Contents
Download PDF
pdf Download XML
45 Views
30 Downloads
Share this article
Research Article | Volume 16 Issue 5 (May, 2026) | Pages 100 - 109
Determination of Echocardiography Derived Cardiac Power Output in the Immediate Preoperative Period in Adult Patients with Severe Mitral Stenosis Undergoing Mitral Valve Replacement: A Prospective, Observational Study
 ,
 ,
 ,
 ,
 ,
 ,
1
MBBS. Junior Resident. Department of Anaesthesia and Intensive Care. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
2
MD DM. Associate Professor. Department of Cardiac Anaesthesia and Intensive Care. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
3
MD DM. Professor. Department of Cardiac Anaesthesia and Intensive Care. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
4
MD. Associate Professor. Department of Anaesthesia and Intensive Care. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
5
MD DM FESC. Professor. Department of Cardiology. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
6
MS MCh. Additional Professor. Department of Cardiothoracic and Vascular Surgery. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012
7
MD DM. Assistant Professor. Department of Anaesthesia and Intensive Care. Postgraduate Institute of Medical Education and Research. Chandigarh. Chandigarh, India. Pin- 160012.
Under a Creative Commons license
Open Access
Received
April 1, 2026
Revised
April 15, 2026
Accepted
May 15, 2026
Published
May 29, 2026
Abstract

Background: Cardiac power output (CPO) has significant prognostic utility in patients with heart failure [1-3], cardiogenic shock [4], patients undergoing transcatheter aortic valve replacement (TAVR) [5,6]. CPO, however, has been evaluated scarcely in the perioperative period of cardiac surgical patients. CPO values in severe mitral stenosis (MS) patients undergoing mitral valve replacement (MVR) surgery is not known. This study aimed to find out the value of in severe MS patients undergoing MVR in comparison with patients with no known cardiac disease undergoing non-cardiac surgery. Methods: Transthoracic echocardiography (TTE) was performed to measure cardiac output (CO) prior to induction of anaesthesia in 50 patients with severe MS undergoing MVR (MS group) and 50 patients with no known cardiac disease undergoing major non-cardiac surgery (Non cardiac group). Mean arterial pressure (MAP) readings were simultaneously obtained from invasive arterial pressure monitor. CPO was calculated and compared between the two groups. Correlation between CPO and EuroSCORE 2 predicted mortality risk was evaluated in the MS group. Results: The median (IQR) CPO found in the MS group 0.62 (0.49-0.77) W was significantly less (p 0.000) than the CPO of 1.03 (0.80-1.24) W obtained in the non-cardiac group. CPO in the MS group had a moderately strong inverse correlation (Spearman’s rho -0.345, p= 0.014) with EuroSCORE 2 predicted mortality risk. Conclusion: CPO in severe MS patients undergoing MVR is significantly lower than that in adult patients with no known cardiac disease undergoing major non-cardiac surgery. CPO in severe MS patients undergoing MVR has moderately strong inverse correlation with EuroSCORE 2 predicted perioperative mortality risk.

Keywords
INTRODUCTION

Cardiac Power Output (CPO) is the hydraulic energy delivered by the left ventricle (LV) to the systemic circulation per unit time [7]. It has the immense advantage of combining both cardiovascular flow and intravascular pressure, thereby more accurately reflecting the efficiency of the cardiovascular system [4]. CPO has been shown to be a powerful predictor of adverse cardiovascular outcome in patients with cardiogenic shock [4], chronic heart failure [8], heart failure with preserved ejection fraction (HFpEF) [1], as well sepsis [9].

 

Valvular heart disease (VHD)-related heart failure (HF) is a special subtype of HF with an increasingly concerned heterogeneity in pathophysiology, clinical phenotypes, and outcomes. In patients undergoing transcatheter aortic valve replacement (TAVR) due to symptomatic severe aortic stenosis, a strong and significant correlation between CPO and mortality has been shown by several studies [5,10].

 

Mitral stenosis (MS) significantly increases the risk of left ventricular diastolic dysfunction (LV DD). Left atrial failure (LAF) is the critical pathophysiological process in the early stage of HFpEF in MS patients. In MS patients, increased left atrial (LA) pressure, which induces LA eccentric remodelling, simultaneously results in LA pumping dysfunction and eventually led to LAF when decompensation occurs [11]. As HFpEF is often associated with reduced CPO, which is again linked to poor prognosis, proportion of severe MS patients are likely to be associated with reduced CPO, which, may be associated with poor prognosis, especially in the patients undergoing corrective surgery for the same. However, the literature is scarce regarding the CPO values in severe MS patients.

 

Therefore, we aimed to find out CPO values in adult patients with severe MS undergoing mitral valve replacement surgery and compare it with CPO values in patients having no known cardiac disease.

MATERIALS AND METHODS

After obtaining clearance from the Institutional Ethics Committee and written informed consent from the participants, adult (18-65 years) severe MS patients undergoing elective mitral valve replacement (MVR) surgery (MS group) and adult (18-65 years) patients with no known cardiac disease and having normal sinus rhythm, undergoing major non-cardiac surgery, requiring intra-operative invasive arterial pressure monitoring (Non-Cardiac group)- were included for the study. Patients declining consent, having body mass index (BMI) > 30 Kg.m-2 and having end stage major organ dysfunction- were excluded. Additionally, patients having concomitant moderate or severe mitral regurgitation, having moderate or severe aortic valve disease, undergoing redo or emergency surgery, having inotropic/mechanical support in the preoperative period, undergoing concomitant coronary artery bypass grafting (CABG)- were excluded in the MS group. As per institutional protocol, patients in both the groups were kept nil per os (NPO) for 6 hours for solids and for 2 hours for clear liquids prior to surgery. In the MS group, all the morning doses of the pre-operative cardiac drugs except heparin (if being given) were continued. In the Non-cardiac group, morning doses of medications being taken for any co-morbid illness were continued/discontinued according to departmental/institutional protocol. In both the groups, after the patients entered the operating room 5-lead electrocardiography (ECG) and pulse oximeter (SpO2) were attached. Invasive arterial catheter was inserted after infiltration of 2% lignocaine over the intended insertion site and the invasive arterial mean arterial pressure (MAP) was noted. Immediately prior to induction of anaesthesia, transthoracic echocardiography (TTE) was performed in both the groups using GE Vivid E9 workstation (GE Healthcare Vingmed Ultrasound AS, Horten, Norway) with M5S-D (1.5-4.5 MHz) transthoracic probe with the patient in supine/left lateral position to acquire images and video loops required for measurement of left ventricular outflow tract (LVOT) diameter, LVOT velocity time integral (VTI), left ventricular (LV) mass, LVEF, inferior vena cava (IVC) diameter and collapsibility. Additionally, images and loops were also acquired for measuring peak left ventricular global longitudinal strain (LV GLS), left atrial (LA) diameter, LA volume, tricuspid annular plane systolic excursion (TAPSE), tricuspid regurgitation (TR) severity, right ventricular systolic pressure (RVSP) in the MS group. Loops/images of at least 3 and 5 cardiac cycles, respectively, were stored for patients in normal sinus rhythm (NSR) and atrial fibrillation (AF), respectively. Subsequently, all the required measurements were performed offline by a single, experienced (> 5 years’) observer using the stored loops and images. The acquisition, interpretation and measurement of all the required parameters were done according to the recommendations made by the American Society of Echocardiography (ASE) in the relevant guidelines [12-15]. Values of the parameters averaged over 3 cardiac cycles (for patients having NSR) and 5 cardiac cycles (for patients having AF) were taken as the final values. Cardiac output (CO) was calculated as CO = 0.785 x [LVOT diameter (in cm)]2 x LVOT VTI x Heart rate (HR). SVRI (in dynes.s-2.cm-5) was calculated as SVRI = [(MAP-CVP)/CO] x 80. CVP was estimated from the IVC diameter and collapsibility [15]. CPO (in W) was calculated as CPO = [CO (in L) x MAP (in mm Hg)]/451. Cardiac power index (CPI), CPO per 100g LV mass, CPI per 100g LV mass- were also calculated. Stored loops and images were reviewed by the same observer after one month from the date of initial measurement (For intra-observer variability). Loops and images were also reviewed by a second independent, experienced (> 5 years’) observer (For inter-observer variability). Appropriate demographic, clinical and laboratory data were collected for calculation of EuroSCORE 2 and Society of Thoracic Surgeons (STS) score predicted perioperative mortality risk in the MS group. Statistical analysis: In order to demonstrate that the mean echocardiography derived CPO in severe MS patients is different by 0.15 W from a mean echocardiography derived CPO of 0.83 with a pooled standard deviation of 0.25 in population with no cardiac disease [3,16], 45 patients each were required in the MS arm and control arm of the cohort for a 1:1 allocation at 80% power and 0.05 alpha for a two-sample t test. Inflating this sample size for 20% dropouts (poor echocardiography window and missed data), we required 54 patients each in the MS arm and the non-cardiac control arm. Categorical data were presented as Number (Percentage) and were compared between the two groups using chi square test. Normal distribution of numerical data was checked by both Kolmogorov-Smirnov test and visual Q-Q plotting. Numerical data were presented as Mean (SD) for normally distributed data and as Median (Interquartile range, IQR) for non-normally distributed data and were compared between the two groups using two-samples t-test and Mann Whitney U test, respectively. Correlation between CPO in the MS group with age, EuroSCORE 2, STS score, LVEF, Peak LV GLS, TAPSE, LA diameter, LA volume, RVSP- were seen by creating scatter-plots and also by calculation of Pearson’s correlation coefficient and Spearman’s rank correlation coefficient for normally and non-normally distributed parameters, respectively. CPO in the MS group was compared between patients having NSR vs patients having AF and between patients having non-significant (Absent/trivial/mild) vs patients having significant (Moderate/severe) TR, using Welch’s t-test. Inter-rater and intra-rater reliability of the echocardiographic measurements were evaluated using the intraclass coefficient (ICC) from a two-way mixed-effects model with absolute agreement. An ICC value of more than 0.80 was considered as good reliability. All the statistical analyses were performed using SPSS (IBM) 22.0 software.

RESULTS

68 and 62 patients were approached for the MS group and the Non-cardiac group, respectively. After exclusions, a total of 50 patients were analysed in each group (Fig 1). The demographic parameters were comparable among the two groups, except female patients were more in number in the Non-cardiac group (Table 1). Carcinoma of urinary bladder was the most common diagnosis (26%) and lobectomy for malignant as well as benign lung lesions was the most commonly planned surgical procedure (42%) in the non-cardiac group (Table 2).

 

Median (IQR) EuroSCORE 2 and STS score predicted perioperative mortality risks in the MS group were 1.35 (1.07-1.88) % and 2.89 (2.18-4.91) %, respectively. 30 (60%) and 20 (40%) patients in the MS group were in AF and NSR, respectively, while 34 (68%) and 16 (32%) patients had non-significant and significant TR, respectively. Only 4 (8%) patients in the MS group had severe TR. All the patients in the MS group were receiving either single or a combination of cardiac medications. Diuretics were the most common class of medication, being received by 48 (96%) of patients, followed by Beta blocker, being received by 44 (88%) of patients. Beta Blocker with Diuretics was the most common medication combination, being received by 18 (36%) of patients.

 

Table 3 depicts the comparison of hemodynamic and common echocardiographic parameters along with CPO and its derived parameters between the MS group and the Non-cardiac group. While heart rate and LVEF was comparable between the two groups, MAP, LVOT diameter, LVOT VTI, stroke volume, stroke index, cardiac output, cardiac index- were significantly less in the MS group in comparison to those of the Non-cardiac group. SVRI was significantly higher in the MS group in comparison to the Non-cardiac group. CPO and its derivatives, i.e, CPI, CPO per 100 gm LV mass, CPI per 100 gm LV mass- were significantly low in the MS group in comparison to the Non-cardiac group.

 

Table 4 depicts the various echocardiographic parameters of the MS group. Peak LV GLS in majority of patients was abnormal, i.e, less negative than -16 % [17]. LA was severely dilated in all the patients, indicated by left atrial volume index (LAVI) more than 40 ml.m-2 [18]. RV function was normal in majority of patients, indicated by TAPSE > 1.7 cm [15]. Majority of the patients had mild to moderately elevated RVSP, indicated by RVSP between 34 to 69 mm Hg [15]. CPO and all its derivatives were not significantly different between patients in NSR vs patients in AF and also between patients having significant ns non-significant TR (Tables 5,6).

 

Fig 2 depicts the correlation of CPO with Age, EuroSCORE 2, STS score, LVEF, Peak LV GLS, LA volume, TAPSE, RVSP- in the MS group. CPO had moderately strong inverse correlation with EuroSCORE 2 predicted mortality risk (Figure 2B). However, it did not have any significant linear correlation with any other parameters.

 

All the measured echocardiographic parameters showed good inter- as well as intra-observer reliability, indicated by ICC > 0.8.

Table 1: Demographic parameters of the study population. Data presented in both Mean (SD) [€] and Median (IQR) [¶] format, except Sex (presented in number). [#- by Mann Whitney U test, ^- by Unpaired t test, $- by Chi Square test, *- p < 0.05]

(Abbreviations: BSA- Body surface area, BMI- Body mass index, SD- Standard deviation, IQR- Inter-quartile range)

 

Parameters

MS group (n=50)

Non cardiac group (n=50)

P value

Age (yrs)

45 (35-56)

47 (32-54)

0.909#

Weight (Kg) €

56 (14)

61 (15)

0.104^

Height (cm)

157 (154-166)

165 (154-170)

0.070#

BSA (m2)

1.6 (1.4-1.7)

1.7 (1.5-1.8)

0.054#

BMI (Kg/m2)

21.7 (18.4-24.5)

21.6 (19.9-25.5)

0.340#

Sex (M/F)

22/28

19/31

0.000*$

 

Table 2: Primary diagnoses and surgical procedures in the non-cardiac group. Data presented in Number (percentage) format.

(Abbreviations: SCC- Squamous cell carcinoma, CA- Carcinoma)

Diagnosis

Number (%)

Surgical Plan

Number (%)

Mediastinal tumour

9 (18%)

Tumour excision

9 (18%)

Carcinoma Urinary Bladder

13 (26%)

Radical cystectomy + Ileal bladder formation

13 (26%)

Malignant Lung lesion

11 (22%)

Lobectomy

21 (42%)

Benign lung lesion

10 (20%)

Miscellaneous

Chest wall defect

Thyroid mass

Renal carcinoma

SCC leg

CA larynx

 

2 (4%)

2 (4%)

1 (2%)

1 (2%)

1 (2%)

Free flap

Mass excision

Radical nephrectomy

Free flap

Total laryngectomy

 

2 (4%)

2 (4%)

1 (2%)

1 (2%)

1 (2%)

Total

50

 

50

 

 

Parameters

MS group (n=50)

Non cardiac group (n=50)

P value

HR (bpm)

79 (69-91)

77 (67-93)

0.967#

MAP (mm Hg)

88 (82-100)

98 (90-110)

0.000*#

LVOT diameter (cm)

1.9 (1.8-2.1)

2.0 (1.9-2.2)

0.009*#

LVOT VTI (cm) €

14.4 (3.9)

17.7 (3.8)

0.000*^

LVEF (%)

54 (48-60)

55.0 (50-60)

0.472#

Stroke Volume (ml)

42.9 (16.4)

59.6 (18.5)

0.000*^

Stroke Index (ml.m-2) €

27.2 (8.8)

35.8 (9.7)

0.000*^

CO (L.min-1)

3.0 (2.5-3.8)

4.7 (3.6-5.5)

0.000*#

CI (L.min-1.m-2) €

2.1 (0.8)

2.8 (0.7)

0.000*^

LV Mass (g)

97.6 (86.9-127.6)

72.9 (59.9-100.7)

0.000*#

SVRI (dyne.s.cm-5.m-2)

3224 (2562-4058)

2640 (2310-3100)

0.000*#

CPO (W)

0.62 (0.49-0.77)

1.03 (0.80-1.24)

0.000*#

CPI (W.m-2) €

0.42 (0.16)

0.64 (0.19)

0.000*^

CPO (W) per 100 gm LV mass

0.58 (0.46-0.77)

1.39 (0.94-1.69)

0.000*#

CPI (W.m-2) per 100 gm LV Mass

0.36 (0.29-0.51)

0.87 (0.60-1.04)

0.000*#

 

Table 3: Comparison of hemodynamic, echocardiographic and cardiac power output parameters between the Mitral Stenosis (MS) group and the Non-cardiac group. [Data presented in both Mean (SD) {€} and Median (IQR) {¶} format. #- By Mann Whitney U test, ^- By independent samples t-test, *- p < 0.05]

 

(Abbreviations: HR- Heart rate, MAP- Mean arterial pressure, LVOT- Left ventricular outflow tract, VTI- Velocity time integral, LVEF- Left ventricular ejection fraction, CO- Cardiac output, CI- Cardiac index, LV- Left ventricular, SVRI- Systemic vascular resistance index, CPO- Cardiac power output, CPI- Cardiac power index)

 

Table 4: Various echocardiographic parameters of the Mitral Stenosis (MS) group. Data presented in both Mean (SD) [€] and Median (IQR) [¶] format.

 

(Abbreviations: LV GLS- Left ventricular global longitudinal strain, LA- Left atrial, LAVI- Left atrial volume index, TAPSE- Tricuspid annular plain systolic excursion, RVSP- Right ventricular systolic pressure)

 

Parameters

Value

Peak LV GLS (%) €

-12.9 (3.3)

LA diameter (cm) ¶

5.0 (4.3-5.5)

LA volume (ml) ¶

139.5 (97.9-223.8)

LAVI (ml.m-2) ¶

88.5 (63.9-144.7)

TAPSE (cm) €

2.0 (0.5)

RVSP (mm Hg) ¶

41 (30-55)

 

Table 5: Comparison of CPO and its derivatives between patients with NSR and with AF in the Mitral Stenosis (MS) group. Data presented in Median (IQR) format. [^- By Mann Whitney U test]

 

(Abbreviations: CPO- Cardiac power output, CPI- Cardiac power index, LV- Left ventricular)

 

Parameter

Patients with NSR

Median (IQR)

N=20

Patients with AF

Median (IQR)

N=30

P Value^

 

CPO (W)

0.63 (0.52-0.77)

0.61 (0.46-0.77)

0.593

CPI (W.m-2)

0.39 (0.31-0.59)

0.39 (0.29-0.49)

0.566

CPO per 100 gm LV mass (W)

0.54 (0.45-0.81)

0.62 (0.48-0.72)

0.751

CPI per 100 gm LV mass (W.m-2)

0.35 (0.26-0.57)

0.38 (0.29-0.51)

0.566

 

Table 6: Comparison of CPO and its derivatives between patients with non-significant (Absent/Trivial/Mild) and significant (Moderate/Severe) Tricuspid regurgitation in the Mitral Stenosis (MS) group. Data presented in Median (IQR) format. [^- By Mann Whitney U test]

 

(Abbreviations: CPO- Cardiac power output, CPI- Cardiac power index, LV- Left ventricular)

 

Parameter

Patients with Insignificant TR

Median (IQR)

N=34

Patients with Significant TR

Median (IQR)

N=16

P Value^

 

CPO (W)

0.65 (0.53-0.81)

0.56 (0.39-0.63)

0.081

CPI (W.m-2)

0.39 (0.32-0.53)

0.34 (0.27-0.44)

0.124

CPO per 100 gm LV mass (W)

0.59 (0.47-0.79)

0.56 (0.45-0.71)

0.618

CPI per 100 gm LV mass (W.m-2)

0.36 (0.29-0.52)

0.34 (0.26-0.48)

0.603

 

FIGURE CAPTIONS

Fig 1 A schematic flow diagram summarizing the selection of the study population

(Abbreviations: MS- Mitral stenosis, TTE- Transthoracic echocardiography, CABG- Coronary artery bypass grafting)

 

Fig 2 Correlation of CPO in the Mitral Stenosis (MS) group with age (Fig 2A), EuroSCORE 2 (Fig 2B), STS mortality score (Fig 2C), LVEF (Fig 2D), Peak LV GLS (Fig 2E), LA volume (Fig 2F), TAPSE (Fig 2G), RVSP (Fig 2H) of patient (ρ- Spearman’s rho, P- p value, *- p < 0.05)

 

(Abbreviation: CPO- Cardiac power output, STS- Society of Thoracic Surgeons, LVEF- Left ventricular ejection fraction, LV GLS- Left ventricular global longitudinal strain, LA- Left atrial, TAPSE- Tricuspid annular plane systolic excursion, RVSP- Right
ventricular systolic pressure)

 

       
       
 


Fig 1

 

 

 

 

 
   


Fig

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

 

DISCUSSION

The primary aim of our study was to get the reference values for CPO and its derivatives in severe MS patients undergoing elective MVR surgery and compare them with patients with no cardiac disease undergoing major non-cardiac surgery. The reference [Median (IQR)] values of echocardiography derived CPO, CPI, CPO per 100g of LV mass and CPI per 100 gm of LV mass in the MS group were found as 0.62 (0.49-0.77) W, 0.39 (0.30-0.50) W.m-2, 0.58 (0.46-0.77) W and 0.36 (0.29-0.51) W.m-2, respectively. All the values were significantly less in comparison to the corresponding values obtained from adult patients with no known cardiac disease.

 

All the patients in the MS group were in stage D heart failure, i.e, had symptoms of heart failure secondary to mitral stenosis. As per 2020 ACC/AHA guidelines for management for management of valvular heart disease

 

[19], patients with mitral stenosis having stage D symptoms require intervention. While impaired CPO value indicates impairment of hydraulic power of heart and therefore, decompensation of cardiac function, its strong association with poor prognosis indicates that impaired hydraulic power of heart is associated with poor prognosis. As untreated symptomatic severe MS is associated with poor prognosis compared to normal, healthy population, the hydraulic power of heart in severe MS is expected to be impaired. However, the amount and severity of such impairment is not known. Our study aimed to fill this knowledge gap in literature.

 

We found significant impairment of CPO and all its derivatives in the patients with severe MS compared to that in patients with no known cardiac disease. Both the components of CPO, i.e, cardiac output and MAP, were found to be significantly lower in the patients in MS group in comparison to the patients in the non-cardiac group. Stroke volume was found to be significantly lower in the MS group than that of the non-cardiac group, whereas, heart rate was comparable between the two groups. Therefore, the impaired cardiac output in the MS group was primarily contributed by impaired stroke volume. Impaired stroke volume in severe mitral stenosis results mainly from fixed reduction in LV preload from mitral valvular impedance to LV filling (20). Reduction in preload is also contributed in severe MS patients by use of diuretics in these patients. Use of diuretics is almost ubiquitous in severe MS patients for relieving heart failure symptoms by reducing pulmonary congestion [21]. 96% of our patients in the MS group were on diuretics. Use of beta blockers also contribute to reduction of stroke volume in these patients due to negative inotropic effects, despite their utility in augmenting LV preload by increasing diastolic filling time through reduction in heart rate [22]. As 88% of our patients in the MS group were receiving beta blockers, the reduction in stroke volume might have been contributed, at least partially, by the negative inotropic effect imparted by them.

 

The lower MAP in the MS group was primarily contributed by low cardiac output in this group as the SVRI was found to be higher in this group compared to the non-cardiac group. Increased systemic vascular resistance in the MS group is expected as all our patients were in stage D heart failure secondary to severe MS and peripheral vasoconstriction is a usual neurohumoral and hyper-adrenergic compensatory response found in heart failure patients [23]. Therefore, the low CPO and all its derivatives in severe MS patients is contributed primarily by reduced stroke volume and cardiac output in these patients. Apart from fixed reduction in preload and reduced inotropy from use of beta blockers, reduced peak LV GLS in these patients also indicates towards a possible role of intrinsic myocardial dysfunction in causing low cardiac output. Rheumatic MS leads to depressed LV function due to chronic rheumatic myocarditis, which is frequently overlooked by conventional echocardiographic parameters, like LVEF. Speckle tracking based peak LV GLS can identify subclinical alterations in LV function in these patients that traditional echocardiography techniques, like LVEF, frequently overlook [24]. The patients of the MS group in our study also had LVEF in normal range. However, the peak LV GLS was significantly lower than normal values, indicating intrinsic myocardial dysfunction had also contributed in lowering cardiac output in this group.

 

While impaired values of CPO as well as its various derivatives have been seen to be associated with poor prognosis in patients with heart failure in multiple studies [1, 3, 25], its utility in predicting perioperative outcome in cardiac surgical patients has remained largely unexplored. CPI < 0.48 W.m-2 has been associated with higher 1-year mortality among patients undergoing TAVR.  Although our study was not designed to evaluate prognostic utility of CPO in severe MS patients undergoing MVR, correlation of CPO with EuroSCORE 2 and STS score, which are used universally for predicting perioperative mortality of adult cardiac surgical patients [26], were seen. There was moderately strong inverse correlation of CPO values with EuroSCORE 2 predicted mortality in patients with severe MS in our study. However, we could not find such correlation between STS score predicted mortality and CPO values in these patients. As CPO reflects hydraulic force generation by heart, low CPO indicates lower force generation, i.e, cardiac decompensation. While degree of cardiac decompensation prior to cardiac surgery definitely affects perioperative mortality, non-cardiac factors, like age, functions of other major organ systems, fraility, co-morbidities, surgical complexity- also have significant impact on the perioperative mortality in cardiac surgical cohort [27]. Therefore, both EuroSCORE 2 as well as STS score incorporates several non-cardiac factors for predicting prognosis after cardiac surgery. Number of non-cardiac risk factors considered are relatively more in the STS score than the EuroSCORE 2 [26]. This could possibly explain the modest correlation of CPO in MS group with EuroSCORE 2 predicted mortality risk and also the absence of significant correlation with STS score predicted mortality risk in our patient population. Moreover, majority of the patients of MS group in our study had low to intermediate risk of predicted mortality. Study with larger sample size involving patients with all tiers of predicted mortality, i.e, low, intermediate and high- would possibly have found more significant correlation.

 

The absence of significant correlation of CPO in MS group with age, RVSP, LA volume and parameters of LV and RV function, i.e, LVEF, peak LV GLS and TAPSE- in our study can be primarily attributed to small sample size, which precluded achievement of adequate power to detect any significant correlation. Evaluation of a larger sample size involving adequate number and mix of patients of different age and having different grades of LV as well as RV function, RVSP and LA volume is required to adequately delineate their correlation with CPO in severe MS patients. Moreover, CPO can vary widely in patients with normal LVEF, as seen in studies involving patients having HFpEF [1]. Besides that, cardiac output and mean arterial pressure depend heavily upon loading conditions apart from myocardial function alone [28, 29]. Therefore, any significant correlation between CPO and parameters of ventricular function may be inherently difficult to find out.

 

While AF is known to significantly reduce cardiac output (CO) in MS patients, thereby worsening symptoms as it eliminates the crucial atrial kick needed to push blood through the narrowed valve, with the effect being more pronounced in severe MS where the atrium struggles to overcome valve resistance [30], we did not find any significant difference in CPO between patients with atrial fibrillation and patients with normal sinus rhythm in the MS group. Again, increasing TR severity worsens heart function, significantly reducing forward cardiac output (CO) by causing right heart strain, volume overload, and impeding systemic venous return and poorer clinical outcomes [31]. While the values of CPO in the subset of MS patients with significant TR were definitely lower than those with insignificant TR in our study, the difference did not reach statistical significance. These apparent lack of difference in CPO between patients with AF vs patients with NSR and between patients having significant vs insignificant TR in the MS group- were most likely caused by a small study population. A larger sample population may successfully find a significant difference between these subsets of patients.

 

There were several limitations of our study. It included a small sample size from only a single, tertiary-care centre. Therefore, its results may not be generalised. However, despite having a small sample size, our study could pick up significant difference of CPO and its derivatives between patients having MS and those not having any cardiac disease. All our patients in the MS group had rheumatic pathology of the mitral valve. Therefore, the CPO values measured in our study population might not be reflective in MS of other pathology, e.g, calcific MS. While rheumatic myocarditis plays a role in reducing cardiac efficiency in patients with MS of rheumatic etiology, it may not be the case in MS of other etiology. However, in low and middle income countries, rheumatic etiology accounts for the major burden of MS [32] and therefore, our results will be valid for severe MS patients from these countries. Although CPO is mainly used as a prognostic parameter, we did not evaluate the association of CPO with either perioperative or long term prognosis in severe MS patients undergoing MVR. Our primary aim, however, was to find reference values of CPO and its derivatives in severe MS patients, which is scarcely available in current literature and we were able to find that. We could also find the prognostic potential of CPO in these patients in finding correlation of it with one of the well established prognostic score. We did not measure any subsequent values in the perioperative or postoperative period apart from the pre-induction values. Further studies, however, in this aspect can be hypothesized based on our findings. We did not measure the most essential component of CPO, i.e, cardiac output by the gold standard method of pulmonary artery catheter. However, use of pulmonary artery catheter requires invasive procedure and its use in perioperative period is diminishing [33]. Use of TTE by anesthesiologists in the perioperative period is, on the other hand, is emerging rapidly [34] and cardiac output measured by TTE is reliable as well as accurate in comparison to that measured by pulmonary artery catheter with an added advantage of being non-invasive [35]. Our results, are, therefore, reproducible and applicable in current cardiac surgical perioperative practice.

CONCLUSION

The median (IQR) values of echocardiography derived CPO, CPI, CPO per 100g of LV mass and CPI per 100 gm of LV mass in the immediate preoperative period of adult patients with severe rheumatic MS undergoing MVR surgery are 0.62 (0.49-0.77) W, 0.39 (0.30-0.50) W.m-2, 0.58 (0.46-0.77) W and 0.36 (0.29-0.51) W.m-2, respectively with all the values being significantly lower than the corresponding values in adult patients with no known cardiac disease undergoing major non-cardiac surgery. CPO measured in the immediate preoperative period of adult patients with severe MS undergoing MVR has a moderately strong inverse correlation with EuroSCORE 2 predicted perioperative mortality risk. Study with larger sample size is needed to establish the relation of CPO in MS patients with age, STS score predicted risks of mortality, LVEF, Peak LV GLS, TAPSE, LA volume, RVSP and to compare CPO values between patients in NSR versus patients in AF and between patients with significant TR versus patients with insignificant TR. Conflicts of interest: Shruti Rajlaxmi, Indranil Biswas, Banashree Mandal, Venkata Ganesh, Parag Barwad, Pankaj Aggarwal and Ira Dhawan declare that they have no conflict of interest. Human rights statements and informed consent: All procedures followed were in accordance with the ethical standards of the responsible committee on human experimentation (institutional and national) and with the Helsinki Declaration of 1964 and later versions. Informed consent was obtained from all patients for being included in the study.

REFERENCES

1.      Harada T, Yamaguchi M, Omote K, et al. Cardiac Power Output Is Independently and Incrementally Associated With Adverse Outcomes in Heart Failure With Preserved Ejection Fraction. Circ Cardiovasc Imaging. 2022;15:e013495.

2.      Wang S, Chen A, Duan X. Resting Cardiac Power Predicts Adverse Outcome in Heart Failure Patients With Preserved Ejection Fraction: A Prospective Study. Front Cardiovasc Med. 2022;9:915918.

3.      Takizawa D, Harada T, Obokata M, et al. Pathophysiologic and prognostic importance of cardiac power output reserve in heart failure with preserved ejection fraction. Eur Heart J Cardiovasc Imaging. 2024;25:220-8.

4.      Fincke R, Hochman JS, Lowe AM, et al; SHOCK Investigators. Cardiac power is the strongest hemodynamic correlate of mortality in cardiogenic shock: a report from the SHOCK trial registry. J Am Coll Cardiol. 2004;44:340–8.

5.      Agasthi P, Arsanjani R, Mookadam F, et al. Does Resting Cardiac Power Index Affect Survival Post Transcatheter Aortic Valve Replacement? J Invasive Cardiol. 2020;32:129-37.

6.      Miyahara D, Izumo M, Sato Y, et al. Cardiac power output is associated with adverse outcomes in patients with preserved ejection fraction after transcatheter aortic valve implantation. Eur Heart J Imaging Methods Pract. 2024;2:qyae048.

7.      Lim H.S. Cardiac power output revisited. Circ Heart Fail 2020;13:e007393.

8.      Williams S, Cooke G, Wright D, et al. Peak exercise cardiac power output; a direct indicator of cardiac function strongly predictive of prognosis in chronic heart failure. Eur. Heart J. 2001;22:1496–1503.

9.      Kimmoun A, Ducrocq N,  Mory S, et al. Cardiac Contractile Reserve Parameters Are Related to Prognosis in Septic Shock. BioMed Res. Int. 2013;2013:930673.

10.   Agasthi P, Pujari S.H, Mookadam F, et al. Does a Gradient-Adjusted Cardiac Power Index Improve Prediction of Post-Transcatheter Aortic Valve Replacement Survival Over Cardiac Power Index? Yonsei Med. J. 2020;61:482–91.

11.   Triposkiadis F, Pieske B, Butler J, et al. Global left atrial failure in heart failure. Eur J Heart Fail. 2016;18:1307–20.

12.   Mitchell C, Rahko PS, Blauwet LA, et al. Guidelines for Performing a Comprehensive Transthoracic Echocardiographic Examination in Adults: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr 2019;32:1-64.

13.   Lang RM, Badano LP, Mor-Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. J Am Soc Echocardiogr. 2015;28:1-39.e14.

14.   Zoghbi WA, Adams D, Bonow RO, et al. Recommendations for Noninvasive Evaluation of Native Valvular Regurgitation: A Report from the American Society of Echocardiography Developed in Collaboration with the Society for Cardiovascular Magnetic Resonance. J Am Soc Echocardiogr. 2017;30:303-371.

15.   Mukherjee M, Rudski LG, Addetia K, et al. Guidelines for the Echocardiographic Assessment of the Right Heart in Adults and Special Considerations in Pulmonary Hypertension: Recommendations from the American Society of Echocardiography. J Am Soc Echocardiogr. 2025;38:141-86.

16.   Ghahremani-Nasab L, Toufan-Tabrizi M, Javanshir E, et al. Assessing cardiac power output values in a healthy adult population. Int J Cardiovasc Imaging. 2024;40:517-26.

17.   Nyberg J, Jakobsen EO, Østvik A, et al. Echocardiographic Reference Ranges of Global Longitudinal Strain for All Cardiac Chambers Using Guideline-Directed Dedicated Views. JACC Cardiovasc Imaging. 2023;16:1516-31.

18.   Parajuli P, Alahmadi MH, Ahmed AA. Left Atrial Enlargement. [Updated 2025 Jan 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK553096/

19.   Otto CM, Nishimura RA, Bonow RO, et al. 2020 ACC/AHA Guideline for the Management of Patients With Valvular Heart Disease: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. Circulation. 2021;143:e72-e227.

20.   El Sabbagh A, Reddy YNV, Barros-Gomes S, et al. Low-Gradient Severe Mitral Stenosis: Hemodynamic Profiles, Clinical Characteristics, and Outcomes. J Am Heart Assoc. 2019;8:e010736.

21.   Carabello BA. Modern management of mitral stenosis. Circulation. 2005;112:432-7.

22.   Cramer CK, Shaw LJ, Chandrashekhar Y. Progress in Cardiovascular Imaging. JACC: Cardiovascular Imaging. 2018;11:1883-914.

23.   Delong C, Sharma S. Physiology, Peripheral Vascular Resistance. [Updated 2023 May 1]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538308/

24.   Rahaman SA, Nath RK, Kumawat A, et al. A Comparative Study of Detection of Alteration of Left Ventricular Strain by Speckle Tracking Echocardiography in Adult Patients with Rheumatic Mitral Stenosis. Eur J Cardiovasc Med. 2024;14:307-13.

25.   Cortigiani L, Sorbo S, Miccoli M, et al. Prognostic value of cardiac power output to left ventricular mass in patients with left ventricular dysfunction and dobutamine stress echo negative by wall motion criteria. Eur Heart J Cardiovasc Imaging. 2017;18:153-158.

26.   Subramaniam K, Balasubramanian, Castor E, et al. Role of risk prediction scores in preoperative assessment of cardiac surgical patients. Best Pract Res Clin Anaesthesiol. 2025;39:83-9.

27.   Tan H, Qi X. A retrospective study on factors affecting early prognosis after mitral stenosis surgery. Curr Probl Surg. 2025;70:101841.

28.   King J, Lowery DR. Physiology, Cardiac Output. [Updated 2023 Jul 17]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470455/

29.   DeMers D, Wachs D. Physiology, Mean Arterial Pressure. [Updated 2023 Apr 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2025 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK538226/

30.   Karthikeyan G. The value of rhythm control in mitral stenosis. Heart. 2006;92:1013-6.

31.   Shiran A, Sagie A. Tricuspid regurgitation in mitral valve disease incidence, prognostic implications, mechanism, and management. J Am Coll Cardiol. 2009;53:401-8.

32.   Simpson MT, Kachel M, Neely RC, et al. Rheumatic Heart Disease in the Developing World. Struct Heart. 2023;7:100219.

33.   Marik PE. Obituary: pulmonary artery catheter 1970 to 2013. Ann Intensive Care. 2013;3:38.

34.   Subramaniam K, Boisen ML, Yehushua L, et al. Perioperative Transthoracic Echocardiography Practice By Cardiac Anesthesiologists-Report of a "Start-Up" Experience. J Cardiothorac Vasc Anesth. 2021;35:222-32.

35.  Mercado P, Maizel J, Beyls C, et al. Transthoracic echocardiography: an accurate and precise method for estimating cardiac output in the critically ill patient. Crit Care. 2017;21:136.

Recommended Articles
Research Article
Published: 29/05/2026
Download PDF
Research Article
Clinical Profile and Therapeutic Management of Gynaecomastia in Indian Males: A Cross-Sectional Study of 100 Cases
Published: 29/05/2026
Download PDF
Research Article
Psychiatric Morbidity and Quality of Life in Patients with Chronic Medical Illness: An Observational Analysis
Published: 19/05/2020
Download PDF
Research Article
STUDY OF EARLY POSTOPERATIVE COMPLICATIONS AND SHORT-TERM MORBIDITIES OF MODIFIED RADICAL MASTECTOMY WITH SPECIAL FOCUS ON MODIFICATIONS OF SURGICAL TECHNIQUE
...
Published: 29/01/2026
Download PDF
Chat on WhatsApp
Copyright © EJCM Publisher. All Rights Reserved.