulation in cases complicated by bleeding. Long-term strategies for secondary prevention are examined, including antithrombotic regimens tailored to the dual risk of thrombosis and bleeding, as well as lipid-lowering and blood pressure management. Future perspectives highlight the potential of novel pharmacological agents, neuroprotective therapies, and AI-driven tools to enhance patient outcomes. This review underscores the importance of integrated, multidisciplinary care and identifies key areas for future research to optimize the management of these high-risk patients.

A wide range of etiologies, both ischemic and nonischemic, can produce an electrocardiographic pattern of ST-segment elevation (STE), including Takotsubo syndrome (TTS) and electrolyte imbalances. Instances of hypocalcemia-induced TTS and STE are exceedingly rare in medical literature. This paper presents the case of a 75-year-old woman with advanced ovarian cancer and no prior heart issues, who exhibited diffuse STE on electrocardiogram, resembling acute coronary syndrome. Additionally, echocardiography suggested left ventricle apical ballooning, as per TTS, in the context of severe hypocalcemia and elevated troponin I level. After confirming no coronary artery disease via angiography, we administered calcium supplementation. Subsequently, the electrocardiogram displayed widespread giant T-wave inversions, and the patient’s cardiac function fully recovered on normalization of calcium levels within few days. This case serves to highlight the importance of recognizing rare causes of STE (eg, hypocalcemia-induced cardiomyopathy), particularly in patients with neoplastic condition. However, the precise mechanism underlying a potential hypocalcemia-induced TTS remains to be elucidated, and there are only a limited number of case reports in the literature. In light of the aforementioned considerations, we propose a comprehensive examination of cases associated with hypocalcemia and STE and left ventricular systolic impairment.