Aims: This study aimed to determine the impact of left ventricular mass (LVM) on discordant stress cardiac magnetic resonance (CMR) imaging and invasive coronary angiography (ICA) in patients with suspected coronary artery disease (CAD) at coronary computed tomography angiography (CCTA).
Methods and results: In this substudy of the Dan-NICAD 2 trial (NCT03481712), 354 patients with suspected obstructive CAD on CCTA were examined with both rest and stress CMR and ICA for invasive physiological measurements. An abnormal stress CMR was defined as ≥2 contiguous segments with a stress perfusion defect, late gadolinium enhancement, or wall motion abnormality. CMR-derived LVM was sex-adjusted by conversion from grams to per cent. Haemodynamically obstructive CAD at ICA was defined as visual diameter stenosis >90% or FFR ≤0.80. LVM was higher in patients with an abnormal stress CMR compared to those with a normal CMR (median difference = 8.0%, P < 0.001). Patients with or without haemodynamically obstructive CAD had similar LVM (median difference = 2%, P = 0.222). Within four binary groups based on normal/abnormal stress CMR and ICA, both median LVM and index of microvascular resistance were higher in patients with discordant abnormal stress CMR and normal ICA than in patients with concordant normal stress CMR and ICA (124% vs. 111%, P = 0.001, and 29 vs. 19, P = 0.072, respectively).
Conclusion: In patients with suspected obstructive CAD, increased LVM can potentially confound concordance between stress CMR and ICA. This is due to increased microvascular resistance, which decreases the pressure gradient across an epicardial stenosis, resulting in a false high FFR and thus, normal ICA.
Aims: Structural valve degeneration (SVD) is the leading cause of late bioprosthetic valve failure. Lipoprotein(a) [Lp(a)] contributes to native aortic valve calcification, but its role in SVD is unclear. We investigated whether elevated Lp(a) is associated with SVD after bioprosthetic aortic valve replacement (AVR) and whether this differs between stenotic and regurgitant phenotypes.
Methods and results: We studied 174 bioprosthetic AVR patients with available Lp(a) levels over a median echocardiographic follow-up of 7.3 years (1372 studies). SVD was defined by VARC-3 criteria, and associations were analysed with Fine-Gray competing risk models. Lp(a) was evaluated categorically (≤ or > 125 nmol/L) and continuously using spline modelling. During follow-up, 40 patients developed SVD (22 stenotic, 9 mixed, and 9 regurgitant). The 15-year cumulative incidence was 51% with a median onset at 14.8 years. Elevated Lp(a) was associated with a higher risk of overall SVD (62% vs. 47%; SHR 2.06, 95% CI 1.09-3.91; P = 0.026) and specifically with stenotic/mixed phenotypes (SHR 2.57, 95% CI 1.26-5.23; P = 0.009). No association was observed with regurgitant phenotypes (SHR 0.85, 95% CI 0.19-3.92; P = 0.84). After multivariable adjustment, elevated Lp(a) remained an independent predictor of stenotic/mixed SVD (adjusted SHR 3.00, 95% CI 1.48-6.07; P = 0.002). Spline modelling showed a linear dose-response, with each 25 nmol/L increase in Lp(a) conferring 13% higher risk.
Conclusion: Elevated Lp(a) is independently associated with long-term risk of stenotic/mixed SVD. These findings highlight Lp(a) as a promising biomarker of prosthetic valve vulnerability and support investigation of emerging Lp(a)-lowering therapies to improve valve durability.
Valvular heart disease (VHD) is traditionally assessed through gradients, regurgitant volumes, and ejection fraction-but these valve-centric indices miss the earliest and most decisive signal: myocardial injury. Contemporary evidence shows that VHD is a myocardial disease, where outcomes are driven far more by the ventricle's biological response than by the valve lesion itself. This state-of-the-art review redefines VHD through a myocardium-first lens, highlighting tools that expose dysfunction long before conventional thresholds fail. A focused triad-LV global longitudinal strain (LV-GLS), RV strain with RV-PA coupling, and LA reservoir strain-detects injury at its inception and sharply improves prognostic precision. Cardiac magnetic resonance adds mechanistic depth through native T1, extracellular volume, and late gadolinium enhancement, identifying diffuse and focal fibrosis that dictate timing and reversibility of remodelling. Next-generation technologies extend this paradigm: CT-derived ECV as a scalable fibrosis surrogate, molecular imaging revealing active calcification and fibro-inflammation, and AI-driven models that fuse imaging, biomarkers, and clinical variables into personalized risk trajectories. We propose a serial, multiparametric, AI-enhanced strategy centred on myocardial protection-using LV-GLS tracking, RV-PA coupling, atrial mechanics, and fibrosis imaging to intervene during the true therapeutic window. This review positions a simple but transformative concept: managing VHD means managing the myocardium. Adopting this shift is essential for preserving cardiac health-not merely correcting valve anatomy.
Aims: Research has shown that the corrected proximal isovelocity surface area (PISA) method yields larger values for regurgitant volume (RegVol) and effective regurgitant orifice area (EROA) than conventional PISA method. However, it remains unclear whether new threshold values are needed for the corrected PISA method to effectively categorize the severity of secondary tricuspid regurgitation (STR). This study sought to identify threshold values for EROA and RegVol measured by the corrected PISA method for a three-grade classification of STR severity.
Methods and results: We used three-dimensional echocardiography to determine the volumetric regurgitant fraction (RegFr), calculated as the difference between the right (RV) and left ventricular (LV) stroke volumes (SV) divided by the RVSV. A total of 213 patients (78 ± 10 years; 64% women) with isolated STR were enrolled. Based on RegFr, we classified STR severity into mild (RegFr < 16%), moderate (RegFr 16-49%), and severe (RegFr > 49%) grades. EROA and RegVol were measured using conventional (EROACONV, RegVolCONV) and corrected (EROACORR, RegVolCORR) PISA methods. The threshold values for identifying patients with mild, moderate, and severe STR were <0.22, 0.22-0.46, and >0.46 cm² for EROACORR, respectively; and <18, 18-42, and >42 mL for RegVolCORR, respectively. The accuracy of these new threshold values in predicting STR severity based on RegFr was 99% for EROACORR and 94% for RegVolCORR. These accuracies were significantly higher than those of EROACONV (90%, P < 0.001) and RegVolCONV (41%, P < 0.001).
Conclusion: New threshold values for the corrected PISA method must be considered to improve the classification of STR severity.
Aims: This study aims to investigate the prognostic role of Stage 3 and 4 cardiac damage (CD) after transcatheter aortic valve intervention (TAVI), dependent on whether comorbidities contributing to right heart dysfunction were present.
Methods and results: Patients with severe aortic stenosis (AS) undergoing TAVI were included. Patients were divided into three groups: Stage 0-2 CD; Stage 3-4 CD, isolated AS (Stage 3-4 CD without significant concomitant chronic obstructive pulmonary disease, mitral annular calcification, mitral stenosis, mitral regurgitation, previous coronary artery bypass graft surgery, or cardiac amyloidosis); Stage 3-4 CD, AS with comorbidities (Stage 3-4 CD with ≥ 1 of these comorbidities). Futility was defined as death or Stage 3-4 New York Heart Association class dyspnoea 1 year after TAVI.Of 985 included patients, 822 (83%) had Stage 1-2 CD; 101 (10%) had Stage 3-4 CD, isolated AS; and 62 (6%) had Stage 3-4 CD, AS with comorbidities. Futility was not more common in Stage 3-4 CD groups (Stage 1-2 CD, 10%; Stage 3-4 CD, isolated AS, 17%; Stage 3-4 CD, AS with comorbidities, 15%, P = 0.09). Baseline and 1-year NYHA class were higher in Stage 3-4 CD compared with Stage 1-2 CD (P < 0.01). The 6 min walking test distance increased similarly in all groups at 1 year.
Conclusion: Potential comorbidities contributing to right heart dysfunction were common among patients in Stage 3-4 CD undergoing TAVI. Stage 3-4 CD was not associated with a significantly higher risk of futility, irrespective of comorbidities, and they experienced a similar functional improvement after TAVI.

