Acute impairment of basal left ventricular rotation but not twist and untwist are involved in the pathogenesis of acute hypertensive pulmonary oedema

Transcription

1 Acute impairment of basal left ventricular rotation but not twist and untwist are involved in the pathogenesis of acute hypertensive pulmonary oedema A.D. Margulescu 1,2, R.C. Sisu 1,2, M. Florescu 2, M. Cinteza 1,2, D. Vinereanu 1,2 1 University of Medicine and Pharmacy 'Carol Davila' (Bucharest, RO) 2 Department of Cardiology, University and Emergency Hospital of Bucharest (Bucharest, RO)

2 Disclosures This study was supported by: Grant 242/2007 (CNCSIS - UEFISCSU); Grant 135/2007 of the Romanian Ministry of Education and Research. ClinicalTrials identifier: NCT

3 Background Method Results Conclusions

4 Left ventricular twist mechanics LV twist is of paramount importance for efficient LV systolic and diastolic function - Subendocardial layer generates counterclockwise rotation of the base - Subepicardial layer generates clockwise rotation of the apex - The larger radius predominates over subendocardium, and is responsible for most of the LV twist Diastolic untwist mostly originates from the elastic energy stored during systolic twist - Delayed untwist is associated with diastolic dysfunction Sengupta et al. J Am Coll Cardiol Img 2008;1:366 76

5 LV twist and its relation to LV function Studies in Chronic Heart Failure (HF): - HF with normal ejection fraction - preserved magnitude of LV twist, but - delayed untwist - Systolic HF (i.e. Dilated cardiomyopathy) - reversed direction of apical rotation negative (counterclockwise) overall LV twist No studies evaluated LV twist in pulmonary edema Aim of the study to evaluate the role of LV twist mechanics in the pathogenesis of AHPE, using speckle tracking echocardiography

6 Background Method Results Conclusions

7 Inclusion criteria All consecutive patients with: 1. acute onset of dyspnoea within the preceding 8 hours; 2. pulmonary rales; 3. systolic blood pressure 160 mmhg at admission; 4. sinus rhythm; 5. informed consent (waiver for the acute event)

8 Study protocol 120 minutes Acute onset of dyspnoea 8 hours Treatment started by the Ambulance or the ED team Call the on-call cardiologist ED Provisional diagnosis of AHPE by the ED medical team Call the on-call investigator Provisional diagnosis of AHPE by the on-call cardiologist Admit patient to CCU Investigator's home - to - hospital time CCU Echo Chest X-ray Time-to-echo was 66 ± 39 min

9 Exclusion criteria 86 patients underwent screening Echo during acute event 35 patients excluded: - 15 acute myocardial infarction (CKMB, TnI). Angina was not excluded - 12 patients with moderate left-sided valvar disease - 1 pneumonia and consolidation - 1 exacerbation of chronic obstructive pulmonary disease - 1 acute lung injury during sepsis - 1 death and 4 patients discharged before 48h 51 patients included in the main study Echo at 48-92h LV twist assessed in 20 patients with good quality echo (LV short axis of both basal and apical levels)

10 Measured parameters LV systolic function (conventional and tissue Doppler echo) Global LVEF, Cardiac power Longitudinal - Mean strain of 6 basal LV segment (ST) LV rotational parameters Systolic Basal LV rotation (RotB) Apical LV rotation (RotA) LV twist (LVT = RotB RotA) Time-to-peak LV twist (TT) Twist rate (TR) Diastolic Untwist rate (UTR) Time from AVC-to-UTR LV torsion (LV tor = LVT / LV length)

11 TT LVT LV twist Apex Base RotB = basal LV rotation (º) RotA RotA = Apical LV rotation (º) LVT = LV twist (º) TT = time-to-lv twist (ms) RotB TR TR = Twist rate (º/s) UTR = Untwist rate (º/s) AVC-UR = time from AVC to UTR (ms) AVC-UR UTR

12 Background Method Results Conclusions

13 General characteristics Demographic characteristics Age (years) 69 (11) Men (%) 20 (40) Medical history, n (%) Coronary artery disease 25 (49) Ischaemic stroke 8 (16) Diabetes mellitus 22 (43) Hypertension 45 (88) Chronic heart failure 18 (35) Acute pulmonary oedema 16 (31) Data in the graphs are presented as mean (SD)

14 General characteristics N Acute episode Follow-up p-value (t-test) Heart rate (beats per minute) (21) 75 (13) < Mean BP (mm Hg) (18) 102 (17) 0.91 Data in the graphs are presented as mean (SD)

15 LV rotation Acute event Follow-up 0 p = p = 0.96 p = (2.1) -5.4 (3.0) (5.2) 3.9 (5.2) (4.9) 9.1 (5.2) RotB 0 RotA 0 LVT Data in the graphs are presented as mean (SD)

16 LV systolic longitudinal and global function Acute event Follow-up 0 p = p = p = (7.0) (7.1) (0.12) 0.36 (0.13) (0.4) 1.0 (0.3) -20 Basal LV strain (%) 0 LVEF 0 CP (W) Data in the graphs are presented as mean (SD)

17 LV systolic function vs. twist Acute event Follow-up Correlation of LV Twist with LVEF Correlation of RotB with basal LV strain R = 0.64, R 2 = 0.41 P < R = 0.33, R 2 = 0.11 P = Data in the graphs are presented as mean (SD)

18 Other parameters of LV twist N Acute episode Followup P-value (t test) TT (ms) (110) 288 (100) 0.49 TR ( /s) (28) 71 (25) 0.81 UTR ( /s) (32) -64 (29) 0.94 AVC-UR (ms) (78) 127 (122) 0.60 LVTor ( /cm) (6.3) 12.8 (7.5) 0.22 Data in the graphs are presented as mean (SD)

19 R = 0.80, p < R = 0.82, p < Reproducibility of twist measurements Bland-Altman of twist Bland-Altman of twist rate Bland-Altman of untwist rate Correlation twist R = 0.94, p < Correlation twist rate R = 0.81, p < Correlation untwist rate R = 0.84, p < Coefficient of Variation between 15% and 20%

20 Study limits Echo was performed 66 min after initiation of Rx, but Patients were still in pulmonary oedema when the first echo was performed, and It is unlikely that acute changes to be entirely reversible in that time Low number of patients, but First study to assess LV twist mechanics during AHPE

21 Background Method Results Conclusions

22 Conclusions 1. Acute hypertensive pulmonary oedema (AHPE) is associated with: LV longitudinal dysfunction, and Decreased basal LV rotation, BUT Preserved apical LV rotation and LV twist This might explain why global LV function is preserved during AHPE 2. Acute alteration of LV untwisting properties is not involved in AHPE

23 Thank you!