Effect of permanent right internal mammary artery occlusion on right coronary artery supply: A randomized placebo-controlled clinical trial.

Natural, nonsurgical internal mammary artery (IMA) bypasses to the coronary circulation have been shown to function as extracardiac sources of myocardial blood supply. The goal of this randomized, placebo-controlled, double-blind trial was to test the efficacy of permanent right IMA (RIMA) device occlusion on right coronary artery (RCA) occlusive blood supply and on clinical and electrocardiographic (ECG) signs of myocardial ischemia. METHODS: This was a prospective superiority trial in 100 patients with chronic coronary artery disease randomly allocated (1:1) to RIMA vascular device occlusion (verum group) or to RIMA sham procedure (placebo group). The primary study end point was RCA collateral flow index (CFI) as obtained during a 1-minute ostial RCA balloon occlusion at baseline before and at follow-up examination 6 weeks after the trial intervention. CFI is the ratio between simultaneous mean coronary occlusive divided by mean aortic pressure both subtracted by central venous pressure. Simultaneously obtained secondary study end points were the registration of angina pectoris and quantitative intracoronary ECG ST-segment shift. RESULTS: CFI change during the follow-up period was +0.036 ±â€¯0.068 in the verum group and -0.021 ±â€¯0.097 in the placebo group (P = .0011). Angina pectoris during the same RCA balloon occlusions had disappeared at follow-up in 14/49 patients of the verum group and in 4/49 patients of the placebo group (P = .0091). Simultaneous intracoronary ECG ST-segment shift change revealed diminished myocardial ischemia at follow-up in the verum group and more severe ischemia in the placebo group. CONCLUSIONS: Permanent RIMA device occlusion augments RCA supply to the effect of diminishing clinical and electrocardiographic signs of myocardial ischemia during a brief controlled coronary occlusion.

Association of Palmar Arch Collateral Function and Radial Artery Occlusion After Transradial Access.

The prevalence and implications of radial artery occlusion (RAO) after transradial catheterization are an intensely discussed topic, resulting in numerous preventive strategies such as adjusted anticoagulation, residual-patency hemostasis, or distal puncture site. The present study aimed at assessing an association of palmar arch, in particular radial artery collateral function and RAO after transradial access (TRA) catheterization. Radial artery collateral function was determined using radial artery pressure signals in the nonobstructed vessel and during brief manual occlusion of the more proximal radial artery. Collateral flow index, the ratio of mean occlusive divided by mean nonocclusive arterial blood pressure, both subtracted by central venous pressure, was determined during manual RAO (radial artery collateral flow index [CFIrad]). The presence or absence of RAO was determined by Doppler ultrasound at least 3 months after TRA. A total of 630 patients with TRA coronary angiography underwent palmar arch, that is, radial and radial plus ulnar artery collateral function assessment. CFIrad was equal to 0.808 ± 0.144 (95% confidence interval 0.797 to 0.819). A total of 200 patients underwent Doppler ultrasound examination of their forearm arterial circulation 301 ± 140 days after TRA. Eight (4%) patients showed signs of RAO, 4 of whom (2%) had a complete RAO and 4 (2%) a stenosis above 30%. Patients with RAO showed a higher CFIrad than those without RAO: 0.900 ± 0.074 versus 0.801 ± 0.154 (p = 0.006). In conclusion, complete RAO as determined by Doppler ultrasound later than 3 months after TRA is rare (2%). In the long run, RAO appears to be related to a very well-developed radial artery collateral function.

Extracardiac coronary steal induced by upper limb hyperemia: a feature of internal mammary artery arteriogenesis.

Function of naturally existing internal mammary artery (IMA)-to-coronary artery anastomoses has been shown by augmented blood supply to the coronary collateral circulation in response to IMA occlusion. Theoretically, this beneficial functional connection is invertible and can be linked to coronary steal, the verification of whose hypothesis would provide alternate proof to the mentioned functional evidence. This was an observational study including 40 patients with chronic coronary syndrome, distal IMA occlusion, and upper limb hyperemia (verum group), and 40 propensity score matched controls (placebo group) without IMA occlusion or hyperemia. Primary study end point was the intergroup difference and temporal development in coronary collateral function (i.e., collateral flow index; CFI) as obtained at 30, 45, and 60 s following a proximal coronary artery balloon occlusion. CFI is the ratio between simultaneous mean coronary occlusive pressure divided by mean aortic pressure both subtracted by central venous pressure. To provoke a steal phenomenon, upper limb hyperemia was induced by upper arm blood pressure cuff deflation following a 5-min suprasystolic inflation ipsilateral to the sensor-wired coronary artery with release immediately after the first CFI measurement. Between the first and the second CFI measurement, CFI change (i.e., CFI@45s - CFI@30s) was absent in the verum group whereas there was CFI recruitment in the placebo group: 0.000 ± 0.023 and +0.009 ± 0.013, respectively; P = 0.032. Among patients with artificial distal IMA occlusion, induction of ipsilateral upper limb hyperemia provokes extracardiac coronary steal as expressed by temporarily absent collateral recruitment as it normally takes place without upper limb hyperemia.NEW & NOTEWORTHY Induction of ipsilateral upper limb hyperemia provokes extracardiac coronary steal among patients with artificial distal internal mammary artery occlusion. Coronary steal via the occluded internal mammary arteries serves as alternate proof of concept of the already existing evidence of their functional extracoronary collateral supply.

Functional assessment of myocardial ischaemia by intracoronary ECG.

INTRODUCTION: In patients with chronic coronary syndrome, percutaneous coronary intervention targets haemodynamically significant stenoses, that is, those thought to cause ischaemia. Intracoronary ECG (icECG) detects ischaemia directly where it occurs. Thus, the goal of this study was to test the accuracy of icECG during pharmacological inotropic stress to determine functional coronary lesion severity in comparison to the structural parameter of quantitative angiographic per cent diameter stenosis (%S), as well as to the haemodynamic indices of fractional flow reserve (FFR) and instantaneous wave-free ratio (iFR). METHOD: The primary study endpoint of this prospective trial was the maximal change in icECG ST-segment shift during pharmacological inotropic stress induced by dobutamine plus atropine obtained within 1 min after reaching maximal heart rate(=220 - age). IcECG was acquired by attaching an alligator clamp to the angioplasty guidewire positioned downstream of the stenosis. For the pressure-derived stenosis severity ratios, coronary perfusion pressure and simultaneous aortic pressure were continuously recorded. RESULTS: There was a direct linear relation between icECG ST-segment shift and %S: icECG=-0.8+0.03*%S (r2=0.164; p<0.0001). There were inverse linear correlations between FFR and %S: FFR=1.1-6.1*10-3*%S (r2=0.494; p<0.0001), and between iFR and %S: iFR=1.27-8.6*10-3*%S (r2=0.461; p<0.0001). Using a %S-threshold of ≥50% as the reference for structural stenosis relevance, receiver operating characteristics-analysis of absolute icECG ST-segment shift during hyperemia showed an area under the curve (AUC) of 0.678±0.054 (p=0.002; sensitivity=85%, specificity=50% at 0.34 mV). AUC for FFR was 0.854±0.037 (p<0.0001; sensitivity=64%, specificity=96% at 0.78), and for iFR it was 0.816±0.043 (p<0.0001;sensitivity=62%, specificity=96% at 0.83). CONCLUSIONS: Hyperaemic icECG ST-segment shift detects structurally relevant coronary stenotic lesions with high sensitivity, while they are identified highly specific by FFR and iFR.

Invasive Assessment of the Human Arterial Palmar Arch and Forearm Collateral Function During Transradial Access.

BACKGROUND: The present study aimed to quantitatively measure the pressure-derived function of the palmar arch and forearm arterial collateral circulation during transradial access. METHODS AND RESULTS: Palmar arch and forearm collateral function was determined using radial artery pressure signals in the nonobstructed vessel and during brief manual occlusions of the more proximal radial artery and of the radial plus ulnar arteries. Collateral flow index (CFI), the ratio of mean occlusive divided by mean nonocclusive arterial blood pressure, both subtracted by central venous pressure, was determined for CFI during radial artery occlusion (CFIrad) and CFI during radial plus ulnar artery occlusion. Before invasive CFI measurements, arterial palmar arch and forearm function was tested noninvasively by the modified Allen test (MAT). Two hundred fifty patients undergoing transradial access coronary angiography were included in the study. CFIrad was equal to 0.802±0.150 (95% CI, 0.783-0.820). CFI during radial plus ulnar artery occlusion was equal to 0.424±0.188 (95% CI, 0.400-0.447). There was an inverse linear relation between CFIrad and MAT in seconds (s): MAT=64-63×CFIrad ( r2=0.229; P<0.0001). Two hundred eleven patients had a normal and 39 patients an abnormal (>15 seconds) MAT. The group with normal MAT had a CFIrad of 0.830±0.111, and patients with abnormal MAT had a CFIrad of 0.648±0.224 ( P<0.0001). CONCLUSIONS: Direct invasive hemodynamic assessment of the palmar arch and forearm arterial function reveals collateral supply to the briefly occluded in comparison to the patent radial artery of 0.802. During external occlusion of both radial and ulnar artery, CFI amounts to an unexpectedly high value of 0.424.

Endothelialization of sirolimus-eluting stents with slow and extended drug release in the porcine overstretch model.

BACKGROUND: Vascular healing of intracoronary stents has been shown to be delayed in drug-eluting stents (DES) due to the cytotoxic compounds on the stent surface that prevent stent ingrowth and endothelialization. The lack of endothelialization explains the occurrence of late and very late stent thrombosis in DES. MATERIALS AND METHODS: In 11 house swines (body weight 38-45 kg), 3 stents were implanted randomly into the 3 large epicardial coronary arteries, namely a bare-metal stent (BMS), a sirolimus-eluting stent with slow-release (SES) and a SES with extended-release (SESXR). Stent length was 18 mm, and stent diameter 3 mm. All stents were of identical design. Animals were followed for 3 (n = 3), 7 (n = 4) and 14 (n = 4) days, respectively. One animal died before implantation due to hyperthermia. On the day of explantation, the animals were euthanized and endothelialization was tested by scanning electron microscopy after drying and sputtering the samples. Endothelial coverage was determined semiquantitatively by 2 observers. RESULTS: Endothelialization was more rapid with BMS and SESXR than SES at 3 and 14 days. At 7 days there were no significant differences between the 2 SES. CONCLUSIONS: Endothelialization of intracoronary stents is faster with BMS and SESXR at 3 days than with SES. These differences persist at 14 days, suggesting delayed vascular healing with the slow-release SES.