Citations

Abstract Aims Cardiogenic shock (CS) is characterized by impaired left ventricular (LV) mechanical performance and adverse remodelling. We evaluated whether transthoracic echocardiography (TTE)-derived modified cardiac efficiency (mCE), integrating stroke work and residual LV volume, is associated with short- and long-term mortality in CS and whether its prognostic value differs by shock aetiology. Methods and results In this retrospective cohort study, consecutive adults admitted with CS to the cardiac intensive care unit at Mayo Clinic (2007–2018) were included if TTE was performed within 24 h. mCE was calculated as (stroke volume × estimated LV end-systolic pressure) divided by LV end-systolic volume and categorized into quartiles. Primary outcome was in-hospital mortality; secondary outcome was 1-year mortality. Multivariable logistic and Cox models adjusted for illness severity, comorbidity burden, shock aetiology, cardiac arrest, vasoactive therapy, and mechanical circulatory support. Among 667 patients, median mCE was 48 mmHg (IQR 32–74). In-hospital mortality was 28% and increased stepwise across decreasing mCE quartiles. The lowest quartile had a 2.5-fold higher adjusted odds of in-hospital death (OR 2.53; 95%CI: 1.49–4.37; P < 0.001). One-year mortality was 41%; the lowest quartile had a two-fold higher adjusted hazard of death (HR 2.05; 95%CI: 1.45–2.89; P < 0.001). Associations were stronger in acute coronary syndrome-related CS (interaction P = 0.035 for in-hospital; P = 0.015 for 1-year). Within the lowest quartile, reduced systolic pressure further amplified mortality risk. Conclusion Early TTE-derived mCE was independently associated with short- and long-term mortality in CS, particularly in acute coronary syndrome-related CS, and captured the interaction between ventricular remodelling and mechanical performance underlying high-risk phenotypes.

Abstract Background Hypotension is a recognized predictor of mortality in the cardiac intensive care unit (CICU) (1-3). Although prior studies link lower mean/averaged mean arterial pressure (MAP) to adverse outcomes, they highlight the need for dedicated research on the minimum MAP (mMAP), as mean data may fail to capture the clinical significance of brief, severe hypotensive episodes. Purpose This study aims to investigate the mortality outcomes associated with the mMAP within the first 24 hours of CICU admission and further stratified according to admission diagnoses. Methods This retrospective cohort study included adult CICU patients with available mMAP data (2007-2018). Patient data were extracted including admission diagnoses, critical care therapies (hemodynamic/ventilatory support, continuous renal replacement therapy), comorbidities, vital signs, lab values, and mortality outcomes. MAP was measured either invasively (arterial catheter) or non-invasively (blood pressure cuff). Primary exposure was mMAP, defined as the lowest recorded MAP in first 24 hours of CICU admission. Primary outcome was in-hospital mortality analyzed using logistic regression, before and after multivariable adjustment. Mortality outcomes were analyzed according to mMAP and stratified by admission diagnoses (not mutually exclusive). Results 11,930 patients were included. Median age was 69.4 (58.1, 79.2) years and 37.7% were female. Admission diagnoses included heart failure (48.7%), acute coronary syndrome (42.7%), shock (14.9%), and cardiac arrest (11.8%). Critical care therapies were used in 58.5%. Median mMAP was 54 (47, 62) mmHg. 1080 (9.1%) patients died during hospitalization, including 672 (5.6%) in the CICU. Median mMAP was lower in patients who died in the CICU (46 vs. 55 mmHg, p<0.001) and during the hospitalization (47 vs. 55 mmHg, p<0.001). In the overall cohort, the lowest mortality was at mMAP of 71-75 mmHg. Patients with lower mMAP had higher mortality across admission diagnosis subgroups (Fig1). The mMAP associated with the nadir mortality was slightly higher for acute coronary syndrome or cardiac arrest patients (66-70 mmHg) than for heart failure or cardiogenic shock patients (61-65 mmHg) (Fig2). Each 5 mmHg increase in mMAP was associated with lower in-hospital mortality in patients with (unadj OR 0.81 [0.79-0.84], AUC 0.64) and without (unadj OR 0.76 [0.71-0.82], AUC 0.67) critical care therapies. Conclusion Our findings re-affirm that hypotension is a significant predictor of mortality, consistent across all admission diagnoses. Notably, the mMAP range associated with the lowest in-hospital mortality was slightly lower for patients with circulatory failure (heart failure or cardiogenic shock) compared to those with acute coronary syndromes or cardiac arrest. This difference may represent an optimal balance between maintaining perfusion and preventing excessive afterload in the setting of circulatory failure, but further investigation is required.1) Mortality Per mMAP & Admission Diag 2) Nadir Mortality Point

Background The prognostic significance of an adverse acid–base milieu despite venoarterial extracorporeal membrane oxygenation support in patients with cardiogenic shock remains poorly defined. We examined metabolic and respiratory disturbances in the ELSO (Extracorporeal Life Support Organization) Registry among patients who received venoarterial extracorporeal membrane oxygenation support for refractory cardiogenic shock. Methods Arterial blood gas acid–base values at 24 hours following venoarterial extracorporeal membrane oxygenation initiation were analyzed, with patients classified by pH, arterial partial pressure of carbon dioxide, and bicarbonate. Multivariable logistic regression and exploratory machine learning analyses were used to assess predictors of in‐hospital mortality. Results Among 15 144 adult patients, 74.6% (10 860) had neither respiratory nor metabolic acidosis, 13.1% (1909) had isolated respiratory acidosis, 11.6% (1684) had isolated metabolic acidosis, and 0.7% (100) had combined acidosis. In‐hospital mortality occurred in 7719 (51.0%) patients and increased incrementally across patients with lower pH (adjusted odds ratio [OR], 2.03 with each 0.1‐unit decrease in pH, using 7.4 as a reference point [95% CI, 1.82–2.26]), bicarbonate (adjusted OR, 1.93 per each 5‐mEq/L <24 mEq/L [95% CI, 1.76–2.12]) or base excess (adjusted OR, 1.90 per each 5‐mEq/L <0 mEq/L [95% CI, 1.75–2.07]) (all P <0.01). Mortality varied significantly, being highest for the low‐pH metabolic acidosis cluster (adjusted OR, 1.90 [95% CI, 1.70–2.12], P <0.01). Conclusions Survival decreased progressively with worse acidemia or metabolic acidosis despite 24 hours of hemodynamic support with venoarterial extracorporeal membrane oxygenation among patients with cardiogenic shock. Our findings emphasize the prognostic significance of metabolic parameters as potentially modifiable risk factors and underscore the need for early recognition and interventions to mitigate severe metabolic derangements.

Background There is limited evidence on the epidemiology and prognostic significance of acid-base disorders in the cardiovascular intensive care unit (CICU). This study examines the association of acid-base status at admission with in-hospital mortality among CICU patients. Methods We conducted a retrospective analysis of adults admitted to the Mayo Clinic CICU from 2007-2018 with available blood gas data, utilizing values obtained closest to CICU admission. Arterial pH, serum bicarbonate, base excess, and partial pressure of carbon dioxide (PaCO 2 ) were examined as predictors of in-hospital mortality. Multivariable logistic regression was used to assess associations, with adjustment for demographics, comorbidities, illness severity, and interventions. Results Among 3229 patients included for analysis, acidemia (pH < 7.35) emerged as the strongest predictor of in-hospital mortality (adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI] 1.29-1.98, P < .003). Metabolic acidosis (HCO3 < 20 mEq/L, aOR 1.55, 95% CI 1.24-1.95, P < .001) and respiratory acidosis (PaCO2 > 45 mm Hg, aOR 1.44, 95% CI 1.14-1.81, P = .002) were associated with higher in-hospital mortality, whereas metabolic and respiratory alkalosis were not. After adjustment, lower pH and more negative base excess were associated with higher in-hospital mortality (both P < .001), whereas HCO3 and PaCO2 were not ( P = .053 and P = .051, respectively). Patients with combined metabolic and respiratory acidosis had the highest in-hospital mortality (56.3%). Conclusions Short-term survival in CICU patients decreases progressively with worse acidemia, especially in the context of combined metabolic and respiratory acidosis. Incorporating metabolic acid-base disorders as key therapeutic targets in randomized cardiogenic shock trials may improve outcomes in this complex population by addressing hemometabolic shock.

Introduction: Pressure-adjusted heart rate (PAHR) provides an integrated assessment of hemodynamic decompensation in critically ill patients. Research Question: How does PAHR perform in critically ill patients with cardiovascular disease? Aims: We sought to evaluate the prognostic value of PAHR on mortality in patients admitted to the cardiovascular intensive care unit (CICU). Methods: A retrospective cohort of patients admitted to the CICU at a tertiary-care academic institution, between 2007 and 2018, who had a transthoracic echocardiogram (TTE) within one day of admission were evaluated. Heart rate (HR), right atrial pressure (RAP), and mean arterial pressure (MAP), obtained from TTE, were used to calculate PAHR as RAP * HR / MAP. Results: Among 5411 patients included for analysis (median age 70.1 years, 38.6% female, 92.4% White), higher PAHR was associated with greater severity of acute illness, burden of comorbidities, and use of critical care therapies. Median values (25 th percentile, 75 th percentile) for HR were 73.0 (63.0, 87.0) beats per minute (bpm), RAP 10.0 (5.0, 14.0) mm Hg, and MAP 81.3 (72.3, 91.7) mm Hg. Median PAHR was significantly higher among patients who died during hospitalization (14.3 bpm vs 6.8 bpm, p <0.001). In addition, TTE measurements of biventricular function, intracardiac filling pressures, and cardiac output were worse among those with higher PAHR (Table). Adjusted in-hospital mortality increased incrementally with higher PAHR, regardless of admission diagnosis, biventricular function, and critical care therapies (adjusted odds ratio [OR] 1.03 per 1 bpm higher, 95% confidence interval [CI] 1.01-1.05, p = 0.001; adjusted OR per quartile 1.37, 95% CI 1.19-1.59, p <0.001, Figure 1). Similarly, one-year mortality increased incrementally with higher PAHR (adjusted hazard ratio 1.03 per 1 bpm higher, 95% CI 1.02-1.04, p <0.001, Figure 2). When compared to component values, including the modified shock index, which is defined by HR / MAP, PAHR had the highest area under the curve (C-statistic 0.75). Conclusions: PAHR is a readily determinable composite measure of filling pressures and vascular resistance that enhances clinical risk stratification of critically ill patients by TTE. Among a diverse cohort of CICU patients, higher PAHR was associated with greater in-hospital and one-year mortality, regardless of admission diagnosis, biventricular function, or illness severity.

Background: Little is known about the epidemiology and prognostic significance of acid-base disturbances in the cardiovascular intensive care unit (CICU). This study examines the association of acid-base status at admission with in-hospital mortality among CICU patients. Methods: We conducted a retrospective analysis of adults admitted to the Mayo Clinic CICU from 2007-2018 who had available blood gas data, utilizing laboratory values obtained closest to the time of CICU admission. Arterial pH, serum bicarbonate, base excess, and partial pressure of carbon dioxide (PaCO 2 ) were examined as predictors of in-hospital mortality. Logistic regression models were used to assess associations, with adjustment for demographics, comorbidities, illness severity, and interventions. A composite acidosis score (CAS, range 0–5), incorporating predefined cut-offs for arterial pH, base excess, and anion gap was calculated to quantify acid-base disturbance severity. Results: A total of 3,229 patients were included for analysis. Of all acid-base variables, acidemia (pH<7.35) emerged as the strongest predictor of in-hospital mortality (adjusted odds ratio [aOR] 1.60, 95% confidence interval [CI] 1.29-1.98, p <0.003). Metabolic acidosis (HCO 3 <20 mEq/L) aOR 1.55, 95% CI 1.24-1.95, p <0.001) and respiratory acidosis (PaCO 2 >45 mmHg, aOR 1.44, 95% CI 1.14-1.81, p =0.002) were associated with worse adjusted in-hospital mortality, whereas alkalemia, metabolic alkalosis, and respiratory alkalosis were not (Fig. 1A-C). After adjustment, lower pH and more negative base excess were associated with higher in-hospital mortality (both p <0.001), whereas HCO 3 and PaCO 2 were not ( p =0.053&p=0.051, respectively; Fig. 2). Patients with combined metabolic and respiratory acidosis had the highest in-hospital mortality (56.3%), followed by patients with isolated or compensated metabolic acidosis (Fig.1D). Patients with severe acidosis (CAS>1) had higher mortality (aOR 2.34, 95% CI 1.88–2.90; p<0.001, Fig. 3AB). In-hospital mortality rose with increasing CAS (aOR 1.36 per point higher, 95% CI 1.26–1.47; p<0.001), with consistent effects across admission diagnoses (Fig. 3C). Conclusions: Acidemia, especially in the context of combined metabolic and respiratory acidosis, strongly predicts in-hospital mortality in the CICU. Incorporating combined acid-base disorders into risk stratification scores may facilitate earlier recognition and prevent progression of hemometabolic shock, thereby improving prognosis.

Background Patients with cardiohepatic syndrome are at higher risk of adverse outcomes in the cardiac intensive care unit. We hypothesized that cardiohepatic syndrome phenotypes would exhibit differences in their clinical and transthoracic echocardiogram hemodynamic profiles, portending a higher risk of mortality. Methods We included unique CICU patients with an admission diagnosis of heart failure from 2007 to 2018 with available data for 1 or more admission liver function tests. Echocardiographic variables were extracted from patients who had a transthoracic echocardiogram within 1 day of admission. We assigned patients to 1 of 4 mutually exclusive cardiohepatic syndrome phenotype groups: normal, hepatocellular, cholestasis, and combined. Results We included 3992 CICU patients; 2483 had an available transthoracic echocardiogram. Patients with cholestasis had more right ventricular systolic dysfunction and congestion, whereas those with hepatocellular injury had more left ventricular systolic dysfunction and poor forward flow; hemodynamics and biventricular function were worst in the combined group. In‐hospital mortality occurred in 14.6% and was higher for patients with cholestasis or hepatocellular injury, especially those with greater extent/severity and worse biventricular function or poor hemodynamics. After adjustment, only the group with hepatocellular injury (adjusted odds ratio [OR], 1.35 [95% CI, 1.04–1.75], P =0.03) and the combined group (adjusted OR, 1.75 [95% CI, 1.30–2.34], P <0.001) remained at higher risk. One‐year mortality was highest in the combined group (adjusted hazard ratio [HR], 1.29 [95% CI, 1.10–1.51], P =0.002). Conclusions Cardiohepatic syndrome phenotypes are associated with distinct echocardiographic profiles. Patients with the combined cardiohepatic syndrome phenotype were at highest risk of mortality, particularly if this was combined with poor cardiac function.