Author + information
- Joo Myung Lee1,
- Hyun Kuk Kim2,
- Kyung Seob Lim3,
- Ki Hong Choi4,
- Jonghanne Park5,
- Doyeon Hwang6,
- Tae-Min Rhee7,
- Jeong Hoon Yang4,
- Eun-Seok Shin8,
- Chang-Wook Nam9,
- Joon-Hyung Doh10,
- Joo-Yong Hahn4,
- Bon-Kwon Koo6 and
- Myung Ho Jeong3
- 1Heart Vascular Stroke Institute, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Korea, Republic of
- 2Chosun University Hospital, Gwangju, Korea, Republic of
- 3Chonnam National University Hospital, Gwangju, Korea, Republic of
- 4Samsung Medical Center, Seoul, Korea, Republic of
- 5Ministry of Health and Welfare, Seoul, Korea, Republic of
- 6Seoul National University Hospital, Seoul, Korea, Republic of
- 7National Maritime Medical Center, Seoul, Korea, Republic of
- 8Ulsan University Hospital, Ulsan, Korea, Republic of
- 9Keimyung University Dongsan Medical Center, Daegu, Korea, Republic of
- 10Inje University Ilsan Paik Hospital, Seoul, Korea, Republic of
Although fractional flow reserve (FFR)-guided decision-making for the non-culprit stenosis in patients with acute myocardial infarction (AMI) has been reported to be better than angiography-guided revascularization, there have been debates regarding the influence of microvascular dysfunction on measured FFR in non-culprit vessels. The aim of this study was to investigate the influence of microvascular damage in one vessel territory on invasively measured physiologic parameters in the other vessel, using a porcine microvascular damage model.
In Yorkshire swine, microvascular damage was induced with selective intracoronary injection of microspheres into the left anterior descending artery (LAD). Coronary stenosis was created in both LAD and left circumflex artery (LCX) using balloon catheters. Coronary physiologic changes were assessed with index of microcirculatory resistance (IMR) and FFR at baseline and at each subsequent injection of microsphere up to 5th dose in both LAD and LCX. Measurement was repeated 5 times at each stage and a total of 424 measurements were made in 12 Yorkshire swine models.
The median area stenosis in LAD and LCX were 48.1% (Q1-Q3 40.8-50.4) and 47.9% (Q1-Q3 31.1-62.9), respectively. At baseline, FFR in LAD was lower than that in the LCX (0.89±0.01 and 0.94±0.01, p<0.001). There was no difference in IMR (18.4±5.8U and 17.9±1.2U, p=0.847). With repeated injections of microsphere, IMR in LAD was significantly increased, up to 77.7±15.7U (p<0.001). Given the same stenosis, FFR in LAD was also significantly increased, up to 0.98±0.01 along with IMR increase (p<0.001). Conversely, IMR and FFR were not changed in the LCX throughout repeated injury to the LAD territory (p=0.105 and p=0.286 for IMR and FFR, respectively). The increase in LAD IMR was mainly driven by the increase in hyperemic mean transit time (p<0.001).
In Yorkshire swine models, local microvascular damage increased both FFR and IMR in a vessel supplying target myocardial territory. However, IMR and FFR were maintained in the other vessel. These results support the use of FFR-guided strategy for non-culprit lesions in patients with AMI.
IMAGING: FFR and Physiologic Lesion Assessment