Cardiac Pumping Capability Research Articles

Prognostic value of resting cardiac power index depends on mean arterial pressure in dilated cardiomyopathy.

AimsIn recent decades, haemodynamic parameters have been estimated for risk stratification and determining treatment strategies for patients with non‐ischaemic dilated cardiomyopathy (DCM). In various invasive procedures, the cardiac pumping capability is defined as cardiac power output (CPO), which is calculated by multiplying cardiac output by the mean arterial pressure. Lower CPO values in advanced heart failure predict adverse outcomes. However, few studies discuss the prognostic value of CPO in mild‐to‐moderate phase patients. This study aimed to determine the value of the cardiac power index (CPI) obtained from the resting CPO for predicting the prognosis of patients with New York Heart Association Functional Class II or III DCM.Methods and resultsFrom March 2000 to January 2020, a total of 623 cardiomyopathy patients were evaluated for haemodynamic parameters. Patients with secondary cardiomyopathy, ischaemic cardiomyopathy, valvular heart disease, and Class IV cardiomyopathy were excluded. A total of 176 DCM patients fulfilled the criteria for inclusion. Patients were 51.7 ± 12.5 years old (mean ± standard deviation) with a mean left ventricular ejection fraction of 32.1 ± 9.2%. The patients were divided into two groups by their median CPI (CPI < 0.52, low‐CPI; CPI ≥ 0.52, high‐CPI). No significant differences were found in the left ventricular end‐diastolic diameter, left ventricular ejection fraction, or pulmonary arterial wedge pressure between the groups. The probability of cardiac event‐free survival was significantly lower for low‐CPI than for high‐CPI groups by Kaplan–Meier analysis (P = 0.012), even with no significant difference between the high and low cardiac index groups (P = 0.069). Furthermore, Cox proportional hazards regression analysis revealed that, in addition to the CPI, the systolic and mean arterial pressure involved in CPI calculation were independent predictors of cardiac events. Indeed, among these factors, mean arterial pressure had the strongest prognostic ability.ConclusionsAlthough CPI is effective for stratifying DCM and predicting cardiac events in patients with Class II/III DCM, this prognostic value depends on mean arterial pressure.

Investigation of non‐Newtonian blood flow with power‐law model: Effects of coronary congenital heart defect on a specific age type

Nowadays, humans are suffering from chronic cardiovascular diseases, including Congenital Heart Defect (CHD). These diseases have far-reaching consequences, such as disruption of the daily life of humans by reducing their ability to perform daily routines. This problem is due to impaired cardiac pumping capability. The present numerical simulation studied the effects of CHDs on pressure drop and AWSS. Numerical calculation of non-Newtonian blood flow parameters, including power-law indices and the Reynolds number, were also investigated. To construct a 3D model of CHDs, an OSS program using DICOM and MRI was used. Besides, the vessel wall was assumed as solid. The non-Newtonian blood flow was assumed as a laminar flow with the slip boundary conditions at the vessel wall. AWSS, pressure drop, and dimensionless heat transfer coefficient are directly correlated with power-law indices, Reynolds number, and constant heat flux boundary conditions of the body. CHDs increased velocity, pressure drop, and AWSS in all steps of the simulation process.

CARDIAC POWER AS A PREDICTOR OF MORTALITY IN SEPSIS

The inflammatory response in sepsis results in end stage damage to tissues and a shock state with increasing circulatory failure. Myocardial depression is one of the many complications seen during severe sepsis and septic shock. Cardiac power output (CPO) is a measure of cardiac pumping capability

P339 Gradient adjusted cardiac power index does not improve prediction of survival post transcatheter aortic valve replacement compared to cardiac power index alone

Abstract Funding Acknowledgements None Background Cardiac Power Index (CPI) is an integrative hemodynamic measure of cardiac pumping capability and is the product of the simultaneously measured mean arterial pressure (MAP) and cardiac output (CO). In patients with aortic stenosis (AS), MAP is not reflective of mean systolic left ventricular (LV) pressure due to the transvalvular gradient. Non-invasive assessment of mean systolic LV pressure is challenging in severe aortic stenosis. CPI assessed using systemic MAP was previously shown to predict survival post transcatheter aortic valve replacement (TAVR). Purpose We evaluated the utility of a gradient adjusted CPI in predicting survival post TAVR compared to CPI alone Methods A retrospective study was performed including patients undergoing TAVR with 1 year follow-up. Baseline demographics, clinical, and echocardiographic data were abstracted from a cohort of 1,011 patients. CPI was calculated, (CO x MAP)/ (451 x BSA) Watts/m2. Gradient adjusted CPI was calculated using an augmented MAP i) adding aortic valve mean gradient(AVMG) to systolic blood pressure (CPI1); ii) adding aortic valve maximal instantaneous gradient to systolic blood pressure (CPI2) and iii) adding AVMG to MAP (CPI3). Patient survival score was calculated using a step up technique to identify the cut off value for CPI and gradient adjusted CPI to identify, where the maximum difference in mortality occurred. Multivariate cox-regression analysis was performed to adjust for baseline covariates. Receiver operator curves(ROC) for CPI and gradient adjusted CPI were calculated to predict survival post TAVR. Results The mortality rate at 1 yr was 16%. Mean age and AVMG of survivors was 81 +/- 9 yrs and 43 +/-14 mmHg vs 80 +/-9 yrs and 42 +/- 13 mmHg in the deceased group. Proportion of female patients was similar in both groups (p = 0.7). Patients in the deceased group at baseline had a higher prevalence of chronic lung disease, atrial fibrillation, heart failure within 2-weeks of procedure, higher STS-PROM score, lower serum albumin level, higher prevalence of moderate to severe tricuspid regurgitation, higher right ventricular systolic pressure and higher prevalence of dialysis. Both CPI and gradient adjusted CPI were independently associated with survival at 1 year. The area under ROC for CP, CP1, CP2 and CP3 were 0.67 (95% confidence interval [CI] 0.62 - 0.72), 0.65 (95% CI 0.60 – 0.70), 0.66 (95% CI 0.61 – 0.71) and 0.63 (95% CI 0.58 – 0.68) respectively. Conclusion Gradient adjusted CPI did not improve accuracy of predicting post TAVR survival at 1 year compared to CPI alone. Abstract P339 Figure. Area under ROC

36 Direct Measurement of Cardiac Compensation in Valvular Heart Disease

<h3>Purpose</h3> The natural history of valvular heart disease (VHD) suggests that the heart initially adapts to compensate for valve lesions and thereby maintain physiological function. When these compensatory mechanisms become exhausted, cardiac decompensation commences. We tested the hypothesis that all VHD patients with normal exercise capacity are in the compensatory phase with no symptoms and normal cardiac reserve. <h3>Methods</h3> Unselected consecutive male patients with VHD performed cardiopulmonary exercise (CPX) testing with non-invasive central haemodynamic measurements during symptom-limited treadmill exercise. Exercise capacity was represented by peak oxygen consumption (VO_2max) and cardiac pumping capability by peak exercise cardiac power output (CPO_max). Data are given as mean±SD. <h3>Results</h3> Of the entire VHD patient cohort (n = 215), 81.4% (n = 175) had VO_2max which were within or above the reference range of healthy male sedentary controls (n = 101). This is shown in Figure 1A where individual patient VO_2max is expressed as a percentage of the average VO_2max of age- and sex-matched controls. These 175 patients with normal VO_2max had a mean age of 63.1 ± 14.0 years, and consisted of 98 (56%) who were asymptomatic (NYHA class I) and 77 (44%) who were discordantly symptomatic in NYHA II+ (.001). As shown in Figure 1B, 117 patients (66.9%) had CPO_max within the normal range, of whom 80 (45.7%) were asymptomatic, but 37 (21.1%) were in NYHA II+ despite having normal VO_2max and CPO_max (.001). Conversely, 58 (33.1%) had CPO_max below the normal range, and yet 18 (10.3%) of these were discordantly still in NYHA I (P &lt; 0.001). These patients were classified asymptomatic by their responsible clinicians but our results revealed they had early, objective evidence of cardiac decompensation. <h3>Conclusions</h3> This investigation demonstrates that it is now possible to directly and objectively measure whether patients are in the compensated or decompensated phases of VHD. There were discrepancies between subjective symptomatic statuses and objectively measured cardiac and physical functional statuses. The possibility to determine whether patients are in the compensatory phase or not, might help in the management of difficult VHD cases.

Atrial Fibrillation reduces the Functional REServe of the Heart by a fifth: A pilot FRESH-AF study

The advent of catheter ablation has reignited the controversy about whether rhythm or rate control should be the preferred mode of therapy for atrial fibrillation (AF) [1]. It is well known that compared to sinus rhythm (SR), AF is associated with increased mortality and morbidity including stroke, heart failure, and impaired quality of life. Furthermore, patients may experience adverse effects from drug treatment that may negate thebeneficial effects ofmaintaining SR [2].What is still unknown is inwhatways and by howmuch overall cardiac function is impairedwhen the atrial “kick” in SR is lost after the onset of AF. To fill this gap in knowledge, it is essential to assess cardiac functionnot onlyat rest but also during maximal stress, and not merely piecemeal aspects of cardiac function. This can be achieved by conducting full cardiopulmonary exercise testing (CPX) in combination with non-invasive evaluation of central haemodynamics [3]. Thiswouldprovide a quantitative assessment of aerobic physical exercise capacity represented by peak O2 consumption (VO2max), together with peak cardiac power output (CPOmax) which measures the overall cardiac dysfunction [4], and is by far the strongest predictor of prognosis in heart failure patients [5]. As metabolic and circulatory demands increase during severe exercise, patients with AF have lower cardiovascular reserve. Previous studies have shown that VO2max improved by 5–13% after restoration of SR in patients with AF [6], buthowmuchcardiac functional gain is achieved thereby is still unknown. We therefore measured changes in CPOmax after successful DC cardioversion (DCCv) in patients with optimally rate-controlled AF. In so doing, we tested the hypothesis that the cardiac pumping capability of patients in AF is diminished by about a fifth. Twelve unselected ambulatory patients (10 males, age: 57.5 ± 13.7 (mean ± SD) years) with symptomatic persistent AF recruited from outpatient clinics underwent full CPX with measurements of non-invasive haemodynamics before and after successful DCCv. The aetiologies (including overlaps) of their AF were ischaemic heart disease (17%), hypertension (25%), LV dysfunction (42%), valve disease (25%), lone AF (25%), and obesity (BMI N 35, 25%). None of the patients had previous catheter ablation, or any contraindication to undergomaximal exercise, such as significant outflow obstruction, haemodynamically serious structural heart disease, uncontrolled ventricular tachyarrhythmia, uncontrolled hypertension, limiting symptoms of ischaemic heart disease, inability or deemed unsafe to exercise on treadmill, contraindications to electrical cardioversion or full anticoagulation, or inability to provide full informed consent. Standardexerciseparametersweremeasuredaspartof an incremental cardiopulmonary exercise test performed on a Trackmaster TMX425 treadmill (Full Vision, Kansas, USA) using the Bruce or modified Bruce protocol, as previously described [3]. Rates of oxygen consumption (VO2) and other gaseous exchanges were recorded breath-by-breath using the Medgraphics Ultima CardiO2 analytic system (Medgraphics, Minnesota, USA). Using the CO2-rebreathing technique (indirect Fick), cardiac output were measured at rest and during peak exercise. Mean arterial pressure was calculated from the equation, MAP=DBP+ 0.412 ∗ (SBP− DBP) [7]. CPOmax in watts is the product of peak cardiac output (COmax in l.min−1)multiplied by theMAP inmm Hg at peak exercisemultiplied by a conversion factor (2.22 × 10−3) [8]. A paired sample t-test was used to assess the change in cardiac reserve variables pre and post DCCv. This study was approved by the National Research Ethics Service Committee for Yorkshire & Humber in Leeds East. After successful cardioversion, subjectively all patients claimed to feel better and more energetic and, as shown in Table 1, objectively their treadmill exercise duration increased by 19.3% (P b 0.05), coupled with an improvement in peak O2 consumption by 16.5% (P b 0.01). Their resting ventricular rate decreased from 83.1 ±20.3 to 66.9 ± 20.5 min− 1 (P b 0.05), while peak exercise HR decreased from 163 ± 42 to 128 ± 18 min−1 to (P b 0.05). Secondarily, these negative chronotropic effects led to heightened stroke volume at peak exercise by 46% (P b 0.0001), thereby raising the peak cardiac output by 16.5% (P b 0.0001). Due to a concomitantly greater

Cardiac power output and its response to exercise in athletes and non‐athletes

Cardiac power output (CPO) is an integrative measure of overall cardiac function as it accounts for both, flow- and pressure-generating capacities of the heart. The purpose of the present study was twofold: (i) to assess cardiac power output and its response to exercise in athletes and non-athletes and (ii) to determine the relationship between cardiac power output and reserve and selected measures of cardiac function and structure. Twenty male athletes and 32 age- and gender-matched healthy sedentary controls participated in this study. CPO was calculated as the product of cardiac output and mean arterial pressure, expressed in watts. Measures of hemodynamic status, cardiac structure and pumping capability were assessed by echocardiography. CPO was assessed at rest and after peak bicycle exercise. At rest, the two groups had similar values of cardiac power output (1·08±0·2W versus 1·1±0·24W, P>0·05), but the athletes demonstrated lower systolic blood pressure (109·5±6·2mmHg versus 117·2±8·2mmHg, P<0·05) and thicker posterior wall of the left ventricle (9·8±1mm versus 9±1·1mm, P<0·05). Peak CPO was higher in athletes (5·87±0·75W versus 5·4±0·69W, P<0·05) as was cardiac reserve (4·92±0·66W versus 4·26±0·61W, P<0·05), respectively. Peak exercise CPO and reserve were only moderately correlated with end-diastolic volume (r=0·54; r=0·46, P<0·05) and end-diastolic left ventricular internal diameter (r=0·48; r=0·42, P<0·05), respectively. Athletes demonstrated greater maximal cardiac pumping capability and reserve than non-athletes. The study provides new evidence that resting measures of cardiac structure and function need to be considered with caution in interpretation of maximal cardiac performance.

Relationship between peak cardiac pumping capability and indices of cardio-respiratory fitness in healthy individuals.

Cardiac power output (CPO) is a unique and direct measure of overall cardiac function (i.e. cardiac pumping capability) that integrates both flow- and pressure-generating capacities of the heart. The present study assessed the relationship between peak exercise CPO and selected indices of cardio-respiratory fitness. Thirty-seven healthy adults (23 men and 14 women) performed an incremental exercise test to volitional fatigue using the Bruce protocol with gas exchange and ventilatory measurements. Following a 40-min recovery, the subjects performed a constant maximum workload exercise test at or above 95% of maximal oxygen consumption. Cardiac output was measured using the exponential CO(2) rebreathing method. The CPO, expressed in W, was calculated as the product of the mean arterial blood pressure and cardiac output. At peak exercise, CPO was well correlated with cardiac output (r=0·92, P<0·01), stroke volume (r=0·90, P<0·01) and peak oxygen consumption (r=0·77, P<0·01). The coefficient of correlation was moderate between CPO and anaerobic threshold (r=0·47, P<0·01), oxygen pulse (r=0·57, P<0·01), minute ventilation (r=0·53, P<0·01) and carbon dioxide production (r=0·56, P<0·01). Small but significant relationship was found between peak CPO and peak heart rate (r=0·23, P<0·05). These findings suggest that only peak cardiac output and stroke volume truly reflect CPO. Other indices of cardio-respiratory fitness such as oxygen consumption, anaerobic threshold, oxygen pulse, minute ventilation, carbon dioxide production and heart rate should not be used as surrogates for overall cardiac function and pumping capability of the heart.

Discrepancy Between Cardiac and Physical Functional Reserves in Stroke

Understanding the physiological limitations to exercise after stroke will assist the development of targeted therapies to improve everyday function. This study defines (1) whether exercise capacity is limited by the cardiovascular system (oxygen supply) or skeletal muscles (oxygen utilization); and (2) cardiac function and pumping capability in people with stroke. Twenty-eight male participants with mild ischemic stroke (70 ± 6 years of age, 18 ± 20 months poststroke) and 25 male, age-matched healthy control subjects performed a graded cardiopulmonary exercise test with gas exchange and noninvasive hemodynamic measurements. Maximal oxygen extraction was calculated as the ratio between peak oxygen consumption and peak cardiac output. Cardiac function and pumping capability were assessed by peak exercise cardiac power output (expressed in watts) and cardiac output. Peak oxygen consumption (18.4 ± 4.6 versus 26.8 ± 5.5 mL/kg/min, P<0.01) and arterial-venous O(2) difference (9.3 ± 2.5 versus 12.6 ± 1.9 mlO(2)/100 mL of blood, P<0.01) were both reduced in stroke participants compared with healthy control subjects. In contrast, peak exercise cardiac power output (4.79 ± 0.79 versus 4.51 ± 0.96 W, P=0.49), cardiac output (16.4 ± 3.1 versus 17.1±2.5 L/min, P=0.41), and the pressure-generating capacity of the heart (127±11 versus 125 ± 14 mm Hg, P=0.97) were similar between stroke participants and healthy control subjects. The ability of skeletal muscles to extract oxygen is diminished after stroke. However, cardiac function and pumping capability are maintained. Appropriate therapies targeting muscle oxygen uptake such as exercise rehabilitation may improve exercise capacity after stroke.

Relationship between peak cardiac pumping capability and selected exercise‐derived prognostic indicators in patients treated with left ventricular assist devices

Exercise-derived variables have been used in the assessment of functional capacity and prognosis in patients with chronic heart failure. The aim of this study was to assess the relationship between cardiac pumping capability represented by peak cardiac power output and peak oxygen consumption, anaerobic threshold, ventilatory efficiency slope, and peak circulatory power in patients undergoing the 'Harefield Protocol'. Haemodynamic and gas exchange measurements were undertaken during a graded treadmill exercise test. They were performed on 54 patients-18 implanted with left ventricular assist devices (LVADs), 16 explanted (recovered), and 20 moderate-to-severe heart failure patients. Peak oxygen consumption was only highly correlated with peak cardiac power output in explanted LVAD (r = 0.85, P< 0.01), but not in implanted LVAD and heart failure patients (r = 0.55 and 0.53, P< 0.05). The anaerobic threshold was only modestly correlated with peak cardiac power output in heart failure and explanted (r = 0.46 and 0.54, P< 0.05) and weakly in implanted LVAD patients (r = 0.37, P< 0.05). Peak cardiac power output was well correlated with peak circulatory power in LVAD explanted and implanted (r = 0.82, P< 0.01; r = 0.63, P< 0.01) but not in heart failure patients (r = 0.31, P> 0.05). Ventilatory efficiency slope was only moderately correlated with peak cardiac power output in LVAD-explanted patients (r = -0.52, P< 0.05). Exercise-derived prognostic indicators demonstrate limited capacity in reflecting cardiac pumping capability in patients treated with LVADs and should therefore be used with caution in interpretation of cardiac organ function.

Cardiac pumping capability in patients with peripheral vascular disease

Peripheral vascular disease (PVD) is a condition characterized by atherosclerotic occlusive disease of the lower extremities, low functional capacity and low exercise tolerance. Less empirical data are available concerning the cardiovascular response to maximum exercise tests in patients with PVD. The purpose of this study was to examine cardiovascular variables in patients with peripheral vascular disease. Fifty patients (67 +/- 9 years) completed an incremental exercise test (2 min stages, 3.2 km h(-1), with increases of 2% every 2 min) to maximum claudication pain. Maximal oxygen consumption (VO2) was assessed on a breath-by-breath basis by online expiratory gas analysis (CardiO2, Medical Graphics Co.). Blood pressure was recorded at peak exercise. Following a 30-min rest period, patients exercised at the highest level attained during the first test and cardiac output (QT) was measured using the exponential non-invasive rebreathing method. Cardiac power output peak (CPOpeak) in Watts (W), was then computed. Mean +/- SD values were; 13.85 +/- 4.14 ml kg min(-1); maximal walk time 357 +/- 227 s; peak mean arterial pressure 127 +/- 15 mmHg; 9.8 +/- 2.39 (l min(-1)); CPO 2.86 +/- 0.87 W. Patients with peripheral vascular disease demonstrate attenuated levels of cardiovascular capacity. This group of patients should be given exercise therapy in order to improve cardiovascular status and ambulatory function.

Comparison and Relation of Indirect and Direct Dynamic Indexes of Cardiac Pumping Capacity in Chronic Heart Failure

Cardiac power output (CPO), the product of cardiac output (CO) and mean arterial pressure (MAP), is a direct measure of cardiac pumping capability and is strongly indicative of prognosis and exercise ability in patients with chronic heart failure (CHF). However, it is not as easily measured as indirect indicators of cardiac function, such as peak oxygen consumption (VO(2)) or peak "circulatory power" (CircP), the product of VO(2) and MAP. The relation between direct and indirect indexes of cardiac pumping capacity was evaluated in 219 ambulatory patients with CHF. CircP was found to have a direct and consistent relation with CPO, overall (R = 0.93, p <0.0001) and at peak exercise (R = 0.84, p < 0.0001). The results suggest CircP to be an adequate measure of cardiac pumping capacity when the more directly measured CPO is not available.

Role of cardiac power in heart failure.

The heart is a muscular mechanical pump with an ability to generate both flow (cardiac output) and pressure. The product of flow output and systemic arterial pressure is the rate of useful work done, or power output. Cardiac pumping capability can be defined as the cardiac power output (CPO(max)) achieved by the heart during maximal stimulation. Cardiac reserve is the increase in power output as the cardiac performance is increased from the resting to the maximally stimulated state. Recently, several studies have shown that CPO(max), a direct indicator of overall cardiac function, measured directly or as an approximation, is a major determinant of exercise capacity and a most powerful predictor of prognosis for patients with chronic heart failure. The same holds true in acute heart failure, where it is also useful in subclassifying the conditions to select the appropriate treatment.

Clinical and research implications of new concepts in the assessment of cardiac pumping performance in heart failure.

Every cardiac pump has its own maximum performance, which denotes its pumping capability. The difference between the performance in the resting state and that at maximum is called pumping reserve. Cardiac pumping performance is therefore best quantified by its hydraulic power output. Cardiac pumping capability is predictive of the ultimate prognosis of patients in severe heart failure whereas pumping reserve is a major determinant of exercise capacity. The therapeutic efficacy of cardiotonic drugs used in the treatment of ambulant heart failure patients should be evaluated with reference to the way they alter the relation between cardiac pumping reserve and exercise capacity.