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. Author manuscript; available in PMC: 2025 Oct 1.
Published in final edited form as: Am Heart J. 2024 Jul 10;276:60–69. doi: 10.1016/j.ahj.2024.07.002

Race, Hypertensive Disorders of Pregnancy and Outcomes in Peripartum Cardiomyopathy

Vincenzo B Polsinelli a, Agnes Koczo b, Amber E Johnson c, Uri Elkayam d, Leslie T Cooper e, John Gorcsan III f, Joan Briller g, James Fett b, Dennis M McNamara b; IPAC investigators
PMCID: PMC11437515  NIHMSID: NIHMS2008481  PMID: 38996860

Abstract

Background:

Black women with peripartum cardiomyopathy (PPCM) have a higher prevalence of hypertensive disorders of pregnancy (HDP) and worse clinical outcomes compared with non-Black women. We examined the impact of HDP on myocardial recovery in Black women with PPCM.

Methods:

A total of 100 women were enrolled into the Investigation in Pregnancy Associated Cardiomyopathy (IPAC) study. Left ventricular ejection fraction (LVEF) was assessed by echocardiography at entry, 6, and 12-months post-partum (PP). Women were followed for 12 months postpartum and outcomes including persistent cardiomyopathy (LVEF≤35%), left ventricular assist device, (LVAD), cardiac transplantation, or death were examined in subsets based on race and the presence of HDP.

Results:

Black women with HDP were more likely to present earlier compared to Black women without HDP (days PP HDP: 34±21 vs 54±27 days, P=0.03). There was no difference in LVEF at study entry for Black women based on HDP, but better recovery with HDP at 6 (HDP:52±11% vs no HDP: 40±14%, P=0.03) and 12-months (HDP:53±10% vs no HDP:40±16%, P=0.02). At 12-months, Black women overall had a lower LVEF than non-Black women (P<0.001), driven by less recovery in Black women without HDP compared to non-Black women (P<0.001). In contrast, Black women with HDP had a similar LVEF at 12 months compared to non-Black women (P=0.56).

Conclusions:

In women with PPCM, poorer outcomes evident in Black women were driven by women without a history of HDP. In Black women, a history of HDP was associated with earlier presentation and recovery which was comparable to non-Black women.

Keywords: cardiomyopathies, heart failure, peripartum cardiomyopathy, pregnancy

Introduction

Peripartum cardiomyopathy (PPCM) is a rare complication of pregnancy, which remains a significant cause of morbidity and mortality. With an incidence in the United States of approximately 1 in 2000 live births, it is even greater cause of maternal mortality worldwide (1,2). Hypertensive disorders of pregnancy (HDP) are a major risk factor for PPCM, and occur in 5–8% of live births (3). Furthermore, HDP occurs more frequently in Black women who are also at increased risk of PPCM (2,4,5). The exact pathophysiology of PPCM remains uncertain, but several hypotheses exist such as immune, inflammatory, vascular, or genetic causes (6–12). Recovery after PPCM, defined as a return of left ventricular ejection fraction (LVEF) >50%, is frequently evident however 7–13% of patients experience adverse cardiac events during the first year postpartum (PP) including durable left ventricular assist device (LVAD), cardiac transplantation, or death (13–15).

An accumulating volume of evidence suggests PPCM and HDP have a shared pathophysiology, and that PPCM in women with co-morbid HDP is driven by a shared mechanism. Racial differences in PPCM have been described (16,17) and studies have demonstrated that Black women have worse outcomes compared to white counterparts (17,18). These differences have been attributed to health disparities including barriers to accessing care, delays in presentation, and higher rates of comorbid conditions such as diabetes, and greater risk of HDP (19). In Nigeria rates of PPCM are estimated around 1 in 100 live births, based in part on cultural practices such as high salt ingestion in the perinatal period (20). In this study, we evaluated the impact of race and HDP on disease severity, myocardial recovery, and outcomes for women with PPCM in the Investigations of Pregnancy Associated Cardiomyopathy (IPAC) study.

Methods

Cohort:

Between December 2009 and September 2012, the IPAC multi-center registry enrolled 100 women with newly diagnosed PPCM within 13 weeks PP (15). Enrollment criteria included 18 years of age or older, no history of cardiac disease, left ventricular ejection fraction (LVEF) ≤ 45% at the time of enrollment, and evaluation consistent with recent onset non-ischemic cardiomyopathy. Women with significant valvular disease, coronary disease, bacterial septicemia, ongoing drug or alcohol use disorders, history of chemotherapy, chest radiation within 5 years, or a history of previous cardiomyopathy were excluded.

At the time of enrollment, demographic information including self-described race, pertinent delivery details, previous clinical evaluation, and current medical therapy were recorded. As all women were enrolled PP, baseline medical therapy was only recorded PP and information on medical therapy during the pregnancy was not obtained. Women were followed until 1 year PP. All hospitalizations and major cardiac events including implantation of a durable left ventricular assist device (LVAD), cardiac transplantation, or death were recorded. The study protocol was reviewed by the institutional review board of all participating centers, and informed consent was obtained from all subjects.

Echocardiographic assessment:

Women enrolled in IPAC had an echocardiogram to assess LVEF at study entry, 6, and 12 months. Echocardiographic measurements including LVEF were assessed in a core laboratory (University of Pittsburgh). LVEF was calculated by biplane Simpson’s rule using a manual tracing of digital images. LV end-systolic and LV end-diastolic diameters (LVEDD) were assessed in the parasternal long-axis view and left atrial diameter (LAD) was assessed in the apical 4-chamber view.

Subset analysis:

HDP were defined as having a diagnosis during the index pregnancy of pre-eclampsia, or gestational hypertension prior to the diagnosis of PPCM. Women with chronic hypertension (occurring prior to index pregnancy) were not included into the HDP subgroup but were included in the no-HDP subgroup. Women who self-identified as Black or African American were included in the Black subgroup and were compared with all other groups combined (women identifying as White, Asian or other).

Outcomes:

Persistent cardiomyopathy was defined as an LVEF ≤ 35% at 12 months postpartum or the last recorded LVEF. Partial or full recovery was defined as LVEF>35%. Survival free from major cardiovascular events (LVAD, cardiac transplantation, or death) was determined for up to 12 months PP. A composite outcome of persistent cardiomyopathy, durable LVAD, cardiac transplantation, or death was used at 12 months.

Statistical Analysis:

Differences in continuous variables between subgroups were assessed using ANOVA. Differences in categorical variables between subgroups were calculated using Pearson’s Chi square test. P-values <0.05 were considered statistically significant. A two-way ANOVA was performed to analyze the interaction of self-designated race and HDP on six month and 12-month LVEF. Survival free from major events (death, durable LVAD, or cardiac transplantation) was compared in women with and without a history of HDP by Kaplan-Meier log rank analysis. Women achieving the composite endpoint of major event or persistent cardiomyopathy were compared by self-designated race (Black versus non-Black) and by history of HDP by Pearson’s Chi square test. Statistical analyses and graphics were completed using R, and Stata 12 (Stata Statistical Software: Release 12. College Station, TX: StataCorp LP.).

Support:

This study was supported by the National Heart, Lung, and Blood Institute through contract HL102429. Dr. Polsinelli is supported by NIH T32HL007822. Dr. Koczo is supported by the American Heart Association (24CDA1266475). Dr. Johnson is supported by NIH K23HL165110. The authors are solely responsible for the design and conduct of this study, all study analyses, the drafting and editing of the paper and its final contents.

Results

Baseline Characteristics:

Mean age in the overall PPCM cohort was 30 ± 6 years, with a baseline LVEF of 34% ± 10. Of the cohort, 30% of the women were self-designated as Black, 65% White, 1% Asian and 4% other. Of the non-Black cohort, 13 (18.6%) women identified as Hispanic, while 2 (6.7%) of women in the Black cohort identified as Hispanic. HDP was evident in the index pregnancy in 37% of women overall and HDP was more common in Black women (53% vs 30%, p=0.04). Differences between HDP subgroups are outlined in Table 1. Among non-Black women, women with HDP delivered via caesarian more often than did non-Black women without HDP (non-Black: HDP: 15/21 vs non-HDP: 22/49; P=0.04). Among Black women with HDP, there were significantly higher rates of breastfeeding and twin-gestation compared with Black women without HDP (Breastfeeding: Black: HDP=4/16 vs non-HDP=0/14; P=0.04, Twin gestation: Black: HDP=4/16 vs non-HDP=0/14; P=0.04).

Table 1.

Clinical and demographic characteristics by HDP and race.

Entire Cohort (n = 100) Non-Black (n = 70) Black (n = 30)
Characteristic No HDP HDP No HDP HDP No HDP HDP
n 63 37 49 21 14 16
Age, years 31 (25,35) 30 (24,34) 31 (25,35) 30 (25,33) 31 (29,34) 32 (23,34)
Diabetes (%) 5 (8) 6 (16) 3 (6) 3 (14) 2 (14) 3 (19)
Smoking (%) 23 (37) 11 (30) 17 (35) 7 (33) 6 (43) 4 (25)
Beta Blocker (%) 55 (87) 33 (89) 42 (86) 17 (81) 13 (93) 16 (100)
ACE inhibitor/ARB (%) 48 (76) 33 (89) 38 (78) 18 (86) 10 (71) 15 (94)
MRA (%) 16 (25) 11 (30) 13 (27) 8 (38) 3 (21) 3 (18)
C-section (%) 27 (43) 23 (62) 22 (45) 15 (71)* 5 (36) 8 (50)
Breastfeeding (%) 7 (11) 8 (22) 7 (14) 4 (19) 0 (0) 4 (25)*
Twin gestation (%) 9 (14) 10 (27) 9 (18) 6 (29) 0 (0) 4 (25)*
Gravida 3 (1,4) 2 (1,3) 2 (1,4) 1 (1,2) 3 (2,4.8) 3 (1.8,4.3)
Para 2 (1,3) 2 (1,3) 2 (1,3) 2 (1,2) 2 (1,3) 2 (1.8,3)
Systolic BP, mmHg 106(98,118) 110(105,130)* 106 (98,116) 109(106,130) 111(99,125) 120(104,135)
Diastolic BP, mmHg 66(59,76) 73(68,80)* 63 (58, 75) 73 (68, 78)* 73 (67, 78) 73 (69, 89)
Body Mass Index, kg/m2 29 (23,35) 27 (24,32) 27 (23,34) 26 (22,30) 34 (29,35) 28 (26,33)
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Categorical variables are displayed as number (%), continuous variables as median and interquartile range (IQR), (*) denotes P-value <0.05. ACE = angiotensin converting enzyme, ARB = angiotensin receptor blocker, MRA = mineralocorticoid receptor antagonist, BP = blood pressure.

In the overall cohort, women with HDP had a higher systolic and diastolic blood pressure (Systolic: 110mmHg vs 106mmHg; P=0.046, Diastolic: 73mmHg vs 66mmHg; P=0.004). Among non-Black women, women with HDP had a significantly higher diastolic blood pressure (Diastolic: 73mmHg vs 63mmHg; P=0.04). There were no differences in systolic or diastolic blood pressure among Black women, and no differences in prior pregnancies (gravida or para) between any of the cohorts. Medical therapy for heart failure was similar between the four subgroups.

Time to presentation:

Differences in time to presentation post-partum are shown in Figure 1. Black women presented later than non-Black women (Black=43±25 days vs non-Black=27±23 days; P=0.002). Overall, for women with or without HDP days postpartum at presentation was not significantly different (HDP=28 ±21 days vs no-HDP=34 ±26 days; p=0.28). Black women with HDP were more likely to present earlier compared to Black women without HDP (days PP HDP: 34±21 vs 54±27 days, P=0.03). Among women without HDP Black women presented significantly later than non-Black women (no-HDP: Black=54±27 days vs non-Black=28±24 days; P<0.001). However, among women with HDP, there was no significant difference between Black, and non-Black women (HDP: Black=34±21 days vs non-Black= 24±21 days; P=0.16).

Figure 1:

Figure 1:

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Days PP at study entry by race and HDP -- Boxplots represent the interquartile range from the first to the third quartile. Median represented by a thick Black line across the interquartile range, and error bars represent 1.5 times the interquartile range. Days PP are shown between Black and non-Black women and by subgroups based on a history of HDP during index pregnancy. Significant differences between pairs of subgroups are shown using vertical hash (|) to represent comparison group, connected by a horizontal bar. HDP = hypertensive disorder of pregnancy; PP = post-partum. Among Black women, women with no history of HDP presented later than women with a history of HDP (P=0.03). Among women with no history of HDP, Black women presented significantly later than non-Black women (P<0.001).

Remodeling and myocardial recovery:

Assessment of myocardial recovery, by measurement of LVEF at enrollment, 6, and 12 months in each subgroup is shown in Figure 2.

Figure 2:

Figure 2:

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LVEF (%) by race and HDP at baseline, 6-, and 12-months PP -- Boxplots represent the interquartile range from the first to the third quartile. Median represented by a thick Black line across the interquartile range, and error bars represent 1.5 times the interquartile range. LVEF is shown between Black and non-Black women and by subgroups based on a history of HDP during index pregnancy. (A) Baseline. (B) Six-months (C) Twelve-months. Significant differences between pairs of subgroups are shown using vertical hash (|) to represent comparison group, connected by a horizontal bar. LVEF = left ventricular ejection fraction; HDP = hypertensive disorder of pregnancy; PP = post-partum.

(A) At baseline, Black women with a history of HDP had a significantly lower mean LVEF than non-Black women with a history of HDP (P=0.001).

(B) At 6 months PP, Black women with no history of HDP had a significantly lower mean LVEF than Black women with a history of HDP (P=0.03), non-Black women with a history of HDP (p=0.008) and non-Black women with no history of HDP (P<0.001).

(C) At 12 months PP, Black women with no history of HDP had a significantly lower mean LVEF than Black women with a history of HDP (P=0.02), non-Black women with a history of HDP (p=0.001) and non-Black women with no history of HDP (P<0.001).

Enrollment:

At study enrollment, Black women had lower LVEF than non-Black (Black=30.6±9.2% vs non-Black=36.0±9.3%; P=0.009) but there was no difference between HDP and non-HDP subgroups (HDP=34.3±9.8% vs no-HDP=34.4±9.5%; P=0.94). Among women without HDP, there was no difference in LVEF at enrollment between women who were Black compared to non-Black (no-HDP: Black=32.8±10.4% vs non-Black=34.9±9.3%; P=0.46). However, among women with HDP, women who were Black had lower LVEF at time of enrollment (HDP: Black=28.7±7.8% vs non-Black=38.5±9.0%; P=0.001).

6-month follow-up:

At 6 months follow-up, Black women had a significantly lower LVEF (Black=46.2±14.0% vs non-Black=53.3±8.2%; P=0.006). Overall, the LVEF at 6 months with and without HDP were not significantly different (no-HDP=50.5±10.9% vs HDP=52.6±10.3%; P=0.41). Among women without HDP, Black women had significantly lower LVEF at 6 months compared to non-Black women (no-HDP: Black=39.6±14.1% vs non-Black=53.5±7.8%; P<.001). Black women with no HDP had a significantly lower LVEF than Black women with HDP (Black women: no HDP=39.6±14.1% vs HDP=52.2±11.5%; P=0.03). There was no significant difference between Black and non-Black women with HDP (HDP: Black 52.2 ± 11.5% vs non-Black=53.0±9.6%; P=0.83).

12-month follow-up:

Similar results were evident at 12 months postpartum with a lower mean LVEF for Black women (Black=46.9±14.3% vs non-Black=55.6±7.0%; P<0.001). For the overall cohort, LVEF was not different based on HDP status (HDP=54.2±7.9% vs non-HDP=52.4±11.7%; P=0.46). Among women without HDP, Black women had a significantly lower LVEF at 12 months compared to non-Black women (no-HDP: Black=39.5±15.9% vs non-Black=55.9±7.2%; P<0.001), but there was no race-based difference among women with HDP (HDP: Black=53.1±9.7% vs non-Black=54.9±6.6%; P=0.56). Black women with no HDP had a significantly lower LVEF than Black women with HDP (Black women: no HDP=39.5±15.9% vs HDP=53.1±9.7%; P=0.02). Compared to all other groups, Black women without HDP had the worst rates of myocardial recovery at 12 months.

Interaction of Race and History of HDP:

There was a significant interaction of self-designated race and HDP for the outcome of LVEF at six months (p=0.01). The interaction of self-designated race and a history of HDP for the outcome of LVEF at 12 months was even more significant (p=0.002). For non-Black women, there was no difference in mean `LVEF at 12 months based on the history of HDP, while in contrast Black women without a history of HDP had a significantly lower mean LVEF at 12 months compared to Black women with a history of HDP (figure 3). The mean LVEF at 12 months for Black women with a history of HDP was very similar to non-Black women with and without a history of HDP.

Figure 3:

Figure 3:

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Interaction of Self-designated Race (Black women versus non-Black women) with HDP for the determination of mean LVEF at 12 months PP. Y axis represents the LVEF (%) at 12 months PP. X axis compares non-Black versus Black women. Women with a history of HDP represented in red, those without a history of HDP in blue. Small circles represent the mean LVEF at 12 months PP for the 4 subgroups, with the thin vertical lines and error bars representing 95% confidence intervals. Solid thick lines connect means for non-Black and Black women for HDP groups (red) and non-HDP (blue). The non-parallel nature of the lines connecting the means represents graphically the significant interaction between Race and history of HDP for the determination of 12 month LVEF (p=0.002).

Remodeling:

Differences in cardiac remodeling including left ventricular diastolic diameter (LVEDD) and left atrial diameter (LAD) in each subgroup are shown in Figure 4. The greatest degree of remodeling was evident in Black women without a history of HDP. Among those who did not have a history of HDP, Black women had a greater LVEDD compared to non-Black (no-HDP: Black=60±7mm vs non-Black=54±6mm; P=0.005), and a greater LAD (no-HDP: Black=42±6 mm vs non-Black=37 ± 7mm; P=0.04). Among Black women, those without HDP also had more remodeling than women with a history of HDP in terms of LAD (P=0.03) but not LVEDD (P=0.18).

Figure 4:

Figure 4:

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LVEDD (A) and LAD (B) (mm) by race and HDP at baseline -- Boxplots represent the interquartile range from the first to the third quartile. Median represented by a thick Black line across the interquartile range, and error bars represent 1.5 times the interquartile range. LVEDD and LAD are shown between Black and non-Black women and by subgroups based on a history of HDP during index pregnancy. Significant differences between pairs of subgroups are shown using vertical hash (|) to represent comparison group, connected by a horizontal bar. LVEDD = left ventricular end-diastolic diameter; LAD = left atrial diameter; HDP = hypertensive disorder of pregnancy.

(A) At baseline, Black women with no history of HDP had a significantly greater LVEDD than non-Black women with n history of HDP (P=0.005).

(B) At baseline, Black women with no history of HDP had a significantly greater LAD than non-Black women with no history of HDP (P=0.04).

Survival and outcomes:

Follow up was available for 92 women through 12 months postpartum Twelve women reached the composite endpoint of major event or persistent cardiomyopathy including 6 women with their last LVEF ≤ 35%, and 6 women who required a durable LVAD or died. More Black women met the composite endpoint than non-Black women (Black women 7 of 27 (26%) non-Black 5 of 65 (8%), P=0.02). More women without a history of HDP reached the composite endpoint (HDP= 1 of 33 (3%); no-HDP 11 of 59 (19%), P=0.03). There was no difference in event-free survival in women with versus without HDP, however no women with HDP experienced an event of LVAD or cardiac transplantation, or death (Log-Rank; P=0.06).

Discussion

IPAC is the largest prospective registry of PPCM ever completed in North America, and confirmed in a prospective study the poorer outcomes previously reported in Black women with PPCM. This current study furthers our understanding by investigating the interaction of self-designated race and HDP for outcomes in PPCM. In IPAC Black women without HDP had later presentation, more cardiac remodeling and lower rates of LVEF recovery. Moreover, these women had an increased risk of major events or persistent cardiomyopathy at 12 months compared to Black women with HDP, and non-Black women. In contrast, Black women with HDP had no difference in mean LVEF during follow up compared to non-Black women with or without a history of HDP. Women with HDP were less likely to experience a major events or persistent cardiomyopathy. Prior studies have suggested both race and HDP have impacts on LVEF recovery and outcomes in PPCM (16,21). Our study suggests HDP may attenuate racial differences seen in PPCM, possibly by facilitating an earlier diagnosis and treatment which may improve myocardial recovery and outcomes.

These data are concordant with several studies which demonstrate worse myocardial recovery and outcomes among Black women with PPCM. (17,21,22), however for the first time the current study suggests that racial differences may be driven primarily by the subset of Black women without a history of HDP. Reports from Germany and Japan from mostly non-Black cohorts have observed better recovery and LVEF among women with HDP. (23,24) Our study found the presence of HDP among Black women was associated with earlier presentations and better outcomes compared to Black women without HDP. Two studies of Black women from South Africa showed an association of higher baseline systolic blood pressure in survivors compared to non-survivors. However, these studies excluded women with hypertension, and speculated lower baseline blood pressure may be related to cardiogenic shock rather than an absence of HDP (25,26).

There are several possible explanations for our findings. The earlier presentation of patients with HDP may suggest that developing HDP during pregnancy leads to closer follow up care postpartum, potentially attenuating barriers to the access of medical care. Lewey et. al. (21) showed delayed time to diagnosis was associated with worse outcomes among women with PPCM, a finding that was maintained in Black and non-Black subgroups irrespective of HDP status. Our study found no significant difference in guideline directed medical therapies for heart failure women with and without a history of HDP. However, the earlier presentation evident in women with HDP likely resulted in earlier initiation of medical therapies for heart failure limiting cardiac remodeling and improving myocardial recovery. An alternative hypothesis may be that the insult causing heart failure in patients with HDP is a temporary increase in blood pressure, and resolution of hypertension leads to clinical improvement. This has been demonstrated in a report from South Africa which compared 30 cases of PPCM with 53 cases of hypertension-associated heart failure during pregnancy(27). The authors noted the women with hypertensive-associated heart failure often presented earlier and were associated with a better prognosis. In contrast, we do not observe better outcomes with HDP in our subset of non-Black women and consistent with the hypothesis that time to presentation affects outcomes there was no difference in time to presentation by HDP among non-Black women.

There are several limitations to the current study. The IPAC study represents the largest prospective North American registry of women with PPCM, however the numbers for subset analysis are small. IPAC was conducted across 30 different centers throughout the United States and Canada and there may be heterogeneity in practice patterns and medical therapy was left to the discretion of the managing physician. Further, race as a social construct is connected to other social determinants of health such as socioeconomic status. The IPAC study did not collect data on social determinants of health, and this remains a major limitation of the present analysis. Finally, while we have data on the time to presentation we do not have data on when exactly treatments were initiated. All women in the IPAC study were enrolled postpartum and detailed information regarding medical therapy during pregnancy, in particular the presentation and management of HDP, were not available.

The current analysis from the IPAC study demonstrates that poorer outcomes for Black women with PPCM were primary driven by the subset without a history of HDP. Black women without HDP had a later presentation postpartum, worse remodeling at presentation and were less likely to demonstrate myocardial recovery during follow up. HDP was more prevalent among Black women, however women with HDP showed no difference based on race in either time to presentation or subsequent myocardial recovery. These data suggest the presence of HDP may actually attenuate the racial differences observed in PPCM. Our findings also suggest that early diagnosis and treatment for women at risk PPCM could limit adverse outcomes and diminish health care disparities. Further studies are required to investigate alterative biologic mechanisms for the better outcomes evident in women with HDP.

Sources of Funding:

This study was supported by the National Heart, Lung, and Blood Institute through contract HL102429. Dr. Polsinelli is supported by NIH T32HL007822. Dr. Koczo is supported by the American Heart Association (24CDA1266475). Dr. Johnson is supported by NIH K23HL165110.

Industry Relationships: Dr. Johnson has a minor consultant relationship with Sanofi and Edwards Lifesciences, the nature of which does not relate to the contents of this manuscript.

APPENDIX:

IPAC Investigators

University of Pittsburgh Medical Center (10) Dennis M McNamara, MD; James D. Fett, MD; Jessica Pisarcik, RN, BSN; Charles McTiernan, PhD; Karen Hanley-Yanez, BS; John Gorcsan III, MD; Erik Schelbert, MD. Intermountain Medical Center (8) Rami Alharethi, MD; Kismet Rasmusson, CRNP; Kim Brunisholz; Amy Butler, BS, CCRP; Deborah Budge; A.G. Kfoury, MD; Benjamin Horne, PhD; Joe Tuinei; Heather Brown. Vanderbilt University (7) Julie Damp, MD; Allen J. Naftilan, MD; Jill Russell, RN, MSN; Darla Freehardt, LPN, BS, CCRP. Cleveland Clinic (7) Eileen Hsich, MD; Cynthia Oblak, CCRC. Washington University, St. Louis (6) Greg Ewald, MD; Donna Whitehead, RN; Jean Flanagan, RN; Anne Platts. University of Southern California (6) Uri Elkayam, MD; Jorge Caro, MPH; Stephanie Mullin, RN. Brigham and Women’s Hospital (5) Michael M. Givertz, MD; M. Susan Anello, RN, BS. University of Kentucky (5) Navin Rajagopalan, MD; David Booth, MD; Tiffany Sandlin, RN; Wendy Wijesiri, RN. Mayo Clinic (4) Leslie T. Cooper, MD; Lori A. Blauwet, MD; Joann Brunner, RN; Mary Phelps; Ruth Kempf. Louisiana State University (4) Kalgi Modi, MD; Tracy Norwood. University of Illinois (4) Joan Briller, MD; Decebal Sorin Griza, MD. Duke University (4) G. Michael Felker, MD; Robb Kociol, MD; Patricia Adams, RN. Wake Forest (4) Gretchen Wells, MD; Vinay Thohan, MD; Deborah Wesley-Farrington, RN, BSN, CCRC, CCA; Sandra Soots, RN, CCRC. Jewish General (3) Richard Sheppard, MD; Caroline Michel, MD; Nathalie Lapointe, RN, PhD; Heather Nathaniel. University of Calgary (3) Angela Kealey, MD. Massachusetts General (2) Marc Semigran, MD; Maureen Daher, RN. Penn State Milton S. Hershey Medical Center (2) John Boehmer, MD; David Silber, MD; Eric Popjes, MD; Patricia Frey, RN; Todd Nicklas, RN. University of Rochester (2) Jeffrey Alexis, MD; Lori Caufield, RN, BSN, CCRC. Georgia Health Sciences University (2) John W. Thornton III, MD; Mindy Gentry, MD; Vincent J.B. Robinson, MBBS; Gyanendra K. Sharma, MD; Joan Holloway, BS; Maria Powell, LPN, CCRC. University of Texas, Southwestern (2) David Markham, MD; Mark Drazner, MD; Lynn Fernandez, RN. Newark Beth Israel Medical Center (2) Mark Zucker, MD; David A. Baran, MD; Martin L. Gimovsky, MD; Natalia Hochbaum, MD; Bharati Patel, RN, CCRC; Laura Adams, RN, BSN. University of Maryland (2) Gautam Ramani, MD; Stephen Gottlieb, MD; Shawn Robinson, MD; Stacy Fisher, MD; Joanne Marshall, BSN, MS. Columbia University (2) Jennifer Haythe, MD; Donna Mancini, MD; Rachel Bijou, MD; Maryjane Farr, MD; Marybeth Marks, Henry Arango. Baylor College (2) Biykem Bozkurt, MD, PhD, FACC, FAHA; Mariana Bolos. Thomas Jefferson (1) Paul Mather, MD; Sharon Rubin, MD; Raphael Bonita, MD; Susan Eberwine, RN. Stony Brook University Medical Center (1) Hal Skopicki, MD, PhD; Kathleen Stergiopoulos, MD; Ellen McCathy-Santoro, MD; Jennifer Intravaia, RN, CCRCII; Elizabeth Maas. Morristown Hospital (0) Jordan Safirstein, MD; Audrey Kleet, RN, MS, ACNP-BC, CCRN, CCTC; Nancy Martinez, RN; Christine Corpoin, RN; Donna Hesari, RN. University of Miami (0) Sandra Chaparro, MD; Laura J. Hudson, MA, MPH, CCRC. Harper University Hospital (0) Jalal K. Ghali, MD; Zora Injic, RN, BSc, MSA. Johns Hopkins Hospital (0) Ilan S. Wittstein, MD.

Footnotes

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