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Objectives: In this study, we sought to assess safety of symptom-limited exercise stress tests the day after coronary stenting., Background: Isolated cases of coronary stent thrombosis have been linked to early exercise stress testing, thereby questioning the safety of unrestricted physical activity after the coronary procedure., Methods: At a single center, 1,000 patients were randomized to a symptom-limited stress test the day after coronary stenting or no stress test. The antiplatelet regimen consisted of acetylsalicylic acid and postprocedural ticlopidine or clopidogrel. The primary end point of the study was the incidence of clinical stent thrombosis at 14 days. The secondary end point was the occurrence of access site complications., Results: Clinical stent thrombosis occurred in five patients (1%) undergoing stress test and in five patients (1%) randomized to no stress test (p = 1.0). Access site complications were detected in 4% and 5.2% of cases, respectively (p = 0.37)., Conclusions: Symptom-limited exercise stress testing the day after coronary stenting does not increase the risk of clinical stent thrombosis or access site complications. Further investigations on safety of early vigorous exercise after coronary stenting in a non-supervised setting are warranted.

Background: Beta-adrenergic blocking agents are the cornerstone in the treatment of coronary artery disease (CAD). The exact pathophysiologic mechanism is not clear but depends largely on the oxygen-sparing effect of the drug. Thus, the effect of metoprolol on coronary flow reserve and coronary flow velocity reserve (CFVR) was determined in patients with CAD., Methods: Coronary blood flow velocity was measured with the Doppler flow wire in 23 patients (age: 56 +/- 10) undergoing percutaneous transluminal coronary angioplasty for therapeutic reasons. Measurements were carried out at rest, after 1-min vessel occlusion (postischemic CFVR) as well as after intracoronary adenosine (pharmacologic CFVR) before and after 5 mg intravenous metoprolol. In a subgroup (n = 15), absolute flow was measured from coronary flow velocity multiplied by coronary cross-sectional area., Results: Rate-pressure product decreased after metoprolol from 9.1 to 8.0 x 10(3) mm Hg/min (p < 0.001). Pharmacologic CFVR was 2.1 at rest and increased after metoprolol to 2.7 (p = 0.002). Likewise, postischemic CFVR increased from 2.6 to 3.3 (p < 0.001). Postischemic CFVR was significantly higher than pharmacologic CFVR before as well as after metoprolol. Coronary vascular resistance decreased after metoprolol from 3.4 +/- 2.0 to 2.3 +/- 0.7 mm Hg x s/cm (p < 0.02)., Conclusions: The following conclusions were drawn from this study. Metoprolol is associated with a significant increase in postischemic and pharmacologic CFVR. However, postischemic CFVR is significantly higher than pharmacologic CFVR. The increase in CFVR by metoprolol can be explained by a reduction in vascular resistance. The increase in CFVR (= increased supply) and the reduction in oxygen consumption (= decreased demand) after metoprolol explain the beneficial effect of this beta-blocker in patients with CAD.

Objectives: The purpose of this investigation in patients with poorly and well developed coronary collaterals was to assess the influence of collateral and collateral adjacent vascular resistances and, in part, a stenotic lesion of the collateral supplying vessel on the hemodynamic collateral responses to adenosine., Background: In humans, little is known about the functional behavior of the coronary collateral circulation., Methods: In 50 patients with one- and two-vessel coronary artery disease (CAD) undergoing percutaneous transluminal coronary angioplasty (PTCA), collateral flow index (CFI, no unit) changes and vascular resistance index (R, cm/mm Hg) changes of the collateral (R(coll)) and the distal collateral receiving (R4) vessel in response to adenosine (140 microg/min/kg IV) were measured by intracoronary (i.c.) Doppler and pressure guidewires. The variables were determined at baseline and during adenosine in patients with poor (angiographic collateral degree before PTCA <2 of 0 to 3) and good coronary collaterals., Results: Pressure-derived CFI (CFI(p)) decreased under adenosine in patients with poor collaterals, and it increased in the group with good collaterals. There were inverse correlations between the adenosine-induced change in CFI(p) and the change in R(coll) (r = 0.61, p = 0.0001). In the group with good, but not with poor collaterals, there was also a significant correlation between CFI(p) increase and the decrease in R4, between the severity of the contralateral stenosis and CFI(p) augmentation and among the left versus right coronary artery as ipsilateral vessel and CFI(p) change., Conclusions: Overall, patients with well, versus poorly developed coronary collaterals do better regarding the capacity to increase collateral flow in response to adenosine. In patients with good, but not poor, collaterals, an adenosine-induced collateral flow increase depends on the ipsilateral distal vascular resistance decrease, but is also directly influenced by the severity of a contralateral stenosis and probably by the size of the collateralized vascular bed.

Objectives: The purpose of this study in patients with quantitatively determined, poorly developed coronary collaterals was to assess the contribution of ischemic as well as adenosine-induced preconditioning and of collateral recruitment to the development of tolerance against repetitive myocardial ischemia., Background: The development of myocardial tolerance to repeated ischemia is nowadays interpreted to be due to biochemical adaptation (i.e., ischemic preconditioning)., Methods: In 30 patients undergoing percutaneous transluminal coronary angioplasty, myocardial adaptation to ischemia was measured using intracoronary (i.c.) electrocardiographic (ECG) ST segment elevation changes obtained from a 0.014-in. (0.036 cm) pressure guidewire positioned distal to the stenosis during three subsequent 2-min balloon occlusions. Simultaneously, an i.c. pressure-derived collateral flow index (CFI, no unit) was determined as the ratio between distal occlusive minus central venous pressure divided by the mean aortic minus central venous pressure. The study patients were divided into two groups according to the pretreatment with i.c. adenosine (2.4 mg/min for 10 min starting 20 min before the first occlusion, n = 15) or with normal saline (control group, n = 15)., Results: Collateral flow index at the first occlusion was not different between the groups (0.15 +/- 0.10 in the adenosine group and 0.13 +/- 0.11 in the control group, p = NS), and it increased significantly and similarly to 0.20 +/- 0.14 and to 0.19 +/- 0.10, respectively (p < 0.01) during the third occlusion. The i.c. ECG ST elevation (normalized for the QRS amplitude) was not different between the two groups at the first occlusion (0.25 +/- 0.13 in the adenosine group, 0.25 +/- 0.19 in the control group). It decreased significantly during subsequent coronary occlusions to 0.20 +/- 0.15 and to 0.17 +/- 0.13, respectively. There was a correlation between the change in CFI (first to third occlusion; deltaCFI) and the respective ST elevation shift (deltaST): deltaST = -0.02 to 0.78 x deltaCFI; r = 0.54, p = 0.02., Conclusions: Even in patients with few coronary collaterals, the myocardial adaptation to repetitive ischemia is closely related to collateral recruitment. Pharmacologic preconditioning using a treatment with i.c. adenosine before angioplasty does not occur. The variable responses of ECG signs of ischemic adaptation to collateral channel opening suggest that ischemic preconditioning is a relevant factor in the development of ischemic tolerance.

Objectives: This study evaluated two methods for the quantitative measurement of collaterals using intracoronary (IC) blood flow velocity or pressure measurements., Background: The extent of myocardial necrosis after coronary artery occlusion is substantially influenced by the collateral circulation. So far, qualitative methods have been available to assess the human coronary collateral circulation, thus restraining the conclusive investigation of, for example, therapies to promote collateral development., Methods: Fifty-one patients with a coronary artery stenosis to be treated by percutaneous transluminal coronary angioplasty (PTCA) were investigated using IC PTCA guidewire-based Doppler and pressure sensors positioned distal to the stenosis. Simultaneous measurements of aortic pressure, IC velocity and pressure distal to the stenosis during and after PTCA provided the variables for calculating collateral flow indices (CFIv and CFIp) that express collateral flow as a fraction of flow via the patent vessel. Both CFIv and CFIp were compared with conventional methods for collateral assessment, among them ST-segment changes >1 mm on IC and surface electrocardiogram (ECG) at PTCA. Also, CFIv and CFIp were compared with each other., Results: In 11 patients without ECG signs of ischemia during PTCA (sufficient collaterals), relative collateral flow amounted to 46% as determined by Doppler and pressure wire. Patients with insufficient collaterals (n=40) had relative collateral flow values of 18%. Using a threshold of CFI=30%, sufficient and insufficient collaterals could be diagnosed with 100% sensitivity and 93% specificity by IC Doppler, and 75% sensitivity and 92% specificity by IC pressure measurements. The agreement between Doppler and pressure measurements was good: CFIv=0.08 + 0.8 CFIp, r=0.80, p=0.0001., Conclusions: Intracoronary flow velocity or pressure measurements during routine PTCA represent an accurate and, at last, quantitative method for assessing the coronary collateral circulation in humans.

Objectives: This prospective, cross-sectional study sought to determine an association between the level of long-term physical activity as well as other clinical and angiographic variables and an index of collateral flow to the vascular region undergoing percutaneous transluminal coronary angioplasty (PTCA)., Background: There is limited and conflicting information about the effect of physical exercise on the coronary collateral circulation in humans, partly because previous studies lacked a quantitative means of assessing collateral channels., Methods: In 79 patients (mean [+/-SD] age 58 +/- 10 years) with coronary artery disease undergoing PTCA (no transmural myocardial infarction), a coronary collateral flow index was determined as the ratio between the intracoronary (IC) distal flow velocity time integral during (Vi(occl)[cm]) and after (Vi(occl) [cm]) PTCA of the stenosis. Vi(occl)/Vi(occl) was measured by a 0.014-in. Doppler guide wire, from which an IC electrocardiogram (ECG) was also recorded. Patients without ECG ST-T wave changes during PTCA were considered to have sufficient collateral channels (n = 29); those with ST-T wave changes were considered to have insufficient collateral channels (n = 50). The level of long-term physical activity was determined by a structured interview (score from 1 to 4). Univariate and multivariate analyses were used to find associations between physical activity as well as 30 other clinical and angiographic variables and the collateral flow index., Results: Long-term physical activity during leisure time, but not during work hours, and the severity of the stenosis undergoing PTCA were found to be independently and directly associated with sufficient versus insufficient collateral channels and with Vi(occl) Vi(occl) (leisure time physical activity [LTPA] score 3.3 +/- 0.9 vs. 2.4 +/- 1.0, p = 0.0002; percent diameter stenosis 88 +/- 12% vs. 80 +/- 14%, p = 0.001; Vi(occl)/Vi(occl) = 0.1 +/- 0.1 LTPA score, p = 0.0002 for trend)., Conclusions: In patients with coronary artery disease, the level of long-term physical activity during leisure time and the severity of the stenosis undergoing PTCA are directly associated with the quantitative degree of collateral flow.