Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

Preeclampsia is a Heart Disease

2,256 views

Published on

Is the heart having permanent modifications when preeclampsia or gestational hypertension occurs?

Published in: Health & Medicine

Preeclampsia is a Heart Disease

  1. 1. PREECLAMPSIAIS A HEART DISEASE HERBERT VALENSISETor Vergata University Rome Italy
  2. 2. IUGR preterm delivery proteinuria abruptio placentae decreased GFR Glomerulo capillary endotheliosis renal failure alterated liver function test subcapsular hemorrhage fibrin deposition HELLP endothelium damage hematological changes humoral factors decreased plasma volume leaky capillaries pulmonary edema increased SVR ARDS increased PA decreased CVP hypertensive encephalopathy ischemia and vasospasm hemorrhage edema eclampsiamultisystem changes in pre-eclampsia
  3. 3. CENTRAL HEATING DOESN’T WORK:IS A BOILER PROBLEM OR THE PIPES ARE NOT WORKING ?
  4. 4. WE SHOULD START OUR TALKFROM THE END OF THE STORY
  5. 5. CONCLUSIONS 1- PATIENTS THAT DEVELOP PREECLAMPSIA HAVE A SIGNIFICANT HIGH RISKOF DEVELOPING CARDIOVASCULAR ISCHEMIC DISEASE IN THE FOLLOWING YEARS OF THEIR LIFE
  6. 6. What are the effects ofpreeclampsia on maternal cardiac function?
  7. 7. Left Atrial Fractional Area Change LA FAC %= (LAmax-LAmin)/LAmax LAmax LAmin
  8. 8. LA FAC% in normal and hypertensive 60 50 * 40 * p <0.001 30 LA FAC% 20 10 0 I TRIM II TRIM III TRIM III TRIM N/GHLAFAC% is reduced in hypertensive patients,suggesting a difficult voiding from left atrium in theleft ventricle Valensise et al Hypertension, 2001
  9. 9. Diastolic dysfunction in HYPERTENSION• Recent data suggest a diastolic dysfunction in Gestational Hypertension Vazquez Blanco Am J Hypertens 2001 Valensise et al. Hypertension; 2001• Transmitral flow is altered with a prolongation of IVRT and a bimodal distribution of DtE Vazquez Blanco Am J Hypertens 2001 Valensise et al. Hypertension 2001• Pulmonary vein flow shows a prevalence of the systolic fraction (confirming the altered compliance suggested by transmitral flow modifications Valensise et al. Hypertension 2001
  10. 10. Diastolic function: Transmitral flow and IVRTNormal E A E GH A Ao Ao DtE dA DtE dA IVRT IVRT• IVRT is prolonged in GH patients because of ahigher left ventricular end-systolic pressure; alonger time is therefore necessary for the leftventricular pressure to fall below the atrial Valensise et al. Hypertension 2001pressure.
  11. 11. ISOVOLUMETRIC RELAXATION TIME 100 90 * 80 70 60IVRT 50 40 30 20 10 0 I TRIM II TRIM III TRIM III TRIM N/GH NORMAL GH Valensise Ultrasound Obstet Gynecol 2000 Valensise Hypertension 2001 * p<0.0001 GH III TRIM vs. NORM III TRIM
  12. 12. Left ventricular geometric pattern and cardiac function• Some Author suggest that the geometric pattern may be altered in Gestational Hypertension Vazquez Blanco Am J Hypertens 2000 Valensise et al. Hypertension; 2001 Novelli et al. Hypertension 2003• Concentric geometry appears to identify patients at high risk for complications during Gestational Hypertension Novelli et al. Hypertension 2003• Cardiac output and stroke volume may be reduced during subsequently complicated Gestational Hypertension compared to uneventful gestational hypertension
  13. 13. GEOMETRIC ASPECTS OF LEFT VENTRICLE
  14. 14. Geometric pattern in complicated hypertensive pregnancy Normal Geometry Eccentric Hypertrophy(LVMi<50g/m2.7, SRP<0.45) (LVMi>50g/m2.7, SRP<0.45) Concentric Concentric Remodeling Hypertrophy (LVMi<50g/m2.7, (LVMi>50g/m2.7, SRP>0.45) SRP>0.45)
  15. 15. Geometric pattern of the left ventricle Novelli et al. Hypertension, 2003Uneventful GH (101) Complicated GH (47) n=31 n=1030.7 % 22.3 % n=70 n=37 69.3 % 78.7% Non concentric Geometry Non concentric geometry Concentric geometry Concentric Geometry
  16. 16. Hemodynamic features of the two groups : Parameter Uneventful Complicated P-value GH GH N=101 N=47 Heart Rate(bpm) 84+/-11 82+/-14 nsSystolic BP(mmHg) 144+/-11 146+/-9 nsDiastolic BP (mmHg) 82+/-13 82+/-14 ns Mean BP (mmHg) 103+/-9 103+/-11 nsTVR (dyne•sec•cm-5) 1403+/-375 1653+/-536 0.002 EDV (mL) 104+/-13 101+/-15 Ns ESV (mL) 30+/-8 33+/-8 0.023Stroke Volume (mL) 74+/-12 67+/-16 0.007Cardiac Output (L) 6.1+/-1.2 5.6+/-2.0 0.046 Novelli et al. Hypertension 2003
  17. 17. What is Total Vascular Resistance (TVR)?TVR is the steady component of the cardiacafterload determined by the cross-sectionaldiameter of the resistance vasculature. How is TVR calculated? TVR is calculated by dividing Mean Blood Pressure with Cardiac Output. Diastolic BP+1/3(Systolic BP-Diastolic BP ) TVR= Cardiac Output (Stroke volume x Heart rate) X 80
  18. 18. LVOT: Left ventricular outflow tract Integral of the aortic flow AOA LV LA
  19. 19. Cardiac OutputCO=5.664 L/min Blood Pressure=110/60 mmHg Mean Blood Pressure=76.6 mmHg TVR=80xMBP/CO TVR=1083 dyn
  20. 20. Cardiac OutputCO=5.664 L/min Blood Pressure=130/85 mmHg Mean Blood Pressure=100 mmHg TVR=80xMBP/CO TVR=1412 dyn
  21. 21. Cardiac OutputCO=5.664 L/min CO=4.5 L/min Blood Pressure=130/85 mmHg Blood Pressure=110/70 mmHg Mean Blood Pressure=100 mmHg Mean Blood Pressure=83.33 mmHg TVR=80xMBP/CO TVR=1412 dyn TVR=1481 dyn
  22. 22. CONCLUSIONS 1- PATIENTS THAT DEVELOP PREECLAMPSIA HAVE A SIGNIFICANT HIGH RISK OF DEVELOPING CARDIOVASCULAR ISCHEMIC DISEASE IN THE FOLLOWING YEARS OF THEIR LIFE2.MATERNAL HEART DURING PREECLAMPSIA AND HYPERTENSION ADAPTS SHOWING - DIASTOLIC DYSFUNCTION - REDUCED LA%FAC AND INCREASED IVRT - INCREASED RELATIVE WALL THICKNESS - REDUCED STROKE VOLUME - REDUCED CARDIAC OUTPUT - INCREASED TOTAL VASCULAR RESISTANCES
  23. 23. Is maternal cardiac function different in patients that will and will not develop clinical complications?
  24. 24. Maternal heart evaluation 268 emGH pregnanciesbetween 28 and 31 weeks Echocardiography: TVR Geometric pattern of LV Follow up for maternal andfeto- neonatal complications Valensise et al, BJOG 2006
  25. 25. Main maternal and fetal/neonatal complicationssubsequently developed in women with gestational hypertension Valensise et al, BJOG 2006
  26. 26. M-mode-derived and 2D-derived parameters at 28–31 weeks Valensise et al, BJOG 2006
  27. 27. Blood Pressure levels and TVR in uncomplicated and complicated early mild gestational hypertension *P<0.05 vs controls; °P<0.05 vs. uncomplicated EMGH °* * *160 1800 1754 144 145140 1600120 1400 * 111 * * 1200 1138100 83 85 1000 94980 80060 62 60040 40020 200 0 0 SBP DBP TVR Controls Uncomplicated EMGH Complicated EMGH Valensise et al, BJOG 2006
  28. 28. Relative wall thickness of the left ventricle (geometric pattern) °* 00:50 * 00:46 00:43 00:41 00:38 RWT>0.45 00:36 Concentric geometry of the 00:28 left ventricle 00:21 00:14 00:07 00:00 RWT Controls Uncomplicated EMGH Complicated EMGH*P<0.05 vs controls; °P<0.05 vs. uncomplicated EMGH Valensise et al, BJOG 2006
  29. 29. ROC CURVE for Blood Pressure Values 100% 80%Sensitivity 60% SBP DBP 40% MBP 20% 0% 0% 50% 100% 1-Specificity
  30. 30. ROC CURVE Relative Wall Thickness Cut off 0.45 Valensise et al, BJOG 2006
  31. 31. ROC CURVE Total Vascular Resistance Cut off 1340 dyn.s.cm-5 Valensise et al, BJOG 2006
  32. 32. Cutoff values for TVR in multiparas e primiparas with sensitivity, specificity, PPV, NPV and accuracy Valensise et al, BJOG 2006
  33. 33. Univariate and multivariate binary logistic regression analysis for the prediction of complicated EMGH Valensise et al, BJOG 2006
  34. 34. TVR in Intrauterine Growth Restriction andSmall for Gestational Age
  35. 35. ISOLATED FGR inNormotensive Total VascularPregnancy Resistance TVR=80 x MAP/CO ** 1800 1600 1400 1200The high mean blood 1000pressure and the low 800 600cardiac output 400explain the elevated 200TVR in the IUGR 0 CONTROL IUGRgroup ** p <0.0001
  36. 36. Parameter Normal Fetal FGR GrowthMaternal Heart rate Cardiac Output Total Vascular ResistanceLeft Ventricular Mass
  37. 37. Differentiation through TVRof FGR from SGA
  38. 38. TAKE HOME MESSAGE: If we find a fetus with an AC <10 thcentile and normal PI of UA at 27-31weeks1. If the mother shows LOW TVR, thepregnancy will probably procede withoutcomplications (SGA).2. If the mother shows HIGH TVR thefetus will develop a Growth Restriction(FGR).
  39. 39. TVR=80 x MAP/CO TVRSGA:normal Cardiac 1800Output coupled with a 1600 **lower Mean Arterial 1400Pressure contributes 1200to maintain a reduced 1000TVR 800 600FGR: low cardiac 400 200Output and relatively 0high Mean Arterial SGA FGRpressure ** p <0.0001
  40. 40. CONCLUSIONS 1. PATIENTS THAT DEVELOP PREECLAMPSIA HAVE A SIGNIFICANT HIGH RISK OF DEVELOPING CARDIOVASCULAR ISCHEMIC DISEASE IN THE FOLLOWING YEARS OF THEIR LIFE 2.MATERNAL HEART DURING PREECLAMPSIA AND HYPERTENSION ADAPTS SHOWING - DIASTOLIC DYSFUNCTION WITH REDUCED LA%FAC AND INCREASED IVRT - INCREASED RELATIVE WALL THICKNESS - REDUCED STROKE VOLUME AND CARDIAC OUTPUT - INCREASED TOTAL VASCULAR RESISTANCES 3. ALTERED CARDIAC FUNCTION MIGHT HELPTO DIFFERENTIATE AMONG THE AFFECTED PATIENTS THOSE WHO WILL DEVELOP COMPLICATIONS
  41. 41. Is maternal cardiac function altered prior to the onset of preeclampsia?
  42. 42. Echocardiograpphy identifies at 24 weeks gestationNormotensive patients with subsequent maternal and/or fetal complications through TVR
  43. 43. Uterine Artery Doppler and maternal TotalVascular Resistance (TVR) and Left ventricularMorphology Vasapollo et al. Hypertension 2008
  44. 44. TVR and CO at 24 weeks’ gestation in the asymptomatic phase High TVR Low CO1600 1570 7 6.571400 dyne 6 L/min1200 51000 1009 4 4.51 L/min800600 dyne 3 2400200 1 0 0 Uncomplicated Complicated Uncomplicated Complicated Vasapollo et al. Hypertension 2008
  45. 45. •Total Vascular Resistance (>1400dynes) appears to be the bestpredictive parameter (PPV: 77%) forcomplications in pregnancy at 24weeks’ gestation in pts selectedthrough uterine artery Doppler. Vasapollo et al. Hypertension 2008
  46. 46. TVR in the latentphase ofEarly and LatePreeclampsia Valensise et al. Hypertension 2008
  47. 47. Model of the asymtomatic phase of Preeclampsia•Our data show that early maternal and fetal complications areassociated to high TVR and low CO in the latent phase of thedisease•Previous and recent data on the latent phase of preeclampsiadescribe a model with low TVR and high CO.Easterling 1990; Bosio 1999; Nicolaides 2008•Early and late PE should be regarded as different forms of thedisease: Early PE (before 34 weeks) associated with abnormaluterine artery Doppler, FGR, and adverse maternal andneonatal outcomes. Late PE (after 34 weeks) associated with normal or slightincrease in uterine resistance index, mild maternal disease,a low rate of fetal involvement.Murphy 2000, Ness 2006, Sibai 2005
  48. 48. EARLY AND LATE PREECLAMPSIAAre Early and Late PE hemodynamically different?Can we link a particular type of PE with aspecific haemodynamic model?
  49. 49. PATIENT SELECTION1345 normotensiveprimigravidas with 24 weeksnotching at 20-22 weeks Uterine artery Doppler+ Maternal Echocardiography X 119 other1119 normal complicationsoutcome 107 PE (8%) (9%)(Controls) 32 Late 75 Early PE PE
  50. 50. ASYMPTOMATIC 24 WEEKS PATIENTS
  51. 51. TVR, CO, bilateral notching, and BMI in the asymptomatic phase of Early and Late PE EARLY PE CO 40%9,008,00 8.96 LATE PE7,00 L/min 60% P<0.05 16%6,005,004,003,00 4.492,00 L/min1,00 84%0,00 Bilateral Notch Normal Doppler EARLY PE LATE PE Pre-pregnancy TVR BMI 281800 281600 1605 27 Kg/m²14001200 dyne 261000 25800600 739 24 24400 dyne200 23 Kg/m² 0 EARLY PE LATE PE 22 EARLY PE LATE PE
  52. 52. EARLY AND LATE PREECLAMPSIA at 24 weeks’ (latent phase) Controls Early PE Late PE TVR 990±179 1605±248* 739±244*° CO 6.61±1.10 4.49±1.09* 8.96±1.83*° Pre-preg. 23±4 24±2 28±6*° BMI Bilateral 67 (6.0%) 45 (60.0%)* 5 (15.6%)*° Notch Birthweight 46±23 18±12* 48±20° centile*P<0.05 vs. controls; °P<0.05 vs. Early PE
  53. 53. CONCLUSIONS EARLY AND LATE PREECLAMPSIA Early and Late PE appear to be hemodynamically different!Early PE is characterized by high TVR and low COLate PE is charachterized by low TVR and high CO IN THE FUTURE: No more PE without CO and TVR values!
  54. 54. CONCLUSIONS 1. PATIENTS THAT DEVELOP PREECLAMPSIA HAVE A SIGNIFICANT HIGH RISK OF DEVELOPING CARDIOVASCULAR ISCHEMIC DISEASE IN THE FOLLOWING YEARS OF THEIR LIFE 2.MATERNAL HEART DURING PREECLAMPSIA AND HYPERTENSION ADAPTS SHOWING- DIASTOLIC DYSFUNCTION WITH REDUCED LA%FAC AND INCREASED IVRT - INCREASED RELATIVE WALL THICKNESS - REDUCED STROKE VOLUME AND CARDIAC OUTPUT - INCREASED TOTAL VASCULAR RESISTANCES 3.ALTERED CARDIAC FUNCTION MIGHT HELP TO DIFFERENTIATE AMONG THE AFFECTED PATIENTS THOSE WHO WILL DEVELOP COMPLICATIONS 4. ALTERED CARDIAC FUNCTION IS ALREADY IDENTIFIABLE IN ASYMPTOMATIC PATIENTS BEFORE THE APPEARANCE OF THE CLINICAL SIGNS
  55. 55. Is maternal cardiac function so difficult to investigate?
  56. 56. IS IT SO DIFFICULT TO GET INFORMATIONSON CARDIAC FUNCTION DURING PREGNANCY?
  57. 57. How to calculate Stroke Volume, Cardiac Output and TVR? E wave A wave IVRT DtE Aortic flow Left Ventricular Out-flow Tract (LVOT) integral (Ao int)Stroke volume (SV)=Area LVOT x Ao intCardiac output (CO)=SV x heart rate Calculation of Total Vascular Resistance: TVR=80 x (Mean Arterial Pressure/Cardiac Output)
  58. 58. JUST ONE MINUTE OF TIMETO MEASURE TOTAL SISTEMIC VASCULAR RESISTANCE
  59. 59. AND LATER?• INDIVIDUAL CONTROL• FOLLOW THE VALUE IN FOLLOWING DAYS/WEEKS• EVALUATE IF THERE IS A TENDENCY TO REDUCE TVR OR INCREASE TVR• ADAPT THERAPY?
  60. 60. To study or not to study the heart this is the question
  61. 61. IN THE FUTURE: Please do take care of theMaternal Cardiac function and be able to evaluate its parameters The heart function might be A good key to understand Preeclampsia vascular status

×