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Abstract Background Ventricular-arterial coupling (VAC) has garnered increasing interest in critical care. The prognostic significance of left ventricular-arterial coupling (LVAC) in this context remains a topic of debate. Objective This study aimed to explore the association between LVAC and patient outcomes in sepsis. Methods Patients with sepsis or septic shock admitted to the intensive care unit (ICU) were included. LVAC was evaluated using the arterial elastance (Ea)/left ventricular end-systolic elastance (Ees) ratio. Prognostic indicators, including 30-day mortality, length of ICU stay, mechanical ventilation (MV), changes in delta lactate levels, and oxygen index were also collected. Results A total of 388 patients were enrolled in this study. A U-shaped relationship was observed between LVAC and 30-day mortality, with an optimal LVAC value of 1.19 identified. For LVAC values above 1.19, the odds ratio (OR) for 30-day mortality was 1.07 (95% confidence interval [CI] 1.01–1.14). Below this threshold, OR was 0.85 (95% CI 0.73, 0.99). Similarly, in the curve for ICU-free days, a β value of − 8.64 (95% CI − 16.53, − 0.76) was noted for LVAC values over 1.26. For ventilator-free time, the kink point was 1.24, with significant β values on both sides of this threshold [− 226.49 (95% CI − 411.59, − 41.38) and 147.67 (95% CI 12.40, 282.93), respectively]. Conclusions This study established U-shaped associations between LVAC and various clinical outcomes in septic patients. Optimizing LVAC could potentially enhance patient prognosis. Given the slight variations in optimal LVAC values across different patient populations, individualized LVAC titration may be beneficial in improving clinical outcomes.

Background: Cardiovascular (CV) diseases are a cause of increased long-term morbidity and mortality in childhood cancer survivors (CCSs) treated with anthracyclines. These drugs may affect not only the heart, but also the vascular system. Left ventricular-arterial coupling (LVAC) represents a reliable parameter of altered ventricular and vascular performance, with validated prognostic value and never investigated in this setting. Aim of this study was to assess, in CCSs and matched controls, LVAC changes, performed with different echocardiographic modalities, and their relationship with endothelial function. Methods: Twenty survivors treated with anthracyclines for childhood malignancies and a matched control group of 20 healthy subjects were enrolled. Arterial elastance (Ea), end-systolic elastance (Ees), Ea/Ees ratio, as well as three-dimensional (3D) LVAC (assessed by measurement of End Systolic Volume [ESV]/Stroke Volume [SV] ratio) were performed at rest. Endothelial function was evaluated by measurement of flow-mediated dilatation (FMD) of the brachial artery. Results: 3D SV and 3D ESV/SV ratio resulted respectively significantly lower and higher in CCSs than in controls, while Ea, Ees and Ea/Ees ratio were not different among groups. A positive correlation between 3D ESV/SV ratio and cumulative anthracycline doses, as well as with time after drug exposure were also found. Mean FMD was similar in CCSs and controls (8.45 ± 1.79 versus 9.41 ± 3.41, p = 0.34). Conclusions: In conclusion, conventional LVAC parameters were not shown to be significantly different between CCSs and controls; however, 3D SV and LVAC were significantly impaired in our population. In these patients, endothelial function was comparable to controls. Larger validation studies are therefore needed. [ABSTRACT FROM AUTHOR]

Background: Cardiovascular (CV) diseases are a cause of increased long-term morbidity and mortality in childhood cancer survivors (CCSs) treated with anthracyclines. These drugs may affect not only the heart, but also the vascular system. Left ventricular-arterial coupling (LVAC) represents a reliable parameter of altered ventricular and vascular performance, with validated prognostic value and never investigated in this setting. Aim of this study was to assess, in CCSs and matched controls, LVAC changes, performed with different echocardiographic modalities, and their relationship with endothelial function. Methods: Twenty survivors treated with anthracyclines for childhood malignancies and a matched control group of 20 healthy subjects were enrolled. Arterial elastance (Ea), end-systolic elastance (Ees), Ea/Ees ratio, as well as three-dimensional (3D) LVAC (assessed by measurement of End Systolic Volume [ESV]/Stroke Volume [SV] ratio) were performed at rest. Endothelial function was evaluated by measurement of flow-mediated dilatation (FMD) of the brachial artery. Results: 3D SV and 3D ESV/SV ratio resulted respectively significantly lower and higher in CCSs than in controls, while Ea, Ees and Ea/Ees ratio were not different among groups. A positive correlation between 3D ESV/SV ratio and cumulative anthracycline doses, as well as with time after drug exposure were also found. Mean FMD was similar in CCSs and controls (8.45 ± 1.79 versus 9.41 ± 3.41, p = 0.34). Conclusions: In conclusion, conventional LVAC parameters were not shown to be significantly different between CCSs and controls; however, 3D SV and LVAC were significantly impaired in our population. In these patients, endothelial function was comparable to controls. Larger validation studies are therefore needed.

Background. In order to provide personalized medicine and improve cardiovascular outcomes, a method for predicting adverse left ventricular remodeling (ALVR) after ST-segment elevation myocardial infarction (STEMI) is needed. Methods. A total of 125 STEMI patients, mean age 51.2 (95% CI 49.6; 52.7) years were prospectively enrolled. The clinical, laboratory, and instrumental examinations were performed between the 7th and 9th day, and after 24 and 48 weeks, including plasma analysis of brain natriuretic peptide (BNP), transthoracic echocardiography, analysis of left ventricular-arterial coupling, applanation tonometry, ultrasound examination of the common carotid arteries with RF signal amplification. Results. Patients were divided into 2 groups according to echocardiography: "ALVR" (n = 63)—end-diastolic volume index (EDVI) >20% and/or end-systolic volume index (ESVI) >15% after 24 weeks compared with initial values; "non-ALVR" (n = 62)—EDVI <20% and ESVI <15%. In the ALVR group, hard endpoints (recurrent myocardial infarction, unstable angina, hospitalization for decompensated heart failure, ventricular arrhythmias, cardiac surgery, cardiovascular death) were detected in 19 people (30%). In the non-ALVR group, hard endpoints were noted in 3 patients (5%). The odds ratio of developing an adverse outcome in ALVR vs. non-ALVR group was 8.5 (95% CI 2.4–30.5) (p = 0.0004). According to the multivariate analysis, the contribution of each of the indicators to the relative risk (RR) of adverse cardiac remodeling: waist circumference, RR = 1.02 (95% CI 1.001–1.05) (p = 0.042), plasma BNP—RR = 1.81 (95% CI 1.05–3.13) (p = 0.033), arterial elastance to left ventricular end-systolic elastance (Ea/Ees)—RR = 1.96 (95% CI 1.11–3.46) (p = 0.020). Conclusion. Determining ALVR status in early stages of the disease can accurately predict and stratify the risk of adverse outcomes in STEMI patients. [ABSTRACT FROM AUTHOR]

Background. In order to provide personalized medicine and improve cardiovascular outcomes, a method for predicting adverse left ventricular remodeling (ALVR) after ST-segment elevation myocardial infarction (STEMI) is needed. Methods. A total of 125 STEMI patients, mean age 51.2 (95% CI 49.6; 52.7) years were prospectively enrolled. The clinical, laboratory, and instrumental examinations were performed between the 7th and 9th day, and after 24 and 48 weeks, including plasma analysis of brain natriuretic peptide (BNP), transthoracic echocardiography, analysis of left ventricular-arterial coupling, applanation tonometry, ultrasound examination of the common carotid arteries with RF signal amplification. Results. Patients were divided into 2 groups according to echocardiography: “ALVR” (n = 63)—end-diastolic volume index (EDVI) >20% and/or end-systolic volume index (ESVI) >15% after 24 weeks compared with initial values; “non-ALVR” (n = 62)—EDVI p = 0.0004). According to the multivariate analysis, the contribution of each of the indicators to the relative risk (RR) of adverse cardiac remodeling: waist circumference, RR = 1.02 (95% CI 1.001–1.05) (p = 0.042), plasma BNP—RR = 1.81 (95% CI 1.05–3.13) (p = 0.033), arterial elastance to left ventricular end-systolic elastance (Ea/Ees)—RR = 1.96 (95% CI 1.11–3.46) (p = 0.020). Conclusion. Determining ALVR status in early stages of the disease can accurately predict and stratify the risk of adverse outcomes in STEMI patients.

Aim. To study the effects of sacubitril/valsartan on left ventricular-arterial coupling (LVAC) and arterial stiffness in HFrEF patients.Material and methods. Arterial stiffness by applanation tonometry and LVAC – by two-dimensional echocardiography were evaluated in 18 patients with compensated HFrEF (age 69Ѓ}9 years, 89% male, arterial hypertension – 83%, diabetes – 39%, myocardial infarction – 89%, left ventricular ejection fraction 32Ѓ}4%) initially and after 6 and 12 months of therapy based on sacubitril/valsartan. LVAC was calculated as the Ea (arterial elastance)/ Ees (left ventricular elastance) ratio. Differences were considered statistically significant at p10 m/s). The decrease in PWV (from 11.5Ѓ}2.9 to 10.2Ѓ}2.9 m/s, p

The objective of this study was to define alterations in ventricular–arterial (V-A) coupling early in the development of tachycardia-induced heart failure (HF). Although HF is characterized by impaired V-A coupling, the temporal relationship of these derangements to overt left ventricular (LV) dysfunction is unknown. Six anesthetized dogs instrumented with LV manometers and piezoelectric crystals were studied before and after 24 h of rapid ventricular pacing (RVP). V-A coupling was indexed by the ratio between the end-systolic pressure–volume relation slope (endsystolic elastance, E ES) and effective arterial elastance ( E A), and mechanical efficiency by the ratio of stroke work (SW) to pressure–volume area (PVA). After RVP, there was no significant depression of LV function, but E A and total peripheral resistance ( R T) were increased ( P < 0.05), indicating increased arterial load. After RVP, E ES/ E A and SW/PVA were maintained during unstressed conditions, but upon changes in load induced by phenylephrine, E ES/ E A declined more precipitously with equivalent increases in R T (slope E ES/ E A– R T relation −16.7 ± 4.6 vs −5.8 ± 4.0 ml/mmHg·min, P < 0.025). Furthermore, after RVP there was significant ( P < 0.05) blunting of dobutamine-induced augmentation of E ES, E ES/ E A, and SW/PVA. Thus, after RVP there was a distinct loss of V-A coupling reserve during afterload and catecholamine stress. V-A coupling defects occur early in the development of tachycardia-induced HF prior to significant pump dysfunction, and are manifested primarily during hemodynamic and inotropic stress. [ABSTRACT FROM AUTHOR]

The purpose of this study was to assess the effect of heart rate on left ventricular (LV)–arterial coupling and LV mechanical efficiency before and after heart failure (CHF). The production of LV stroke work (SW) and mechanical efficiency depends on the coupling of the LV and arterial system. The response of LV–arterial coupling to tachycardia may be altered in heart failure. We compared the response of LV–arterial coupling to increased heart rate (HR) in six conscious, instrumented dogs before and after pacing-induced CHF. Coupling was quantified as EES/EA, where EES is the slope of end-systolic pressure (P)–volume (V) relation, and EA is arterial elastance. Mechanical efficiency was determined as the ratio of SW to a total P–V area (PVA). Before CHF, EES and EA increased similarly with increased heart rate to 180 min-1. Thus, EES/EA remained unaltered (0.96 ± 0.08 vs 0.94 ± 0.35), and SW/PVA was unchanged (0.62 ± 0.03 vs 0.59 ± 0.06). Compared with the results prior to CHF and after CHF the resting EES was decreased, thus both EES/EA (0.58 ± 0.09) and SW/PVA (0.48 ± 0.06) were less (P ≪ 0.05) than baseline. After CHF, an increase in HR to 180 min-1 increased EA but not EES, thus EES/EA fell to 0.44 ± 0.06 (P ≪ 0.05) and SW/PVA fell to 0.41 ± 0.05 (P ≪ 0.05). Under normal conditions, LV–arterial coupling remains optimal during increases in HR. After CHF, tachycardia exacerbates the suboptimal baseline LV–arterial coupling, reducing the efficiency of producing SW. [ABSTRACT FROM AUTHOR]

Purpose: To investigate the predictive value of left ventricular-arterial coupling (VAC) for clinical prognosis of elderly patients with septic shock., Materials and Methods: This was a single-center prospective cohort study of 63 elderly patients with septic shock treated between August 2014 and January 2016 at the 30-bed intensive care unit (ICU) of Zhejiang Hospital (China). Left VAC was evaluated by transthoracic echocardiography (TTE). End-systolic elastance (Ees) and left ventricular ejection fraction (LVEF) were measured; arterial elastance (Ea) was calculated. The 28-day survival was evaluated., Results: Compared with non-survivors, survivors had a significantly lower Ea/Ees ratio (P<0.01), mainly because survivors had higher Ees values (P<0.01), but without difference in Ea (P=0.720). LVEF was greater (47.5±7.3 vs. 43.6±6.4, P=0.03); LVESV was smaller in survivors compared to non-survivors (P<0.05). The multivariate Cox proportional regression analysis showed that APACHEII scores (hazard ratio (HR)=1.12, 95% confidence interval (95%CI):1.01-1.25, P=0.04), blood lactate levels (HR=1.21, 95%CI:1.07-1.36, P=0.002), and VAC (HR=2.57, 95%CI:1.29-5.13, P=0.007) were independently associated with 28-day mortality of elderly patients with septic shock. The optimal cutoff point of VAC for predicting 28-day mortality was 2.14 with 56.7% sensibility and 87.9% specificity; the area under the curve was 0.74., Conclusions: Left VAC has prognostic value in elderly patients with septic shock., (Copyright © 2017. Published by Elsevier Inc.)