Unveiling the impact of cirrhotic cardiomyopathy on portal hemodynamics and survival after transjugular intrahepatic portosystemic shunt: a prospective study.

BACKGROUND AND AIMS: The placement of Transjugular intrahepatic portosystemic shunt (TIPS) results in a sudden increase in central circulating blood volume, which requires proper regulation of the cardiovascular system. We aimed to investigate the impact of TIPS on cirrhotic cardiomyopathy (CCM). METHOD: A consecutive case series of patients with cirrhosis who underwent TIPS were evaluated by echocardiography and pressure measurements before, immediately after TIPS and 2-4 days later (delayed). Furthermore, all patients underwent a one-year follow-up. RESULTS: In this study, 107 patients were enrolled, 38 (35.5%) with CCM. Echocardiography revealed an increase in postoperative left ventricular filling pressure accompanied by an elevation in left ventricular ejection fraction (LVEF). However, patients in the CCM group exhibited lower LVEF and mean arterial pressure (MAP) compared to the non-CCM group. Post-TIPS, CCM patients showed increased right atrium pressure (RAP) that normalized within 2-4 days, whereas non-CCM patients had lower RAP than baseline. Compared to patient without CCM, CCM patients revealed lower immediate (16.7 ± 4.4 vs. 18.9 ± 4.8, p = 0.022) and delayed 15.9 ± 3.7 vs. 17.7 ± 5.3, p = 0.044) portal vein pressures (PVP) and portal pressure gradients (PPG) (7.7 ± 3.4 vs. 9.2 ± 3.6, p = 0.032 and 10.1 ± 3.1 vs. 12.3 ± 4.9, p = 0.013). The 1-year mortality rates were 13.2% for CCM patients and 4.3% for non-CCM patients (log-rank test, p = 0.093), with MELD score, and preoperative RAP significantly associated with the mortality. CONCLUSION: Cirrhotic patients with CCM exhibit lower PVP and PPG immediately after TIPS and 2-4 days later, without significantly impacting one-year survival outcomes.

In vitro and clinical validation of different correction algorithms for the two-dimensional proximal isovelocity surface area method in a low-velocity flow field for quantifying tricuspid regurgitation.

Background: The 2-dimensional proximal isovelocity surface area (2D PISA) method underestimates tricuspid regurgitation (TR) severity. Previously proposed correction algorithms should be further scrutinized. Methods: Two correction algorithms were tested. One approach involves dividing the 2D PISA effective regurgitant orifice area by a constant of 0.7 (EROA0.7). Another approach involves multiplying the unadjusted EROA by Vorifice/(Vorifice - Valiasing), where Vorifice denotes the TR jet velocity, and Valiasing represents the color aliasing velocity (EROAVo-Va). In vitro validation was performed on a commercially available multifunctional valve tester with different size orifices and peak pressure gradients. A true EROA was derived through the regurgitant volume (RVol) calculated from the tester. For clinical validation, RVol was calculated as the difference between the overall stroke volume and the forward stroke volume of the right ventricle. Volumetric EROA was derived by dividing the RVol by the TR velocity-time integral (VTI). The vena contracta area (VCA) was obtained through direct planimetry with 3D echocardiography. The mean of volumetric EROA and VCA served as the reference in clinical validation. Results: Excellent correlation between the calculated EROAs and the true EROA was observed in vitro (r=0.98, r=0.97, and r=0.98 for uncorrected EROA, EROAVo-Va, and EROA0.7, respectively; all P values <0.0001). EROAVo-Va underestimated the true EROA and averaged 33% (P=0.3163), while EROA0.7 overestimated the true EROA and averaged 8% (P=0.0032). Clinically, these methods consistently exhibited a notable underestimation that varied with the reference EROA. This systematic underestimation was mitigated by both algorithms when either the VCA (biases of 19.6, 15.1, and 11.8 mm2 for uncorrected EROA, EROAVo-Va, and EROA0.7, respectively) or the volumetric EROA (biases of 10.1, 5.6, and 2.3 mm2 for uncorrected EROA, EROAVo-Va, and EROA0.7, respectively) served as the reference. Their ability to distinguish severe TR was similar, with area under the curve values of 0.905, 0.903, and 0.893 for uncorrected EROA, EROAVo-Va, and EROA0.7, respectively. No statistically significant differences were observed for diagnostic accuracy (all P values >0.05). Conclusions: Using a correction factor of 0.7 in quantifying TR provides similar accuracy when compared to other techniques. This represents a valuable clinical tool for quickly correcting the underestimation of the 2D PISA method in TR. This simple method may increase the frequency of applying the correction and earlier recognition of patients with severe TR.

Echocardiographic parameters recommended for assessing the severity of tricuspid regurgitation: concordance and discordance.

Background: Current guidelines recommend integrating several echocardiographic indices to evaluate the severity of tricuspid regurgitation (TR). Discordance of indices, including qualitative and quantitative methods, commonly exists in practice. The discordance among these parameters has not yet been fully elucidated. Methods: A total of 127 patients with recognizable TR jets without pulmonary regurgitation or intracardiac shunt were prospectively enrolled. We evaluated 8 parameters by 2-dimensional (2D) echocardiography: proximal iso-velocity surface area (PISA)-derived regurgitant volume (RVol), PISA-derived effective regurgitant orifice area (EROA), PISA radius, vena contracta width (VCW), color Doppler jet area, tricuspid valve annular diameter, inferior vena cava (IVC) diameter, and peak E wave. According to current guidelines, each echocardiographic parameter was determined to represent either severe or non-severe TR. A concordance score was calculated as the number of concordant parameters divided by 8, with a higher score reflecting better concordance. Data were further categorized into 3 subgroups: complete concordance (0 discordant parameters), high concordance (1-2 discordant parameters), and low concordance (3-4 discordant parameters). Results: The mean concordance score was 81%±17% for the entire cohort. There were 48 (38%) patients with complete concordance, including 6 patients with severe TR. In contrast, the low concordance group (n=43, 34%) mostly comprised severe TR patients (36 patients). When considering only EROA, RVol, and VCW, concordance improved, with 98 patients (77%) in complete agreement. Conclusions: Concordance seems limited when using echocardiographic parameters to assess TR severity. Applying only EROA, RVol, and VCW results in better concordance, as recommended by the current guidelines.

Gene-echocardiography: refining genotype-phenotype correlations in hypertrophic cardiomyopathy.

AIMS: This study aims to clarify the association between hypertrophic patterns and genetic variants in hypertrophic cardiomyopathy (HCM) patients, contributing to the advancement of personalized management strategies for HCM. METHODS AND RESULTS: A comprehensive evaluation of genetic mutations was conducted in 392 HCM-affected families using Whole Exome Sequencing. Concurrently, relevant echocardiographic data from these individuals were collected. Our study revealed an increased susceptibility to enhanced septal and interventricular septal thickness in HCM patients harbouring gene mutations compared with those without. Mid-septal hypertrophy was found to be associated predominantly with myosin binding protein C3 (MYBPC3) variants, while a higher septum-to-posterior wall ratio correlated with myosin heavy chain 7 (MYH7) variants. Mutations in MYH7, MYBPC3, and other sarcomeric or myofilament genes (troponin I3 [TNNI3], tropomyosin 1 [TPM1], and troponin T2 [TNNT2]) showed a relationship with increased hypertrophy in the anterior wall, interventricular septum, and lateral wall of the left ventricle. In contrast, alpha kinase 3 (ALPK3)-associated hypertrophy chiefly presented in the apical region, while hypertrophy related to titin (TTN) and obscurin (OBSCN) mutations exhibited a uniform distribution across the myocardium. Hypertrophic patterns varied with the type and category of gene mutations, offering valuable diagnostic insights. CONCLUSION: Our findings underscore a strong link between hypertrophic patterns and genetic variants in HCM, providing a foundation for more accurate genetic testing and personalized management of HCM patients. The novel concept of 'gene-echocardiography' may enhance the precision and efficiency of genetic counselling and testing in HCM.

Effects of arterial blood supply and venous return on multi-territory perforator flap survival.

This study aimed to design arterial ischemic and venous congested areas on the same multi-territory perforator flap, assessing the effects of arterial blood supply and venous return on flap survival. Totally 68 rats were randomly divided into the experimental (Exp) and control (Con) groups. In the Exp group, flaps were based on left superficial epigastric artery and right superficial epigastric vein. In the Con group, flaps were based on the left superficial epigastric artery and vein. Immediate postoperative ink-gelatin angiography, epidermal metabolite levels detection, tissue edema measurement, survival rate evaluation in half of the flaps and average microvessel density assessment were performed. Blood in the Exp group flowed through most angiosomes, but only flowed around pedicled vessels in the Con group; metabolite levels of left halves in the Con and Exp groups were comparable with those of right halves. Angiosomes with high water contents occurred in the Exp group. Survival rates of left halves in the Con and Exp groups were higher than those of right halves, and more microvessels were found in the left ventral areas of both groups compared with the right ventral area in the Exp group. These findings revealed that on the same multi-territory perforator flap, arterial blood supply, affected by venous return, is a prerequisite for flap survival.