Cardiovascular Disease in Special Populations: From Basic Science to Clinical Practice

Myocardial infarction (MI) is defined as a clinical event in which myocardial damage is evidenced in the setting of myocardial ischemia. However, patients without occlusive coronary artery stenosis can also have myocardial infarction, which is titled Myocardial Infarction with Non-Obstructive Coronary Arteries (MINOCA). In our study, we aimed to evaluate oxidative stress and inflammation responses between MINOCA and MI with coronary artery disease (CAD) patients. In this prospective, cross-sectional study, patients with elevated cardiac markers who were admitted to the cardiology clinic between March 2024 and May 2024 with the preliminary diagnosis of acute coronary syndrome were included. Patients were consecutively collected as those with an occlusive lesion on coronary angiography and those without. Routine blood samples and oxidative stress parameters were obtained and compared between groups. A total of 88 patients, including 44 MINOCA and 44 MI-CAD patients, were included in the study. The MINOCA group was significantly younger than the MI-CAD group (56.2 ± 12.5, vs. 64.7 ± 9.3, p: 0.001). While inflammatory parameters were similar between groups, dityrosine (5708 FU/mL (5311–6417) vs. 4488 FU/mL (3641–5238), p < 0.001), lipid hydroperoxide (3.6 nmol/mL (3.4–3.9) vs. 3.4 nmol/mL (3.1–3.9), p: 0.023), kynurenine (3814 ± 621 FU/mL vs. 3319 ± 680 FU/mL, p: 0.001), and malondialdehyde (17.4 nmol/mL (13.7–19.1) vs. 13.1 nmol/mL (12–14.9), p < 0.001) levels were higher in the MI-CAD group than in the MINOCA group. Although inflammation parameters did not differ between MI-CAD and MINOCA patients, oxidative stress parameters were higher in the MI-CAD group. Regardless of the presence and severity of inflammation, oxidative markers can help to assess the level of myocardial cell damage, risk stratification, and diagnosis of myocardial infarction. Full article

Background: Severe aortic stenosis (AS) stratified by sex has been increasingly studied in the European population. Sex-specific outcomes in Asian patients with AS remain poorly defined. Hence, we aimed to study the clinical characteristics and impact of sex in moderate-to-severe AS, undergoing both invasive and conservative interventions in an Asian cohort over 10 years. Methods: Consecutive data with echocardiographic diagnoses of AS were stratified according to gender in a tertiary academic center between 2011 and 2021. Demographics, comorbidities, and clinical outcomes were compared. Results: Seven hundred and three (703) patients were included (56%, n = 397 were female). Calcific AS was the dominant etiology in both genders. Females had higher incidences of anemia (p < 0.001) and chronic kidney disease (p = 0.026); although, females had lower incidences of cardiovascular complications of coronary artery disease (CAD) (p = 0.002) and prior acute myocardial infarction (AMI) (p = 0.015). Echocardiographically, females had a smaller left ventricular outflow tract diameter (LVOTd) (p < 0.001), LV mass (p < 0.001), and left ventricle end diastolic volume (LVEDV) (p < 0.001). Conversely, the left atrial (LA) area (p < 0.001) and volume index (LAVI) (p < 0.001) were larger in females. Females had higher average E/e’ (p = 0.010) ratios compared to males. The mean follow-up duration between genders was 4.1 ± 3.3 years. Upon univariate analysis, a greater proportion of female AS patients encountered cardiovascular (CV) hospitalization during follow-up (female: 27.5%, n = 109 vs. male: 18.3%, n = 56; p = 0.005) compared to male patients, but there were no significant differences for the outcomes of heart failure (p = 0.612), stroke (p = 0.664), and all-cause mortality (p = 0.827). Fewer females underwent aortic valve (AV) intervention compared to males (21.2% vs. 27.8%, p = 0.042), albeit with a longer duration to AV intervention (3.6 years ± 2.4 vs. 2.6 years ± 2.3, p = 0.016). In the severe AS cohort, female sex remained an independent predictor for subsequent heart failure (aHR 2.89, 95% CI 1.01–8.29, p = 0.048) and CV hospitalization (aHR 20.0, 95% CI 1.19–335, p = 0.037) after adjustments for age, ethnicity, body mass index (BMI), comorbidities, left ventricular ejection fraction (LVEF), and AV intervention. Conclusions: There was no difference in heart failure, stroke, and all-cause mortality outcomes between male and female Asian patients with moderate-to-severe AS. However, there were more cardiovascular hospitalizations, with fewer and longer duration to AV intervention in females compared to males in our cohort. Full article

Objective: Cardiac computed tomography (CT) helps screen coronary artery stenosis in cases with dilated cardiomyopathy (DCM). Extracellular volume fraction (ECV) analysis has recently been eligible for CT. Method: We evaluated the impact of ECV on the CT to predict the prognosis in DCM patients with heart failure with reduced ejection fraction (HFrEF). Patients or Materials: We analyzed 101 consecutive DCM cases with HFrEF who underwent cardiac CT. All the patients had a lower left ventricular (LV) ejection fraction (LVEF) of less than 40%. We evaluated the effect of ECV to predict the patients’ prognosis. Cardiovascular death, hospitalization due to heart failure, and fatal arrhythmic events were included in the major adverse cardiac events (MACE). Results: MACE occurred in 27 cases (27%). The patients with MACE (27 cases) had an increased ECV on the LVM on the CT (37.2 ± 6.7 vs. 32.2 ± 3.6%, p = 0.0008) compared to the others (74 cases). Based on the receiver operating characteristics curve analysis, the best cutoff value of the ECV on the LVM to predict the MACE was 32.3%. The patients with ECV ≥ 32.3% had significantly higher MACE based on the Kaplan–Meier analysis. The ECV on the LVM was a significant marker to predict MACE based on the univariate Cox proportional hazard model (hazard ratio of 8.00, 95% confidence interval 1.88–33.97, p = 0.0048). Conclusions: ECV by CT is helpful to predict MACE in cases with DCM and HFrEF. Full article

We here sought to assess thrombotic and hemorrhagic complications and associated risk factors during pregnancy, delivery, and postpartum in women with prosthetic heart valves (PHV). Methods: The retrospective cohort study covered January 2011 to December 2022. The objective of the study was to assess the risk factors and frequency of thrombotic and hemorrhagic complications during pregnancy, delivery, and the postpartum period in women with PHV based on the experience of one perinatal center. We included 88 pregnancies with 77 prosthetic heart valves (PHV), which were divided into two groups, mechanical valve prostheses (MVP) (n = 64) and biological valve prosthesis (BVP) (n = 24). In the study we analyzed pregnancy outcomes, as well as thrombotic and hemorrhagic complication frequencies. Results: Of 88 pregnancies, 79 resulted in live births. In the MVP group, there were six miscarriages (9.4%) and two medical abortions (3.1%), including one due to Warfarin’s teratogenic effects. No miscarriages were reported in the BVP group, but one fetal mortality case (4.2%) occurred. During pregnancy, 11 MVP cases (17.2%) experienced thrombotic complications. In the BVP group, one patient (4.2%) had transient ischemic attack (TIA). Two MVP cases required surgical valve repair during pregnancy, and one in the post-delivery stage was caused by thrombotic complications. Postpartum, two MVP cases had strokes, and in one MVP patient, pulmonary embolism was registered, while no thrombotic complications occurred in the BVP group. Hemorrhagic complications affected 15 MVP cases (17.9%) in the postpartum period. There were no registered cases of maternal mortality. Conclusions: The effective control of anti-factor Xa activity reduced thrombotic events. However, the persistently high incidence of postpartum hemorrhagic complications suggests a need to reassess anticoagulant therapy regimens, lower target levels of anti-Xa, and reduce INR levels for discontinuing heparin bridge therapy. Despite the heightened mortality risk in MVP patients, our study cohort did not have any mortality cases, which contrasts with findings from other registries. Full article

Background/Objectives: In recent years, a possible connection between HLA-Cw6 and a distinctive cardiometabolic (CM) profile in patients with psoriatic disease (PsD) has been proposed, although there is still little support for this. Our aim was to further investigate this possible association by studying a large population of PsD patients. Methods: For this study, three different cohorts of patients with PsD were analyzed: two with a majority of cutaneous psoriasis, pooled n: 600, and a third with only psoriatic arthritis—PsA—cases, n: 340. Potential relationships between HLA-Cw6 and the different CM risk factors (hypertension, diabetes, obesity, dyslipidemia) were analyzed using univariate and multivariate regression models, while the final net effect was assessed using fixed- or random-effects meta-analyses, as appropriate. Results: In the PsA cohort, no association was detected between HLA-Cw6 carriership and any of the CM comorbidity factors. In psoriasis cohorts, after correcting for age, sex, disease duration, and arthritis, HLA-Cw6 carriers had a reduced diabetes risk (OR 0.49, 95%CI: 0.26–0.91, p = 0.026). This latter effect was confirmed by a fixed-effects meta-analysis of the included cohorts (pooled OR: 0.50, 95%CI: 0.27–0.90). Conclusions: This work demonstrates a potential protective effect of the HLA-Cw6 allele on the risk of diabetes in PsD. Our findings together with those of others seem to confirm the existence of a novel HLA-Cw6-linked cardiometabolic endotype in this disease. Full article

Trastuzumab, a monoclonal antibody which works against human epidermal growth factor receptor 2 (HER2), possibly causes cardiotoxicity through mitochondrial dysfunction. The usefulness of isolated peripheral blood mononuclear cells (PBMCs) in the assessment of trastuzumab-induced cardiotoxicity remains uncertain. This study aimed to determine the temporal changes in mitochondrial function, oxidative stress, and cell death in the isolated PBMCs of HER2-positive breast cancer patients during breast cancer treatment and to compare the changes with HER2-negative breast cancer patients who did not receive trastuzumab therapy. Eighteen newly diagnosed HER2-positive breast cancer women who received sequential doxorubicin and trastuzumab were consecutively recruited. Age- and gender-matched controls with HER2-negative breast cancer were selected. Echocardiography was carried out, and blood samples for the study of cardiac biomarkers and PBMCs were collected periodically during treatment. Only one patient in our cohort developed asymptomatic left ventricular dysfunction during trastuzumab treatment. However, trastuzumab following doxorubicin aggravated subclinical cardiac injury, determined by cardiac troponin and echocardiography. Cellular and mitochondrial oxidative stress in isolated PBMCs remained unchanged throughout breast cancer treatment. Regarding mitochondrial respiration, the maximal respiration and spare respiration capacity was significantly increased in controls after doxorubicin treatment but not in patients who received trastuzumab therapy. Moreover, the percentage of apoptosis and necroptosis in isolated PBMCs was dramatically decreased in the control, compared to patients with trastuzumab treatment. In conclusion, trastuzumab caused subtle myocardial injury and impaired mitochondrial respiration and cell viability in isolated PBMCs. Full article