Article

Coronary collateral quantitation in patients with coronary artery disease using intravascular flow velocity or pressure measurements

Inselspital, Universitätsspital Bern, Berna, Bern, Switzerland
Journal of the American College of Cardiology (Impact Factor: 15.34). 11/1998; 32(5):1272-1279. DOI: 10.1016/S0735-1097(98)00384-2

ABSTRACT Objectives. This study evaluated two methods for the quantitative measurement of collaterals using intracoronary (IC) blood flow velocity or pressure measurements.Background. The extent of myocardial necrosis after coronary artery occlusion is substantially influenced by the collateral circulation. So far, qualitative methods have been available to assess the human coronary collateral circulation, thus restraining the conclusive investigation of, for example, therapies to promote collateral development.Methods. Fifty-one patients with a coronary artery stenosis to be treated by percutaneous transluminal coronary angioplasty (PTCA) were investigated using IC PTCA guidewire-based Doppler and pressure sensors positioned distal to the stenosis. Simultaneous measurements of aortic pressure, IC velocity and pressure distal to the stenosis during and after PTCA provided the variables for calculating collateral flow indices (CFIv and CFIp) that express collateral flow as a fraction of flow via the patent vessel. Both CFIv and CFIp were compared with conventional methods for collateral assessment, among them ST-segment changes >1 mm on IC and surface electrocardiogram (ECG) at PTCA. Also, CFIv and CFIp were compared with each other.Results. In 11 patients without ECG signs of ischemia during PTCA (sufficient collaterals), relative collateral flow amounted to 46% as determined by Doppler and pressure wire. Patients with insufficient collaterals (n = 40) had relative collateral flow values of 18%. Using a threshold of CFI = 30%, sufficient and insufficient collaterals could be diagnosed with 100% sensitivity and 93% specificity by IC Doppler, and 75% sensitivity and 92% specificity by IC pressure measurements. The agreement between Doppler and pressure measurements was good: CFIv = 0.08 + 0.8 CFIp, r = 0.80, p = 0.0001.Conclusions. Intracoronary flow velocity or pressure measurements during routine PTCA represent an accurate and, at last, quantitative method for assessing the coronary collateral circulation in humans.

Download full-text

Full-text

Available from: Bernhard Meier, Mar 31, 2014
0 Followers
 · 
67 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Therapeutic augmentation of collateral artery growth (arteriogenesis) is of tremendous clinical interest. Since monocytes home to areas of arteriogenesis and create a local arteriogeneic milieu by secreting a wide range of growth factors, we followed the idea of utilizing these cells for augmentation of collateral growth. For that purpose, we adoptively transferred both syngeneic (same strain) and allogeneic (different strain) bone marrow derived monocytes (BMDMs) into balb/c mice 24 h after femoral artery ligation. Restoration of hind-limb perfusion was determined by Laser Doppler Perfusion Imaging and histological workup. While syngeneic cell transplantation did not augment arteriogenesis in comparison to non-transplanted animals (PI = 0.56 ± 0.06 vs. 0.48 ± 0.09, respectively, ns), allogeneic monocytes massively promoted the collateralization (PI = 0.85 ± 0.14, p < 0.001). Homed monocytes were visualized near growing collateral vessels by staining the cells with the lipophil fluorochrome DiI prior to transplantation. To analyze whether the effect of allogeneic BMDM transplantations is due to local inflammation triggered by a host-versus-graft reaction, transplant recipients were pre-treated with the immunosuppressive drug cyclosporine A, which completely prevented the effect of allogeineic monocyte transplantation (PI = 0.45 ± 0.06, p < 0.001). Here, we have demonstrated murine allogeneic monocytes to be an attractive way to trigger local inflammatory responses near growing collateral vessels and stimulate their adaption, overcoming the endogenous restriction of collateral vessel growth.
    American Journal of Translational Research 01/2013; 5(2):155-69. · 3.23 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: We discover ed and validated medium sized apolipoprotein(a) as a marker for good myocardial collaterization. A total of 80 subjects were investigated in two serial studies: a discovery study (n=14) applying a pooling strat- egy to a gel and label free proteomics platform followed by a validation study (n=80) measuring apolipoprotein(a) isoforms and concentration in individual subjects. Degree of myocardial collaterization as well as apolipoprotein(a) concentration and isoform determination were performed by state-of-the-art methodologies. As apolipoprotein(a) concentration negatively correlates with isoform size (variable number of Kringle-IV type 2 repeats in human population), subjects were grouped into patients with small, medium and large apolipoprotein(a) isoforms for the statistical analysis. Among the 70 subjects with medium and large apolipoprotein(a) isoforms (>17 Kringle-IV type 2 repeats), subjects with insufficient collaterization (n=57) had a median apolipoprotein(a) concentration of 11.9 nmol/L, while patients with sufficient collaterization (n=13) had a median concentration of 31.3 nmol/L (p=0.033, Mann-Whitney U-test). Among the 52 subjects with medium sized apolipoprotein(a) isoforms (30< Kringle IV type 2 repeats >17) the difference in concentration was even more significant (13.4 vs 33.5 nmol/L, p=0.008).
    Journal of Proteomics & Bioinformatics 11/2008; 01(08). DOI:10.4172/jpb.1000048
  • Source
    European Heart Journal 12/2000; 21(21):1730-2. DOI:10.1053/euhj.2000.2194 · 14.72 Impact Factor