BackgroundProlonged invasive mechanical ventilation (IMV) following out-of-hospital cardiac arrest (OHCA) is associated with increased mortality, complications, and long-term functional impairment. Identification of early interventions that may reduce the duration of IMV is therefore clinically relevant.ObjectiveTo evaluate the association between the timing of bronchoscopy and the duration of IMV in patients successfully resuscitated after OHCA.MethodsWe performed a retrospective observational study of patients admitted to a cardiac intensive care unit after successful cardiopulmonary resuscitation for OHCA who required IMV for more than 24 h. Patients receiving mechanical circulatory support or those with poor neurological prognosis were excluded. The primary outcome was the total duration of IMV according to the timing of bronchoscopy. Secondary outcomes included associations between IMV duration and return of spontaneous circulation (ROSC) time, initial serum lactate levels, and the impact of bronchoscopy on antibiotic therapy.ResultsA total of 38 patients (29 men and 9 women; median age 53 years) were included. Bronchoscopy performed within 24 h of ICU admission was associated with a significantly shorter duration of IMV compared with delayed bronchoscopy (98 ± 15 vs 243 ± 49 h; p < .05). A moderate positive correlation was observed between ROSC duration and IMV duration (Pearson r = .44; p = .006). Initial serum lactate levels were not significantly correlated with IMV duration. Early bronchoscopy led to modification of antibiotic therapy in 56% of patients.ConclusionsEarly bronchoscopy after OHCA was associated with a substantial reduction in the duration of IMV. These findings suggest that early bronchoscopic evaluation may represent a readily available ICU intervention to reduce the risk of prolonged mechanical ventilation in selected post-cardiac arrest patients.

Immediate initiation of extracorporeal membrane oxygenation (ECMO) has not demonstrated benefit in individuals diagnosed with cardiogenic shock based on the presence of hypotension. The relationship between other hemodynamic or metabolic parameters and clinical outcomes, with or without ECMO, is not fully understood. The Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock (ECMO-CS) trial randomly assigned 117 patients diagnosed with cardiogenic shock to 2 groups: immediate initiation of ECMO or early conservative strategy. The present post-hoc analysis investigated the clinical efficacy of immediate ECMO therapy in subgroups with cardiogenic shock-more specific characteristics: low cardiac index, low venous oxygen saturation (SvO2) and high partial carbon dioxide pressure (pCO2) gap. The primary endpoint for this analysis was 1-year all-cause mortality; the secondary endpoint was a composite of mortality or hemodynamic worsening requiring ECMO. Data regarding cardiac index were available for 58 patients. In the subgroup with cardiac index < 2.2 L/min/m2, immediate ECMO initiation was associated with a reduced risk for all-cause death (hazard ratio [HR] 0.48 [95

AimsAmong patients with cardiogenic shock, immediate initiation of extracorporeal membrane oxygenation (ECMO) did not demonstrate any benefit at 30 days. The present study evaluated 1‐year clinical outcomes of the Extracorporeal Membrane Oxygenation in the therapy of Cardiogenic Shock (ECMO‐CS) trial.Methods and resultsThe ECMO‐CS trial randomized 117 patients with severe or rapidly progressing cardiogenic shock to immediate initiation of ECMO or early conservative strategy. The primary endpoint for this analysis was 1‐year all‐cause mortality. Secondary endpoints included a composite of death, resuscitated cardiac arrest or implantation of another mechanical circulatory support device, duration of mechanical ventilation, and the length of intensive care unit (ICU) and hospital stays. In addition, an unplanned post‐hoc subgroup analysis was performed. At 1 year, all‐cause death occurred in 40 of 58 (69.0%) patients in the ECMO arm and in 40 of 59 (67.8%) in the early conservative arm (hazard ratio [HR] 1.02, 95% confidence interval [CI] 0.66–1.58; p = 0.93). The composite endpoint occurred in 43 (74.1%) patients in the ECMO group and in 47 (79.7%) patients in the early conservative group (HR 0.83, 95% CI 0.55–1.25; p = 0.29). The durations of mechanical ventilation, ICU stay and hospital stay were comparable between groups. Significant interaction with treatment strategy and 1‐year mortality was observed in subgroups according to baseline mean arterial pressure (MAP) indicating lower mortality in the subgroup with low baseline MAP (<63 mmHg: HR 0.58, 95% CI 0.29–1.16; pinteraction = 0.017).ConclusionsAmong patients with severe or rapidly progressing cardiogenic shock, immediate initiation of ECMO did not improve clinical outcomes at 1 year compared to the early conservative strategy. However, immediate ECMO initiation might be beneficial in patients with advanced haemodynamic compromise.

An elevated left atrial pressure at rest and especially at stress is the main cause of symptoms and an increased risk of hospitalization and death in patients with heart failure. The mechanistic approach with implantation of interatrial shunt device (IASD) to reduce left atrial pressure in the patients with heart failure with mildly reduced and preserved ejection fraction was feasible and safe in a pilot study. In a non-randomized REDUCE LAP-HF and a randomized REDUCE LAP-HF I study the implantation of IASD was associated with improved symptoms and hemodynamic parameters. The effect of IASD on the risk of cardiovascular events including death and risk of heart failure hospitalizations was the objective of a multicentric randomized sham procedure controlled REDUCE LAP-HF II study. The review article is focused on the rationale of the method and the results of essential studies.

There are substantial differences in autonomic nervous system activation among heart (cardiac) failure (CF) patients. The effect of acute CF on autonomic function has not been well explored. The aim of our study was to assess the effect of experimental acute CF on heart rate variability (HRV). Twenty-four female pigs with a mean body weight of 45 kg were used. Acute severe CF was induced by global myocardial hypoxia. In each subject, two 5-min electrocardiogram segments were analyzed and compared: before the induction of myocardial hypoxia and >60 min after the development of severe CF. HRV was assessed by time-domain, frequency-domain and nonlinear analytic methods. The induction of acute CF led to a significant decrease in cardiac output, left ventricular ejection fraction and an increase in heart rate. The development of acute CF was associated with a significant reduction in the standard deviation of intervals between normal beats (50.8 [20.5–88.1] ms versus 5.9 [2.4–11.7] ms, p < 0.001). Uniform HRV reduction was also observed in other time-domain and major nonlinear analytic methods. Similarly, frequency-domain HRV parameters were significantly changed. Acute severe CF induced by global myocardial hypoxia is associated with a significant reduction in HRV.

Transcatheter aortic valve replacement (TAVR) is a minimally invasive therapeutic procedure with a consistent, linear increase in the number of implantations worldwide. Recently, TAVR has been rapidly expanding into lower-risk populations. Sporadic cases of late prosthesis-related Stanford type A dissection have been documented in self-expanding, as well as balloon-expandable TAVR valves, manifested primarily as acute aortic syndrome. We present the case of a 76-year-old male, who experienced refractory in-hospital cardiac arrest with non-shockable rhythm due to the obstruction of coronary flow caused by aortic dissection type A, with entry directly adjacent to the aortic prosthesis according to autopsy. The patient died despite the engagement of extracorporeal cardiopulmonary resuscitation. Aortic dissection developed one year after a transfemoral TAVR procedure using an Edwards SAPIEN 3 29 mm self-expanding valve. TAVR-associated late aortic dissection type A represents a rare, life-threatening condition with various clinical manifestations. The risk factors have not been well described and the differential diagnosis may be challenging. As the number of TAVR recipients and their life expectancy is increasing, we may face this complication more often in future.

Background: Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is increasingly being used for circulatory support in patients with cardiogenic shock, although the evidence supporting its use in this context remains insufficient. The ECMO-CS trial (Extracorporeal Membrane Oxygenation in the Therapy of Cardiogenic Shock) aimed to compare immediate implementation of VA-ECMO versus an initially conservative therapy (allowing downstream use of VA-ECMO) in patients with rapidly deteriorating or severe cardiogenic shock. Methods: This multicenter, randomized, investigator-initiated, academic clinical trial included patients with either rapidly deteriorating or severe cardiogenic shock. Patients were randomly assigned to immediate VA-ECMO or no immediate VA-ECMO. Other diagnostic and therapeutic procedures were performed as per current standards of care. In the early conservative group, VA-ECMO could be used downstream in case of worsening hemodynamic status. The primary end point was the composite of death from any cause, resuscitated circulatory arrest, and implementation of another mechanical circulatory support device at 30 days. Results: A total of 122 patients were randomized; after excluding 5 patients because of the absence of informed consent, 117 subjects were included in the analysis, of whom 58 were randomized to immediate VA-ECMO and 59 to no immediate VA-ECMO. The composite primary end point occurred in 37 (63.8%) and 42 (71.2%) patients in the immediate VA-ECMO and the no early VA-ECMO groups, respectively (hazard ratio, 0.72 [95% CI, 0.46–1.12]; P=0.21). VA-ECMO was used in 23 (39%) of no early VA-ECMO patients. The 30-day incidence of resuscitated cardiac arrest (10.3.% versus 13.6%; risk difference, –3.2 [95% CI, –15.0 to 8.5]), all-cause mortality (50.0% versus 47.5%; risk difference, 2.5 [95% CI, –15.6 to 20.7]), serious adverse events (60.3% versus 61.0%; risk difference, –0.7 [95% CI, –18.4 to 17.0]), sepsis, pneumonia, stroke, leg ischemia, and bleeding was not statistically different between the immediate VA-ECMO and the no immediate VA-ECMO groups. Conclusions: Immediate implementation of VA-ECMO in patients with rapidly deteriorating or severe cardiogenic shock did not improve clinical outcomes compared with an early conservative strategy that permitted downstream use of VA-ECMO in case of worsening hemodynamic status. Registration: URL: https://www.clinicaltrials.gov; Unique identifier: NCT02301819.

Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Eight female swine (45 kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure–volume catheter. Data are expressed as median (interquartile range). Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9–3.1) L/min and LV ejection fraction to 15.2% (10.5–19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2–34.9) to 56.0 (51.9–73.3) mmHg (P ˂ 0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2–40.0) to 19.1 (15.2–29.0) mmHg (P ˂ 0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0–53.4) to 72.5 (51.4–77.1) mmHg (P ˂ 0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7–19.1) to 20.8 (16.3–25.6) mmHg (P ˂ 0.01). Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.

Veno-venous extracorporeal membrane oxygenation (VV-ECMO) is a life-saving treatment for respiratory failure that may serve as a bridge to patient recovery or lung transplantation. In COVID-19, recovery is somewhat unpredictable and occasionally occurs after >100 days on VV-ECMO support. Thus, determining therapy cessation may be difficult. We report the case of a 59-year-old male without specific risk factors admitted to a tertiary center for rapidly progressive respiratory failure due to severe COVID-19, despite aggressive mechanical ventilatory support. Immediate insertion of VV-ECMO was associated with prompt resolution of hypoxemia and hypercapnia; however, all therapeutic efforts to wean the patient from VV-ECMO failed. During the prolonged hospitalization on VV-ECMO, sepsis was the most life-threatening complication. The patient overcame roughly 40 superinfections, predominantly affecting the respiratory tract, and spent 183 days on antimicrobial treatment. Although the function of other organ systems was generally stable, gradually progressive right ventricular dysfunction due to precapillary pulmonary hypertension required increasing doses of inotropes. A successful lung transplantation was performed after 207 days of VV-ECMO support. The present case provides evidence for prolonged VV-ECMO therapy as a bridge to lung transplantation in severe COVID-19 despite numerous, predominantly infectious complications.

Abstract Background Venoarterial extracorporeal membrane oxygenation (VA-ECMO) is widely used in the treatment of patients experiencing cardiogenic shock (CS). However, increased VA-ECMO blood flow (EBF) may significantly impair left ventricular (LV) performance. The objective of the present study was to assess the effect of VA-ECMO on LV function in acute CS with concomitant severe aortic stenosis (AS) or mitral regurgitation (MR) in a porcine model. Methods Eight female swine (45kg) underwent VA-ECMO implantation under general anaesthesia and mechanical ventilation. Acute CS was induced by global myocardial hypoxia. Subsequently, severe AS was simulated by obstruction of the aortic valve, while severe MR was induced by mechanical destruction of the mitral valve. Haemodynamic and LV performance variables were measured at different rates of EBF rates (ranging from 1 to 4 L/min), using arterial and venous catheters, a pulmonary artery catheter, and LV pressure-volume catheter. Data are expressed as median (interquartile range). Results Myocardial hypoxia resulted in declines in cardiac output to 2.7 (1.9–3.1) L/min and LV ejection fraction to 15.2% (10.5–19.3%). In severe AS, increasing EBF from 1 to 4 L/min was associated with a significant elevation in mean arterial pressure (MAP), from 33.5 (24.2–34.9) to 56.0 (51.9–73.3) mmHg (P˂0.01). However, LV volumes (end-diastolic, end-systolic, stroke) remained unchanged, and LV end-diastolic pressure (LVEDP) significantly decreased from 24.9 (21.2–40.0) to 19.1 (15.2–29.0) mmHg (P˂0.01). In severe MR, increasing EBF resulted in a significant elevation in MAP from 49.0 (28.0–53.4) to 72.5 (51.4–77.1) mmHg (P˂0.01); LV volumes remained stable and LVEDP increased from 17.1 (13.7–19.1) to 20.8 (16.3–25.6) mmHg (P˂0.01). Conclusion Results of this study indicate that the presence of valvular heart disease may alleviate negative effect of VA-ECMO on LV performance in CS. Severe AS fully protected against LV overload, and partial protection was also detected with severe MR, although at the cost of increased LVEDP and, thus, higher risk for pulmonary oedema.

The evidence supporting surgical aneurysmectomy in ischemic heart failure is inconsistent. The aim of the study was to describe long-term effect of minimally invasive hybrid transcatheter and minithoracotomy left ventricular (LV) reconstruction in patients with ischemic cardiomyopathy. Twenty-three subjects with transmural anterior wall scarring, LV ejection fraction 15-45%, and New York Heart Association class ≥ II were intervened using Revivent TC anchoring system. LV end-systolic volume index was reduced from 73.2 ± 27 ml at baseline to 51.5 ± 22 ml after 6 months (p < 0.001), 49.9 ± 20 ml after 2 years (p < 0.001), and 56.1 ± 16 ml after 5 years (p = 0.047). NYHA class improved significantly at 5 years compared to baseline. Six-min walk test distance increased at 2 years compared to the 6-month visit. Hybrid LV reconstruction using the anchoring system provides significant and durable LV volume reduction during 5-year follow-up in preselected patients with ischemic heart failure. Legend: Hybrid left ventricular reconstruction using the anchoring system provides significant and durable LV volume reduction throughout 5-year follow-up in preselected patients with ischemic heart failure.

Aims Inappropriate control of blood volume redistribution may be a mechanism responsible for exercise intolerance in heart failure with preserved ejection fraction (HFpEF). We propose to address this underlying pathophysiology with selective blockade of sympathetic signalling to the splanchnic circulation by surgical ablation of the right greater splanchnic nerve (GSN). Methods and results In a single-arm, prospective, two-centre trial, 10 patients with HFpEF (50% male, mean age 70 +/- 3 years) all with New York Heart Association (NYHA) class III, left ventricular ejection fraction >40%, pulmonary capillary wedge pressure (PCWP) >= 15 mmHg at rest or >= 25 mmHg with supine cycle ergometry, underwent ablation of the right GSN via thoracoscopic surgery. Patients were evaluated at baseline, 1, 3, 6 and 12 months after the procedure. The primary endpoint was a reduction in exercise PCWP at 3 months. There were no adverse events related to the blockade of the nerve during 12-month follow-up but three patients had significant peri-procedural adverse events related to the surgical procedure itself. At 3 months post-GSN ablation, patients demonstrated a reduction in 20 W exercise PCWP when compared to baseline [-4.5 mmHg (95% confidence interval, CI -14 to -2); P = 0.0059], which carried over to peak exercise [-5 mmHg (95% CI -11 to 0; P = 0.016). At 12 months, improvements were seen in NYHA class [3 (3) vs. 2 (1, 2); P = 0.0039] and quality of life assessed with the Minnesota Living with Heart Failure Questionnaire [60 (51, 71) vs. 22 (16, 27); P = 0.0039]. Conclusion In this first-in-human study, GSN ablation in HFpEF proved to be feasible, with a suggestion of reduced cardiac filling pressure during exercise, improved quality of life and exercise capacity.

Abstract Introduction Extracorporeal cardiopulmonary resuscitation (ECPR) has been introduced as a life-saving procedure in refractory cardiac arrest. Methods Eligible patients for this analysis had to undergo ECPR after unsuccessful cardiopulmonary resuscitation with a minimum of three defibrillation attempts. For extracorporeal life support (ECLS) was used Cardiohelp system or Levitronix CentriMag blood pump. LUCAS II system was used for chest compressions during cardiac arrest. The relations of blood lactate and pH levels, measured before ECPR insertion and after 24 hours as well as comorbities (diabetes, hypertension, BMI) to the clinical outcomes at 2 years were evaluated. Results We analyzed data from 59 patients treated with ECPR for refractory cardiac arrest. The mean age of our patients was 61 years. Out-of-hospital cardiac arrest (OHCA) occurred in 33 patients, 26 patients suffered from in-hospital arrest (IHCA). Baseline value of lactate was 11.57±4.22 mmol/l, initial pH 6.95±0.31. In comparison with survivors, patients who died had significantly higher initial lactate levels (12.05±0.81 vs. 8.01±0.77; P<0.05). Moreover, survivors had significantly lower lactate levels after 24 hours (7.39 vs 2.56) and lower BMI (27.4 vs 31.2; P<0.05). Diabetes or hypertension in our group have no influence on the mortality. The difference of mortality in the group of OHCA or IHCA was also not significant. 32% patients survived one month with good neurological outcome (CPC 1–2), 30% six months, 23% one year and 21% two years. Conclusions ECPR give the last chance to survive refractory cardiac arrest. The levels of blood lactate are significantly associated with clinical outcomes of ECPR. Obesity was associated with significantly higher mortality in our group. Funding Acknowledgement Type of funding source: Public grant(s) – National budget only. Main funding source(s): MH CZ DRO (Nemocnice Na Homolce - NNH, 00023884)

Abstract Introduction Continuous reliable evaluating of left ventricular (LV) contractile function in patients with advanced heart failure requiring intensive care remains challenging. Recently, continual monitoring of dP/dtmax from arterial line became available for hemodynamic monitoring. However, the relation between arterial dP/dtmax and LV dP/dtmax measurement is not fully understood. Purpose The aim of our study was to determine the relation of arterial dP/dtmax and LV dP/dtmax assessed by echocardiography in patients with acute heart failure. Methods Forty-eight patients with acute heart failure requiring intensive care and hemodynamic monitoring were recruited into the study (mean age 70.4 years, 65% were males). Hemodynamic variables including arterial dP/dtmax were continually monitored using arterial line pressure waveform analysis. LV dP/dtmax was assessed using continuous-wave Doppler analysis of mitral regurgitation flow. Results The values from continual arterial dP/dtmax monitoring significantly correlated with the LV dP/dtmax assessed by echocardiography (r=0.72, 95% confidence interval [CI] 0.54–0.83, P<0.0001). Linear regression revealed that (LV dP/dtmax) = 0.87×(arterial dP/dtmax) + 291, P<0.0001. Arterial dP/dtmax significantly correlated also with the stroke volume (r=0.55, P<0.0001), cardiac output (r=0.32, P=0.0289), mean arterial blood pressure (r=0.43, P=0.0155) and systolic blood pressure (r=0.79, P<0001). On the other hand arterial dP/dtmax did not correlate with the systemic vascular resistance (SVR), heart rate, dynamic arterial elastance, diastolic blood pressure or central venous pressure. Conclusion Our results revealed that arterial dP/dtmax values tightly and highly significantly correlate with LV dP/dtmax. Arterial dP/dtmax could be, therefore, used for continual monitoring of LV contractility. Acknowledgement/Funding Institutional grant MH CZ - DRO (Na Homolce Hospital- NNH, 00023884), IG150501

BackgroundHyperuricemia is associated with a poorer prognosis in heart failure (HF) patients. Benefits of hyperuricemia treatment with allopurinol have not yet been confirmed in clinical practice. The aim of our work was to assess the benefit of allopurinol treatment in a large cohort of HF patients.MethodsThe prospective acute heart failure registry (AHEAD) was used to select 3160 hospitalized patients with a known level of uric acid (UA) who were discharged in a stable condition. Hyperuricemia was defined as UA ≥500 μmoL/L and/or allopurinol treatment at admission. The patients were classified into three groups: without hyperuricemia, with treated hyperuricemia, and with untreated hyperuricemia at discharge. Two‐ and five‐year all‐cause mortality were defined as endpoints. Patients without hyperuricemia, unlike those with hyperuricemia, had a higher left ventricular ejection fraction, a better renal function, and higher hemoglobin levels, had less frequently diabetes mellitus and atrial fibrillation, and showed better tolerance to treatment with angiotensin‐converting enzyme inhibitors/angiotensin receptor blockers and/or beta‐blockers.ResultsIn a primary analysis, the patients without hyperuricemia had the highest survival rate. After using the propensity score to set up comparable groups, the patients without hyperuricemia had a similar 5‐year survival rate as those with untreated hyperuricemia (42.0% vs 39.7%, P = 0.362) whereas those with treated hyperuricemia had a poorer prognosis (32.4% survival rate, P = 0.006 vs non‐hyperuricemia group and P = 0.073 vs untreated group).ConclusionHyperuricemia was associated with an unfavorable cardiovascular risk profile in HF patients. Treatment with low doses of allopurinol did not improve the prognosis of HF patients.

Abstract Background Continuous, reliable evaluation of left ventricular (LV) contractile function in patients with advanced heart failure requiring intensive care remains challenging. Continual monitoring of dP/dtmax from the arterial line has recently become available in hemodynamic monitoring. However, the relationship between arterial dP/dtmax and LV dP/dtmax remains unclear. This study aimed to determine the relationship between arterial dP/dtmax and LV dP/dtmax assessed using echocardiography in patients with acute heart failure. Methods Forty-eight patients (mean age 70.4 years [65% male]) with acute heart failure requiring intensive care and hemodynamic monitoring were recruited. Hemodynamic variables, including arterial dP/dtmax, were continually monitored using arterial line pressure waveform analysis. LV dP/dtmax was assessed using continuous-wave Doppler analysis of mitral regurgitation flow. Results Values from continual arterial dP/dtmax monitoring were significantly correlated with LV dP/dtmax assessed using echocardiography (r = 0.70 [95% confidence interval (CI) 0.51–0.82]; P < 0.0001). Linear regression analysis revealed that LV dP/dtmax = 1.25 × (arterial dP/dtmax) (P < 0.0001). Arterial dP/dtmax was also significantly correlated with stroke volume (SV) (r = 0.63; P < 0.0001) and cardiac output (CO) (r = 0.42; P = 0.0289). In contrast, arterial dP/dtmax was not correlated with SV variation, dynamic arterial elastance, heart rate, systemic vascular resistance (SVR), or mean arterial pressure. Markedly stronger agreement between arterial and LV dP/dtmax was observed in subgroups with higher SVR (N = 28; r = 0.91; P < 0.0001), lower CO (N = 26; r = 0.81; P < 0.0001), and lower SV (N = 25; r = 0.60; P = 0.0014). A weak correlation was observed in the subjects with lower SVR (N = 20; r = 0.61; P = 0.0004); in the subgroups with higher CO (N = 22) and higher SV (N = 23), no significant correlation was found. Conclusion Our results suggest that in patients with acute heart failure requiring intensive care with an arterial line, continuous calculation of arterial dP/dtmax may be used for monitoring LV contractility, especially in those with higher SVR, lower CO, and lower SV, such as in patients experiencing cardiogenic shock. On the other hand, there was only a weak or no significant correlation in the subgroups with higher CO, higher SV, and lower SVR.