Cardiac calcified amorphous tumor (CAT) is an uncommon nonneoplastic intracardiac lesion associated with end-stage renal disease; mobile lesions carry an embolic risk and are generally resected. A 62-year-old man on maintenance hemodialysis was found to have a mobile verrucous mass 17 mm long on the anterior mitral leaflet and a separate immobile calcified lesion, 19 × 12 mm, at the base of the posterior mitral leaflet, together with moderate aortic regurgitation, left ventricular dilatation, a left ventricular ejection fraction of 41%, and pulmonary hypertension. Infective endocarditis was considered unlikely because blood cultures were negative and there was no inflammatory response; a noninfective thrombotic lesion was suspected, but four months of warfarin produced no regression of either lesion. Because open-heart surgery was required for the mobile mass, the aortic valve was addressed at the same operation. Each prosthetic option carried a disadvantage: a bioprosthesis could undergo accelerated structural deterioration in the same calcifying environment, and a mechanical valve would require lifelong anticoagulation, which in dialysis carries a bleeding hazard and may itself promote calcification. Aortic valve neocuspidization with glutaraldehyde-treated autologous pericardium was therefore chosen as an individualized alternative, with transaortic resection of the mobile mass; the immobile lesion was left unresected because of its proximity to the atrioventricular groove and left circumflex artery. Histology confirmed CAT. Aspirin was continued while warfarin was not resumed. Over three years of echocardiographic and 45 months of clinical follow-up, the reconstructed valve remained free of stenosis and paravalvular leak, ventricular function improved, the unresected lesion did not enlarge, and no thromboembolic or bleeding event occurred, although aortic regurgitation progressed to a mild-to-moderate degree.

Rheumatic heart disease (RHD) remains a major cause of maternal cardiovascular morbidity and mortality in low-resource settings, particularly among women of reproductive age. Physiological changes during pregnancy can unmask previously undiagnosed disease or precipitate decompensation in those with established valvular lesions. We present a case series of three women with RHD during pregnancy and the early postpartum period, highlighting the burden, clinical presentation, and management challenge in a resource-limited setting. All patients presented with advanced disease, including severe mitral stenosis, atrial fibrillation, and heart failure, with one case complicated by multivalvular involvement and reduced left ventricular function. Management focused on hemodynamic stabilization using diuretics, rate control, anticoagulation, and multidisciplinary care. Definitive interventions such as percutaneous balloon mitral valvotomy or valve replacement were indicated but deferred due to limited availability and financial constraints. All three mothers were clinically stabilized and remained alive at short-term follow-up, although one preterm neonate died from respiratory distress syndrome and Case 3 required readmission because of medication nonadherence. This series underscores the persistent burden of RHD in pregnancy in sub-Saharan Africa and highlights critical gaps in access to definitive cardiac interventions and anticoagulation monitoring. Strengthening health systems, improving access to specialized cardiac care, and implementing preventive strategies are essential to reduce morbidity and mortality associated with RHD in pregnancy in resource-limited settings.

To determine whether higher Hounsfield unit (HU) thresholds for computed tomography-derived aortic valve calcium (CT-AVC) scoring provide additional hemodynamic or discriminatory value beyond conventional 130-HU Agatston scoring in classical high-flow/high-gradient severe aortic stenosis (AS). This single-center retrospective cohort included 63 consecutive pre-TAVI patients with trileaflet, classical high-flow/high-gradient severe AS. CT-AVC was quantified on non-contrast ECG-gated CT at 130, 200, 500, 800, and 1000 HU within a manually defined leaflet/annulus region of interest, excluding left ventricular outflow tract and mitral annular calcification. Associations with peak gradient, mean gradient, and aortic valve area were assessed using correlation and multivariable linear regression.Exploratory ROC analysis assessed discrimination of very severe hemodynamic burden, defined as a mean gradient ≥ 60 mmHg, within the established severe-AS cohort, with ROC areas compared using DeLong testing. CT-AVC at all HU thresholds was independently associated with higher peak gradient (β, 0.010 at 130 HU to 0.144 at 1000 HU; all P ≤ 0.005) and higher mean gradient (β, 0.0059 at 130 HU to 0.073 at 1000 HU; all P ≤ 0.024). Associations with aortic valve area were not statistically significant. Within-cohort discrimination of very severe hemodynamic burden was modest and comparable across thresholds (AUC 0.65-0.67), with no statistically significant difference by DeLong testing (P = 0.68). In classical high-flow/high-gradient severe AS, CT-AVC demonstrated consistent associations with transvalvular gradients across HU thresholds. Higher HU thresholds did not outperform conventional 130-HU scoring and showed only modest, comparable performance for within-severity hemodynamic stratification. These thresholds should be interpreted as complementary densitometric analyses rather than alternative diagnostic cut-offs.

Intraoperative ventilatory failure is most often attributed to airway or equipment problems, but rare pleural complications can produce abrupt obstructive physiology. We report an 85-year-old woman with severe mitral and aortic stenosis, end-stage renal disease (ESRD) on hemodialysis, and recurrent pleural effusions undergoing video-assisted thoracoscopic surgery (VATS) with bilateral PleurX catheter placement who developed sudden ventilation failure immediately after left-sided catheter placement. Despite prompt airway reassessment and emergent pleural decompression, she progressed to cardiopulmonary arrest with echocardiographic findings consistent with profound hemodynamic compromise. This case highlights tension hydrothorax as a critical diagnostic consideration when unexplained ventilatory failure follows pleural instrumentation, particularly in patients with limited preload reserve.

In humans, surgical repair is commonly performed for infective endocarditis (IE) associated with mitral valve destruction. However, extensive valve destruction may make repair impossible and require prosthetic valve replacement. In small-breed dogs, appropriately sized prosthetic valves are lacking, and complete surgical mitral valve reconstruction in dogs has not been reported. We encountered a Chihuahua that developed IE after mitral valve repair. During reoperation for progressive mitral regurgitation recurrence, the mitral leaflets were extensively destroyed and torn, and re-repair using native tissue was impossible; the entire valve was therefore reconstructed with fresh autologous pericardium. A graft was harvested and fashioned into a cylindrical valve based on a design previously described in a human study. Intraoperative saline testing and immediate postoperative echocardiography confirmed adequate opening and closure of the reconstructed pericardial valve, with only mild mitral regurgitation and no stenosis. The dog died on the second day after reoperative day of an uncontrolled infection caused by extended-spectrum beta-lactamase-producing Escherichia coli. This case demonstrates that an autologous pericardial valve can provide short-term mechanical function as a mitral valve in a small-breed dog and indicates that infection control is the principal determinant of outcome.

Left atrial myxoma is the most common primary cardiac tumor, although intratumoral hemorrhage remains exceedingly rare. We recently treated a 55-year-old man with a 37-year smoking history who presented with progressive dyspnea and leg edema caused by acute heart failure. Echocardiography revealed a large, pedunculated left atrial mass (54 × 27 mm) protruding into the left ventricle during diastole, causing functional mitral stenosis, as well as moderate mitral and tricuspid regurgitation. Contrast-enhanced computed tomography revealed a 30 × 46 mm intracardiac mass without definite feeding vessels or signs of hemorrhage. The patient underwent semi-urgent surgery 1 week after diagnosis, with complete tumor excision and concomitant mitral and tricuspid annuloplasty. Histopathological examination revealed a 5.5 cm myxoid tumor containing multiple intratumoral hemorrhagic foci with hemosiderin deposition, consistent with hemorrhagic myxoma. The postoperative course was uneventful. Intratumoral bleeding within a myxoma may result from rupture of fragile neovessels, potentially leading to sudden enlargement and mitral inflow obstruction. Awareness of this rare condition is essential for timely clinical recognition and appropriate surgical decision-making in patients with deteriorating left atrial myxoma.

Mitral regurgitation (MR) frequently coexists with severe aortic stenosis and may persist or worsen after surgical aortic valve replacement (SAVR) despite afterload reduction. Following SAVR, abrupt ventricular unloading can unmask hyperdynamic ventricular function, promote systolic anterior motion and left ventricular outflow tract (LVOT) obstruction, resulting in dynamic MR and hemodynamic instability. A thorough preoperative assessment of ventricular geometry and mitral valve anatomy is crucial to identify patients at increased risk of post-SAVR LVOT obstruction. We describe a case of severe dynamic MR and LVOT obstruction following SAVR, successfully managed through comprehensive echocardiographic evaluation and tailored hemodynamic optimization, ultimately avoiding unnecessary percutaneous mitral intervention.

Cardiac myxoma is the most common primary cardiac tumor and typically arises in the left atrium. Large, mobile myxomas may prolapse through the mitral valve and produce functional mitral stenosis with secondary pulmonary hypertension. We report a 57-year-old woman with cardiovascular risk factors (hypercholesterolemia and obesity) who presented with New York Heart Association class III dyspnea and palpitations. First-line transthoracic echocardiography revealed a giant, mobile left atrial mass (4.7 x 4.8 cm) attached to the basal third of the interatrial septum, prolapsing into the left ventricle and producing a mean transmitral gradient of 16 mmHg with severe pulmonary hypertension (estimated pulmonary artery systolic pressure approximately 80 mmHg). Preoperative coronary computed tomography (CT) angiography, performed to exclude significant coronary artery disease given her cardiovascular risk factors and to characterize the intracardiac mass non-invasively, confirmed the mass and showed coronary atheromatosis without significant stenosis. The mass was surgically resected within two weeks of diagnosis via a minimally invasive thoracoscopic approach, decided in a multidisciplinary heart team meeting, with femoro-femoral cannulation, without preoperative anticoagulation; activity restriction and close clinical monitoring were maintained while awaiting surgery. The postoperative course was uncomplicated, with early extubation and rapid mobilization. At one-month follow-up, the transmitral gradient and pulmonary artery pressures had normalized, with a stable, mild residual mitral regurgitation and complete symptom resolution. Histopathological examination showed a well-circumscribed, non-encapsulated, smooth-surfaced proliferation of spindle-to-stellate cells within an abundant myxoid stroma, without atypia, mitoses, or necrosis; immunohistochemistry was positive for calretinin, confirming the diagnosis of myxoma. This case illustrates the diagnostic and hemodynamic impact of a giant left atrial myxoma and the feasibility of a minimally invasive thoracoscopic resection in a carefully selected patient.