Abstract:Background—The objective of this study is to test the effect of permanent right internal mammary artery device closure on coronary collateral function and myocardial ischemia.Methods and Results—This was a prospective, open-label clinical trial in 50 patients with coronary artery disease. The primary study end point was coronary collateral flow index as obtained during a 1-minute proximal right coronary artery (RCA) and left coronary artery balloon occlusion at baseline before and at follow-up examination 6 we… Show more
“…Recently investigated have been the function of mammary‐to‐coronary artery anastomoses and their effects on myocardial ischemia in humans by occluding the IMAs with an angioplasty balloon. In the presence versus absence of IMA occlusion, the collateral flow index was significantly higher, intracoronary ECG ST elevation significantly less, and angina diminished while occluding the right IMA for 3 weeks even improved fractional flow reserve . Hence, these studies have confirmed the theory that a functional ischemia‐reducing extracardiac coronary artery supply exists via naturally‐occurring IMA anastomoses.…”
Internal mammary arteries (IMAs), via angiogenesis/arteriogenesis, have great potential for developing collaterals. This generally occurs when ischemia involves the inferior limbs or heart. Although this phenomenon may be spontaneous, it seems to be promoted by iatrogenic or voluntary occlusion of the IMAs. We present a patient who underwent triple coronary artery bypass grafting with two saphenous vein grafts and a free-graft left IMA and suffered an acute myocardial infarction 6 weeks after surgery. Emergency coronary angiography revealed occlusion of the grafts and an amazing branch arising from the proximal stump of the surgically-cut and clipped IMA, leading to the anterior wall of the heart, functionally creating an effective natural bypass, probably stimulated both by anterior wall ischemia and interrupted flow within the proximal left IMA. K E Y W O R D S angiogenesis, coronary artery bypass grafting, internal mammary artery, occlusion, refractory angina
“…Recently investigated have been the function of mammary‐to‐coronary artery anastomoses and their effects on myocardial ischemia in humans by occluding the IMAs with an angioplasty balloon. In the presence versus absence of IMA occlusion, the collateral flow index was significantly higher, intracoronary ECG ST elevation significantly less, and angina diminished while occluding the right IMA for 3 weeks even improved fractional flow reserve . Hence, these studies have confirmed the theory that a functional ischemia‐reducing extracardiac coronary artery supply exists via naturally‐occurring IMA anastomoses.…”
Internal mammary arteries (IMAs), via angiogenesis/arteriogenesis, have great potential for developing collaterals. This generally occurs when ischemia involves the inferior limbs or heart. Although this phenomenon may be spontaneous, it seems to be promoted by iatrogenic or voluntary occlusion of the IMAs. We present a patient who underwent triple coronary artery bypass grafting with two saphenous vein grafts and a free-graft left IMA and suffered an acute myocardial infarction 6 weeks after surgery. Emergency coronary angiography revealed occlusion of the grafts and an amazing branch arising from the proximal stump of the surgically-cut and clipped IMA, leading to the anterior wall of the heart, functionally creating an effective natural bypass, probably stimulated both by anterior wall ischemia and interrupted flow within the proximal left IMA. K E Y W O R D S angiogenesis, coronary artery bypass grafting, internal mammary artery, occlusion, refractory angina
“…[ 5 ] The collateral flow index, fractional flow reserve, intracoronary ECG, and anginal symptoms have all been recently demonstrated to improve when the ipsilateral IMA is occluded. [ 6 ] These recent findings confirm that the old principle of IMA occlusion had a strong rationale, and suggest that it would be worthwhile further studying its effects in RA.…”
“…In comparison, the absolute change in CFI during short‐term treatment with G‐CSF was +0.049 ± 0.062 (−0.010 ± 0.060 in the placebo group), whereby the CFI responses during follow‐up were more consistent, and thus, statistically more relevant in the previous than the actual study. The average CFI response to other forms of coronary arteriogenesis, such as heart rate reduction by ivabradine, physical exercise, external counterpulsation, or extracardiac coronary collateral supply augmentation via the native internal mammary artery compares as follows: +0.059 ± 0.050, +0.069 ± 0.050, and +0.067 ± 0.064, respectively. Thus, the effects appear more sizeable and less variable than the response induced by pegfilgrastim, both of which may be related to a possible fading effect of the pro‐arteriogenic action of pegfilgrastim linked to a longer period of administration over 6 months vs only 6 weeks to 3 months.…”
Objective
To test the effect of long‐term pegfilgrastim on collateral function and myocardial ischaemia in patients with chronic stable coronary artery disease (CAD).
Methods
This was a prospective clinical trial with randomized 2:1 allocation to pegfilgrastim or placebo for 6 months. The primary study endpoint was collateral flow index (CFI) as obtained during a 1‐minute ostial coronary artery balloon occlusion. CFI is the ratio of mean coronary occlusive divided by mean aortic pressure both subtracted by central venous pressure (mm Hg/mm Hg). Secondary endpoints were signs of myocardial ischaemia determined during the same coronary occlusion, that is quantitative intracoronary (i.c.) ECG ST‐segment shift (mV) and the occurrence of angina pectoris. Endpoints were obtained at baseline before and at follow‐up after three subcutaneous study drug injections.
Results
Collateral flow index in the pegfilgrastim group changed from 0.096 ± 0.076 at baseline to 0.126 ± 0.070 at follow‐up (P = 0.0039), while in the placebo group CFI changed from 0.157 ± 0.146 to 0.122 ± 0.043, respectively (P = 0.29); the CFI increment at follow‐up was +0.030 ± 0.075 in the pegfilgrastim group and −0.034 ± 0.148 in the placebo group (P = 0.0172). In the pegfilgrastim group, i.c. ECG ST‐segment shift changed from +1.23 ± 1.01 mV at baseline to +0.93 ± 0.97 mV at follow‐up (P = 0.0049), and in the placebo group, it changed from +0.98 ± 1.02 mV to +1.43 ± 1.09 mV, respectively (P = 0.05). At follow‐up, the fraction of patients free from angina pectoris during coronary occlusion had increased in the pegfilgrastim but not in the placebo group.
Conclusion
Pegfilgrastim given over the course of 6 months improves collateral function in chronic stable CAD, which is reflected by reduced myocardial ischaemia during a controlled coronary occlusion.
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