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Figure 1.  Simultaneous Assessment of Ejection Times in the Pulmonary Artery and Aorta
Simultaneous Assessment of Ejection Times in the Pulmonary Artery and Aorta

A, Tracings from a patient with constrictive pericarditis showing significantly decreased ejection time of the aorta in inspiration corresponding with a significantly increased ejection time of the pulmonary artery. B, Tracings from a patient with restrictive cardiomyopathy, showing no respiratory variation in ejection time in the aorta and a slight decrease in ejection time with inspiration in the pulmonary artery.

Figure 2.  Scatterplot of Assessment for Ventricular Interdependence
Scatterplot of Assessment for Ventricular Interdependence

Ventricular interdependence is reflected by comparing the respirophasic differences in ejection times (ET) in the aorta (Ao; A), pulmonary artery (PA; B), and the difference between the 2 (C) in patients with constrictive pericarditis and those without. There were significant differences between groups for ETs in the PA, as well as the difference in Ao ET and PA ET.

Table.  Patient Characteristics and Hemodynamics
Patient Characteristics and Hemodynamics
1.
Connolly  DC, Wood  EH.  Cardiac catheterization in heart failure and cardiac constriction.   Trans Am Coll Cardiol. 1957;7:191-201.PubMedGoogle Scholar
2.
Nishimura  RA, Connolly  DC, Parkin  TW, Stanson  AW.  Constrictive pericarditis: assessment of current diagnostic procedures.   Mayo Clin Proc. 1985;60(6):397-401. doi:10.1016/S0025-6196(12)60850-7PubMedGoogle ScholarCrossref
3.
Geske  JB, Anavekar  NS, Nishimura  RA, Oh  JK, Gersh  BJ.  Differentiation of constriction and restriction: complex cardiovascular hemodynamics.   J Am Coll Cardiol. 2016;68(21):2329-2347. doi:10.1016/j.jacc.2016.08.050PubMedGoogle ScholarCrossref
4.
Nishimura  RA.  Constrictive pericarditis in the modern era: a diagnostic dilemma.   Heart. 2001;86(6):619-623. doi:10.1136/heart.86.6.619PubMedGoogle ScholarCrossref
5.
Syed  FF, Schaff  HV, Oh  JK.  Constrictive pericarditis—a curable diastolic heart failure.   Nat Rev Cardiol. 2014;11(9):530-544. doi:10.1038/nrcardio.2014.100PubMedGoogle ScholarCrossref
6.
Miranda  WR, Oh  JK.  Constrictive pericarditis: a practical clinical approach.   Prog Cardiovasc Dis. 2017;59(4):369-379. doi:10.1016/j.pcad.2016.12.008PubMedGoogle ScholarCrossref
7.
Nishimura  RA, Carabello  BA.  Hemodynamics in the cardiac catheterization laboratory of the 21st century.   Circulation. 2012;125(17):2138-2150. doi:10.1161/CIRCULATIONAHA.111.060319PubMedGoogle ScholarCrossref
8.
Hurrell  DG, Nishimura  RA, Higano  ST,  et al.  Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis.   Circulation. 1996;93(11):2007-2013. doi:10.1161/01.CIR.93.11.2007PubMedGoogle ScholarCrossref
9.
Talreja  DR, Nishimura  RA, Oh  JK, Holmes  DR.  Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory.   J Am Coll Cardiol. 2008;51(3):315-319. doi:10.1016/j.jacc.2007.09.039PubMedGoogle ScholarCrossref
10.
Kligfield  P, Okin  P, Devereux  RB, Goldberg  H, Borer  JS.  Duration of ejection in aortic stenosis: effect of stroke volume and pressure gradient.   J Am Coll Cardiol. 1984;3(1):157-161. doi:10.1016/S0735-1097(84)80443-XPubMedGoogle ScholarCrossref
11.
Weissler  AM, Peeler  RG, Roehll  WH  Jr.  Relationships between left ventricular ejection time, stroke volume, and heart rate in normal individuals and patients with cardiovascular disease.   Am Heart J. 1961;62:367-378. doi:10.1016/0002-8703(61)90403-3PubMedGoogle ScholarCrossref
12.
Gonzalez  MS, Basnight  MA, Appleton  CP.  Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration.   J Am Coll Cardiol. 1991;18(1):243-252. doi:10.1016/S0735-1097(10)80246-3PubMedGoogle ScholarCrossref
13.
Gorlin  R, Gorlin  SG.  Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves, and central circulatory shunts. I.   Am Heart J. 1951;41(1):1-29. doi:10.1016/0002-8703(51)90002-6PubMedGoogle ScholarCrossref
14.
Leighton  RF, Zaron  SJ, Robinson  JL, Weissler  AM.  Effects of atrial pacing on left ventricular performance in patients with heart disease.   Circulation. 1969;40(5):615-622. doi:10.1161/01.CIR.40.5.615PubMedGoogle ScholarCrossref
15.
Shabetai  R, Fowler  NO, Guntheroth  WG.  The hemodynamics of cardiac tamponade and constrictive pericarditis.   Am J Cardiol. 1970;26(5):480-489. doi:10.1016/0002-9149(70)90706-XPubMedGoogle ScholarCrossref
Brief Report
September 22, 2021

A Simplified Method for the Diagnosis of Constrictive Pericarditis in the Cardiac Catheterization Laboratory

Author Affiliations
  • 1Department of Cardiovascular Medicine, Mayo Clinic, Rochester, Minnesota
  • 2Department of Cardiovascular Medicine, Mayo Clinic, Jacksonville, Florida
JAMA Cardiol. 2022;7(1):100-104. doi:10.1001/jamacardio.2021.3478
Key Points

Question  In patients being evaluated for possible constrictive pericarditis, is there a simpler way to assess for enhanced ventricular interdependence in the catheterization laboratory?

Findings  In this diagnostic study including 20 patients with and without constrictive pericarditis, comparison of ejection times in the pulmonary artery and ascending aorta was an accurate method to assess for enhanced ventricular interdependence.

Meaning  Evaluation of ejection times can simplify the invasive assessment for constriction, particularly when high-fidelity micromanometers are not available and frequent catheter-induced ventricular ectopy or mechanical aortic prostheses are present.

Abstract

Importance  Enhanced ventricular interdependence is a highly sensitive and specific criterion for the diagnosis of constrictive pericarditis (CP), but simultaneous ventricular measurements can be challenging at cardiac catheterization. Ejection times (ETs) correlate with stroke volumes and can be easily measured from arterial pressure tracings.

Objective  To assess respirophasic changes in pulmonary artery (PA) ETs and aorta (Ao) ETs as a marker for enhanced ventricular interdependence.

Design, Setting, and Participants  Retrospective analysis of simultaneous left-side and right-side heart catheterizations between January 2006 and January 2017 was performed. The data were analyzed in June 2020. All catheterizations were performed at the Mayo Clinic, Rochester, Minnesota. This study evaluated patients undergoing left-side and right-side heart catheterization for assessment of CP after noninvasive evaluation was inconclusive.

Main Outcomes and Measures  Measurements of the PA and Ao ETs were made during inspiration and expiration. Ventricular interaction was mainly assessed by evaluating the difference of ETs from expiration to inspiration as well as the difference in Ao minus the difference in PA.

Results  A total of 10 patients with surgically proven CP and 10 patients without CP (restrictive cardiomyopathy or severe tricuspid regurgitation) were identified. Of these 20 included patients, 10 (50%) were female, and the median (interquartile range) age was 59.5 (47.0-67.5) years. There were no significant differences in demographic characteristics or baseline hemodynamic measurements. In patients with CP compared with those without CP, there was a significantly greater decrease in PA ET (mean [SD], −31.8 [28.6] vs 5.1 [9.5]; P < .001) and a nonsignificantly greater increase in Ao ET (mean [SD], 19.0 [15.7] vs 10.5 [9.1]; P = 0.20) during expiration vs inspiration. Thus, the difference in Ao ET minus the difference in PA ET during expiration vs inspiration was significantly greater in those with CP compared with those without CP (mean [SD], 50.8 [22.5] milliseconds vs 5.4 [15.2] milliseconds; P < .001).

Conclusions and Relevance  In this study, PA and Ao measurements of ETs throughout the respiratory cycle were a simple, easily obtainable, and accurate parameter for the diagnosis of CP.

Introduction

Constrictive pericarditis (CP) remains a difficult diagnostic challenge. It must be differentiated from other diseases that present with predominant right-sided heart failure, such as restrictive cardiomyopathy (RCM) and severe tricuspid valve regurgitation (TR).1-4 Despite advances in multimodality imaging, invasive catheterization may still be needed, but conventional criteria of early rapid filling and end equalization of diastolic pressures have been shown to be nondiagnostic. Enhanced ventricular interaction determined by analysis of left ventricular (LV) and right ventricular (RV) pressure contours during the respiratory cycle is a highly sensitive and specific finding in individuals with CP.2,5-7 However, this subtle finding frequently requires simultaneous high-fidelity micromanometer tracings in the LV and RV, which are limited to operators and cardiac laboratories that are facile with their use.8,9 The ability to detect enhanced ventricular interaction may also be impaired by catheter-induced ectopy or mechanical impediments to direct ventricular measurements (eg, prosthetic valves). Thus, it would be valuable to have easily obtained, reliable parameters to determine the presence or absence of enhanced ventricular interaction.

Aortic and pulmonic ejection time (ET) measurements are a reflection of left-sided and right-sided stroke volumes, respectively.10,11 Accordingly, we sought to evaluate ETs in the pulmonary artery (PA) and aorta (Ao) as surrogates for respirophasic changes in RV and LV stroke volumes9 in patients undergoing catheterization for evaluation of severe right-sided heart failure.

Methods

Retrospective analysis of patients undergoing left-sided and right-sided heart catheterization for invasive assessment for CP was performed at the Mayo Clinic, Rochester, Minnesota, between January 2006 through January 2017. All patients underwent cardiac catheterization for further evaluation when noninvasive testing was inconclusive. Ten consecutive patients with surgically proven CP, 5 patients with RCM, and 5 patients with severe TR who had simultaneous Ao and PA tracings available for review were selected. This study was approved by the Mayo Clinic Institutional Review Board and only patients who provided written informed consent were included. The study followed Standards for Reporting of Diagnostic Accuracy (STARD) reporting guideline.

Clinical history, laboratory, and imaging data were abstracted from the medical record. Invasive hemodynamic pressures were recorded as computerized means and averaged over 6 to 8 consecutive beats. ETs (measured in milliseconds) were manually recorded from systolic upstroke to dicrotic notch with a sweep speed of 100 mm/s. Measurements were taken at peak inspiration and expiration in patients breathing spontaneously (Figure 1) with care taken to avoid split beats.12 Peak inspiration was defined as the diastolic nadir of pressures over a respiratory cycle while peak expiration was defined as the maximum systolic pressure. The difference of ETs from expiration to inspiration was calculated. All measurements were performed in blinded fashion by 1 author (W.R.M.). Subsequent measurements of 5 consecutive patients were also performed by 2 of us (C.C.J. and W.R.M.) for assessment of intra- and interobserver variability.

Given the sample size, statistical analysis was performed using rank sum and Fisher exact test. Matched pair analysis was used to compare difference of timing intervals between inspiration and expiration. Interclass correlation coefficients were assessed for intraobserver and interobserver variability. P values were 2-tailed with a level of significance of P < .05, and the statistical software used was JMP, version 14.1 (SAS Institute).

Results

Of the 20 included patients, 10 (50%) were female, and the median (interquartile range) age was 59.5 (47.0-67.5) years. There were no significant differences in demographic characteristics between those with CP and those without CP (Table). Invasive hemodynamics revealed comparable resting measurements of atrial and ventricular pressures between groups. The differences in PA ETs from expiration to inspiration were significantly lower among those with CP vs without CP (mean [SD]−31.8 [28.6] milliseconds vs 5.1 [9.5] milliseconds; P < .001). The differences in Ao ETs from expiration to inspiration were nonsignificantly higher among those with CP vs without CP (mean [SD]−19.0 [15.7] milliseconds vs 10.5 [9.1] milliseconds; P = .20). Thus, there was more variation in the Ao and PA ET during the respiratory cycle in individuals with CP vs without CP; the difference in Ao ET minus the difference in PA ET during expiration vs inspiration was significantly higher in individuals with CP vs without CP (mean [SD], 50.8 [22.5] milliseconds vs 28.1 [29.9] milliseconds; P < .001) (Figure 2).

Intraclass coefficients for intraobserver and interobserver variability were excellent at 0.96 (95% CI, 0.40-0.99) and 0.97 (95% CI, 0.68-0.99), respectively.

Discussion

We present a simple method for the diagnosis of CP using respiratory changes in ETs (as surrogate for stroke volumes) in the PA and Ao. Our results demonstrate significant variation in ETs between respiratory phases in those with CP and not in those with RCM or severe TR, consistent with significant ventricular interdependence—one of the hallmarks of CP.

Clinically, CP, RCM, and severe TR can present similarly, and many patients have overlapping features on noninvasive assessment. Invasive assessment can provide clarity in these challenging cases by demonstrating enhanced ventricular interaction.7 However, this subtle finding may require high-fidelity micromanometer-tipped catheters in LV and RV and can be challenged by ectopy, as well as a growing number of patients with aortic valve prostheses.

ETs are a well-established surrogate for stroke volumes, as they reflect ventricular performance.10 This relationship between ETs and stroke volumes was shown to be linear in both health and disease.11 Indeed, ETs are critical in calculation of invasively derived valve areas by the Gorlin equation.13 In healthy individuals with inspiration, ET may increase slightly in the RV and decrease slightly in the LV, thus reflecting minimal ventricular interdependence.14

Enhanced ventricular interdependence is a phenomenon in which ventricular stroke volumes vary significantly over the respiratory cycle.8,9 In individuals with CP, the noncompliant pericardium impairs ventricular filling, preferentially increasing RV stroke volume with inspiration at the expense of LV stroke volume, and the inverse applying during expiration.3,15 We previously reported on the accuracy of analyzing LV and RV contours during the respiratory cycle as a marker of beat-to-beat stroke volume.8,9 We showed that respiratory changes in peak LV and RV pressures8 as well as ratio of the systolic area in the left and right ventricles9 were significantly higher in those with CP vs those without CP. These dynamic respiratory findings were significantly more sensitive and specific for CP compared with traditional hemodynamic criteria.8,9 In the present study, we evaluated ETs in the great arteries as the surrogate for enhanced ventricular interaction. This assessment of ETs was strongly discriminative in diagnosing CP (mean [SD], 50.8 [22.5] milliseconds vs 18.4 [8.2] milliseconds; P < .001). As in the study by Talreja et al,9 we also assessed a comparable ratio of respirophasic changes using ETs, and found comparable discriminative ability. Thus, ETs in the PA and Ao were accurate assessments for ventricular interdependence. Using PA and Ao parameters to evaluate ventricular interdependence offers several advantages. These tracings can be obtained efficiently, without the need to access both ventricles, and confront ventricular ectopy or fluid-filled catheter whip artifact.

Limitations

The major limitation of this study is the small sample size, as the evaluation of CP has shifted toward echocardiography and less so invasively. This is also related to our operators not routinely recording simultaneous PA and Ao pressures during constriction studies. As most patients in this cohort had normal pulmonary vascular resistance, it remains unclear if an elevated pulmonary vascular resistance could impact PA ETs. The small sample size limited the assessment of sensitivity and specificity for the difference in Ao minus the difference in PA. Lastly, as with other markers of ventricular interdependence, discordance of ETs is not specific for CP and cannot be used in isolation to diagnose CP.

Conclusions

The findings of this study show simultaneous assessment of ETs in PA and Ao has diagnostic capability comparable with simultaneous ventricular assessment. These measurements could easily be integrated into routine practice and are particularly of value in patients for which simultaneous biventricular measurements is challenging. Further studies could be performed both invasively using simultaneous PA and Ao tracings, as well as noninvasively with use of echocardiographic Doppler imaging.

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Article Information

Accepted for Publication: June 16, 2021.

Published Online: September 22, 2021. doi:10.1001/jamacardio.2021.3478

Corresponding Author: Rick A. Nishimura, MD, Department of Cardiovascular Medicine, Mayo Clinic, 200 First St SW, Rochester, MN 55905 (rnishimura@mayo.edu).

Author Contributions: Drs Jain and Miranda had full access to all the data in the study and take responsibility for the integrity of the data and the accuracy of the data analysis.

Concept and design: Miranda, El Sabbagh, Nishimura.

Acquisition, analysis, or interpretation of data: Jain, Miranda, El Sabbagh.

Drafting of the manuscript: Jain.

Critical revision of the manuscript for important intellectual content: All authors.

Statistical analysis: Jain.

Administrative, technical, or material support: Nishimura.

Supervision: Miranda.

Conflict of Interest Disclosures: None reported.

References
1.
Connolly  DC, Wood  EH.  Cardiac catheterization in heart failure and cardiac constriction.   Trans Am Coll Cardiol. 1957;7:191-201.PubMedGoogle Scholar
2.
Nishimura  RA, Connolly  DC, Parkin  TW, Stanson  AW.  Constrictive pericarditis: assessment of current diagnostic procedures.   Mayo Clin Proc. 1985;60(6):397-401. doi:10.1016/S0025-6196(12)60850-7PubMedGoogle ScholarCrossref
3.
Geske  JB, Anavekar  NS, Nishimura  RA, Oh  JK, Gersh  BJ.  Differentiation of constriction and restriction: complex cardiovascular hemodynamics.   J Am Coll Cardiol. 2016;68(21):2329-2347. doi:10.1016/j.jacc.2016.08.050PubMedGoogle ScholarCrossref
4.
Nishimura  RA.  Constrictive pericarditis in the modern era: a diagnostic dilemma.   Heart. 2001;86(6):619-623. doi:10.1136/heart.86.6.619PubMedGoogle ScholarCrossref
5.
Syed  FF, Schaff  HV, Oh  JK.  Constrictive pericarditis—a curable diastolic heart failure.   Nat Rev Cardiol. 2014;11(9):530-544. doi:10.1038/nrcardio.2014.100PubMedGoogle ScholarCrossref
6.
Miranda  WR, Oh  JK.  Constrictive pericarditis: a practical clinical approach.   Prog Cardiovasc Dis. 2017;59(4):369-379. doi:10.1016/j.pcad.2016.12.008PubMedGoogle ScholarCrossref
7.
Nishimura  RA, Carabello  BA.  Hemodynamics in the cardiac catheterization laboratory of the 21st century.   Circulation. 2012;125(17):2138-2150. doi:10.1161/CIRCULATIONAHA.111.060319PubMedGoogle ScholarCrossref
8.
Hurrell  DG, Nishimura  RA, Higano  ST,  et al.  Value of dynamic respiratory changes in left and right ventricular pressures for the diagnosis of constrictive pericarditis.   Circulation. 1996;93(11):2007-2013. doi:10.1161/01.CIR.93.11.2007PubMedGoogle ScholarCrossref
9.
Talreja  DR, Nishimura  RA, Oh  JK, Holmes  DR.  Constrictive pericarditis in the modern era: novel criteria for diagnosis in the cardiac catheterization laboratory.   J Am Coll Cardiol. 2008;51(3):315-319. doi:10.1016/j.jacc.2007.09.039PubMedGoogle ScholarCrossref
10.
Kligfield  P, Okin  P, Devereux  RB, Goldberg  H, Borer  JS.  Duration of ejection in aortic stenosis: effect of stroke volume and pressure gradient.   J Am Coll Cardiol. 1984;3(1):157-161. doi:10.1016/S0735-1097(84)80443-XPubMedGoogle ScholarCrossref
11.
Weissler  AM, Peeler  RG, Roehll  WH  Jr.  Relationships between left ventricular ejection time, stroke volume, and heart rate in normal individuals and patients with cardiovascular disease.   Am Heart J. 1961;62:367-378. doi:10.1016/0002-8703(61)90403-3PubMedGoogle ScholarCrossref
12.
Gonzalez  MS, Basnight  MA, Appleton  CP.  Experimental cardiac tamponade: a hemodynamic and Doppler echocardiographic reexamination of the relation of right and left heart ejection dynamics to the phase of respiration.   J Am Coll Cardiol. 1991;18(1):243-252. doi:10.1016/S0735-1097(10)80246-3PubMedGoogle ScholarCrossref
13.
Gorlin  R, Gorlin  SG.  Hydraulic formula for calculation of the area of the stenotic mitral valve, other cardiac valves, and central circulatory shunts. I.   Am Heart J. 1951;41(1):1-29. doi:10.1016/0002-8703(51)90002-6PubMedGoogle ScholarCrossref
14.
Leighton  RF, Zaron  SJ, Robinson  JL, Weissler  AM.  Effects of atrial pacing on left ventricular performance in patients with heart disease.   Circulation. 1969;40(5):615-622. doi:10.1161/01.CIR.40.5.615PubMedGoogle ScholarCrossref
15.
Shabetai  R, Fowler  NO, Guntheroth  WG.  The hemodynamics of cardiac tamponade and constrictive pericarditis.   Am J Cardiol. 1970;26(5):480-489. doi:10.1016/0002-9149(70)90706-XPubMedGoogle ScholarCrossref
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