Search Results (5)

Background: Right ventricular (RV) function is inadequately investigated and routinely overlooked in transthyretin amyloid cardiomyopathy (ATTR-CM). Novel imaging distinguishers between intrinsic RV myocardial disease in ATTR-CM and primary RV overload disorder phenotypes may enhance mechanistic and pathophysiological understanding of RV dysfunction. We aimed to investigate RV performance in ATTR-CM employing comprehensive 2D and 3D echocardiography, and to compare these indices with primary RV afterload disease. Methods: We investigated conventional and novel indices of RV contractile function, myocardial work and ventricular–vascular coupling in 21 well-characterized ATTR-CM patients, 10 PAH patients and 12 healthy controls. RV long axis function and pulmonary artery (PA) systolic pressure were evaluated using 2D Doppler echocardiography. RV ejection fraction (RVEF), volumes, global longitudinal strain (GLS) and novel myocardial work indices were analyzed by 3D echocardiography. RV elastance (E_es), afterload (E_a) and RV-PA coupling (E_es/E_a) were estimated using the single-beat volume method. Results: ATTR-CM showed lower RVEF, GLS and E_es, and a higher RV global myocardial work index (GWI), constructive work (GCW), E_a and reduced RV-PA coupling compared with controls. RV EF, stroke volume, GLS and circumferential strain did not differ between ATTR-CM and PAH. However, GWI, GCW, E_es and E_a were lower in ATTR-CM. RV–pulmonary coupling displayed strong association with RV 3D strain (r = 0.84, p < 0.001), whereas RV E_es (contractility) was related to RV GWI (r = 0.54, p < 0.001). Conclusions: ATTR-CM displayed lower RV performance, higher GMW and reduced RV-PA coupling. Myocardial work indices E_es and E_a are novel distinguishers of RV dysfunction phenotypes. The clinical and prognostic value of these novel variables warrant further investigation. Full article

Background: Right ventricular (RV) dysfunction or failure occurs in more than 30% of patients in cardiogenic shock (CS). However, the importance of timely diagnosis of prognostically relevant impairment of RV function is often underestimated. Moreover, data regarding the impact of mechanical circulatory support like the Impella on RV function are rare. Here, we investigated the effects of the left ventricular (LV) Impella on RV function. Moreover, we aimed to identify the most optimal and the earliest applicable parameter for bedside monitoring of RV function by comparing the predictive abilities of three common RV function parameters: the pulmonary artery pulsatility index (PAPi), the ratio of right atrial pressure to pulmonary capillary wedge pressure (RA/PCWP), and the right ventricular stroke work index (RVSWI). Methods: The data of 50 patients with CS complicating myocardial infarction, supported with different flow levels of LV Impella, were retrospectively analyzed. Results: Enhancing Impella flow (1.5 to 2.5 L/min ± 0.4 L/min) did not lead to a significant variation in PAPi (p = 0.717), RA/PCWP (p = 0.601), or RVSWI (p = 0.608), indicating no additional burden for the RV. PAPi revealed the best ability to connect RV function with global hemodynamic parameters, i.e., cardiac index (CI; p < 0.001, 95% CI: 0.181–0.663), pulmonary capillary wedge pressure (PCWP; p = 0.005, 95% CI: −6.721–−1.26), central venous pressure (CVP; p < 0.001, 95% CI: −7.89–5.575), and indicators of tissue perfusion (central venous oxygen saturation (SvO₂); p = 0.008, 95% CI: 1.096–7.196). Conclusions: LV Impella does not impair RV function. Moreover, PAPi seems to be to the most effective and valid predictor for early bedside monitoring of RV function. Full article

Background: Studies had previously identified three cardiogenic shock (CS) phenotypes (cardiac-only, cardiorenal, and cardiometabolic). Therefore, we aimed to understand better the hemodynamic profiles of these phenotypes in acute myocardial infarction-CS (AMI-CS) using pulmonary artery catheter (PAC) data to better understand the AMI-CS heterogeneity. Methods: We analyzed the PAC data of 309 patients with AMI-CS. The patients were classified by SCAI shock stage, congestion profile, and phenotype. In addition, 24 h hemodynamic PAC data were obtained. Results: We identified three AMI-CS phenotypes: cardiac-only (43.7%), cardiorenal (32.0%), and cardiometabolic (24.3%). The cardiometabolic phenotype had the highest mortality rate (70.7%), followed by the cardiorenal (52.5%) and cardiac-only (33.3%) phenotypes, with significant differences (p < 0.001). Right atrial pressure (p = 0.001) and pulmonary capillary wedge pressure (p = 0.01) were higher in the cardiometabolic and cardiorenal phenotypes. Cardiac output, index, power, power index, and cardiac power index normalized by right atrial pressure and left-ventricular stroke work index were lower in the cardiorenal and cardiometabolic than in the cardiac-only phenotypes. We found a hazard ratio (HR) of 2.1 for the cardiorenal and 3.3 for cardiometabolic versus the cardiac-only phenotypes (p < 0.001). Also, multi-organ failure, acute kidney injury, and ventricular tachycardia/fibrillation had a significant HR. Multivariate analysis revealed that CS phenotypes retained significance (p < 0.001) when adjusted for the Society for Cardiovascular Angiography & Interventions score (p = 0.011) and ∆congestion (p = 0.028). These scores independently predicted mortality. Conclusions: Accurate patient prognosis and treatment strategies are crucial, and phenotyping in AMI-CS can aid in this effort. PAC profiling can provide valuable prognostic information and help design new trials involving AMI-CS. Full article

Prostacyclin analogs are among the most effective and widely used therapies for pulmonary arterial hypertension (PAH). However, it is unknown whether they also confer protection through right ventricle (RV) myocardio-specific mechanisms. Moreover, the use of prostacyclin analogs in severe models of PAH has not been adequately tested. To further identify underlying responses to prostacyclin, a prostacyclin analogue, treprostinil, was used in a preclinical rat Sugen-chronic hypoxia (SuCH) model of severe PAH that closely resembles the human disease. Male Sprague–Dawley rats were implanted with osmotic pumps containing vehicle or treprostinil, injected concurrently with a bolus of Sugen (SU5416) and exposed to 3-week hypoxia followed by 3-week normoxia. RV function was assessed using pressure–volume loops and hypertrophy by weight assessed. To identify altered mechanisms within the RV, tissue samples were used to perform a custom RNA array analysis, histological staining, and protein and transcript level confirmatory analyses. Treprostinil significantly reduced SuCH-associated RV hypertrophy and decreased the rise in RV systolic pressure, mean pulmonary arterial (mPAP), and right atrial (RAP) pressure. Prostacyclin treatment was associated with improvements in RV stroke work, maximum rate of ventricular pressure change (max dP/dt) and the contractile index, and almost a complete reversal of SuCH-associated increase in RV end-systolic elastance, suggesting the involvement of load-independent improvements in intrinsic RV systolic contractility by prostacyclin treatment. An analysis of the RV tissues showed no changes in cardiac mitochondrial respiration and ATP generation. However, custom RNA array analysis revealed amelioration of SuCH-associated increases in newly identified TBX20 as well as the fibrotic markers collagen1α1 and collagen 3α1 upon treprostinil treatment. Taken together, our data support decreased afterload and load-independent improvements in RV function following prostacyclin administration in severe PAH, and these changes appear to associate with improvements in RV fibrotic responses. Full article

Right heart-associated hemodynamic parameters including intraoperative pulmonary vascular resistance (PVR) were reported to be associated with patient survival after liver transplantation. We investigated whether intraoperative stroke work indexes of both ventricles could have a better prognostic value than PVR. We reviewed 683 cases at a tertiary care academic medical center. We collected intraoperative variables of baseline central venous pressure, baseline right ventricle end-diastolic volume, mixed venous oxygen saturation, intraoperative PVR and right and left ventricular stroke work indexes. Time-weighted means or area under the curve of intraoperative right and left ventricular stroke work indexes were calculated as exposure variables. One-year all-cause mortality or graft failure was our primary outcome. Cox proportional hazard regression analysis was performed to evaluate the association between exposure variables and one-year all-cause mortality or graft failure. Kaplan–Meier survival curve analysis of our primary outcome was performed for different time-weighted mean ventricular stroke work index groups. Cubic spline curve analysis was performed to evaluate the linear relationship between our exposure variables and primary outcome. Time-weighted mean right ventricular stroke work index was significantly associated with one-year all-cause mortality or graft failure (hazard ratio 1.21, 95% confidence interval (CI) 1.12–1.36, p < 0.001). However, there was no significant association between time-weighted mean left ventricular stroke work index, time-weighted mean PVR, PVR at the end of surgery and one-year mortality. Area under the curve of right ventricular stroke work index was also significantly associated with one-year mortality or graft failure (hazard ratio 1.24, 95% CI 1.15–1.37, p < 0.001). Kaplan–Meier survival curve analysis showed a significant difference in the survival between different mean right ventricular stroke work index groups (Log-rank test: p = 0.002). Cubic spline function curve showed the gradual increase in the risk of mortality with a positive slope with time-weighted mean right ventricular stroke work index. In conclusion, intraoperative elevated right ventricular stroke work index was significantly associated with poor patient or graft survival after liver transplantation. Intraoperative right ventricular stroke work index could be an intraoperative hemodynamic goal and prognostic marker for mortality after liver transplantation. Full article