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.

Reactive myocardial hyperaemia for functional assessment of coronary stenosis severity.

AIMS: Our aim was to compare functional assessment of coronary stenosis severity by fractional flow reserve (FFR) measurement, as induced by systemic adenosine, and by regional reactive myocardial hyperaemia. METHODS AND RESULTS: The primary study endpoints were coronary pressure-derived FFR values in response to intravenous adenosine infusion (140 µg/min/kg), and to a one-minute proximal coronary artery balloon occlusion (reactive hyperaemia) for the same stenosis of interest. The secondary study endpoint was coronary collateral flow index (CFI) during the same occlusion. CFI is the ratio between simultaneous mean arterial occlusive pressure and mean aortic pressure, both subtracted by central venous pressure. As a reference, coronary artery stenoses were assessed quantitatively as percent diameter reduction (%S). One hundred and twenty-five patients with coronary artery disease were included in the study. There was an inverse association between quantitatively determined structural stenosis severity and adenosine-induced FFR as well as post-ischaemic reactive hyperaemia FFR (%S=1-0.004 FFR; both at p<0.0001). Sensitivity and specificity for detecting a stenosis of ≥50% at an FFR threshold of 0.80 was 0.891 and 0.605 (adenosine-induced FFR), and 0.817 and 0.684 (post-ischaemic FFR), respectively. The FFR difference for a given stenosis (post-ischaemic minus adenosine-induced FFR) was directly related to CFI. CONCLUSIONS: Regional reactive hyperaemia FFR is not inferior to systemic adenosine FFR in detecting structurally relevant coronary stenosis. Depending on the absence or presence of functional collaterals, systemic adenosine-induced FFR may underestimate or overestimate stenosis severity, respectively.

Direct quantitative assessment of the peripheral artery collateral circulation in patients undergoing angiography.

BACKGROUND: Despite the fact that numerous studies have pursued the strategy of improving collateral function in patients with peripheral artery disease, there is currently no method available to quantify collateral arterial function of the lower limb. METHODS AND RESULTS: Pressure-derived collateral flow index (CFIp, calculated as (occlusive pressure-central venous pressure)/(aortic pressure-central venous pressure); pressure values in mm Hg) of the left superficial femoral artery was obtained in patients undergoing elective coronary angiography using a combined pressure/Doppler wire (n=30). Distal occlusive pressure and toe oxygen saturation (Sao2) were measured for 5 minutes under resting conditions, followed by an exercise protocol (repetitive plantar-flexion movements in supine position; n=28). In all patients, balloon occlusion of the superficial femoral artery over 5 minutes was painless under resting conditions. CFIp increased during the first 3 minutes from 0.451±0.168 to 0.551±0.172 (P=0.0003), whereas Sao2 decreased from 98±2% to 93±7% (P=0.004). Maximal changes of Sao2 were inversely related to maximal CFIp (r(2)=0.33, P=0.003). During exercise, CFIp declined within 1 minute from 0.560±0.178 to 0.393±0.168 (P<0.0001) and reached its minimum after 2 minutes of exercise (0.347±0.176), whereas Sao2 declined to a minimum of 86±6% (P=0.002). Twenty-five patients (89%) experienced pain or cramps/tired muscles, whereas 3 (11%) remained symptom-free for an occlusion time of 10 minutes. CFIp values were positively related to the pain-free time span (r(2)=0.50, P=0.002). CONCLUSIONS: Quantitatively assessed collateral arterial function at rest determined in the nonstenotic superficial femoral artery is sufficient to prevent ischemic symptoms during a total occlusion of 5 minutes. During exercise, there is a decline in CFIp that indicates a supply-demand mismatch via collaterals or, alternatively, a steal phenomenon. CLINICAL TRIAL REGISTRATION-URL: http://www.clinicaltrials.gov. UNIQUE IDENTIFIER: NCT01742455.