Function of Natural Internal Mammary–to–Coronary Artery Bypasses and Its Effect on Myocardial IschemiaCLINICAL PERSPECTIVE
Background—The function of naturally existing internal mammary (IMA)–to–coronary artery bypasses and their quantitative effect on myocardial ischemia are unknown.
Methods and Results—The primary end point of this study was collateral flow index (CFI) obtained during two 1-minute coronary artery balloon occlusions, the first with and the second without simultaneous distal IMA occlusion. The secondary study end point was the quantitatively determined intracoronary ECG ST-segment elevation. CFI is the ratio of simultaneously recorded mean coronary occlusive pressure divided by mean aortic pressure both subtracted by mean central venous pressure. A total of 180 pairs of CFI measurements were performed among 120 patients. With and without IMA occlusion, CFI was 0.110±0.074 and 0.096±0.072, respectively (P<0.0001). The difference of CFI obtained in the presence minus CFI obtained in the absence of IMA occlusion was highest and most consistently positive during left IMA with left anterior descending artery occlusion and during right IMA with right coronary artery occlusion (ipsilateral occlusions): 0.033±0.044 and 0.025±0.027, respectively. This CFI difference was absent during right IMA with left anterior descending artery occlusion and during left IMA with right coronary artery occlusion (contralateral occlusions): −0.007±0.034 and 0.001±0.023, respectively (P=0.0002 versus ipsilateral occlusions). The respective CFI differences during either IMA with left circumflex artery occlusion were inconsistently positive. Intracoronary ECG ST-segment elevations were significantly reduced during ipsilateral IMA occlusions but not during contralateral or left circumflex artery occlusions.
Conclusion—There is a functional, ischemia-reducing extracardiac coronary artery supply via ipsilateral but not via contralateral natural IMA bypasses.
Clinical Trial Registration—URL: http://www.clinicaltrials.gov. Unique identifier: NCTO1676207.
In patients with chronic coronary artery disease (CAD), prognosis is adversely affected by ischemia.1 Likewise, the extent of ischemia and necrosis is the main determinant of outcome after acute myocardial infarction.2 Both the degree of myocardial ischemia and the resulting infarct size can be estimated by ECG ST-segment shift, in particular and very sensitively by intracoronary ECG.3,4 The absence of intracoronary ECG ST-segment shift during a brief coronary balloon occlusion has been demonstrated to be a beneficial prognosticator of survival.5 Myocardial ischemia in the event of coronary occlusion is influenced by the duration of occlusion, the size of the myocardial area at risk for infarction, the lack of collateral supply to the ischemic zone, the absence of ischemic preconditioning before vascular occlusion, and the level of myocardial oxygen consumption at the time of occlusion.6 The beneficial effect on survival of a well-functioning intercoronary collateral circulation in chronic stable CAD has been well documented.7–9
Clinical Perspective on p 2652
Anatomically, extracardiac coronary collateral supply via internal mammary artery (IMA) branches to the pericardium was described >80 years ago.10,11 In the advent of coronary bypass surgery, bilateral IMA ligation in patients with CAD has been suggested to alleviate angina pectoris and ECG signs of ischemia,12–16 although this finding has been challenged by 2 very small sham-controlled trials.17,18 Using angiographic techniques, a total of 3 case reports have described the structural existence of in vivo naturally occurring anastomoses between one of the IMAs and the coronary circulation.19–21 Very recently, an experimental study in 8 dogs undergoing coronary artery constriction and IMA ligation failed to reveal myocardial microsphere perfusion via IMA in the single animal that survived the entire study protocol.22
Hence, the prevalence, functional relevance, and effect on myocardial ischemia of extracardiac coronary collateral supply via natural IMA bypasses are unknown. The present study in patients without and with CAD tested the hypotheses that coronary collateral function increases in the presence versus the absence of distal IMA balloon occlusion and that the former is reflected by reduced myocardial ischemia.
Study Design and Patients
This was a prospective, observational study in 120 patients undergoing coronary angiography for diagnostic purposes in the context of chest pain. The primary study end point was collateral flow index (CFI; see below for calculation) obtained in 180 instances during two 1-minute coronary artery balloon occlusions (a total of 360 measurements), the first with and the second without simultaneous distal IMA balloon occlusion (Figure 1). Half of the patients with half of the measurements underwent assessment of ipsilateral IMA–to–coronary artery anastomoses (left IMA to left coronary artery and right IMA to right coronary artery), and half of the patients with half of the measurements underwent assessment of contralateral IMA–to–coronary artery anastomoses. Secondary study end points were the quantitatively determined intracoronary ECG ST-segment elevation and angina pectoris during the same 1-minute coronary occlusions. Criteria for study inclusion were age >18 years, written informed consent to participate in the study, and 0- to 3-vessel chronic stable CAD. Exclusion criteria were acute coronary syndrome, previous myocardial infarction in the vascular region undergoing CFI measurement, and severe hepatic or renal failure (creatinine clearance <15 mL·min−1·1.73 m−2).
The study was approved by the ethics committee of the Kanton of Bern, Switzerland, and all patients gave written informed consent to participate.
Cardiac Catheterization and Coronary Angiography
Patients underwent left heart catheterization and coronary angiography for diagnostic purposes from the right femoral artery approach. Biplane left ventriculography was performed, followed by coronary angiography. Coronary artery stenoses were determined quantitatively as percent diameter reduction with the guiding catheter used for calibration. Aortic pressure (Pao) was obtained with a 6F coronary artery guiding catheter. Central venous pressure (CVP) was measured via the right femoral vein.
Invasive Coronary Assessment
Primary Study End Points
Coronary occlusive collateral flow relative to normal antegrade flow through the nonoccluded coronary artery (CFI) was determined from coronary pressure measurements. A 0.014-in pressure-monitoring angioplasty guide wire (Pressure Wire, St. Jude Medical, Eschborn, Germany) was set at zero, calibrated, advanced through the guiding catheter, and positioned in the distal part of the vessel of interest. CFI was determined by simultaneous measurement of mean Pao (mm Hg), the distal coronary artery pressure during balloon occlusion (Poccl; mm Hg), and the CVP (mm Hg; Figure 2) obtained during the last 30 seconds of the 1-minute coronary balloon occlusions. CFI was calculated as (Poccl−CVP) divided by (Pao−CVP).23 The accuracy of pressure-derived CFI measurements compared with ECG signs of myocardial ischemia during occlusion and with absolute myocardial perfusion measurements has been documented previously.5,24,25
Secondary Study End Points
Signs of myocardial ischemia were assessed simultaneously with CFI measurement as quantitatively determined intracoronary ECG ST-segment elevation (mV; Figure 2); the intracoronary ECG lead was obtained from the angioplasty guide wire via a cross-clamp to lead V1.3,5 Myocardial ischemia during the 1-minute coronary occlusions was also characterized by the presence or absence of angina pectoris.
Before the diagnostic examination, 2 puffs of oral isosorbide dinitrate were given. After diagnostic coronary angiography and at the start of the invasive study procedure, all patients received 5000 U heparin intravenously. The left or right IMA was intubated via a second 5F right femoral artery introducer sheath using a 5F mammary artery guiding catheter. IMA angiography was performed (Figure 1). A 2.5-mm angioplasty balloon catheter (20 mm long) was placed distally at or slightly below the level of the heart. The coronary artery subsequently undergoing CFI measurements was chosen on the basis of the presence of a stenotic lesion requiring percutaneous coronary intervention or on the basis of ease of access in case of a nonstenotic vessel. A 6F coronary guiding catheter was used in all cases. Fractional flow reserve was obtained before CFI. Fractional flow reserve was determined with the pressure guide wire positioned distally in the nonoccluded vessel of interest with the use of an intracoronary bolus of ≈70 μg adenosine for hyperemia induction: Fractional flow reserve equals distal coronary pressure divided by Pao. Shortly before the first CFI measurement, the IMA angioplasty balloon was inflated at a pressure of 5 to 7 atm, and complete occlusion was established by angiography. For CFI measurement, an adequately sized angioplasty balloon catheter (diameter ranging from 2.5–4 mm) was positioned in the proximal part of the vessel while the pressure guide wire remained distally, and balloon inflation occurred at a pressure of 1 to 2 atm. Complete coronary occlusion was established by angiography (Figure 1). During this vessel occlusion, simultaneous Poccl, Pao, and CVP were obtained for the calculation of CFI (Figure 2). During the entire procedure, the intracoronary ECG obtained from the guide wire was recorded. At the end of the first 1-minute balloon occlusion, the IMA and the coronary artery angioplasty balloons were released in this sequence. Immediately after CFI measurement, the patient was asked about the occurrence of angina pectoris during the 1-minute coronary artery balloon occlusion. A few minutes after the combined occlusion of the IMA and coronary artery, the second coronary artery occlusion was performed with the angioplasty balloon at the identical location as in the first occlusion. The sequence of coronary occlusions remained unchanged throughout the study: first with and second without simultaneous IMA occlusion.
Intraindividual comparison of CFI, intracoronary ECG ST-segment elevation, and heart rate obtained in the presence versus the absence of IMA occlusion was performed by a paired Student t test. A mixed linear model was used to assess the within-person correlation of repetitive measurements of continuous variables in >1 coronary artery. Because repetitive intraindividual measurements in different coronary arteries were not shown to be related to the study end points, between-group comparisons of continuous demographic, clinical, angiographic, and hemodynamic variables, CFI, and intracoronary ECG data were performed by factorial ANOVA followed by the Bonferroni post hoc test (values of P<0.0033 indicating significance in the context of multiple testing). Study groups were established on the basis of the 6 different combinations of IMA with coronary artery occlusion. The χ2 test or, when applicable, the Fisher exact test was used for comparison of categorical variables among the study groups. Continuous variables are given as mean and SD or SE or as median and interquartile range when applicable (nonnormal distribution of data).
A total of 180 pairs of CFI measurements were performed among the 120 study patients, that is, 60 patients underwent 1 and 60 patients underwent 2 CFI measurements (Table 1). The prevalence of a functional IMA–to–coronary artery connection as defined by a larger CFI in the presence compared with the absence of IMA occlusion was 123 of 180 (68%). During IMA occlusion, CFI was 0.110±0.074; in the absence of IMA occlusion, CFI was 0.096±0.072 (P<0.0001).
Patient Characteristics and Clinical Data
There were no statistically significant differences between the groups in terms of age, occurrence of cardiovascular risk factors, and intake of cardiovascular drugs (Table 1). The proportion of men differed significantly between the study groups (Table 1).
Hemodynamic and Coronary Angiographic Data
There was no difference between the groups in systemic blood pressure, left ventricular ejection fraction, and left ventricular end-diastolic pressure (Table 2). The number of coronary arteries with CAD, the total number of stenotic lesions, the percent diameter narrowing of the stenosis (vessel undergoing CFI measurement), and the fractional flow reserve obtained in the same vessel did not differ statistically between the groups (Table 2).
IMA Occlusion and Related Changes in Study End Points
IMA balloon occlusion time before coronary balloon occlusion was similar between the study groups (Table 3). Heart rate obtained during simultaneous IMA and coronary artery occlusion and during coronary occlusion without IMA occlusion did not differ either intraindividually (P=0.29) or between the groups (Table 3).
Primary Study End Point
CFI obtained simultaneously with IMA occlusion was different between the study groups and was similar in the absence of IMA occlusion (Table 3). Figure 2 exemplifies an augmented CFI in the presence versus the absence of simultaneous IMA balloon occlusion. The individual changes in CFI in the presence versus the absence of IMA occlusion are shown in Figure 3.
The difference of CFI obtained in the presence of IMA occlusion minus CFI in the absence of IMA occlusion was highest and most consistently positive during left IMA with left anterior descending artery (LAD) occlusion and during right IMA with right coronary artery (RCA) occlusion (ipsilateral occlusions): 0.033±0.044 and 0.025±0.027, respectively (Table 3 and Figure 4). This CFI difference was absent during right IMA with LAD occlusion and during left IMA with RCA occlusion (contralateral occlusions): −0.007±0.034 and 0.001±0.023, respectively (Table 3 and Figure 4). The respective CFI differences during either IMA with left circumflex artery (LCx) occlusion were inconsistently positive (Table 3 and Figure 4).
In the 60 patients undergoing 2 coronary artery measurements, the mentioned CFI differences were statistically independent between the 2 coronary arteries: ΔCFI in the first vessel=0.01+0.1 ΔCFI in the second vessel; r2=0.005, P=0.61 (ΔCFI is CFI with IMA occlusion minus CFI without IMA occlusion).
Secondary Study End Points
Figure 2 exemplifies reduced intracoronary ECG ST-segment elevation in the presence versus the absence of simultaneous IMA balloon occlusion. Intracoronary ECG ST-segment elevation normalized for R amplitude was diminished most during ipsilateral left IMA with LAD occlusion and during right IMA with RCA occlusion, whereas it remained unchanged or was worsened during contralateral IMA occlusion or during IMA with LCx occlusion, respectively (Table 3 and Figure 4). Angina pectoris tended to be diminished during ipsilateral IMA with LAD and RCA occlusions (Table 3).
The present clinical study demonstrated for the first time the prevalent in vivo function of natural IMA–to–coronary artery bypasses and their anti-ischemic effect. Functional natural IMA bypasses were consistently present during ipsilateral IMA with coronary artery occlusion (right IMA with RCA and left IMA with LAD); they were absent or inconsistently present during contralateral IMA with coronary artery occlusion or during either IMA with LCx occlusion.
Extracardiac Coronary Collateral Supply
The branches of the IMAs are the pericardiacophrenic arteries with their high takeoff, anterior intercostal arteries, perforating arteries, musculophrenic arteries, and superior epigastric arteries (ie, the continuation of the IMAs), which finally anastomose with the external iliac arteries via the inferior epigastric arteries. In this article, the older term IMA is used instead of the newer term internal thoracic artery in the context of historical aspects relating to IMA surgery. The anatomy of extracardiac coronary arterial anastomoses taking their origin from the bronchial or the internal thoracic arteries was alluded to as early as 1803 by Albrecht von Haller (cited in Loukas et al26). Hudson et al10 rediscovered them accidentally by observing the supply of ink injected into the coronary circulation to the pericardium and to extracardiac arterial regions. Hence, communication between the coronary circulation and pericardiacophrenic branches of the IMAs, but also the anterior mediastinal, phrenic, and intercostal arteries and the esophageal arterial branches of the aorta, was demonstrated.11 The bronchial arteries supply the posterior part of the pericardium, and extracardiac anastomoses to the coronary arteries are preferentially found at sites of pericardial reflections such as entry into the pericardium of the caval veins.27 The most common bronchial artery–to–coronary artery communication has been documented to the left circumflex coronary artery.27 Structurally, this may explain why in our present study functional IMA bypasses to the LCx were present only inconsistently and why, in essence, they had no anti-ischemic effect.
Function of Natural IMA Bypasses
In the context of the first studies of bilateral IMA ligation (see below),12–16,28 canine experiments on the extracorporeal bypass have shown that the procedure as carried out in the second intercostal space led to an average increase in total coronary flow of ≈6 to 10 mL/min.29 It was thought that the hemodynamic effect of IMA ligation was transmitted by a local pressure rise of 12 to 15 mm Hg in the subclavian artery with unchanged systemic pressure.30 If the macroscopic arterial circulation is considered a system of connecting tubes, an instantaneous pressure equilibration would physically be expected rather than the mentioned pressure difference. Conversely, the length of the arterial system between different sections resisting the pressure transmission could serve as an explanation for the findings by Taber and Marchioro.30
Compared with the cited experiments,29,30 the present study protocol did not, for ethical reasons, temporarily block the entire coronary circulation but instead blocked only part of it, that is, 1 of the 3 coronary arteries. Myocardial ischemia was induced twice with and without simultaneous IMA occlusion. The sequence of coronary occlusions with IMA occlusion first was held constant as a conservative measure favoring the null hypothesis of the study that coronary collateral function does not increase in the presence versus the absence of distal IMA balloon occlusion. Possible coronary collateral recruitment or ischemic preconditioning occurring during the second (but not the first) occlusion could be misinterpreted as augmented CFI or diminishing signs of ischemia in the context of IMA occlusion if it occurred during the second but not the first coronary occlusion. Despite this study design, CFI was higher in the presence versus the absence of IMA occlusion in 68% of the measurements, and overall, this difference amounted to 0.025 compared with the absence of IMA occlusion (P<0.0001). The fact that the anatomic vicinity of the occluded IMA and coronary artery rendered this finding more consistent enhances the verification of the hypothesis in the case of the LAD and RCA. The variability in response of either IMA occlusion during LCx occlusion increased rather than decreased, which may be seen in light of the variable supply of the LCx coronary territory by extracardiac sources other than the IMA (bronchial arteries).27 The consistency of the CFI increase during IMA occlusion was slightly less in the case of LAD with left IMA occlusion (25 of 30 measurements) than in the case of RCA with right IMA occlusion (28 of 30 measurements). The most likely explanation for a worsening response in the context of ipsilateral IMA-to-LAD and IMA-to-RCA occlusions is strong collateral recruitment or ischemic preconditioning during the second coronary occlusion in nonfunctional IMA anastomoses. Theoretically, the possibility of the 20-mm-long angioplasty balloon obstructing the takeoff of the pericardiacophrenic branch directly supplying the coronary system is given as an alternative explanation for a diminished CFI during ipsilateral IMA occlusion. However, for this study, it is irrelevant because the IMA occlusion site was always distal at the fifth or sixth intercostal space, where the bifurcation of the superior epigastric and the musculophrenic artery is located (Figure 1A). The bifurcation of the IMA and the pericardiacophrenic artery is, on the other hand, its first or second one at the level of the first or second intercostal space.
Anti-Ischemic Effect of Natural IMA Bypasses
This topography of the IMA-pericardiacophrenic bifurcation provided the rationale for the IMA ligation site chosen in the trials carried out in the late 1950s among ≈500 symptomatic CAD patients.15,17,18,28,31–33 IMA ligation as a treatment for angina pectoris was conceived by Fieschi in 1939, and in 1954, Battezzati et al12 documented anew the existence of connections between both IMAs and the myocardium by methylene blue injection into the IMAs. Transthoracic surgical access to the IMAs was performed under local anesthesia by a small incision between the second and third rib. The primary end point of the clinical trials was angina pectoris and, inconsistently, ECG signs of myocardial ischemia. Battezzati and coworkers28 reported the results of their uncontrolled trial among 304 CAD patients in 1959. Nearly all of the patients improved in terms of their symptoms, and this improvement was sustained during follow-up. In a further uncontrolled trial among 50 CAD patients, Kitchell et al31 reported similarly favorable results, with symptomatic relief in 68% of the patients. The following sham-controlled trials of bilateral IMA ligation in 35 CAD patients coined the phrase “surgery as placebo” in the context of their negative results.17,18,34 Although the introduction of a sham-control study design in the context of surgical trials was seminal,35 the conclusion drawn from the negative results of the IMA ligation trials at hand is questionable in the context of the present investigation. Possibly in this context, the anti-ischemic concept of IMA ligation has been promoted again lately.22,36–38
In the trial by Cobb et al,17 angina pectoris relief was found in 5 of 8 patients (63%) after IMA ligation and in 5 of 7 patients (71%) after IMA sham ligation. Dimond and coworkers18 reported 9 of 13 in the verum and 5 of 5 in the sham-operation group, respectively. In comparison, angina pectoris relief during a 1-minute ipsilateral IMA plus simultaneous coronary balloon occlusion in our study occurred in 6 of 60 measurements among 40 patients; it was absent during contralateral IMA occlusion (P=0.08). From this perspective, the abrupt stop of bilateral transthoracic IMA ligation was likely caused by the advent of IMA bypass grafting rather than by the slim evidence against IMA ligation claimed by the controlled trials. The soft study end point of angina pectoris requires patient numbers that, for meaningful results, are 1 order of magnitude higher than those recruited for the sham-controlled IMA ligation trials. This is even more so in case of an inconsistently applied ischemic stimulus such as daily activities versus the systematically used 1-minute coronary occlusion. In this context, the present study predefined intracoronary ECG ST-segment elevation during coronary occlusion, not angina pectoris, as the first end point for ischemia, the former of which was consistently reduced during ipsilateral IMA with RCA or LAD occlusion. Another drawback of the historical IMA ligation studies was that their patients did not undergo coronary angiography, and it is unknown how many in the verum group had, by chance, their culprit lesion in the LCx, where the effect of IMA ligation from either side is variable and not anti-ischemic. Finally, the systematic IMA ligation at the second intercostal space may have resulted in a variable site of IMA occlusion proximal or distal to the pericardiacophrenic artery, that is, the source of extracardiac supply to the coronary circulation. Occlusion proximal to the bifurcation of the pericardiacophrenic artery likely resulted in a much reduced supply to the pericardium compared with distal occlusion.
The present study performed collateral function measurements of the IMAs themselves in only a small minority of the cases, which does not allow reliable estimation of their CFI for a distinction between the effect of proximal and distal IMA occlusion. Anatomically, there is communication between the IMAs and the iliac external arteries via the superior and inferior epigastric arteries. On the basis of the rare functional IMA CFI measurements of the present study, collateral supply from the caudal side amounted to approximately two thirds during proximal IMA occlusion compared with patency. The absence of systematic proximal IMA occlusion implies a further study limitation, that is, the missing information on the effect of proximal IMA occlusion together with occlusion of the pericardiacophrenic branch. Because the latter has been described as the extracardiac source of coronary arterial supply, the effects found in the present study would have been absent during proximal IMA occlusion at the site of the pericardiacophrenic artery bifurcation. Finally, IMA angiography during distal occlusion was systematically performed, but image quality at the end of the 1-minute occlusion was too inconsistent to allow proper analysis of contrast medium supply to the coronary circulation. In fact, this could be seen in only 2 to 3 patients in our study (see Figure 1).
From the present study findings, an anti-ischemic therapeutic approach alternative to IMA bypass grafting (ie, distal IMA occlusion by invasive techniques) can be considered. In a first step, catheter-based IMA occlusion ought to be investigated conceptually in the setting of the less frequently grafted right IMA among patients with ischemia in the RCA territory.
There is a functional, ischemia-reducing extracardiac coronary artery supply via ipsilateral but not via contralateral natural IMA bypasses.
We thank Hélène Steck, RN, Raphael Grossenbacher, RN, and all members of the catheterization laboratory staff for their expert assistance.
Sources of Funding
This study was supported by grants from the Swiss National Science Foundation for research (grant 3200B_141030/1 to Dr Seiler), and from the Bangerter-Rhyner Foundation, Bern, Switzerland (to Drs Stoller and Seiler).
- Received January 21, 2014.
- Accepted April 10, 2014.
- © 2014 American Heart Association, Inc.
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Until now, the prevalence, functional relevance, and effect on myocardial ischemia of extracardiac coronary collateral supply via natural internal mammary artery (IMA) bypasses have been unknown. The present study in patients without and with coronary artery disease tested the hypotheses that coronary collateral function increases in the presence versus the absence of distal IMA balloon occlusion and that the former is reflected by reduced myocardial ischemia. The study among 120 patients with chronic stable coronary artery disease undergoing coronary angiography found that there is a functional, ischemia-reducing extracardiac coronary artery supply via ipsilateral (ie, during left IMA with left anterior descending artery occlusion and during right IMA with right coronary artery occlusion) but not via contralateral natural IMA bypasses. On the basis of the findings presented here, an anti-ischemic therapeutic approach alternative to IMA bypass grafting, that is, distal IMA occlusion by invasive techniques, can be considered. In a first step, catheter-based IMA occlusion ought to be conceptually investigated in the setting of the less frequently grafted right IMA among patients with ischemia in the right coronary artery territory.