Ventricular function

Left Ventricle

Stroke Volume (SV)

Stroke volume is the amount of blood pumped by one ventricle during a contraction (Silverthorn et al. 2013).

  • Definition: Difference between EDV and ESV.

  • Calculation: LVSV = LVEDV − LVESV

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderReference Value (mL)Note
    (Kawel-Boehm et al. 2020)410male(103, 21)papillary muscles included in mass
    432female(83, 16)papillary muscles included in mass
    832male(91, 18)papillary muscles included in volume
    1064female(73, 13)papillary muscles included in volume
    (Hudsmith et al. 2005)63male(112, 19)
    45female(91, 17)
    (Aquaro et al. 2019)25(69, 16)
    (Suinesiaputra et al. 2018)4413(84.9, 19.2)48% male in full cohort with size 4874
    (Petersen et al. 2017)368male59-132
    432female49-100
    (Le Ven et al. 2016)196male(112, 19)average age 26.7 years
    238female(84, 13)average age 25.8 years
  • Clinical Associations: Stroke volume is reduced in patients with DCM (Carlsson et al. 2007) and HFpEF (Marwick 2018).

  • ICC: 0.76

Ejection Fraction (EF)

In addition to the stroke volume, the volume of blood ejected from the ventricle in one contraction can also be expressed in ejection fraction (EF) (Silverthorn et al. 2013). EF reflects both cardiac functional and remodeling, and is widely recognized as a valuable diagnostic and prognostic tool. Its use in a variety of settings, ranging from heart failure and myocardial infarction to valvular heart disease, has made it a cornerstone of modern cardiology. In general, EF is more informative than stroke volume as a functional marker (Marwick 2018). Patients with symptomatic heart failure (HF) can be classified into those with preserved ejection fraction (HFpEF) and those with reduced ejection fraction (HFrEF). Nevertheless, patients with HFpEF do not have normal systolic function.

  • Definition: The fraction of blood ejected from the left ventricle during systole (stroke volume) relative to the volume present at end-diastole (end-diastolic volume).

  • Calculation: LVEF = LVSV/LVEDV

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderAgeReference Value (%)Note
    (Kawel-Boehm et al. 2020)875male(64, 8)papillary muscles included in mass
    931female(66, 7)papillary muscles included in mass
    51male20-29(60, 7)papillary muscles included in mass
    105male30-39(63, 7)papillary muscles included in mass
    110male40-49(62, 7)papillary muscles included in mass
    78male50-59(63, 7)papillary muscles included in mass
    34male60-69(62, 7)papillary muscles included in mass
    43female20-29(62, 6)papillary muscles included in mass
    110female30-39(64, 6)papillary muscles included in mass
    127female40-49(63, 7)papillary muscles included in mass
    93female50-59(65, 6)papillary muscles included in mass
    41female60-69(65, 6)papillary muscles included in mass
    832male(63, 6)papillary muscles included in volume
    1064female(66, 7)papillary muscles included in volume
    (Assadi et al. 2023)169(62, 11)96 males, 73 females
    (Kono et al. 1991)8(76, 1)5 males, 3 females
    (Rahimtoola et al. 1975)10(64, 5)
    (Suinesiaputra et al. 2018)4413(59.4, 6.4)48% male in full cohort with size 4874
    (Petersen et al. 2017)368male48-69
    432female51-70
    (Hasselberg et al. 2021)16(64, 7)5 males, 11 females, average age 47 years
  • Clinical Associations:

    Ejection fraction is lower in patients with pulmonary arterial hypertension (PAH) (Lindholm et al. 2022). In patients with heart failure, an EF < 35% is significantly associated with malignant arrhythmias and sudden cardiac death (SCD) (Marwick 2018). In HFrEF and ischemic heart disease, both LVEDV and LVESV may increase, leading to preserved LVSV but reduced LVEF (Marwick 2018). Higher LVEF is associated with a linear reduction in mortality up to 45% in patients with HF (Kosaraju et al. 2024). Impaired contractility, reflected by an LVEF < 40%, is a hallmark of dilated cardiomyopathy (DCM) (Mahmaljy, Yelamanchili, and Singhal 2023), while significantly reduced LVEF is also observed in cardiac amyloidosis and left ventricular non-compaction (LVNC) compared with healthy individuals (Bogunovic et al. 2022). Following myocardial infarction (MI), patients without LVEF recovery face a higher risk of SCD (Chew et al. 2018). In those with prior MI and an LVEF < 30%, implantation of an implantable cardioverter-defibrillator (ICD) is associated with a significant reduction in both SCD and all-cause mortality (Kosaraju et al. 2024). In valvular disease, LVEF is critical for decision-making. In severe mitral regurgitation (MR), an LVEF < 60% indicates abnormal LV function (Baumgartner et al. 2017). In aortic regurgitation (AR), an LVEF < 50%, together with regurgitant severity, guides surgical referral, and reduced LVEF confers poorer prognosis even in asymptomatic patients (Dujardin et al. 1999). For aortic stenosis (AS), valve replacement is recommended in asymptomatic patients with severe AS or chronic severe AR when LVEF < 50%, and mitral valve surgery is considered when LVEF ≤ 60% (Kosaraju et al. 2024). Beyond structural disease, LVEF remains the gold standard for diagnosing cardiotoxicity, defined by a value < 50% or a decline of more than 10% from baseline (Park 2019).

  • ICC: 0.52

Cardiac Output (CO)

Cardiac output is one of the approaches to assess the effectiveness of the heart as a pump, by measuring the volume of blood pumped by one ventricle in a given period of time, usually in 1 minute(Silverthorn et al. 2013). There are four determinants of the cardiac output: heart rate, contractility, preload and afterload (Vincent 2008): The heart rate is the simplest determinant of cardiac output, as the faster the heart beats, the more blood can be pumped over the particular period of time. Once the contractility is impaired, the cardiac output will be reduced as well. Preload refers to the degree of myocardial distension prior to shortening. As demonstrated in Frank-Starling law, the greater the stretch within certain limits, the greater the force of contraction, which will increase cardiac output. Afterload is the force against which ventricles must act in order to eject blood. Reducing afterload can increase cardiac output, especially where contractility is impaired.

  • Definition: Percentage of EDV ejected with one contraction

  • Calculation: CO = Heart Rate (HR) × LVSV

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderReference Value (L/min)Note
    (Kawel-Boehm et al. 2020)91male(5.6, 1.1)papillary muscles included in mass
    89female(4.5, 0.9)papillary muscles included in mass
    (Kawel-Boehm et al. 2020)464male(6.1, 1.1)papillary muscles included in volume
    632female(4.9, 1.0)papillary muscles included in volume
  • ICC: 0.64

Cardiac Index (CI)

  • Definition: Cardiac output indexed to BSA

  • Calculation: CI = CO/BSA

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderReference Value (L/min/m<sup>2</sup>)Note
    (Kawel-Boehm et al. 2020)91male(3.0, 0.6)papillary muscles included in mass
    89female(2.9, 0.5)papillary muscles included in mass
    (Kawel-Boehm et al. 2020)464male(3.2, 0.6)papillary muscles included in volume
    632female(2.9, 0.5)papillary muscles included in volume
    (Rahimtoola et al. 1975)10(3.6, 0.9)
  • Clinical Associations: Cardiac index is lower in patients with congestive HF (Carlsson et al. 2012).

  • ICC: 0.51

Peak Filling Rate (PFR)

Once the ventricular volume/time (V/t) curve is obtained by plotting the cavity volumes over time, the corresponding ventricular dV/dt curve can be derived. There are two positive peaks PFR-E and PFR-A, each indicating the maximum speed of passive filling and that secondary to atrial contraction respectively (Aquaro et al. 2019). Between the two peaks, a zone of almost zero speed is normally present and represents the phase of diastasis, where blood flows passively from the atria to the ventricles at a slower rate due to balanced pressures during mid-diastole.

<figure> <img src="/latex/images/ventricle/PFR.png" id="fig:PFR" alt="Volume/time (V/t) curve and dV/dt curve of left ventricle from which early peak filling rate and atrial peak filling rate can be derived (Aquaro et al. 2019)." /><figcaption aria-hidden="true">Volume/time (V/t) curve and dV/dt curve of left ventricle from which early peak filling rate and atrial peak filling rate can be derived <span>(Aquaro et al. 2019)</span>.</figcaption> </figure>

  • Definition: Early peak filling rate (PFR-E) is the first positive peak of the ventricular dV/dt curve. Atrial peak filling rate (PFR-A) is the second positive peak (Aquaro et al. 2019).

  • Acquisition Type: SAX, LAX

  • Reference Range:

    • PFR-E:

      StudyCohort SizeGenderAgeReference Value (mL/s)Note
      (Aquaro et al. 2019)25(375, 63)11 males, 9 females, average age 51 years
      (Ruijsink et al. 2020)304male45-54239-594
      384male55-64202-537
      241male65-74167-496
      297female45-54231-497
      322female55-64207-436
      213female65-74179-425
      (Erdei et al. 2022)12(581, 100)7 males, 5 females, average age 33 years
      (Sharifov et al. 2023)8(324, 97)6 males, 2 females
      (A. Maceira et al. 2006)10male20-29484-1034
      10male30-39392-941
      10male40-49299-848
      10male50-59206-756
      10male60-69114-663
      10female20-29393-967
      10female30-39312-886
      10female40-49231-805
      10female50-59150-724
      10female60-6969-642
      (Grassedonio et al. 2015)43(423,29)19 males, 24 females, average age 41 years
    • PFR-A:

      StudyCohort SizeGenderAgeReference Value (mL/s)Note
      (Aquaro et al. 2019)25(177, 56)11 males, 9 females, average age 51 years
      (Ruijsink et al. 2020)304male45-5477-431
      384male55-64102-436
      241male65-7463-382
      297female45-5454-355
      322female55-6473-373
      213female65-7482-386
      (Erdei et al. 2022)12(220, 101)7 males, 5 females, average age 33 years
      (Sharifov et al. 2023)8(210, 97)6 males, 2 females
      (A. Maceira et al. 2006)10male20-2999-421
      10male30-39144-467
      10male40-49189-512
      10male50-59234-557
      10male60-69279-602
      10male70-79324-647
      10female20-2958-327
      10female30-3995-364
      10female40-49131-400
      10female50-59167-436
      10female60-69203-472
      10female70-79239-508
      (Grassedonio et al. 2015)43(219,107)19 males, 24 females, average age 41 years
  • Clinical Associations: Hypertensive patients with reduced global longitudinal strain exhibit a slower PFR-E and an increased PFR-A (Erdei et al. 2022). Reduced PFR-E is also observed in patients with familial amyloid polyneuropathy (Hongo et al. 1989) and PAH (Göransson, Vejlstrup, and Carlsen 2017).

  • ICC:

    • PFR-E: Note: 0.31

    • PFR-A: Note: 0.20

Right Ventricle

Stroke Volume

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderAgeReference Value (mL)Note
    (A. M. Maceira et al. 2006)10male20-2974-143
    10male30-3974-142
    10male40-4973-141
    10male50-5972-140
    10male60-6971-139
    10male70-7970-138
    10female20-2961-112
    10female30-3959-111
    10female40-4958-109
    10female50-5956-108
    10female60-6955-106
    10female70-7953-105
    (Kawel-Boehm et al. 2020)896male(95, 26)
    977female(74, 18)
    (Petersen et al. 2017)368male62-131
    432female48-99
  • ICC: 0.77

Ejection Fraction

  • Acquisition Type: SAX, LAX

  • Reference Range:

    StudyCohort SizeGenderAgeReference Value (%)Note
    (A. M. Maceira et al. 2006)10male20-2948-74
    10male30-3950-76
    10male40-4952-77
    10male50-5953-79
    10male60-6955-81
    10male70-7957-83
    10female20-2949-73
    10female30-3951-75
    10female40-4953-77
    10female50-5955-79
    10female60-6957-81
    10female70-7959-83
    (Kawel-Boehm et al. 2020)1069male(57, 8)
    1112female(60, 7)
    50male20-29(52, 8)
    55male30-39(55, 7)
    49male40-49(57, 8)
    55male50-59(57, 8)
    47female20-29(56, 11)
    51female30-39(58, 9)
    46female40-49(60, 8)
    46female50-59(61, 8)
    (Petersen et al. 2017)368male45-65
    432female47-68
  • Clinical Associations: RV EF is a powerful and independent predictor of major adverse cardiac events after adjusting for covariates including LV EF, with broad generalizability across patients with known or suspected cardiovascular disease (Purmah et al. 2021). Patients with Ebstein’s anomaly tend to have lower RV EF (Lee et al. 2013).

  • ICC: 0.58

Peak Filling Rate

  • Acquisition Type: SAX, LAX

  • Reference Range:

    • PFR-E:

      StudyCohort SizeGenderAgeReference Value (mL/s)Note
      (A. M. Maceira et al. 2006)10male20-29277-814
      10male30-39223-760
      10male40-49169-706
      10male50-59116-652
      10male60-6962-599
      10male70-798-545
      10female20-29241-701
      10female30-39189-649
      10female40-49137-598
      10female50-5986-546
      10female60-6934-494
    • PFR-A

      StudyCohort SizeGenderAgeReference Value (mL/s)Note
      (A. M. Maceira et al. 2006)10male20-2923-709
      10male30-3970-756
      10male40-49118-804
      10male50-59165-852
      10male60-69213-899
      10male70-79260-947
      10female20-2954-656
      10female30-3959-660
      10female40-4964-665
      10female50-5969-670
      10female60-6974-675
      10female70-7979-680

Strain and Strain Rate*

RV deformation can be quantified as global longitudinal strain, incorporating both the interventricular septum and the RV free wall, or as RV free wall longitudinal strain, which includes only the three free wall segments and is more commonly recommended in clinical practice (Smiseth et al. 2024). RV longitudinal strain is more sensitive to subtle myocardial dysfunction than conventional indices of RV performance such as RV EF (Muraru et al. 2022). Typically, RV deformation measures approximately 30% in the longitudinal direction and 15% in the circumferential direction, while LA deformation tends to be lower longitudinally and higher circumferentially (Muraru et al. 2022).

  • Acquisition Type: SAX, LAX, Tagged MRI

  • Reference Range: Due to the conflicting data and inter-vendor variability of segmental longitudinal strain, it is not possible to propose any reference ranges of segmental RV longitudinal strain for clinical use: A significant base-to-apex segmental strain gradient is observed in the RV free wall in children and in one adult study, while other studies with adult population found all segments of RV free wall having similar RV LS values. Conversely, basal segments are reported as having either the highest or the lowest values among the three RV free wall segments. (Muraru et al. 2022).

    Reported normal values can be found in (Fine et al. 2013), (Chia et al. 2014), (McGhie et al. 2017), (Morris et al. 2017) (Park et al. 2018) and (Addetia et al. 2021)

  • Clinical Associations: The longitudinal and circumferential RV strains are reduced in patients with TOF (Kempny et al. 2012). The reduced RV longitudinal strain is associated with higher risk of mortality for patients with PAH or idiopathic pulmonary fibrosis, and also signals acute pulmonary embolism (PE), RV failure as well as RV myocardial fibrosis (Park 2019).

    In heart failure, RV LS reflects systolic performance and predicts adverse outcomes, including RV failure after left ventricular assist device implantation and poor prognosis in DCM caused by lamin A/C mutations. In arrhythmogenic cardiomyopathy (ACM), RV LS identifies early RV involvement, enhances risk stratification for ventricular arrhythmias, and detects asymptomatic mutation carriers. Reduced RV LS is also observed in athletes with ventricular arrhythmias, mimicking ACM-like remodeling patterns. In pulmonary hypertension (PH), RV LS serves as an independent predictor of functional capacity, RV failure, and survival. In systemic sclerosis (SSc), regional RV LS abnormalities, particularly a basal–apical gradient, are linked to pulmonary fibrosis and PH, even when overall RV function appears preserved. In valvular heart disease, RV LS impairment is common in AS, especially in low-flow, low-gradient AS with reduced LV EF, where it independently predicts mortality. In patients undergoing transcatheter aortic valve replacement (TAVR), pre-procedural reduction in RV LS is associated with low cardiac output and worse post-interventional outcomes. In mitral regurgitation (MR), impaired RV LS relates to elevated pulmonary pressures and worse prognosis after surgery; post-operative recovery of RV LS predicts myocardial recovery and lower risk of heart failure hospitalization. In tricuspid regurgitation (TR), reduced RV LS independently predicts long-term survival and post-operative outcomes, even beyond TR severity. In congenital heart disease, RV LS reflects altered loading conditions and adaptive remodeling: it decreases after atrial septal defect (ASD) closure due to reduced volume load, and in repaired tetralogy of Fallot (TOF), impaired RV LS correlates with pulmonary regurgitation severity and reduced exercise capacity. In patients with transposition of the great arteries (TGA) or congenitally corrected TGA, RV LS is an independent predictor of adverse events, including symptomatic deterioration and arrhythmias (Muraru et al. 2022).

<figure> <img src="/latex/images/strain/RV_strain_disease.png" id="fig:RV_strain_disease" alt="Additive value of RV LS to conventional parameters of RV systolic function in different clinical settings (Muraru et al. 2022)." /><figcaption aria-hidden="true">Additive value of RV LS to conventional parameters of RV systolic function in different clinical settings <span>(Muraru et al. 2022)</span>.</figcaption> </figure>

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