We sought to investigate the relationship between infarct and dyssynchrony post- myocardial infarct (MI), in a porcine model. Mechanical dyssynchrony post-MI is associated with left ventricular (LV) remodeling and increased mortality. Cine, gadolinium-contrast, and tagged cardiovascular magnetic resonance (CMR) were performed pre-MI, 9 ± 2 days (early post-MI), and 33 ± 10 days (late post-MI) post-MI in 6 pigs to characterize cardiac morphology, location and extent of MI, and regional mechanics. LV mechanics were assessed by circumferential strain (eC). Electro-anatomic mapping (EAM) was performed within 24 hrs of CMR and prior to sacrifice. Mean infarct size was 21 ± 4% of LV volume with evidence of post-MI remodeling. Global eC significantly decreased post MI (-27 ± 1.6% vs. -18 ± 2.5% (early) and -17 ± 2.7% (late), p < 0.0001) with no significant change in peri-MI and MI segments between early and late time-points. Time to peak strain (TTP) was significantly longer in MI, compared to normal and peri-MI segments, both early (440 ± 40 ms vs. 329 ± 40 ms and 332 ± 36 ms, respectively; p = 0.0002) and late post-MI (442 ± 63 ms vs. 321 ± 40 ms and 355 ± 61 ms, respectively; p = 0.012). The standard deviation of TTP in 16 segments (SD16) significantly increased post-MI: 28 ± 7 ms to 50 ± 10 ms (early, p = 0.012) to 54 ± 19 ms (late, p = 0.004), with no change between early and late post-MI time-points (p = 0.56). TTP was not related to reduction of segmental contractility. EAM revealed late electrical activation and greatly diminished conduction velocity in the infarct (5.7 ± 2.4 cm/s), when compared to peri-infarct (18.7 ± 10.3 cm/s) and remote myocardium (39 ± 20.5 cm/s). Mechanical dyssynchrony occurs early after MI and is the result of delayed electrical and mechanical activation in the infarct.

Background/Objectives: Lactate, traditionally considered a byproduct of anaerobic metabolism, is increasingly recognized as a biomarker of tissue perfusion and systemic stress. While hyperlactatemia is frequent after pediatric cardiac surgery, evidence regarding its prognostic role remains controversial. This study aimed to evaluate whether serial lactate measurements predict mortality in children undergoing surgery for congenital heart disease in Southeast Mexico. Methods: We conducted a retrospective cohort study including children aged 0–210 weeks with confirmed congenital heart disease who underwent first-time cardiac surgery between January 2022 and December 2024. Serum lactate was measured intraoperatively, at intensive care unit (ICU) admission, and at 12 and 24 h postoperatively using a Gem^® Premier™ 3500 analyzer. Sociodemographic, clinical, and surgical data were recorded. Associations between lactate levels and mortality were analyzed with Cox regression, adjusting for RACHS-2 category and intraoperative complications. Predictive performance was assessed with ROC curves and Harrell’s C-index. Results: 103 patients were included (median age 49.2 weeks; 60% female). Lactate levels overlapped intraoperatively but significantly discriminated against survivors from non-survivors thereafter. ICU admission lactate ≥ 4.2 mmol/L predicted mortality with 100% sensitivity and 60% specificity (AUC = 0.84). Hazard ratios confirmed that lactate at ICU admission (HR 2.17, 95% CI 1.16–4.06; p = 0.015), 12 h (HR 6.37, 95% CI 1.02–39.6; p = 0.047), and 24 h (HR 1.81, 95% CI 1.07–3.09; p = 0.028) were significant predictors of mortality. The model showed excellent discrimination (Harrell’s C = 0.986), though optimism due to the limited number of deaths should be considered. Conclusions: Serial lactate monitoring, particularly upon ICU admission, provides strong prognostic information for in-hospital mortality in pediatric cardiac surgery patients. Incorporating early postoperative lactate into routine monitoring may allow timely therapeutic adjustments. Preoperative lactate assessment warrants further evaluation as a potential risk stratification tool.

Background: Rickettsial diseases are endemic in southeastern Mexico, yet their potential subclinical cardiac effects remain poorly understood. Although severe spotted fever and typhus group infections may cause myocarditis and arrhythmias, limited evidence exists regarding cardiac alterations in individuals previously diagnosed with rickettsiosis who later show Rickettsia spp. IgG seropositivity. Methods: This follow-up observational study was conducted at a tertiary referral hospital in the Yucatan Peninsula. From an initial cohort of 390 patients evaluated for suspected rickettsial disease, 284 were confirmed as IgG-positive during follow-up. Among them, 18 adults who were asymptomatic for acute rickettsiosis at reassessment, but reported mild or nonspecific cardiac symptoms, underwent standardized cardiological evaluation. Procedures included a 12-lead electrocardiogram (ECG), transthoracic echocardiography, and 24 h Holter monitoring. All studies were reviewed independently by two blinded cardiologists with senior adjudication. Results: Global systolic function was preserved in all participants. However, subclinical abnormalities were identified, including right ventricular dilation in 16.7%, clinically relevant QTc prolongation in 22.2%, sinus pauses in 11.1%, reduced heart rate variability in 11.1%, atrial flutter in one patient, and complete left bundle branch block in one patient. QTc prolongation was detected exclusively through Holter monitoring. Conclusions: Adults previously diagnosed with rickettsiosis may exhibit subclinical cardiac involvement despite apparent recovery. Holter monitoring appears more sensitive than ECG for identifying electrical disturbances, warranting larger prospective studies.

An 80-year-old man presented to the cardiology outpatient clinic due to shortness of breath. His past medical history included alcohol intake, hypertension, inferior wall myocardial infarction (five years ago), an ischemic stroke, and permanent atrial fibrillation (diagnosed three years before the current examination). A physical exam revealed a decreased intensity of S1 and S2, irregular rate and rhythm, and no murmurs nor friction rub. X-rays, Computed Tomography, and echocardiography exhibited pericardial calcification, involving mostly the inferior wall and protruding into the left ventricle. A diagnosis of constrictive pericarditis due to pericardial calcification was established and considered idiopathic. Even when it may be related to ischemic heart disease, post-infarction pericarditis could explain how the calcification extended to adjacent territory perfused by the circumflex coronary artery. Combined imaging studies were crucial not only for identifying calcium deposits in the pericardium but also in assessing a patient inherently prone to co-existing and exacerbating conditions. Even though pericardiectomy allows for removal of the clinical manifestations of congestive pericarditis in the most symptomatic patients with pericardial calcification, among patients like ours, with tolerable symptoms, cardiologists should discuss the therapeutic options considering the patient’s choices, potentially including a rehabilitation plan as part of non-pharmacological management.