Basic Clinical Characteristics
Finally, 58 acute SPPCM patients, 29 chronic SPPCM patients, and 45 female DCM patients matched for LVEF and age were included (Fig. 1). Table 1 showed the maternal information of PPCM. More than 60% of these PPCM patients had heart failure symptoms onset after delivery and nearly half of them(49.4%) had cesarean section. During pregnancy, 3(3.4%) patients had pre-eclampsia and 10(11.5%) patients had gemellary pregnancy. As for childbearing history, we found that 28(32.2%) patients gestated at least for twice and 15(17.2%) patients had history of abortion. Besides, 10 SPPCM had family history of cardiovascular disease and 2 of them had family history of DCM.
Age of female DCM(32.6 ± 8.0y) tend to be older than acute SPPCM(29.1 ± 5.4y) but similar with chronic SPPCM(31.3 ± 6.5y), p = 0.070. The median disease duration was 12.0(2.0, 18.0) months for female DCM, 2.0(1.0, 3.0)months for acute SPPCM, 30.0(10.5, 69.0) months for chronic SPPCM. No significant difference was found for heart rate, blood pressure, family history, and so on(all p > 0.05 in Table 1). Use of β-blocker, digoxin, and anticoagulant were less frequent in female DCM(all p < 0.05 in Table 1). As for echocardiography, pulmonary hypertension, mitral regurgitation, tricuspid regurgitation occurred more often in both acute and chronic SPPCM patients than female DCM patients(all p < 0.05 in Table 1). Laboratory test was presented in Table S1. Acute SPPCM have higher cholesterol, low density lipoprotein, and platelet than chronic SPPCM and female DCM(p < 0.001). Besides, active partial thromboplastin time in acute and chronic SPPCM was higher than female DCM(p < 0.001). The other laboratory tests were not significantly different(all p > 0.05)
Table 1
Basic clinical information
Maternal related information for SPPCM(n = 87) |
Gestational DM | 2(2.3%) | Pre-eclampsia | 3(3.4%) |
Cesarean | 43(49.4%) | Gemellary pregnancy | 10(11.5%) |
Abortion | 15(17.2%) | Multi-gestation | 28(32.2%) |
Antepartum onset | 33(37.9%) | Postpartum onset | 54(62.1%) |
Clinical characteristics for SPPCM and matched female DCM |
| Acute SPPCM(n = 58) | Chronic SPPCM(n = 29) | Female DCM(n = 45) | P |
Age, y | 29.1 ± 5.4 | 31.3 ± 6.5 | 32.6 ± 8.0 | 0.070 |
Height, m | 161.5 ± 6.5 | 162.8 ± 4.9 | 160.0 ± 6.0 | 0.137 |
Weight, kg | 62.1 ± 12.9 | 61.2 ± 13.5 | 57.3 ± 10.8 | 0.130 |
BSA | 1.8 ± 0.2 | 1.8 ± 0.2 | 1.7 ± 0.2 | 0.068 |
Heart rate, bp | 92.1 ± 19.7 | 83.1 ± 15.2 | 86.2 ± 21.6 | 0.093 |
SBP, mmHg | 105.6 ± 13.8 | 107.3 ± 17.6 | 109.2 ± 15.9 | 0.514 |
DBP, mmHg | 70.7 ± 12.3 | 69.6 ± 11.5 | 73.0 ± 11.4 | 0.435 |
FCD | 8(13.8%) | 2(6.9%) | 5(11.1%) | 0.682 |
• Hyperlipemia | 8(13.8%) | 2(6.9%) | 3(6.7%) | 0.485 |
NYHA I-II | 9(15.5%) | 5(17.2%) | 12(26.7%) | 0.372 |
NYHA III-IV | 49(84.5%) | 24(82.8%) | 33(73.3%) |
Diuretics | 58(100.0%) | 29(100.0%) | 43(95.6%) | 0.113 |
β-blocker | 55(94.8%) | 29(100.0%) | 38(84.4%) | 0.016 |
ACEI or RRB | 48(82.8%) | 24 (82.8%) | 35(77.8%) | 0.787 |
Digoxin | 38(65.5%) | 18(62.1%) | 10(22.2%) | < 0.001 |
Anticoagulant | 18(31.0%) | 11(37.9%) | 3(6.7%) | 0.002 |
PH | Mild | 9(15.5%) | 7(25.0%) | 1(2.2%) | 0.036 |
Moderate | 3(5.2%) | 1(3.6%) | 2(4.4%) |
Severe | 0 | 1(3.6%) | 2(4.4%) |
MR | Mild | 24(41.4%) | 7(24.1%) | 10(22.2%) | 0.015 |
Moderate | 20(34.5%) | 10(34.5%) | 11(24.4%) |
Severe | 7(12.1%) | 7(24.1%) | 6(13.3%) |
TR | Mild | 28(58.3%) | 15(51.7%) | 7(15.6%) | < 0.001 |
Moderate | 7(14.6%) | 4(13.8%) | 8(17.8%) |
Severe | 4(8.3%) | 4(13.8%) | 4(8.9%) |
AR | Mild | 3(5.2%) | 3(10.3%) | 2(4.4%) | 0.579 |
Moderate | 0 | 0 | 0 |
Severe | 0 | 0 | 0 |
PR | Mild | 3(5.2%) | 2(6.9%) | 3(6.7%) | 0.929 |
Moderate | | 0 | 0 |
| Severe | 2(3.4%) | 02(6.9%) | 03(6.7%) |
Change in T wave or ST-T | 21(36.2%) | 10(34.5%) | 23(51.1%) | 0.227 |
Tachycardia | 12(20.7%) | 2(6.9%) | 5(11.1%) | 0.158 |
VPB | 2(3.4%) | 9(31.0%) | 9(20.0%) | 0.001 |
Conduction block | 1(1.7%) | 7(24.1%) | 5(11.1%) | 0.003 |
Abbreviations: Diabetes Mellitus, DM; High Blood Pressure, HBP; Systolic Blood Pressure, SBP; Diastolic Blood Pressure, DBP; New York Heart Association, NYHA; Angiotensin-Converting Enzyme Inhibitors, ACEI; Calcium Channel Blockers, CCB; Angiotensin Receptor Blockers, ARB; Family Cardiovascular Disease, FCD; Pulmonary Hypertension, PH; Body Surface Area, BSA; Mitral Regurgitation, MR; Tricuspid Regurgitation, TR; Aortic regurgitation, AR; Pulmonary Regurgitation, PR; Ventricular Premature Beat, VPB;* presents significant difference between acute SPPCM and female DCM; # presents significant difference between chronic SPPCM and female DCM;& presents significant difference between acute SPPCM and chronic SPPCM |
Comparison Of Biventricular Structure And Function
Parameters of biventricular structure and function were presented in Table 2. Though there was no statistical difference for LVEF among the three groups, chronic SPPCM had higher indexed LV end systolic volume(LVESVi, 126.1 ± 59.3 ml/m2), indexed LV end diastolic volume(LVEDVi, 166.5 ± 68.2 ml/m2), indexed LV stroke volume(LVSVi, 40.1 ± 24.4 ml/m2) than acute SPPCM and female DCM. Acute SPPCM and female DCM have similar LV volume parameters(all p > 0.05). As for right ventricular function, female DCM had lager indexed right ventricular end diastolic volume(RVEDVi, 96.5 ± 32.0 ml/m2) than acute SPPCM, lager indexed right ventricular stroke volume(RVSVi, 32.0 ± 10.5 ml/m2) and better right ventricular ejection fraction(RVEF, 37.1 ± 20.6%) than SPPCM of the two subgroups. Besides, chronic SPPCM had more dilated transverse diameter(70.0 ± 9.2 mm for LV and 33.6 ± 12.0 mm for RV) of bi-ventricle. But no significant difference was found of longitudinal diameter(all p > 0.05 in Table S2). Thickness of myocardial wall was not significant different among these patients(all p > 0.05).
Table 2
Comparison of biventricular structure and function among acute SPPCM, chronic SPPCM and female DCM
Parameters | Acute SPPCM n = 58 | Chronic SPPCM n = 29 | Female DCM n = 45 | P |
LVEDV, ml | 219.7 ± 61.0& | 297.5 ± 114.3&# | 237.5 ± 67.9# | < 0.001 |
LVEDVi, ml/m2 | 125.4 ± 36.3& | 166.5 ± 68.2&# | 139.0 ± 40.5# | 0.001 |
LVESV, ml | 165.9 ± 60.8& | 224.8 ± 99.5&# | 174.0 ± 63.6# | 0.001 |
LVESVi, ml/m2 | 94.6 ± 35.3& | 126.1 ± 59.3&# | 101.9 ± 38.5# | 0.006 |
LVSV, ml | 53.75 ± 21.4& | 72.3 ± 43.1& | 63.5 ± 21.5 | 0.012 |
LVSVi, ml/m2 | 30.9 ± 12.8& | 40.1 ± 24.4& | 37.1 ± 12.2 | 0.024 |
LVEF, % | 26.0 ± 11.1 | 25.4 ± 12.8 | 28.0 ± 9.2 | 0.526 |
LV massi, g/m2 | 56.1 ± 15.1 | 60.4 ± 17.8 | 62.3 ± 17.2 | 0.055 |
RVEDV, ml | 137.6 ± 45.2& | 164.0 ± 82.5#& | 165.3 ± 54.9# | 0.031 |
RVEDVi, ml/m2 | 79.1 ± 28.6* | 91.9 ± 49.0 | 96.5 ± 32.0* | 0.037 |
RVESV, ml | 98.8 ± 46.2 | 121.2 ± 85.3 | 110.7 ± 61.6 | 0.263 |
RVESVi, ml/m2 | 56.7 ± 28.2 | 68.4 ± 50.2 | 64.5 ± 36.4 | 0.320 |
RVSV, ml | 38.8 ± 19.8* | 42.8 ± 25.3# | 54.8 ± 17.8*# | 0.001 |
RVSVi, ml/m2 | 22.3 ± 11.9* | 23.4 ± 13.1# | 32.0 ± 10.5*# | < 0.001 |
RVEF, % | 30.3 ± 15.1* | 30.8 ± 20.6# | 37.1 ± 20.6*# | 0.006 |
Abbreviations: Left Ventricular End Diastolic Volume, LVEDV; Left Ventricular End Systolic Volume, LVESV; Left Ventricular Stroke Volume, LVSV; Left Ventricular Ejection Fraction, LVEF; Left Ventricle, LV; Right Ventricular End Diastolic Volume, RVEDV; Right Ventricular End Systolic Volume, RVESV; Right Ventricular Stroke Volume, RVSV; Right Ventricular Ejection Fraction, RVEF. * presents significant difference between acute SPPCM and female DCM; # presents significant difference between chronic SPPCM and female DCM;& presents significant difference between acute SPPCM and chronic SPPCM |
Comparison Of Global, Segmental Myocardial Deformation In Left Ventricle
Although there was no statistical difference for global peak longitudinal strain(PLS) among the three groups, acute SPPCM tend to had lower global peak radial strain(PRS), and global peak circumferential strain(PCS) tend to be lower in both acute and chronic SPPCM(p = 0.053 and p = 0.059 respectively, presented in Table 3). Further analysis revealed that basal PRS and middle PCS of acute SPPCM were significant lower than that in female DCM(all p < 0.05). Middle PRS of acute SPPCM(8.1 ± 4.6%) was lower than that in both chronic SPPCM(11.3 ± 9.8%) and female DCM(11.7 ± 7.4%). Besides, we also found that apical PLS and apical PCS in acute SPPCM and chronic SPPCM were significantly lower than that in female DCM(all p < 0.05).
Table 3
Comparison of biventricular structure and function among acute SPPCM, chronic SPPCM and female DCM
Parameters | Acute SPPCM n = 58 | Chronic SPPCM n = 29 | Female DCM n = 45 | P |
Global PRS | 9.5 ± 5.0 | 11.2 ± 6.5 | 12.4 ± 6.7 | 0.053 |
Global PCS | -8.5 ± 3.7 | -8.1 ± 4.7 | -10.0 ± 3.8 | 0.059 |
Global PLS | -5.7 ± 3.2 | -6.1 ± 3.7 | -6.9 ± 3.0 | 0.154 |
Basal PRS | 16.4 ± 8.4* | 17.3 ± 9.6 | 21.4 ± 12.5* | 0.045 |
Basal PCS | -8.1 ± 3.0 | -8.1 ± 3.9 | -8.2 ± 3.3 | 0.995 |
Basal PLS | -4.2 ± 3.9 | -4.0 ± 5.0 | -4.2 ± 4.0 | 0.965 |
Middle PRS | 8.1 ± 4.6&* | 11.3 ± 9.8& | 11.7 ± 7.4* | 0.021 |
Middle PCS | -7.9 ± 3.5* | -8.2 ± 4.9 | -9.9 ± 4.1* | 0.034 |
Middle PLS | -5.2 ± 3.9 | -6.2 ± 3.6 | -6.6 ± 3.7 | 0.151 |
Apical PRS | 7.7 ± 7.4 | 8.1 ± 6.9 | 8.4 ± 7.1 | 0.888 |
Apical PCS | -10.1 ± 5.5* | -8.7 ± 5.5# | -12.5 ± 5.3*# | 0.009 |
Apical PLS | -7.4 ± 3.2* | -7.5 ± 4.0# | -9.4 ± 3.6*# | 0.015 |
Global LGE extent, % | 7.3(3.9, 23.9) | 13.1(4.0, 35.3) | 23.6(3.6, 42.8) | 0581 |
Basal LGE extent, % | 18.5(6.1, 39.4) | 19.8(8.7, 53.9) | 39.8(25.7, 46.4) | 0.231 |
Middle LGE extent, % | 9.3(4.5, 31.1) | 12.9(7.8, 37.8) | 31.8(18.4, 48.9) | 0.074 |
Apical LGE extent, % | 5.3(4.5, 13.6) | 5.5(4.7, 13.2) | 8.6(5.9, 12.1) | 0.172 |
Presence of LGE, n | 15(25.9%)&* | 17(58.6%)& | 23(51.1%)* | 0.004 |
Average segments of LGE | 8.0 ± 6.2 | 9.1 ± 4.8 | 10.1 ± 6.3 | 0.564 |
Abbreviations: Peak Radial Strain, PRS; Peak Circumferential Strain, PCS; Peak Longitudinal Strain, PLS; Late Gadolinium Enhancement, LGE. * presents significant difference between acute SPPCM and female DCM; # presents significant difference between chronic SPPCM and female DCM;& presents significant difference between acute SPPCM and chronic SPPCM |
Segmental difference was found after further comparison for PRS, PCS, and PLS in 16 AHA segments among the three group. Compared with female DCM, significant decrease of PRS in acute PPCM was mainly distributed in segment of AHA1-3,6–8,11–12 and significant decrease of PRS in chronic SPPCM was revealed in segment of AHA5(Fig. 2). Compared with chronic SPPCM, acute SPPCM had lower PRS in segment of AHA 7 and AHA 8 which was the foundation of a lower middle PRS in acute SPPCM. In comparison with female DCM, obvious decrease of PCS in acute SPPCM mainly distributed in segment of AHA 7–8,11–12, 13–16 and decrease of PCS in chronic SPPCM mainly distributed in segment of AHA 4, 7,12–16(Fig. 3). As for PLS, lower value in segment of AHA5,13–15 for acute SPPCM and lower value in segment of AHA 8,13–15 in chronic SPPCM were revealed (Figure S1).
Uniformity Of Myocardial Deformation Dysfunction In Ppcm And Aged-matched Dcm
To explore uniformity of myocardial deformation dysfunction, the absolute difference of myocardial strain between enrolled patients and parous women was calculated and compared among basal, middle, and apical part of LV(shown in Table 4). The mean age of healthy puerparas was 32.1 ± 8.0. And the duration between CMR examination and delivery was 19.6 ± 11.9 months. In acute SPPCM patients, dysfunction of PRS, PCS, and PLS were all inhomogeneous among basal, middle, and apical part of LV. PRS(39.3 ± 8.4) decreased more extensively in basal part. PCS(10.4 ± 3.0) and PLS(8.3 ± 3.9) decreased less severe in basal part among three part of LV(all p < 0.05). For chronic SPPCM, despite decrease of PLS was homogeneous(p = 0.143), dysfunction of PRS and PCS were inhomogeneous (all p < 0.001). PRS dysfunction(38.3 ± 9.6) in basal part of LV was more severer than middle and apical part of LV. PCS dysfunction(10.5 ± 3.9) in basal part was milder among three part of LV. In female DCM, dysfunction of PLS(p = 0.810) and PCS(p = 0.056) were homogeneous among the three part of LV. Only dysfunction of PRS was heterogeneously with a more severer dysfunction in basal part(34.3 ± 12.5) was found.
Table 4
Uniformity of myocardial deformation dysfunction and fibrosis among basal, middle, and apical part of LV for acute SPPCM, chronic SPPCM and female DCM
Group | Basal | Middle | Apical | P |
The extent of myocardial deformation dysfunction for PRS compared among basal, middle, apical part of LV |
acute SPPCM | 39.3 ± 8.4#* | 28.7 ± 4.6#& | 24.4 ± 7.4*& | < 0.001 |
chronic SPPCM | 38.3 ± 9.6#* | 25.5 ± 9.8# | 24.1 ± 6.9* | < 0.001 |
female DCM | 34.3 ± 12.5#* | 25.2 ± 7.4# | 23.8 ± 7.1* | < 0.001 |
The extent of myocardial deformation dysfunction for PCS compared among basal, middle, apical part of LV |
acute SPPCM | 10.4 ± 3.0*# | 14.3 ± 3.5# | 14.8 ± 5.4* | < 0.001 |
chronic SPPCM | 10.5 ± 3.9#* | 14.0 ± 4.9# | 16.2 ± 5.5* | < 0.001 |
female DCM | 10.4 ± 3.3 | 12.2 ± 4.1 | 12.4 ± 5.3 | 0.056 |
The extent of myocardial deformation dysfunction for PLS compared among basal, middle, apical part of LV |
acute SPPCM | 8.3 ± 3.9*# | 10.0 ± 3.9# | 10.8 ± 3.2* | 0.002 |
chronic SPPCM | 8.6 ± 5.0 | 9.0 ± 3.6 | 10.7 ± 4.0 | 0.143 |
female DCM | 8.3 ± 4.0 | 8.6 ± 3.7 | 8.8 ± 3.6 | 0.810 |
The extent of LGE compared among basal, middle, apical part of LV |
acute SPPCM | 16.0 ± 17.9%* | 13.9 ± 15.8% | 3.7 ± 5.3%* | 0.047 |
chronic PPCM | 17.1 ± 21.9%* | 21.2 ± 20.9%& | 3.9 ± 5.4%*& | 0.018 |
female DCM | 26.2 ± 20.2%* | 23.7 ± 20.2%& | 5.4 ± 7.8%*& | < 0.001 |
Abbreviations: as shown in Table 2 and Table 3. # means statistical difference between basal and middle part; * means statistical difference between basal and apical part; & means statistical difference between apical and middle part. |
Comparison Of Global, Segmental Late Gadolinium Enhancement In Left Ventricle
Acute SPPCM(25.9%) had significantly lower incidence of LGE than chronic SPPCM(58.6%) and female DCM(51.1%). After quantification of LGE, we found that global LGE extent tend to increase in acute SPPCM, chronic SPPCM, and female DCM gradually(p = 0.581, as shown in Figure S2). Similar results were found for basal, middle and apical LGE extent as well. Further analysis for 16 AHA segment was conducted, no significant difference was found between acute SPPCM and chronic SPPCM. LGE extent was similar in 16 AHA segments between chronic SPPCM and female DCM. However, LGE extent for segment of AHA 9 in acute SPPCM were less extensive than female DCM (Fig. 4).
LGE extent in segment of AHA 9 in acute SPPCM was less extensive than female DCM. Abbreviations: as shown in Table 3.
Distribution Of Myocardial Fibrosis In Ppcm And Aged Matched Female Dcm
LGE was not homogeneously distributed among basal, middle, and apical part of LV, percentage of LGE was similar in basal and middle part of LV(shown in Table 4). LGE extent was less extensive in apical part for all three groups(all p < 0.05).
Comparison Of Cardiac Function And Myocardial Strain Between Patients With And Without Lge
In order to investigate influence of LGE on cardiac function and myocardial strain, comparison was carried out between patients with and without LGE. In acute SPPCM, patients with positive LGE had significant increased LVESVi(109.9 ± 29.4 vs 89.2 ± 35.9, p = 0.049) and reduced LVEF(20.1 ± 9.5 vs 28.1 ± 11.0). The other cardiac function parameters were similar between acute SPPCM with and without LGE(all p > 0.05 in Table 5). For myocardial strain,
Global PRS(p = 0.013), apical PRS(p = 0.026), global PCS(p = 0.031), middle PCS(p = 0.013), and apical PCS(p = 0.027) in acute SPPCM with LGE also decreased significantly compared with patients without LGE. In chronic SPPCM, only RVEF tended to be lower(23.8 ± 12.7 vs 40.6 ± 25.7, p = 0.054) in patients with positive LGE compared with patients with negative LGE. There was no significant difference in the rest cardiac function indexes between subgroups based on LGE in chronic SPPCM(all p > 0.05 in Table S3). Referring to myocardial strain, global PLS(p = 0.022), basal PLS(p = 0.006), apical PLS(p = 0.047), middle PCS(p = 0.046), and apical PCS(p = 0.026) in chronic SPPCM with LGE was significantly lower than that in patients without LGE. Besides, global PCS tended to be lower in chronic SPPCM with LGE(p = 0.054). In female DCM, biventricular function and myocardial indexes were not significantly different between patients with and without LGE(all p > 0.05 in Table S4). Only LV mass in female DCM with positive LGE was significantly lower than that in female DCM without LGE.
Table 5
Comparison of cardiac function and myocardial strain in acute SPPCM based on LGE presence
Parameters | Positive LGE(n = 15) | Negative LGE(n = 43) | P |
LVEDVi | 136.9 ± 29.6 | 121.4 ± 37.8 | 0.158 |
LVESVi | 109.9 ± 29.4 | 89.2 ± 35.9 | 0.049 |
LVSVi | 26.9 ± 12.0 | 32.2 ± 12.9 | 0.168 |
LVEF | 20.1 ± 9.5 | 28.1 ± 11.0 | 0.015 |
RVEDVi | 87.6 ± 33.6 | 76.1 ± 26.4 | 0.178 |
RVESVi | 65.3 ± 30.7 | 53.7 ± 26.9 | 0.168 |
RVSVi | 22.2 ± 13.5 | 22.4 ± 11.5 | 0.980 |
RVEF | 26.5 ± 14.4 | 31.6 ± 15.2 | 0.260 |
LV massi | 55.2 ± 13.4 | 56.4 ± 15.9 | 0.808 |
GRS | 7.3 ± 3.1 | 10.3 ± 5.3 | 0.013 |
GCS | -6.7 ± 2.7 | -9.1 ± 3.8 | 0.031 |
GLS | -5.0 ± 3.3 | -5.9 ± 3.1 | 0.331 |
BRS | 14.2 ± 6.3 | 17.1 ± 9.0 | 0.249 |
BCS | -7.0 ± 2.6 | -8.5 ± 3.1 | 0.089 |
BLS | -4.3 ± 3.1 | -4.2 ± 4.3 | 0.900 |
MRS | 6.6 ± 3.2 | 8.6 ± 5.0 | 0.145 |
MCS | -6.0 ± 2.6 | -8.5 ± 3.5 | 0.013 |
MLS | -4.9 ± 3.4 | -5.3 ± 4.0 | 0.729 |
ARS | 4.9 ± 4.1 | 8.7 ± 8.0 | 0.026 |
ACS | -8.0 ± 3.5 | -10.9 ± 5.8 | 0.027 |
ALS | -6.2 ± 3.2 | -7.8 ± 3.2 | 0.092 |
Abbreviations: as shown in Table 2 and Table 3 |
Repeatability
Intra- and interobserver reliability analysis of global and segmental strain in the three direction were presented in Table S5. The range of mean bias was from − 4.9–4.7%. Limit of agreement for global strain indexes were narrower than segmental strain indexes, which indicated that global strain indexes were relative more stable.