scholarly journals Grading right ventricular dysfunction in left ventricular disease using echocardiography: a proof of concept using a novel multiparameter strategy

2021 ◽  
Author(s):  
Odd Bech‐Hanssen ◽  
Marco Astengo ◽  
Martin Fredholm ◽  
Niklas Bergh ◽  
Clara Hjalmarsson ◽  
...  
Keyword(s):  
Right Ventricular ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Proof Of Concept

scholarly journals Left and right ventricular dysfunction in patients with COVID-19-associated myocardial injury

Infection ◽  
2021 ◽  
Author(s):  
Stéphanie Bieber ◽  
Angelina Kraechan ◽  
Johannes C. Hellmuth ◽  
Maximilian Muenchhoff ◽  
Clemens Scherer ◽  
...  
Keyword(s):  
Ejection Fraction ◽  
Right Ventricular ◽  
Ventricular Function ◽  
Myocardial Injury ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Ventricular Ejection Fraction ◽  
Strain Echocardiography

Abstract Purpose SARS-COV-2 infection can develop into a multi-organ disease. Although pathophysiological mechanisms of COVID-19-associated myocardial injury have been studied throughout the pandemic course in 2019, its morphological characterisation is still unclear. With this study, we aimed to characterise echocardiographic patterns of ventricular function in patients with COVID-19-associated myocardial injury. Methods We prospectively assessed 32 patients hospitalised with COVID-19 and presence or absence of elevated high sensitive troponin T (hsTNT+ vs. hsTNT-) by comprehensive three-dimensional (3D) and strain echocardiography. Results A minority (34.3%) of patients had normal ventricular function, whereas 65.7% had left and/or right ventricular dysfunction defined by impaired left and/or right ventricular ejection fraction and strain measurements. Concomitant biventricular dysfunction was common in hsTNT+ patients. We observed impaired left ventricular (LV) global longitudinal strain (GLS) in patients with myocardial injury (-13.9% vs. -17.7% for hsTNT+ vs. hsTNT-, p = 0.005) but preserved LV ejection fraction (52% vs. 59%, p = 0.074). Further, in these patients, right ventricular (RV) systolic function was impaired with lower RV ejection fraction (40% vs. 49%, p = 0.001) and reduced RV free wall strain (-18.5% vs. -28.3%, p = 0.003). Myocardial dysfunction partially recovered in hsTNT + patients after 52 days of follow-up. In particular, LV-GLS and RV-FWS significantly improved from baseline to follow-up (LV-GLS: -13.9% to -16.5%, p = 0.013; RV-FWS: -18.5% to -22.3%, p = 0.037). Conclusion In patients with COVID-19-associated myocardial injury, comprehensive 3D and strain echocardiography revealed LV dysfunction by GLS and RV dysfunction, which partially resolved at 2-month follow-up. Trial registration COVID-19 Registry of the LMU University Hospital Munich (CORKUM), WHO trial ID DRKS00021225.

scholarly journals Impact of right ventricular dysfunction after MitraClip treatment as a bridge to heart transplantation: insights from the MitraBridge registry

2021 ◽  
Vol 42 (Supplement_1) ◽  
Author(s):  
A Munafo ◽  
A Scotti ◽  
R Estevez-Loureiro ◽  
D Arzamendi ◽  
N.P Fam ◽  
...  
Keyword(s):  
Heart Transplantation ◽  
Right Ventricular ◽  
Primary Outcome ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Volume Index ◽  
Left Ventricular Ejection ◽  
End Point

Abstract Background MitraClip treatment has been recently proposed as a “bridge strategy” solution for advanced heart failure (HF) patients with significant functional mitral regurgitation (MR), who are potential candidates or are waiting for cardiac replacement therapy (LVAD or heart transplantation, HTx). In this clinical scenario, left-ventricular-related right ventricular dysfunction (RVD) represents an important prognostic factor. Purpose Our study aimed to investigate the possible prognostic implication of RVD in advanced HF patients treated with MitraClip as a bridge to HTx strategy. Methods RVD was assessed using the relationship between tricuspid annular peak systolic excursion (TAPSE) and pulmonary artery systolic pressure (PASP). All patients from the MitraBridge registry for whom these two echocardiographic parameters were available, were included in the study. A cut-off value of TAPSE/PASP ratio <0.36 was used to defined RVD, as previously reported. The primary outcome was a composite end-point of all-cause death or rehospitalization for HF at 2-year. For patients who underwent LVAD implantation or HTx, follow-up data were censored at the time of those events. Results A total of 80 patients were included in the study. The median TAPSE/PASP ratio was 0.35 (25th-75th: 0.27–0.46), with 43 (54%) patients having a TAPSE/PASP ratio <0.36 (RVD group). The latter had a prevalent MR ischemic etiology (49% vs 38%), with a more frequent history of percutaneous coronary intervention (46.5% vs 22%, p=0.02). Except for TAPSE (15.7±3.6 mm vs 19.2±3.7 mm, p=0.001) and PASP (61±14 mmHg vs 39.5±9.5 mmHg, p<0.001), the other echocardiographic characteristics were similar between the two study groups (overall mean left ventricular ejection fraction 26.9±8%, median left ventricular end-diastolic volume index 120.7, 25th-75th: 102.2–146.5 mL/m2). After a median follow-up time of 508 (25th-75th: 160–899) days, elective HTx occurred in 12 patients (7 from the RVD group), while LVAD implantation was performed in 13 patients (7 from the RVD group). The primary outcome occurred in 30 patients (38%) with a 2-year Kaplan-Meier estimate of freedom from the composite end-point of 41%. At univariate (HR 1.3 95% CI 0.6–2.8, p=0.451) and multivariate (HR 1.6 CI 0.7–3.8, p=0.249) Cox-regression analysis, TAPSE/PASP ratio <0.36 was not identified as an independent predictor of primary outcome. Indeed, at follow-up echocardiographic control (median time 252, 25th-75th: 122–365 days), a significant improvement in TAPSE/PASP ratio was observed in the RVD group (baseline median TAPSE/PASP ratio 0.27, 25th-75th: 0.22–0.32 vs follow-up median TAPSE/PASP ratio 0.37, 25th-75th: 0.28–0.47, p<0.001). Conclusion In advanced HF patients with functional MR, MitraClip treatment could prevent or ameliorate left-ventricular-related RVD, allowing safe access to HTx or LVAD. FUNDunding Acknowledgement Type of funding sources: None.

Mechanisms of hypotension produced by platelet-activating factor

1989 ◽  
Vol 66 (6) ◽  
pp. 2681-2690 ◽  
Author(s):  
F. R. Laurindo ◽  
R. E. Goldstein ◽  
N. J. Davenport ◽  
D. Ezra ◽  
G. Z. Feuerstein
Keyword(s):  
Right Ventricular ◽  
Pulmonary Vascular Resistance ◽  
Vascular Resistance ◽  
Ventricular Dysfunction ◽  
Platelet Activating Factor ◽  
Right Ventricular Dysfunction ◽  
Left Ventricular ◽  
Right Ventricular Failure ◽  
Right Atrial ◽  
Ventricular Failure

Platelet-activating factor (PAF) is a phospholipid mediator that induces cardiovascular collapse and release of the secondary mediator thromboxane A2 (TxA2). To clarify mechanisms involved in this collapse and, specifically, the relative contribution of left ventricular and right ventricular dysfunction, we studied 12 open-chest pigs. PAF infusion (0.04–0.28 nmol.kg-1.min-1) induced a 5- to 120-fold increase in pulmonary vascular resistance, a 75–98% fall in cardiac output, and systemic arterial hypotension. Right ventricular failure was indicated by chamber enlargement, decreased shortening, and increased right atrial pressures. In contrast, left ventricular dysfunction was accompanied by decreases in chamber dimensions and filling pressures that were unresponsive to volume expansion. U 46619 (a stable TxA2 analogue) and mechanical pulmonary artery constriction induced changes similar to PAF. In 11 additional closed-chest pigs, TxA2 blockade with indomethacin attenuated the PAF-induced rise in pulmonary vascular resistance, right ventricular dysfunction, and systemic hypotension. A specific TxA2 synthase inhibitor, OKY-046, also diminished hemodynamic effects of PAF in six other pigs. Tachyphylaxis was not observed in five pigs repeatedly given PAF. We conclude that acute right ventricular failure as the result of severe increase in pulmonary vascular resistance is the primary mechanism early in the course of PAF-induced shock in the pig. PAF-induced release of TxA2 may contribute significantly to these events.

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