Cold cardioplegia for acute infarction a viable adjunct to reperfusion therapy?
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Animals↗
Biomedical subjects
Guy R Heyndrickx
Publications and source records attributed to Guy R Heyndrickx.
GLU-27 variant of beta2-adrenergic receptor polymorphisms is an independent risk factor for coronary atherosclerotic disease.
OBJECTIVE: Arg16Gly and Gln27Glu polymorphism of beta(2)-adrenergic receptors (beta 2AR) have been associated with several risk factors for coronary atherosclerotic disease (CAD). Nevertheless, conflicting data have been reported concerning their influence on CAD and cardiovascular clinical events. AIM: To investigate whether (a) beta 2AR polymorphisms are associated with CAD; and (b) the potential impact, if any, of these polymorphisms on cardiovascular clinical events in patients presenting with angina-like pain or silent ischemia. METHODS AND RESULTS: We screened 786 consecutive patients referred to cardiac catheterization because of angina-like pain or silent ischemia for Arg16Gly, Gln27Glu, Thr164Ile beta 2AR polymorphisms. Patients were divided in 2 groups according to the presence or absence of CAD at the angiography. Hundred subjects from blood donor center served as controls. Clinical endpoints were evaluated at baseline and up to 6 years follow-up. Glu-27 homozygous genotype and Glu-27 allele (Glu-27, allele frequency: 47% CAD versus 39% NO CAD, p<0.05) were more frequent in patients with CAD. At multivariate analysis, patients carrying Glu-27 allele showed a significantly higher risk of developing CAD (OR: 1.78, 95% CI: 1.21-2.63, p=0.004). At clinical follow-up, a higher incidence of coronary revascularization was noted in Glu-27 homozygotes as compared with Gln-27 homozygote patients. CONCLUSIONS: In patients at high risk for CAD and/or angina-like pain, Glu-27 allele of beta2 adrenergic receptor polymorphism is an independent risk factor for CAD and appears to be associated with higher incidence of myocardial revascularization.
Aged↗
Pretreatment of adult bone marrow mesenchymal stem cells with cardiomyogenic growth factors and repair of the chronically infarcted myocardium.
The in vivo cardiac differentiation and functional effects of unmodified adult bone marrow mesenchymal stem cells (MSCs) after myocardial infarction (MI) is controversial. We postulated that ex vivo pretreatment of autologous MSCs using cardiomyogenic growth factors will lead to cardiomyogenic specification and will result in superior biological and functional effects on cardiac regeneration of chronically infarcted myocardium. We used a chronic dog MI model generated by ligation of the coronary artery (n = 30). Autologous dog bone marrow MSCs were isolated, culture expanded, and specified into a cardiac lineage by adding growth factors, including basic FGF, IGF-1, and bone morphogenetic protein-2. Dogs underwent cell injection >8 wk after the infarction and were randomized into two groups. Group A dogs (n = 20) received MSCs specified with growth factors (147 +/- 96 x 10(6)), and group B (n = 10) received unmodified MSCs (168 +/- 24 x 10(6)). After the growth factor treatment, MSCs stained positive for the early muscle and cardiac markers desmin, antimyocyte enhancer factor-2, and Nkx2-5. In group A dogs, prespecified MSCs colocalized with troponin I and cardiac myosin. At 12 wk, group A dogs showed a significantly larger increase in regional wall thickening of the infarcted territory (from 22 +/- 8 to 32 +/- 6% in group A; P < 0.05 vs. baseline and group B, and from 19 +/- 7 to 21 +/- 7% in group B, respectively) and a decrease in the wall motion score index (from 1.60 +/- 0.05 to 1.35 +/- 0.03 in group A; P < 0.05 vs. baseline and group B, and from 1.58 +/- 0.07 vs. 1.56 +/- 0.08 in group B, respectively). The biological ex vivo cardiomyogenic specification of adult MSCs before their transplantation is feasible and appears to improve their in vivo cardiac differentiation as well as the functional recovery in a dog model of the chronically infarcted myocardium.
Adult Stem Cells↗
Assessment of renal artery stenosis severity by pressure gradient measurements.
OBJECTIVES: The purpose of this study was to define "significant" renal artery stenosis (i.e., a stenosis able to induce arterial hypertension). BACKGROUND: The degree of renal artery stenosis that justifies an attempt at revascularization is unknown. METHODS: In 15 patients, transstenotic pressure measurements were obtained before and after unilateral stenting. After stenting, graded stenoses were created in the stented segment by progressive inflation of a balloon catheter. Stenosis severity was expressed as the ratio of distal pressure (P(d)) corrected for aortic pressure (P(a)). Balloon inflation pressure was adjusted to create 6 degrees of stenosis (P(d)/P(a) from 1.0 to 0.5, each step during 10 min). Plasma renin concentration was measured at the end of each step in the aorta and in both renal veins. RESULTS: For a P(d)/P(a) ratio >0.90, no significant change in plasma renin concentration was observed. However, when P(d)/P(a) became <0.90, a significant increase in renin was observed in the renal vein of the stenotic kidney, finally reaching a maximal increase of 346 +/- 145% for P(d)/P(a) of 0.50 (p = 0.006). These values returned to baseline when the stenosis was relieved. In addition, plasma renin concentration increased significantly in the vein from the non-stenotic kidney (p = 0.02). CONCLUSIONS: In renal artery stenoses, a P(d)/P(a) ratio of 0.90 can be considered a threshold value below which the stenosis is likely responsible for an up-regulation of renin production and, thus, for renovascular hypertension. These findings might contribute to better patient selection for renal angioplasty.
Aged↗
Results of the first clinical study of adjunctive CAldaret (MCC-135) in patients undergoing primary percutaneous coronary intervention for ST-Elevation Myocardial Infarction: the randomized multicentre CASTEMI study.
AIMS: To examine the safety and efficacy of intravenous caldaret in patients with large acute ST-elevation myocardial infarction (STEMI) undergoing percutaneous coronary intervention (PCI). METHODS AND RESULTS: STEMI patients (n=387) with > or =10 mm summed ST-deviation on electrocardiogram were randomized to receive a 48 h infusion of caldaret 57.5 mg [lower dose (LD)], caldaret 172.5 mg [higher dose (HD)], or placebo, starting before PCI. Both HD and LD were well tolerated. In 247 patients with pre-PCI TIMI 0/1, there was no effect of HD or LD on single photon emission computed tomography infarct size or ejection fraction assessed at Day 7 and Day 30. Subgroup analyses suggest that future work in patients with anterior MI might be warranted. CONCLUSION: This first human experience with caldaret prior to direct PCI for large STEMI shows a good safety profile. No evidence of efficacy was discerned. Subgroup analyses in anterior MI patients showed some effects in endpoints studied, however, these findings require confirmation in a further study if a drug effect is to be established.
Angioplasty, Balloon, Coronary↗
Assessment of renal flow and flow reserve in humans.
OBJECTIVES: The purpose of this work was to establish the normal range of maximal renal hyperemic response in humans and to identify the ideal renal vasodilatory stimuli. BACKGROUND: Stenotic renovascular atherosclerosis is increasingly treated by percutaneous transluminal renal intervention but with an unpredictable outcome. This may be due to hemodynamically non-significant stenosis or the presence of irreversible damage to the glomerular circulation. We propose that the renovascular hyperemic response may help identify appropriate patients. METHODS: In 28 normotensive patients, quantitative angiographic measurements of the renal artery were obtained, and renal artery pressure and flow velocity were continuously recorded after various hyperemic agents. RESULTS: In a first group of 11 patients, a significant increase in renal artery average peak velocity (APV) was observed after intrarenal (IR) bolus injection of 600 microg isosorbide dinitrate (41 +/- 19%), 30 mg papaverine (50 +/- 34%), 50 microg dopamine (94 +/- 54%), 0.8 microg x kg(-1) fenoldopam (80 +/- 25%), and during IR infusion of 1 microg x kg(-1) x min(-1) fenoldopam (86 +/- 28%). A second group of 17 patients received intravenous infusion of dopamine (3, 5, 10, 20, 30, and 40 microg x kg(-1) x min(-1)). The 3 and 5 microg x kg(-1) x min(-1) of dopamine modestly reduced renal resistance index (RI) (-13 +/- 15% and -25 +/- 20%, respectively). At higher dosages, no further decline in RI was observed. No significant change in vessel diameter was observed before and after the administration of the pharmacological stimuli suggesting that changes in APV corresponded with changes in absolute renal blood flow. CONCLUSIONS: The normal renal flow reserve averages approximately 2 in humans with normal renal function. An IR bolus injection of 50 microg x kg(-1) of dopamine is the most convenient means to elicit maximal renal hyperemia.
Adult↗
Timing of intracoronary bone-marrow-derived stem cell transplantation after ST-elevation myocardial infarction.
It is still unclear whether the timing of intracoronary stem cell therapy affects the therapeutic response in patients with reperfused myocardial infarction. The natural course of healing the infarction and the presence of putative homing signals within the damaged myocardium appear to favor cell engraftment during the transendothelial passage in the early days after reperfusion. However, the adverse inflammatory environment, with its high oxidative stress, might be deleterious if cells are administered too early after reperfusion. In addition, current studies use mostly unfractionated cells and it remains to be addressed whether specific cell types, and their enrichment, would be better suited to augmenting the recovery at later time points. Here we highlight several aspects of the timing of intracoronary stem cell therapy and focus on time-related questions that are relevant to the design of future experimental and basic studies.
Animals↗
Early reperfusion phenomena.
Cycles of ischemia-reperfusion are ubiquitous in clinical cardiology. Depending on the duration and intensity of the ischemic episode as well as its repetition mode, several pathophysiologic syndromes have been identified, such as myocardial stunning, hibernation, and preconditioning. It remains a difficult exercise to distinguish ischemic from reperfusion damage. Production of oxygen free radicals and alteration in calcium homeostasis are major players during early reperfusion, responsible for the pathologic and functional alterations. At the molecular level, upregulation and downregulation of a number of genes have been observed in stunned myocardium, pointing toward some inborn survival adaptive mechanism. The no-reflow phenomenon, a most paradoxic event after reperfusion, usually occurs after more prolonged episodes of ischemia. The underlying mechanism involves additional lesions to the microvasculature interacting with myocytes lesions. Further insight into molecular and genomic adaptation to ischemia and reperfusion will undoubtedly help to improve our ability to fight reperfusion injury.
Animals↗
Hyperdynamic myocardial response to beta-adrenergic stimulation in patients with chest pain and normal coronary arteries.
OBJECTIVES: The goal of this study was to test the hypothesis that an abnormal response to beta-adrenergic stimulation may play a role in the pathophysiology of chest pain in patients with normal coronary arteries. BACKGROUND: The mechanism of angina-like (AL) chest pain in patients with angiographically normal coronary arteries remains controversial. METHODS: Fifty-eight patients with AL pain and a normal coronary angiogram underwent dobutamine echocardiography (DE) to evaluate regional wall motion and intraventricular flow velocities (IFV). Control patients consisted of 22 matched patients free of angina and coronary artery disease. Abnormal IFV were defined as dagger-shaped Doppler spectrum > or =3 m/s. RESULTS: Dobutamine-induced regional wall motion abnormalities did not develop in any of the patients. An IFV > or = 3 m/s was found in 28 patients (48%) with AL pain but in only 4 (18%) control patients (p < 0.05). In the subgroup of patients with AL pain and IFV > or =3 m/s, plasma renin concentration (PRC) was higher as compared with those with IFV <3 m/s (18 +/- 17 pg/ml vs. 9 +/- 6 pg/ml, p < 0.05). There were no differences in plasma ADR, NADR, or angiotensin-converting enzyme levels. Fourteen patients with angina and IFV > or =3 underwent control DE and blood sampling after 6 weeks treatment with 10 mg of bisoprolol. In these patients, a decrease in IFV (from 3.4 +/- 0.35 m/s to 2.46 +/- 0.64 m/s, p < 0.001) and a decrease in angina score (from 5.4 +/- 1.5 to 0.6 +/- 1.4, p < 0.001) were observed at follow-up. CONCLUSIONS: The present data suggest that an exaggerated myocardial response to beta-adrenergic stimulation plays a role in the mechanisms of chest pain in some patients with normal coronary arteries.
Adrenergic beta-Agonists↗
Long-term clinical outcome after fractional flow reserve-guided percutaneous coronary intervention in patients with multivessel disease.
OBJECTIVES: In the present study, we analyzed the clinical outcome of patients with multivessel coronary artery disease in whom at least one vessel was treated by percutaneous coronary intervention (PCI) and at least one other vessel was deferred on the basis of fractional flow reserve (FFR) measurements during the same session. BACKGROUND: Myocardial FFR is an established tool for assessing the severity of epicardial stenoses. It has been shown that it is safe to defer an intervention in single vessel disease patients when FFR >0.75. METHODS: One hundred two patients (66 +/- 10 years) with multivessel coronary artery disease were included in the study. In all patients, PCI of at least two vessels was contemplated. Yet in all of them at least one vessel was treated by PCI, whereas at least one other vessel was deferred based on an FFR >0.75. Major adverse cardiac events (MACE) were recorded during an average follow-up of 29 +/- 18 months. RESULTS: In 102 patients, 113 coronary arteries underwent PCI. In these arteries FFR was 0.57 +/- 0.13 and mean diameter stenosis was 68 +/- 14%. One hundred twenty-seven coronary arteries had an FFR >0.75 and PCI was deferred. In these arteries FFR was 0.86 +/- 0.06 and mean diameter stenosis was 47 +/- 12%. No death occurred during the follow-up. A MACE occurred in 9% and 13% of patients after 12 and 36 months, respectively. These MACE were related to 22 (9.2%) arteries. Among them, 8 (6.3%) MACE were related to one of the initially deferred vessels, whereas 14 (12.3%) MACE were related to one of the initially treated coronary artery. CONCLUSIONS: In patients with multivessel disease, PCI of hemodynamically non-significant stenoses can be safely deferred, even if initially planned on the basis of the angiogram.
Aged↗
Pressure-derived measurement of coronary flow reserve.
OBJECTIVES: We aimed to validate the technique of measuring the coronary flow reserve (CFR) with coronary pressure measurements against an established thermodilution technique. BACKGROUND: The CFR has traditionally required measurement of coronary blood flow velocity with the Doppler wire and, more recently, using a thermodilution technique with the coronary pressure wire. However, recent work has suggested that the CFR may be derived from pressure measurements alone (the ratio of the square root of the pressure drop across an epicardial stenosis during hyperemia to that value at rest). This depends on the assumption that friction losses across a coronary stenosis are negligible. METHODS: We compared pressure-derived CFR values with those obtained by the thermodilution technique using the intracoronary pressure wire in 38 stenoses in 34 patients with significant coronary stenoses undergoing percutaneous intervention. We also compared these two techniques of measuring CFR in 25 stenoses (6 vessels) artificially created by inflating small balloons within a stented coronary artery after percutaneous intervention. RESULTS: There is a close linear relationship between pressure-derived and thermodilution CFR in native (r(2) = 0.52; p < 0.001) and artificial stenoses (r(2) = 0.54; p < 0.05), although the pressure-derived technique appears to systematically underestimate CFR values in both situations. This applies to native and artificial stenoses. CONCLUSIONS: Coronary flow reserve cannot be measured merely with pressure alone, and it cannot be safely assumed that friction losses are negligible across a native coronary stenosis. These data suggest that friction loss is an important determinant of the pressure gradient along an atherosclerotic coronary artery.
Aged↗
Angiographic and three-dimensional intravascular ultrasound analysis of combined intracoronary beta radiation and self-expanding stent implantation in human coronary arteries.
This study tested the combination of vascular brachytherapy (VBT) and self-expanding Wallstent implantation in coronary lesions of patients at high risk for restenosis as assessed angiographically by quantitative coronary analysis and by 3-dimensional intravascular ultrasound analysis. Twenty-nine "de novo" lesions were managed with a self-expanding stent alone (n = 19) or with a self-expanding stent after beta-VBT (n = 10) in 27 patients who had been identified by high levels of plasma angiotensin-converting enzyme as being prone to myointimal growth after stent implantation. At 6 months, the increase in stent strut diameter was similar in the 2 groups by quantitative coronary analysis and 3-dimensional intravascular ultrasound (Delta mean stent strut diameter -0.33 +/- 0.3 vs -0.40 +/- 0.3 mm, p = 0.5; Delta stent area -11.8 +/- 6.1 vs -12.0 +/- 6.1 mm(2), p = 0.9; Delta stent volume -96.9 +/- 112 vs -83.5 +/- 73 mm(3), p = 0.7; for groups treated with VBT and self-expanding stents and only self-expanding stents, respectively). In-stent neointimal proliferation was decreased in the group treated with VBT and self-expanding stents (minimal luminal diameter 2.5 +/- 0.8 vs 1.88 +/- 0.8 mm, p = 0.04) by quantitative coronary analysis (minimal luminal area 6.7 +/- 2.5 vs 4.1 +/- 1.9 mm(2), p = 0.01), by intravascular ultrasound, and proliferation volume (84.6 +/- 66.4 vs 159.2 +/- 103.5 mm(3), p = 0.05) by 3-dimensional intravascular ultrasound. Positive vessel and luminal remodelings were observed in 50% of the group treated with VBT and self-expanding stents and in 11% of the group treated only with self-expanding stents (p = 0.02). The combined use of VBT and self-expanding stents is a novel approach that enlarges vascular lumen by preventing vessel constriction and neointimal proliferation. The feasibility and good results of this experimental approach suggest that the simultaneous use of these 2 technologies may be an interesting alternative for difficult vascular districts with high restenosis rates, such as peripheral circulation in the lower limbs.
Angioplasty, Balloon↗
Tissue doppler imaging predicts recovery of left ventricular function after recanalization of an occluded coronary artery.
OBJECTIVES: We tested the hypothesis that the tissue Doppler imaging (TDI)-derived positive preejection velocity (+VIC) can predict the recovery of contractile function after revascularization in patients with a recent myocardial infarction. BACKGROUND: In experimental studies, the presence and extent of TDI-derived +VIC correlated with the extent of viable myocardium. METHODS: Forty-three patients with a large myocardial infarction and an occluded left anterior descending (n = 38) or dominant right coronary (n = 5) artery were selected. The median duration of occlusion was 24 h. Longitudinal myocardial velocities were recorded at rest by pulsed-wave TDI echocardiography 6 +/- 2 h after revascularization. Functional recovery was defined as an increase in segmental chordal shortening > or =10% at three-month follow-up left ventricular angiogram as compared with baseline. RESULTS: A good quality TDI signal was obtained in 309 of 324 analyzed segments (95.4%). Severe dysfunction was present in 198 segments of which 126 (64%) showed recovery at three-month follow-up. Sampling of all dysfunctional segments lasted 11 +/- 4 min per patient. Sensitivity, specificity, and accuracy of the +VIC to predict segmental recovery were 91%, 71%, and 84%, respectively. The percentage of segments that were dysfunctional at angiography but showed a +VIC correlated with improvement of both global left ventricular ejection fraction (r = 0.60, p = 0.001) and wall motion score index (r = -0.78, p < 0.0001) at follow-up. CONCLUSIONS: Assessment of +VIC by pulsed-wave TDI is a simple and accurate method that predicts recovery of contractile function after revascularization in patients with a recent myocardial infarction.
Angioplasty, Balloon, Coronary↗
Alpha-adrenergic receptor blockade and hyperaemic response in patients with intermediate coronary stenoses.
BACKGROUND: Maximal hyperaemia is paramount in the diagnosis of patients with coronary artery disease. However in these patients, enhanced alpha-adrenergic microvascular vasoconstriction may preclude adenosine to induce maximal hyperaemia. AIM: To assess the presence and the clinical relevance of residual microvascular resistance after administration of adenosine. METHODS AND RESULTS: Fractional flow reserve (FFR, calculated by coronary pressure measurements during adenosine-induced hyperaemia) was assessed in 85 patients with an intermediate coronary stenosis (mean diameter stenosis of 50+/-1%) and normal left ventricular function which were divided into the following three groups: (a) 33 patients before and after IC bolus of phentolamine, an alpha1-, alpha2-adrenergic blocker; (b) 32 patients before and after IC bolus of urapidil, a selective alpha1-adrenergic blocker; (c) 20 patients before and after IC bolus of saline. Since minimal luminal diameter remained unchanged before and after phentolamine (1.46+/-0.06 vs. 1.47+/-0.06 mm, ns), urapidil (1.46+/-0.06 vs. 1.39+/-0.08, ns), and saline (1.56+/-0.08 vs. 1.55+/-0.08, ns), changes in FFR reflects changes in microvascular resistance. Overall, phentolamine and urapidil induced a slight but significant decrease in FFR (phentolamine: 0.79+/-0.02 vs. 0.77+/-0.02, p<0.05; urapidil: 0.78+/-0.02 vs. 0.75+/-0.02, p<0.05). However, only 6 patients showed a change in FFR from > or = 0.75 to <0.75 and no patients showed a change in FFR from > or = 0.80 to <0.75 that could have influenced clinical decision making. Saline did not induce any change in FFR. Phentolamine and urapidil induced only transient and negligible haemodynamic changes in heart rate and blood pressure. CONCLUSIONS: The administration of alpha-adrenergic blockers in addition to adenosine unmasks a small, yet clinically irrelevant, degree of residual microvascular tone. The consequential changes in FFR values do not significantly affect clinical decision making.
Adrenergic alpha-Antagonists↗
Effects of intravenous dobutamine on coronary vasomotion in humans.
OBJECTIVES: We sought to investigate the vascular mechanisms of dobutamine-induced myocardial ischemia. BACKGROUND: Dobutamine stress is often used as a surrogate for exercise. The effects of dobutamine on the epicardial arteries are incompletely understood and possibly different from those of physical exercise. METHODS: Intravenous (IV) dobutamine (40 microg/kg per min) was administered in 19 patients with normal, 23 patients with mildly atherosclerotic, and 12 patients with stenotic coronary arteries. In another two groups of patients with stenotic arteries, IV dobutamine was preceded by 1) an intracoronary (IC) bolus of the alpha-adrenergic blocker phentolamine (12 microg/kg, n = 12); and 2) an IC infusion of the nitric oxide substrate L-arginine (150 micromol/l per min for 20 min, n = 11). Intravenous saline instead of dobutamine was infused into eight patients with normal arteries. After dobutamine (or saline), an IC bolus of isosorbide dinitrate (ISDN, 0.2 mg) was given. Coronary vasomotion was evaluated by quantitative coronary angiography on angiograms obtained after each dose of dobutamine, saline, phentolamine, L-arginine, and ISDN. RESULTS: Dobutamine increased the rate-pressure product and heart rate similarly in all patients except those who received saline. Dobutamine induced vasodilation in normal (change in luminal diameter [DeltaLD] vs. baseline: 19 +/- 2%) and in mildly atherosclerotic arteries (DeltaLD: 8 +/- 2%, p < 0.05 vs. normal). In stenotic arteries, dobutamine did not induce significant vasomotion (DeltaLD: -3 +/- 3%); the latter was improved by L-arginine (DeltaLD: 10 +/- 3%, p < 0.05 vs. stenotic arteries) and fully restored by phentolamine (DeltaLD: 19 +/- 3%, p < 0.05 vs. stenotic arteries). CONCLUSIONS: Endothelial dysfunction and enhanced alpha-adrenergic tone contribute to the loss of dobutamine-induced vasodilation in coronary atherosclerosis. In contrast to physical exercise, dobutamine does not induce "paradoxical vasoconstriction" of atherosclerotic coronary arteries.
Adrenergic beta-Agonists↗
Randomized evaluation of polytetrafluoroethylene-covered stent in saphenous vein grafts: the Randomized Evaluation of polytetrafluoroethylene COVERed stent in Saphenous vein grafts (RECOVERS) Trial.
BACKGROUND: Treatment of lesions located in saphenous vein grafts (SVGs) is associated with increased procedural risk and a high rate of restenosis. METHODS AND RESULTS: We conducted a randomized, multicenter trial to evaluate the usefulness of a polytetrafluoroethylene (PTFE)-covered stent compared with a bare stainless steel (SS) stent for prevention of restenosis and major adverse cardiac events (MACE) in patients undergoing SVG treatment. The primary end point was angiographic restenosis at 6 months. Secondary end points were 30-day and 6-month MACE rates, defined as the cumulative of death, myocardial infarction (MI), and target lesion revascularization. Between September 1999 and January 2002, 301 patients with SVG lesions were randomized to either the PTFE-covered JoStent coronary stent graft (PTFE group, n=156) or the SS JoFlex stent (control group, n=145). Angiographic and procedural success rates were similar between the 2 groups (97.4% versus 97.9% and 87.3% versus 93.8%, respectively). The incidence of 30-day MACE was higher in the PTFE group (10.9% versus 4.1%, P=0.047) and was mainly attributed to MI (10.3% versus 3.4%, P=0.037). The primary end point, the restenosis rate at 6-month follow-up, was similar between the 2 groups (24.2% versus 24.8%, P=0.237). Although the 6-month non-Q-wave MI rate was higher in the PTFE group (12.8% versus 4.1%, P=0.013), the cumulative MACE rate was not different (23.1% versus 15.9%, P=0.153). CONCLUSIONS: The study did not demonstrate a difference in restenosis rate and 6-month clinical outcome between the PTFE-covered stent and the SS stent for treatment of SVG lesions. However, a higher incidence of nonfatal myocardial infarctions was found in patients treated with the PTFE-covered stent.
Adult↗
Intracoronary and intravenous adenosine 5'-triphosphate, adenosine, papaverine, and contrast medium to assess fractional flow reserve in humans.
BACKGROUND: Inducing both maximal and steady-state coronary hyperemia is of clinical importance to take full advantage of fractional flow reserve measurements. The present study compares different dosages and routes of administration of adenosine 5'-triphosphate (ATP), adenosine, contrast medium, and papaverine regarding their potential to achieve both maximal and steady-state hyperemia. METHODS AND RESULTS: In 21 patients with an isolated coronary stenosis, coronary vasodilation was induced successively by papaverine (20 mg intracoronary), adenosine (20 and 40 microg intracoronary), ATP (20 and 40 microg intracoronary), iohexol (6 mL intracoronary), adenosine or ATP through an antecubital vein (140 and 180 microg x kg(-1) x min(-1)), or adenosine or ATP through a femoral vein (140 and 180 microg x kg(-1) x min(-1)). Because vessel dimensions did not change, the ratio of distal coronary pressure (Pd) to aortic pressure (Pa) was used as an index of myocardial resistance. Pd/Pa was 0.77+/-0.21 at rest and decreased to 0.61+/-0.21 after papaverine. Pd/Pa decreased to a similar level with all other vasodilators, except with contrast medium (0.68+/-0.21; P<0.01 versus papaverine). Steady-state hyperemia could only be obtained by intracoronary papaverine and by intravenous ATP or adenosine. In another 23 patients, an intravenous infusion of ATP was varied from 0 to 280 microg x kg(-1) x min(-1). At doses >140 microg x kg(-1) x min(-1), there was neither a further decrease in Pd/Pa ratio nor a further increase in coronary flow velocities. CONCLUSIONS: Provided sufficient dosages are used, ATP, adenosine, and papaverine (but not contrast medium) induce maximal hyperemia and are therefore suitable to assess fractional flow reserve. Only intracoronary papaverine and intravenous ATP or adenosine induce steady-state hyperemia enabling a pressure pullback maneuver that is useful in assessing diffuse coronary atherosclerosis.
Adenosine↗
Effect of an anti-PDGF-beta-receptor-blocking antibody on restenosis in patients undergoing elective stent placement.
AIM: The aim of the study was to determine whether a single intravenous infusion of 25 mg/kg CDP860, a humanized di-Fab' fragment against PDGF-beta receptor, leads to a reduction of in-stent restenosis. METHODS: In this phase II, double-blind, placebo-controlled, multicentre study 145 patients presenting with stable or unstable angina were randomized to a single infusion of placebo or active drug (CDP860) before undergoing stenting. Quantitative angiography and 3D intravascular ultrasound (IVUS) were obtained at baseline and follow-up. Primary endpoint was the IVUS assessment of percentage in-stent volume obstruction. RESULTS: At six-month follow-up, the placebo group and CDP860 group did not differ significantly regarding minimal luminal diameter (1.75 +/- 0.68 versus 1.82 +/--0.66 mm), restenosis rate (16.2 versus 14.1%), minimal lumen area (4.71 +/- 1.85 versus 4.41 +/- 1.77 mm(2) ), in-stent neointimal volume (30 +/- 23 versus 31 +/- 31 mm(3)) and in-stent obstruction volume (23.8 +/- 14.4 versus 22.1 +/- 15.3%). Major adverse cardiac events at 210 days were similar in both groups: death 1.5 versus 1.4%, myocardial infarction 5.9 versus 8.1% and target vessel revascularization 16.4 versus 17.6%. CONCLUSION: A single intravenous administration of monoclonal antibody against PDGF-beta receptor failed to reduce the amount of neointimal hyperplasia after stent implantation.
Angina Pectoris↗