Abstract
Background
Valvular heart disease and intracardiac shunts can disrupt the balance between left ventricular (LV) and right ventricular (RV) stroke volumes. However, the prognostic value of such imbalances has not been established among asymptomatic individuals.
Purpose
To assess the association between differential ventricular stroke volumes quantified using cardiac MRI and clinical outcomes in individuals without cardiovascular disease.
Materials and Methods
This secondary analysis of a prospective study included participants without cardiovascular disease at enrollment (July 2000 to July 2002) who underwent cardiac MRI. Differences in stroke volume were calculated as LV stroke volume minus RV stroke volume, and participants were categorized as having balanced (greater than or equal to −30 mL to ≤30 mL), negative (less than −30 mL), or positive (>30 mL) differential stroke volumes. Multivariable Cox proportional hazard regression models were used to test the association between differences in stroke volume and adverse outcomes.
Results
A cohort of 4058 participants (mean age, 61.4 years ± 10 [SD]; 2120 female) were included and followed up for a median of 18.4 years (IQR, 18.3–18.5 years). During follow-up, 1006 participants died, 235 participants developed heart failure, and 764 participants developed atrial fibrillation. Compared with participants who had a balanced differential stroke volume, those with an increased differential stroke volume showed a higher risk of mortality (hazard ratio [HR], 1.73 [95% CI: 1.12, 2.67]; P = .01), heart failure (HR, 2.40 [95% CI: 1.11, 5.20]; P = .03), and atrial fibrillation (HR, 1.89 [95% CI: 1.16, 3.08]; P = .01) in adjusted models. Participants in the negative group, with a decreased differential stroke volume, showed an increased risk of heart failure compared with those in the balanced group (HR, 2.09 [95% CI: 1.09, 3.99]; P = .03); however, this was no longer observed after adjusting for baseline LV function (P = .34).
Conclusion
Participants without cardiovascular disease at the time of study enrollment who had an LV stroke volume exceeding the RV stroke volume by greater than 30 mL had an increased risk of mortality, heart failure, and atrial fibrillation compared with those with balanced stroke volumes.
ClinicalTrials.gov Identifier: NCT00005487
© RSNA, 2024
Supplemental material is available for this article.
See also the editorial by Almeida in this issue.
Summary
Differences between left and right ventricular stroke volumes of greater than 30 mL per heartbeat can be detected among asymptomatic individuals in a general population and are associated with adverse clinical outcomes.
Key Results
■ In this secondary analysis of a multicenter prospective study that included 4058 asymptomatic participants followed for up to 18 years, those with differences in left ventricular (LV) and right ventricular (RV) stroke volumes greater than 30 mL per heartbeat (n = 47) on cardiac MRI scans had an increased risk of mortality, heart failure, and atrial fibrillation compared with participants with differential stroke volumes from −30 to 30 mL (n = 3931) (hazard ratio [HR] range, 1.73–2.40; P value range, .01–.03).
■ Participants with differences in LV and RV stroke volumes less than −30 mL (n = 80) also had an increased risk of heart failure (HR, 2.09; P = .03), which was no longer observed after adjusting for baseline LV function (P = .34).
Introduction
Healthy individuals are expected to have equal left ventricular (LV) and right ventricular (RV) stroke volumes (1). While imbalance between LV and RV stroke volumes can arise under specific physiologic situations, balance is typically restored through length-tension compensatory processes (2). However, valvular heart disease and rarer diseases entailing anomalous communication between the systemic and pulmonary circulatory circuits, such as congenital intracardiac shunts, can produce a persistent imbalance between LV and RV stroke volumes (3,4).
Cardiac MRI provides highly accurate and reproducible assessment of cardiac chamber size and function, from which valvular regurgitation can be measured through the difference between LV and RV stroke volumes (hereafter, ΔSV) (5). In clinical practice, a dedicated cardiac MRI assessment to determine the clinical significance of valvular regurgitation uses phase-contrast imaging. Nevertheless, a key advantage of using ΔSV over other cardiac MRI measures for quantifying valvular regurgitation is its ability to be calculated from a single image acquisition. Current advancements in deep learning algorithms for accurate and reproducible automated quantification of ventricular size and function (6,7) allow greater access to ΔSV determination, making it easier to be integrate into routine cardiac MRI protocols. However, how differences between left and right ventricular stroke volumes impact prognosis remains underexplored.
Thus, the aim of this study was to assess the association between differential ventricular stroke volumes, determined by manual quantification of chamber volumes across the cardiac cycle using cardiac MRI, with clinical outcomes in individuals without a previous history of cardiovascular disease.
Materials and Methods
This secondary analysis of a prospective multicenter study was approved by institutional review boards at each field center, and all participants provided written informed consent (Appendix S1).
Study Participants
Details of the MESA (Multi-Ethnic Study of Atherosclerosis; ClinicalTrials.gov identification no. NCT00005487) study design have been described elsewhere (8). In brief, MESA includes a multiethnic (self-reported race and ethnicity as African American; Asian, predominantly of Chinese descent; Hispanic; and White) prospective cohort of participants aged 45–84 years without cardiovascular disease upon enrollment (July 2000 to July 2002). Individuals were recruited from six U.S. academic field centers (Baltimore, Maryland; Chicago, Illinois; Forsyth County, North Carolina; Los Angeles County, California; northern Manhattan, New York; St Paul, Minnesota). Those who underwent cine cardiac MRI with available LV and RV functional quantification were included in this study and followed up until December 2019. Those with missing ventricular volumes, covariates, or outcome data were excluded. Included participants answered clinical questionnaires and underwent physical examination, cardiac CT and MRI, and laboratory testing.
Participants were grouped based on a negative difference, positive difference, or balanced difference in LV and RV stroke volumes (Fig 1). The primary end point of this study was all-cause mortality, and secondary end points were incident heart failure and atrial fibrillation. Two independent physicians reviewed all records for outcome classification and assignment of event dates. To verify self-reported diagnoses, copies of all death certificates and medical records for all hospitalizations and outpatient cardiovascular diagnoses were requested. Details of studies that included part or all of the same participants as this study are provided in Table S1.
Figure 1:
Example images in participants with various differential ventricular stroke volumes. (A) Noncontrast cardiac MRI scan at end diastole in a 63-year-old Hispanic female participant with diabetes and a differential ventricular stroke volume of 35 mL shows a mitral regurgitant jet. The participant experienced atrial fibrillation 10 years later and died after 15 years of follow-up. (B) Noncontrast cardiac MRI scan at end diastole in a 59-year-old African American male participant with hypertension and a differential ventricular stroke volume of −35 mL shows a tricuspid regurgitant jet. The participant was still living and had not developed atrial fibrillation or heart failure after 17 years of follow-up. (C) Noncontrast cardiac MRI scan at end diastole in a 63-year-old male participant of Chinese descent who had no comorbidities and a differential ventricular stroke volume of 0 mL shows normal cardiac structure. The participant was still living and had not developed atrial fibrillation or heart failure after 19 years of follow-up.
Definitions
The outcomes in MESA were adjudicated by the MESA morbidity and mortality committee (8). Ascertainment protocols are available online (www.mesa-nhlbi.org). The definitions of outcomes are explained in Appendix S1. Follow-up was defined as the time from the initial study visit until the occurrence of end points, loss to follow-up, or end of follow-up.
Cardiac MRI Protocol
The cardiac MRI protocol has been previously reported (9,10) (Appendix S1). Briefly, cardiac MRI was performed using 1.5-T MRI scanners (Signa CV/i or Signa LX [GE HealthCare], Vision or Sonata [Siemens Healthineers]) with electrocardiographic gating and fast gradient-echo cine sequences, with a temporal resolution less than or equal to 50 msec.
Cardiac MRI Analysis
Image analysis was performed by trained MRI technologists, who were blinded to participant characteristics, using QMASS software (version 4.2; Medis Medical Imaging) on dedicated workstations at the central cardiac MRI review center at Johns Hopkins Hospital, Baltimore, Maryland. Methods for quantification of LV and RV structural and functional parameters have been previously described (11) and showed strong interreader and intrareader agreement (9,12). Remodeling parameters, including ventricular mass, atrial volumes, and functional and strain parameters, were also calculated as detailed in previous reports (13–19). ΔSV was calculated by subtracting the RV stroke volume from the LV stroke volume.
Two readers (A.A. and Y.K., with 2.5 and 13 years of experience in cardiac MRI), who were not blinded to participant characteristics, independently examined two-chamber, three-chamber, and four-chamber long-axis and short-axis cine images in participants from the positive and negative ΔSV groups to identify the presence of valvular heart disease. Any discrepancies were resolved by a third reader (J.A.C.L.). Additionally, one reader (A.A.) examined participants in the balanced ΔSV group who had dilation of at least one cardiac chamber to detect valvular regurgitation. A random sample of 200 participants in the balanced ΔSV group who had normal-sized cardiac chambers was also examined as reference. Details of chamber size adjudication are explained in Appendix S1.
Statistical Analysis
Penalized polynomial spline plots generated using unadjusted Cox proportional hazards models were used to define ΔSV cutoffs for clinical outcomes (Fig S1). Participants were categorized as follows: negative group, ΔSV less than −30 mL; balanced group, ΔSV between −30 mL and 30 mL; positive group, ΔSV greater than 30 mL. Continuous variables are presented as means ± SDs or medians with IQRs based on normality, and groups were compared using analysis of variance or the Kruskal-Wallis test. The Tukey-Kramer HSD (honestly significant difference) test and Bonferroni correction were used for pairwise group comparisons. Categorical variables are presented as counts and percentages, and groups were compared using the Fisher exact test or χ2 test. The median follow-up was calculated using the inverse Kaplan-Meier method. Survival, cumulative risk of heart failure, and cumulative risk of atrial fibrillation were deduced from Kaplan-Meier analysis and compared using the log-rank test. Univariable and multivariable Cox proportional hazards models were used to assess the association between time to events and ΔSV group (independent variable). As sensitivity analyses, two supplementary models were constructed to adjust for the LV and RV ejection fraction. Furthermore, Fine-Gray competing risk regression analysis was employed to identify the subdistribution hazard for incident heart failure and atrial fibrillation with death as a competing risk. The proportional hazards assumption was confirmed in each model using statistical methods and graphs based on the Schoenfeld residuals (Fig S2). A two-sided P < .05 was considered indicative of a statistically significant difference. All statistical analyses were performed by an author (A.A.) using R version 4.2.1 (The R Foundation).
Results
Participant Characteristics at Baseline
Of the 6814 participants enrolled in the MESA study, 4204 had cardiac MRI scans interpretable for the LV and RV. Of these, 146 were excluded due to missing stroke volumes, covariates, or outcome data (Fig 2). A total of 4058 participants (mean age, 61.4 years ± 10 [SD]; 2120 female, 1938 male) were included in this study (Table S2). The distribution of ΔSV is illustrated in Figure 3, and the mean ΔSV was 0.09 mL ± 12.3. Of the 4058 participants, 3931 (96.8%) were in the balanced ΔSV group, 47 (1.2%) were in the positive ΔSV group, and 80 (2.0%) were in the negative ΔSV group. The median follow-up period was 17 years (IQR, 16.9–17.1 years) for atrial fibrillation and 18.4 years (IQR, 18.3–18.5 years) for other outcomes. The positive ΔSV group had a higher mean systolic blood pressure (133.4 mm Hg ± 23.5, P = .01), median N-terminal pro–brain natriuretic peptide level (85.8 pg/mL [IQR, 37.9–253.6 pg/mL], P < .01), and mean Framingham risk score (17.1% ± 10.1, P < .01) compared with the balanced ΔSV group (Table 1). The negative ΔSV group had a lower proportion of female participants (13.8% [11 of 80], P < .001) and people who smoke (8.8% [seven of 80], P = .01) compared with both the balanced and positive ΔSV groups. No evidence of a difference in age, race and ethnicity, body mass index, heart rate, diastolic blood pressure, diabetes status, use of lipid-lowering medication, and estimated glomerular filtration rate was observed across ΔSV groups.
Figure 2:
Flowchart of participant selection. CMR = cardiac MRI, LV = left ventricle, MESA = Multi-Ethnic Study of Atherosclerosis, RV = right ventricle.
Figure 3:
Histogram shows the distribution of ΔSV, which was calculated by subtracting right ventricular stroke volume (RVSV) from left ventricular stroke volume (LVSV). Dashed vertical lines indicate a differential ventricular stroke volume of −30 mL and 30 mL, respectively, which is the range of distribution for the majority of the study sample.
Table 1:
Baseline Characteristics of Participants Stratified according to Differential Stroke Volume between the Left and Right Ventricles
Ventricular and Atrial Remodeling across ΔSV Groups at Baseline
Participants in the positive ΔSV group had higher LV volumes, LV mass, and sphericity indexes and lower mass to volume ratios than those in the balanced ΔSV group (Table 2). The mean LV ejection fraction was lower in the negative ΔSV group compared with both the positive and balanced ΔSV groups. Additionally, compared with the balanced ΔSV group, the mean LV global function index was higher in the positive ΔSV group and lower in the negative ΔSV group. Participants in the negative ΔSV group had higher RV volumes, higher RV ejection fractions, and lower RV mass to volume ratios compared with the balanced ΔSV group. Conversely, the positive ΔSV group had a lower mean RV end-diastolic volume and lower mean RV ejection fraction compared with both the balanced and negative ΔSV groups.
Table 2:
Baseline Ventricular and Atrial Remodeling in Participants Stratified according to Differential Stroke Volume between the Left and Right Ventricles
Similarly, the three groups showed differences in left atrial (LA) remodeling (Table 2). Participants in the positive ΔSV group had higher LA volumes than those in the negative or balanced ΔSV groups. In addition, the total LA emptying fraction was lower in the positive and negative ΔSV groups compared with the balanced ΔSV group. LA strain was lower in the negative ΔSV group compared with the balanced ΔSV group. There was no evidence of a difference among the three groups regarding right atrial volumes and function (Table 2).
Outcomes across ΔSV Groups
Long-term survival.—A total of 1006 participants died during follow-up. Participants in the positive ΔSV group had lower survival over 18 years of follow-up (57% [95% CI: 44, 73]) than those in the negative ΔSV (70% [95% CI: 60, 81]) and balanced ΔSV (75% [95% CI: 74, 77]) groups (P = .003) (Fig 4A, Appendix S1). Participants in the positive ΔSV group had a higher risk of mortality than participants in the balanced ΔSV group in the adjusted multivariable model 2 (hazard ratio [HR], 1.73 [95% CI: 1.12, 2.67]; P = .01) (Table 3) and after further adjustment for LV and RV function at baseline (Table S3).
Figure 4:
Kaplan-Meier curves show the (A) survival probability, (B) cumulative rate of heart failure, and (C) cumulative rate of atrial fibrillation stratified according to ΔSV group and compared using the log-rank test. ΔSV is defined as left ventricular stroke volume minus right ventricular stroke volume and categorized as follows: balanced, ΔSV greater than or equal to −30 mL to less than or equal to 30 mL; negative, ΔSV less than −30 mL; positive, ΔSV greater than 30 mL. Participants in the positive ΔSV group had lower survival (P = .003) and an increased rate of heart failure (P < .001) and atrial fibrillation (P < .001) compared with those in the balanced ΔSV group. Participants in the negative ΔSV group had an increased rate of heart failure compared with those in the balanced ΔSV group (P < .001).
Table 3:
Cox Proportional Hazard Analysis Assessing the Association between Severity of Differential Stroke Volume between the Left and Right Ventricles and Long-term Risk of Clinical Outcomes
Incident heart failure.—A total of 235 participants experienced heart failure. The cumulative rate of heart failure over 18 years of follow-up was higher in the positive ΔSV (16.7% [95% CI: 3.4, 28.2]) and negative ΔSV (15% [95% CI: 5.9, 23.3]) groups compared with the balanced ΔSV group (6.5% [95% CI: 5.7, 7.4]) (P < .001) (Fig 4B, Appendix S1). Participants in the positive ΔSV group had a higher risk of developing heart failure than participants in the balanced ΔSV group in the adjusted multivariable model 2 (HR, 2.40 [95% CI: 1.11, 5.20]; P = .03) (Table 3) and after adjusting for LV and RV function at baseline (Table S3). Participants in the negative ΔSV group also had a higher risk of developing heart failure than those in the balanced ΔSV group in the adjusted multivariable model 2 (HR, 2.09 [95% CI: 1.09, 3.99]; P = .03) (Table 3) and after adjusting for RV function at baseline (Table S3). In the multivariable Fine-Gray analysis, the negative ΔSV group still showed greater risk of developing heart failure than the balanced ΔSV group (HR, 2.20 [95% CI: 1.19, 4.07]; P = .01) (Table 4). However, no evidence of a difference was observed between the negative and balanced ΔSV groups in terms of risk of heart failure after adjusting for LV function (Tables S3, S4).
Table 4:
Fine-Gray Subdistribution Hazard Analysis Assessing the Association between Severity of Differential Stroke Volume between the Left and Right Ventricles and Long-term Risk of Clinical Outcomes with a Competing Event of Death
Incident atrial fibrillation.—A total of 764 participants developed atrial fibrillation during follow-up. The cumulative rate of atrial fibrillation was higher in the positive ΔSV group over 18 years of follow-up (41.5% [95% CI: 23.7, 55.1]) than in the negative ΔSV (27.9% [95% CI: 16.6, 37.7]) and balanced ΔSV groups (22.8% [95% CI: 21.3, 24.4]) (P < .001) (Fig 4C, Appendix S1). Participants in the positive ΔSV group had a greater risk of developing atrial fibrillation than those in the balanced ΔSV group in the adjusted multivariable model 2 (HR, 1.89 [95% CI: 1.16, 3.08]; P = .01) (Table 3) and after adjusting for baseline LV and RV function (Table S3). Similarly, in the fully adjusted Fine-Gray analysis, participants in the positive ΔSV group had a greater risk of developing atrial fibrillation than those in the balanced ΔSV group (HR, 1.75 [95% CI: 1.00, 3.07]; P = .05) (Table 4) and this greater risk remained after adjusting for LV and RV function at baseline (Table S4).
Valvular Regurgitation according to Visual Inspection of Cine MRI Scans
In the positive ΔSV group, 87.2% (41 of 47) of participants had visually confirmed mitral regurgitation, and 12.8% (six of 47) had isolated aortic regurgitation (Fig 5A). In the negative ΔSV group, 82.5% (66 of 80) of participants demonstrated tricuspid regurgitation, 2.5% (two of 80) had isolated mitral regurgitation, and 15% (12 of 80) showed no detectable valvular regurgitation on cardiac MRI scans (Fig 5B). In the balanced ΔSV group, 3422 participants had normal-sized cardiac chambers (Appendix S1). Among the 509 participants with at least one dilated cardiac chamber, 58.3% (297 of 509) were free of visually detectable valvular regurgitation, 27.5% (140 of 509) had concurrent mitral regurgitation and tricuspid regurgitation, 5.9% (30 of 509) had isolated mitral regurgitation, 4.5% (23 of 509) had tricuspid regurgitation, and 3.7% (19 of 509) had isolated aortic regurgitation (Fig 5C). In a random sample of 200 participants with normal cardiac chamber sizes, 4.5% (nine of 200) had mitral regurgitation, 1% (two of 200) had isolated tricuspid regurgitation, 1.5% (three of 200) had isolated aortic regurgitation, and the remaining 93% (186 of 200) did not show valvular regurgitation (Fig 5D).
Figure 5:
Pie charts show the distribution of valvular abnormalities among participants in the (A) positive ΔSV group (n = 47), (B) negative ΔSV group (n = 80), (C) balanced ΔSV group with at least one dilated cardiac chamber (n = 509), and (D) balanced ΔSV group with normal-sized cardiac chambers (n = 200). ΔSV is defined as left ventricular stroke volume minus right ventricular stroke volume and categorized as follows: balanced, ΔSV greater than or equal to −30 mL to less than or equal to 30 mL; negative, ΔSV less than −30 mL; positive, ΔSV greater than 30 mL. AR = aortic regurgitation, MR = mitral regurgitation, TR = tricuspid regurgitation.
Discussion
Valvular heart disease and intracardiac shunts associated with congenital heart disease can cause persistent disruption in the balance between ventricular stroke volumes. In this cohort study involving 4058 participants of diverse racial and ethnic backgrounds with no pre-existing cardiovascular disease, we investigated the association between differential ventricular stroke volumes quantified at cardiac MRI and clinical outcomes. Our findings indicate that differences between left ventricular (LV) and right ventricular (RV) stroke volumes can be detected among asymptomatic individuals. Participants with a larger LV stroke volume relative to RV stroke volume had a higher risk of mortality (hazard ratio [HR], 1.73 [95% CI: 1.12, 2.67]; P = .01), heart failure (HR, 2.40 [95% CI: 1.11, 5.20]; P = .03), and atrial fibrillation (HR, 1.89 [95% CI: 1.16, 3.08]; P = .01) during follow-up. Notably, increased risk for these outcomes was independent of both LV and RV function at baseline. Participants with a larger RV stroke volume relative to LV stroke volume had solely a higher risk of heart failure (HR, 2.09 [95% CI: 1.09, 3.99]; P = .03), but this increased risk was no longer observed after adjusting for baseline LV function (P = .34).
In our study cohort, we were able to visually detect mitral regurgitation in 87.2% of participants with ΔSV greater than 30 mL. Notably, these participants displayed larger (mean LV end-diastolic volume index, 87.7 mL/m2; P < .001) and more spherical LVs (mean LV sphericity volume index at end diastole, 0.32; P < .01), indicating eccentric LV remodeling, as well as increased LA dimensions (mean minimal LA volume index, 23.9 mL/m2; P < .001) and decreased LA function (mean total LA emptying fraction, 43.8%; P < .01), reflecting increased mitral regurgitant volume. Most importantly, our findings showed an increase in the risk of mortality, heart failure, and aortic regurgitation for participants with ΔSV greater than 30 mL per heartbeat, a cutoff value suggested by the clinical guidelines to classify mitral regurgitation as moderate to severe (5). Mitral regurgitation is the most common type of clinically significant left-sided valvular heart disease (20). However, individuals with subclinical moderate to severe mitral regurgitation may remain asymptomatic for years (21). With long-standing mitral regurgitation, continuous LV volume overload results in remodeled ventricular geometry, establishing a vicious cycle in which mitral regurgitation perpetuates its own progression (21). As transcatheter interventions for the treatment of mitral regurgitation continue to show promising results (22), early detection of this condition in asymptomatic individuals has become increasingly important. Another pathologic cause of greater LV stroke volume compared with RV stroke volume in asymptomatic individuals is aortic regurgitation (23). Considering the lower prevalence of aortic regurgitation versus mitral regurgitation in community studies (20), and that asymptomatic individuals with severe aortic regurgitation and normal LV function often remain stable for a long period of time (24), mitral regurgitation may be driving adverse outcomes in those with positive ΔSV in this study.
There is a paucity of data regarding the prevalence of pulmonary regurgitation in community-based cohort studies. However, pulmonary regurgitation is unlikely to be commonly found among healthy middle-aged or older individuals who are free of known cardiovascular conditions, including congenital heart disease (25), as in the MESA baseline cohort. Therefore, tricuspid regurgitation is the most common etiology for a relatively greater RV stroke volume compared with LV stroke volume among asymptomatic individuals (26), as suggested by our findings. In our study, 82.5% of participants with ΔSV less than −30 mL was identified as having tricuspid regurgitation, with 45% of them having concurrent mitral regurgitation. Compared with individuals with ΔSV within the −30 to 30 mL range, and those with ΔSV greater than 30 mL, participants with ΔSV less than −30 mL had a lower LV ejection fraction while exhibiting a higher RV ejection fraction, suggesting a compensatory mechanism most commonly associated with tricuspid regurgitation. Also, in the negative ΔSV group, the mean LV global function index, which integrates assessment of LV structure with overall function, was observed to be lower (32.5%) than the 37% threshold previously linked to increased risk of heart failure in MESA (17). While we found that participants with ΔSV less than −30 mL had a greater risk of heart failure, this was no longer observed after adjusting for baseline LV function. Together these findings suggest that the negative ΔSV seen in this group stems from RV eccentric remodeling associated with tricuspid regurgitation, secondary to left heart disease.
Our study had several limitations. First, the cardiac MRI scans used in this analysis were acquired to assess cardiac structure and function, and not specifically for visual assessment of valvular heart disease. Consequently, our capacity to visually identify valvular pathologies was limited, restricting our ability to precisely identify the mechanism of imbalance between LV and RV stroke volumes. Despite such limitations, we visually reviewed all imaging studies with clinically significant stroke volume imbalances, as well as a large sample of studies with balanced stroke volumes, to probe for the presence of valvular heart disease. This strategy was used as an exploratory tool rather than a method to rule in or rule out valve abnormalities. Second, the studies were reviewed by MRI readers who were not blinded to participant data, which may have introduced confirmation bias in determining valvular regurgitation. Third, the same data were used for determining ΔSV cutoffs and correlating them with clinical outcomes.
In conclusion, participants with no known cardiovascular disease at the time of study enrollment who had a left ventricular stroke volume exceeding right ventricular stroke volume by greater than 30 mL, as quantified on cardiac MRI scans, showed an increased risk of mortality, heart failure, and atrial fibrillation compared with participants with balanced stroke volumes during a 17–18-year follow-up period. Quantifying differential ventricular stroke volumes at cardiac MRI could aid in the early detection of valvular heart disease in individuals who would benefit from dedicated assessment, as well as allow identification of those at risk for adverse events, thereby facilitating timely surveillance for progressive valvular heart disease. Further studies are required to determine the mechanisms underlying ventricular stroke volume imbalances and confirm their associations with long-term outcomes in asymptomatic individuals.
Acknowledgments
Acknowledgments
We thank the other investigators, the staff, and the participants of MESA for their valuable contributions. A complete list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org.
Supported by the National Heart, Lung, and Blood Institute (contracts N01-HC-95159, N01-HC-95160, N01-HC-95161, N01-HC-95162, N01-HC-95163, N01-HC-95164, N01-HC-95165, N01-HC-95166, N01-HC-95167, N01-HC-95168, N01-HC-95169) and National Center for Research Resources (grants UL1-TR-000040, UL1-TR-001079) of the National Institutes of Health.
Data sharing: Data analyzed during the study were provided by a third party. Requests for data should be directed to the provider indicated in the Acknowledgment.
Disclosures of conflicts of interest: A.A. No relevant relationships. Y.K. No relevant relationships. H.B. No relevant relationships. V.V. No relevant relationships. O.C. No relevant relationships. R.Z. No relevant relationships. M.R.O. No relevant relationships. C.O.W. No relevant relationships. A.G.B. No relevant relationships. S.J.S. No relevant relationships. B.A.V. No relevant relationships. D.A.B. Editor emeritus for Radiology; member of the RSNA Publications Ethics Committee. J.A.C.L. Associate editor for Radiology.
Abbreviations:
- HR
- hazard ratio
- LA
- left atrium
- LV
- left ventricle
- MESA
- Multi-Ethnic Study of Atherosclerosis
- RV
- right ventricle
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