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Journal of Peking University (Health Sciences) ›› 2024, Vol. 56 ›› Issue (1): 150-156. doi: 10.19723/j.issn.1671-167X.2024.01.023

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Index of microcirculatory resistance is associated with left ventricular remodeling in patients with acute anterior ST-segment elevation myocardial infarction undergoing emergency primary percutaneous coronary intervention

Fangfang WANG1,Fumeng LIANG2,Nan LI3,Xiaoxiao WANG3,Jiangli HAN1,*(),Lijun GUO1,*()   

  1. 1. Department of Cardiology and Institute of Vascular Medicine, Peking University Third Hospital; State Key Laboratory of Vascular Homeostasis and Remodeling, Peking University; NHC Key Laboratory of Cardiovascular Molecular Biology and Regulatory Peptides, Peking University; Beijing Key Laboratory of Cardiovascular Receptors Research, Beijing 100191, China
    2. Department of General Medicine, Peking University Third Hospital, Beifang Branch, Beijing 100089, China
    3. Research Center of Clinical Epidemiology, Peking University Third Hospital, Beijing 100191, China
  • Received:2023-08-06 Online:2024-02-18 Published:2024-02-06
  • Contact: Jiangli HAN,Lijun GUO E-mail:dr_hanjiangli@126.com;guo_li_jun@sohu.com
  • Supported by:
    Capital Health Development Scientific Research Fund(2014-2-4093);Sunshine Cardiovascular Research Fund of Chinese Medical Doctor Association(SCRFCMDA201321)

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Abstract:

Objective: To evaluate whether index of microcirculatory resistance (IMR) is associated with left ventricular (LV) remodeling in acute anterior ST elevation myocardial infarction (STEMI) patients undergoing primary percutaneous coronary intervention (PPCI). Methods: This was a single-center retrospective cohort study. The patients with first anterior STEMI who received PPCI from January 2014 to August 2017 in Peking University Third Hospital was enrolled. After PPCI, IMR was measured immediately by using pressure/temperature guidewire. The success rate of IMR measurement was 100%. Also we collected some related clinical data from the medical records and laboratory results. Infarct size [assessed as creatine kinase (CK) peak], echocardiography at baseline and 1 year follow-up were assessed. LV adverse remodeling (LVAR) was defined as ≥20% increase in LV end-diastolic volume (LVEDV). Results: A total of forty-three patients were enrolled, with an average age of (58.7±12.4) years.The patients were divided into two groups as IMR ≤25 and IMR>25 by normal values recommended by previous literature. Compared with IMR ≤25 group, IMR>25 group had a higher percentage of initial thrombolysis in myocardial infraction (TIMI) grade 0 (95.7% vs. 65.0%, P=0.029), higher serum CK peak value [4 090 (383, 15 833)vs. 1 580 (396, 5 583), P=0.004]. The IMR>25 group suffered higher rates of ventricular aneurysm (30.4% vs. 5.0%, P=0.021). There was no difference in LVEDV [(111.0±18.8) mL vs. (115.0±23.6) mL, P=0.503] between the two groups 1 day after MI, but after 1 year, LVEDV in IMR>25 group was significantly higher than in IMR≤25 group [(141.5±33.7) mL vs. (115.9±27.9) mL, P=0.018]. The incidence of LVAR was more significant in IMR>25 group (47.4% vs. 11.8%, P=0.024). Binary Logistics regression showed that IMR [B=0.079, exp(B) (95%CI)=1.082 (1.018－1.149), P=0.011] and serum triglyceride level [B=1.610, exp(B) (95%CI)=5.005 (1.380－18.152), P=0.014] were the predictors of LVAR 1 year after MI. IMR had a good predictive value for LVAR 1 year after MI [area under the curve (AUC)=0.749, P=0.019], IMR>29 was a good cutoff value with sensitivity 81.8% and specificity 68.0%. Conclusion: Our study elaborates that immediate measurement of IMR after PPCI in patients with STEMI can reflect the microvascular function.And IMR could be used as a quantitative biomarker to predict LVAR after STEMI.

Key words: Acute myocardial infarction, Index of microcirculatory resistance, LV adverse remodeling, Triglyceride

CLC Number: 

  • R542.22

Table 1

The baseline characteristics in patients with IMR≤25 and IMR>25"

Parameters IMR ≤25 (n=20) IMR>25 (n=23) P value
Age/years, $\bar x \pm s$ 55.9±14.7 61.1±9.8 0.205
Male, n (%) 17 (85.0) 18 (78.3) 0.862
Hypertension, n (%) 6 (27.3) 9 (39.1) 0.324
Diabetes mellitus, n (%) 7 (35.0) 6 (26.1) 0.526
Dyslipidemia, n (%) 10 (50.0) 6 (26.1) 0.106
Current smoking, n (%) 15 (75.0) 16 (69.6) 0.692
WBC/(×109/L), $\bar x \pm s$ 11.20±3.89 11.00±4.22 0.584
Neut/%, M (min, max) 78.4 (64.9, 92.0) 82.8 (54.0, 90.4) 0.279
hs-CRP/(mg/L), M (min, max) 4.53 (2.18, 9.42) 4.02 (2.27, 7.74) 0.543
eGFR/(mL/min), $\bar x \pm s$ 93.6±22.1 81.8±20.6 0.079
Cholesterol/(mmol/L), $\bar x \pm s$ 4.80±0.86 4.80±1.38 0.995
LDL-C/(mmol/L), $\bar x \pm s$ 3.08±0.64 2.99±0.92 0.726
HDL-C/(mmol/L), M (min, max) 0.96 (0.61, 1.59) 0.96 (0.74, 1.45) 0.779
TG/(mmol/L), M (min, max) 1.33 (0.61, 4.68) 1.44 (0.65, 3.08) 0.706
Glu/(mmol/L), M (min, max) 5.6 (4.2, 18.1) 6.4 (4.5, 9.2) 0.886
HbA1C/%, M (min, max) 6.05 (5.00, 11.40) 5.70 (4.90, 7.90) 0.057
NT-proBNP/(ng/mL), M (min, max) 815 (20, 3 357) 1030 (70, 4 264) 0.762
Peak CK/(IU/L), M (min, max) 1 580 (396, 5 583) 4090 (383, 15 833) 0.004
Killip≥Ⅱ, n (%) 1 (5.0) 4 (17.4) 0.431

Table 2

Intervention-related results and discharge treatment in patients with IMR≤25 and IMR>25"

Parameters IMR ≤25(n=20) IMR>25(n=23) P value
Procedural characteristics
    TIMI flow grade 0(initial), n (%) 13 (65.0) 22 (95.7) 0.029
    Coronary infused tirofiban, n (%) 5 (25.0) 12 (52.2) 0.069
    Thrombus aspiration, n (%) 1 (5.0) 6 (26.1) 0.146
    TIMI flow grade 3 (final) proximal LAD, n (%) 20 (100.0) 20 (87.0) 0.491
    Multivessel disease, n (%) 14 (70.0) 13 (56.5) 0.270
    IMR, M (min, max) 17.90 (8.96, 23.31) 44.20 (25.08, 87.00) < 0.001
    CFR, M (min, max) 1.85 (0.70, 5.30) 1.30 (0.80, 2.30) 0.027
    FFR, M (min, max) 0.85 (0.72, 0.96) 0.87 (0.70, 1.03) 0.378
Discharge treatment
    ACE inhibitor, n (%) 11 (55.0) 10 (43.5) 0.887
    β-blocker, n (%) 10 (50.0) 11 (47.8) 0.451

Table 3

Echocardiography parameters in Patients with IMR≤25 and IMR>25 at baseline and 1 year follow-up"

Parameters IMR≤25 IMR>25 P
Baseline
    n 20 23
    LVEF/%, $\bar x \pm s$ 47.6±3.7 44.3±4.9 0.02
    Sm/(cm/s), $\bar x \pm s$ 7.2±0.8 9.6±2.4 0.01
    LVEDD/mm, $\bar x \pm s$ 49.2±4.4 48.5±3.6 0.54
    LVEDV/mL, $\bar x \pm s$ 115.0±23.6 111.0±18.8 0.503
    Ventricular aneurysm, n (%) 1 (5.0) 7 (30.4) 0.021
1 year follow-up
    n 17 19
    LVEF/%, $\bar x \pm s$ 57.0±9.0 50.0±7.0 0.01
    Sm/(cm/s), $\bar x \pm s$ 9.7±2.8 8.3±1.8 0.087
    LVEDD/mm, $\bar x \pm s$ 49.3±5.0 53.7±5.3 0.014
    LVEDV/mL, $\bar x \pm s$ 115.9±27.9 141.5±33.7 0.018
    ΔLVEF/%, $\bar x \pm s$ 10.0±9.0 6.0±8.0 0.16
    ΔLVEDV/%, $\bar x \pm s$ -2.0±21.0 27.0±29.0 0.001
    LVAR, n (%) 2 (11.8) 9 (47.4) 0.024

Figure 1

In both the IMR>25 and the IMR≤25 group, LVEF had recovered significantly at 1 year after MI compared with that found at baseline (A), and the two groups had similar changes in LVEF (ΔLVEF, B) ΔLVEF=LVEF1 year-LVEFbaseline. IMR, index of microcirculatory resistance; LVEF, left ventricular ejection fraction."

Figure 2

LVEDV in the IMR>25 group 1 year after MI was significantly larger than that at baseline (P=0.002), but there was no such change in the IMR≤25 group (P=0.566, A), was higher in the IMR≤25 group (P=0.001, B) ΔLVEDV=(LVEDV1 year-LVEDVbaseline)/ LVEDVbaseline. IMR, index of microcirculatory resistance; LVEDV, left ventricular end diastolic volume."

Figure 3

LVEDV in the IMR>25 group increased by more than 20% over baseline, which means the incidence of LVAR was higher than IMR≤25 group IMR, index of microcirculatory resistance; LVEDV, left ventricular end diastolic volume; LVAR, left ventricular adverse remodeling."

Figure 4

Receiver operating characteristic curve (ROC) analysis showed that IMR had diagnostic value for LVAR IMR, index of microcirculatory resistance; LVAR, left ventricular adverse remodeling. Area under the curve (AUC)=0.749, 95% confidence interval: 0.578－0.920, P=0.019."

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