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Biomedical subjects

A Schömig

Publications and source records attributed to A Schömig.

At least 19 recordsLinked to original sources
PubMed2002

Manual compression repair of post-catheterization femoral pseudoaneurysms: an alternative to ultrasound guided compression repair?

BACKGROUND: It is unknown, whether direct guidance by ultrasound is essential for the safety and efficacy of ultrasound-guided compression repair (UGCR) of pseudoaneurysms. We therefore tested, whether clinically guided manual compression repair (MCR) without continuous ultrasound control may represent an equally effective alternative. METHODS: After ultrasound diagnosis of a pseudoaneurysm, direct manual compression was applied to the lesion until the characteristic clinical signs disappeared or for a maximum of 1 hour. Then a compression bandage was applied for 24 hours. If the pseudoaneurysm persisted, MCR was repeated up to a maximum of three times. RESULTS: Of 96 consecutive patients with pseudoaneurysms, ten patients were referred to primary surgery; one patient refused any therapy. The remaining 85 patients (89%) were treated by MCR. MCR was successful in 74 patients (87%). Of these, 74% were cured at the first attempt, while 16% resp. 10% required 2 resp. 3 compression manoeuvers for definite cure. The success rate tended to be somewhat lower in patients on anticoagulants (78%) than in those on aspirin (91%) or those without any antithrombotic medication (89%) (p = 0.14). No major complications were observed. Of the 11 patients in whom MCR was unsuccessful, five patients underwent surgical repair; in four patients the pseudoaneurysms thrombosed spontaneously within 1-3 months and 2 pseudoaneurysms persist without complications. CONCLUSIONS: Our results with MCR are comparable to those published for UGCR. Since MCR requires less technical equipment and seems to be less painful for the patient, a prospective comparison of both methods appears warranted.

Adult↗
PubMed2002

Myocardial blood volume and the amount of viable myocardium early after mechanical reperfusion of acute myocardial infarction: prospective study using venous contrast echocardiography.

BACKGROUND: Myocardial capillary perfusion is a prerequisite of myocellular viability after reperfusion of acute myocardial infarction. It was hypothesised that the magnitude of myocardial capillary perfusion, assessed by transmural signal intensity in venous contrast echocardiography as a corollary of the blood volume of myocardial capillaries, and the amount of viable myocardium, represented by differential levels of contractile function two weeks after reperfusion, are correlated. OBJECTIVES: To evaluate the role of venous contrast echocardiography for the identification of viable myocardium in patients with acute myocardial infarction early after successful mechanical reperfusion. METHODS: 60 patients with a first acute myocardial infarction underwent venous contrast echocardiography several hours after successful mechanical reperfusion (median time interval 190 min.). The relative transmural videointensity (median (25th, 75th percentiles)) of akinetic segments was determined. After two weeks, contractile function was re-evaluated at rest and during dobutamine infusion if segments without functional recovery were present. RESULTS: Relative videointensity early after reperfusion differed significantly between functional groups after two weeks: normokinesia (88% (77%, 100%)), hypokinesia (74% (54%, 99%)), and akinesia with (61% (48%, 76%)) and without contractile reserve (31% (22%, 46%)). Relative videointensity and contractile function were significantly correlated (r = -0.67). The diagnostic accuracy of relative videointensity > 50% for prediction of contractility of initially akinetic segments at rest or during dobutamine was 82% (chi2 = 76.2, p < 0.001). CONCLUSIONS: Early after successful mechanical reperfusion of acute myocardial infarction, the magnitude of capillary perfusion in the perfusion territory of an infarct related artery is correlated with the amount of viable myocardium. Quantitative venous contrast echocardiography can be used for accurate identification of viable myocardium.

Blood Volume↗
PubMed2001

Blocking caspase-activated apoptosis improves contractility in failing myocardium.

Cardiac myocyte apoptosis has been demonstrated in end-stage failing human hearts. The therapeutic utility of blocking apoptosis in congestive heart failure (CHF) has not been elucidated. This study investigated the role of caspase activation in cardiac contractility and sarcomere organization in the development of CHF. In a rabbit model of heart failure obtained by rapid ventricular pacing, we demonstrate, using in vivo transcoronary adenovirus-mediated gene delivery of the potent caspase inhibitor p35, that caspase activation is associated with a reduction in contractile force of failing myocytes by destroying sarcomeric structure. In this animal model gene transfer of p35 prevented the rise in caspase 3 activity and DNA-histone formation. Genetically manipulated hearts expressing p35 had a significant improvement in left ventricular pressure rise (+dp/dt), decreased end-diastolic chamber pressure (LVEDP), and the development of heart failure was delayed. To better understand this benefit, we examined the effects of caspase 3 on cardiomyocyte dysfunction in vitro. Microinjection of activated caspase 3 into the cytoplasm of intact myocytes induced sarcomeric disorganization and reduced contractility of the cells. These results demonstrate a direct impact of caspases on cardiac function and may lead to novel therapeutic strategies via antiapoptotic regimens.

Adenoviridae↗
PubMed2001

Association of a CD18 gene polymorphism with a reduced risk of restenosis after coronary stenting.

Inflammatory mechanisms play an important role in the process of restenosis after percutaneous coronary interventions, with cell adhesion molecules, including Mac-1 (CD11b/CD18), as key mediators. A single nucleotide polymorphism, 1323C/T, located in exon 11 of the CD18 gene has been previously described, but its functional and clinical significances have not yet been studied. We assessed whether an association exists between this polymorphism and restenosis after coronary stenting. Clinical and angiographic measures of restenosis were evaluated over 1 year after coronary stent placement in 1,207 consecutive patients. Angiographic restenosis was defined as a > or =50% diameter stenosis at follow-up angiography. Determination of the CD18 1323C/T genotype was based on the polymerase chain reaction technique. The frequency of the T allele was 0.34 and its presence reduced the 1-year risk of a major adverse cardiac event (death, myocardial infarction, target vessel revascularization) by 29% (p = 0.011). Carriers of the T allele had a significantly lower risk of angiographic restenosis compared with noncarriers (odds ratio 0.71, 95% confidence interval 0.55 to 0.92). The incidence of restenosis decreased as a function of the number of T alleles: 38.1% in patients with genotype CC, 31.7% in patients with genotype CT, and 26.0% in patients with genotype TT (p = 0.004). Thus, the 1323T allele of the CD18 gene is associated, in a gene dose-dependent manner, with a lower incidence of angiographic restenosis after coronary stenting. This finding suggests that Mac-1 is involved in the development of restenosis after coronary stent placement.

Angioplasty, Balloon, Coronary↗
PubMed2001

[Problems of electrocardiographic diagnosis of occlusion of the left circumflex coronary artery].

BACKGROUND AND OBJECTIVE: The electrocardiographic diagnosis of posterior myocardial infarction is difficult. It was the objective of the present study to evaluate ST-segment changes in angiographically documented occlusion of the left RCX in the setting of an acute myocardial infarction and to analyse the value of the posterior chest leads V(7)-V(9). PATIENTS AND METHODS: Data of 120 patients (88 males, on average 61+/-13 years old) with an acute myocardial infarction and angiographically proven occlusion of the left circumflex artery were included in the study. Mean time of pain onset to ECG recording was 5.5 +/- 2.8 hours. The ECGs were analysed for ST-segment changes of > or = 1 mm in two contiguous leads in surface leads I-aVF, > or = 2 mm in the precordial leads V(1)-V(6), and > or = 1 mm in right precordial (V(3)R-V(6)R) and posterior (V(7)-V(9)) leads. These additional leads were recorded only in a subgroup of 36 patients. Maximal creatine kinase activity was determined as a measure of infarct size. RESULTS: Standard leads I-V(6) showed ST-segment elevation in 55 of 120 patients (46 %). In the subgroup of patients with extended chest leads 61 % (11/36) had significant ST-segment elevation, whereas isolated ST-segment elevation in the posterior leads occurred in 8 % (3/36). ST-segment depression in the standard leads was observed in 73 of the 120 patients (54 %), and isolated ST-segment depression was seen in 31 patients (26 %). No significant ST-segment changes in the standard leads were found in 34 patients (28 %). Maximum CK values were not significantly different among the three groups (1107 +/- 815 IU/l vs 953 +/- 651 IU/l vs 816 +/- 553 IU/l; (P = 0.447). CONCLUSION: These findings confirm that the sensitivity of the standard ECG leads is less than 50 % in angiographically documented occlusion of the left RCX. The extended posterior chest leads (V(7)-V(9)) improve sensitivity only marginally (by 8 %). Isolated ST-segment depression or no significant ST-segment depression in the standard leads was observed in 26 % and 28 % respectively. The infarct size - as measured by maximum CK-values - did not differ among the respective groups.

Aged↗
PubMed2001

Modes of initiation of paroxysmal atrial fibrillation from analysis of spontaneously occurring episodes using a 12-lead Holter monitoring system.

Although new, possibly curative radiofrequency ablation techniques for atrial fibrillation (AF) have been developed in recent years, little is known about the mechanisms of spontaneous onset of AF episodes. Using a 12-lead 24-hour Holter monitoring system, we aimed to characterize such episodes. A total of 297 spontaneous episodes of AF in 33 patients with intermittent AF (mean age of 59 +/- 11 years) were analyzed. Two hundred seventy-six episodes (93%) were initiated by atrial premature complexes (APCs), whereas 19 episodes (6.4%) were preceded by typical atrial flutter and 2 (0.7%) by atrial tachycardia. Based on 12-lead electrocardiographic criteria, the origin of ectopic beats initiating AF was classified in 230 episodes (77.5%) as being of left atrial origin, in 6 episodes (2.0%) as being of right atrial origin and in 40 episodes (13.5%) the exact location could not be determined. In 16 of 23 patients (70%) with multiple episodes of AF, ectopic beats that initiated AF were consistently monomorphic. In the 120 seconds (6.2 APCs/min for a 30-second period) before onset of AF, frequency of ectopic beats increased from 0.8 APCs/min in AF-free intervals to 4.1/min (6.2 APCs/min for a 30-second period), (p = 0.003 and p = 0.016, respectively). In 209 of 254 episodes (82%), AF onset occurred during normal sinus rate (60 to 100 beats/min). Thus, paroxysmal AF is triggered most frequently by monomorphic left APCs. In most AF episodes, the increase in the number of ectopic beats that initiated episodes of AF occurred at a normal sinus rate.

Adult↗
PubMed2001

Previous cytomegalovirus infection and restenosis after coronary stent placement.

BACKGROUND: Reactivated cytomegalovirus may promote neointima formation after percutaneous coronary interventions by facilitating cell cycle progression through inhibition of the eukariotic tumor suppressor protein p53. This prospective study sought to investigate the effect of previous cytomegalovirus infection on restenosis after coronary stenting. METHODS AND RESULTS: In 551 consecutive patients with successful stent placement, we determined cytomegalovirus IgG titers. Primary and secondary end points were the rate of angiographic restenosis at 6 months and the rate of target vessel reintervention at 1 year, respectively. Three hundred forty patients (62%) had a positive cytomegalovirus IgG titer. We obtained angiographic follow-up in 82% of all patients. Angiographic restenosis rate was 28.7% in patients with positive cytomegalovirus titers and 34.6% in patients with negative titers (P=0.18). Between the groups with and without positive cytomegalovirus titers, there were no significant differences in late lumen loss (1.16+/-0.90 mm and 1.23+/-0.86 mm, respectively, P=0.44). Target vessel reintervention was performed in 16.8% of the patients with positive cytomegalovirus titers and in 17.5% of those without (P=0.82). Even after correction for potential confounding variables by multivariate analysis, positive cytomegalovirus titers did not manifest as a predictor of angiographic restenosis (adjusted odds ratio [95% confidence interval], 0.78 [0.52 to 1.19]). CONCLUSIONS: Previous cytomegalovirus infection does not carry an increased risk of restenosis after stenting.

Aged↗
PubMed2001

Treatment of Chlamydia pneumoniae infection with roxithromycin and effect on neointima proliferation after coronary stent placement (ISAR-3): a randomised, double-blind, placebo-controlled trial.

BACKGROUND: Vascular infection with Chlamydia pneumoniae might boost inflammatory responses that play a pivotal part in neointima formation, which is the main cause of restenosis after stenting. Our aim was to investigate whether or not treatment of C pneumoniae infection with antibiotics prevents restenosis after coronary stent placement. METHODS: We enrolled 1010 consecutive patients with successful coronary stenting into a randomised, double-blind trial. Patients received the macrolide antibiotic roxithromycin 300 mg once daily for 28 days (506), or placebo (504). Primary endpoint was frequency of restenosis (diameter stenosis >50%) at follow-up angiography, and secondary endpoint was rate of target vessel revascularisation during the year after stenting. A prespecified secondary analysis addressed treatment effect with respect to titre of C pneumoniae in serum. Analysis was by intention to treat. FINDINGS: Rate of angiographic restenosis was 31% (157 lesions) in the roxithromycin group and 29% (148) in the placebo group (relative risk 1.08 [95% CI 0.92-1.26]; p50.43), corresponding to a rate of target vessel revascularisation of 19% (120) and 17% (105), respectively (1.13 [0.95-1.36]; p50.30). The combined 1-year rates of death and myocardial infarction were 7% (36) in the roxithromycin group and 6% (30) in the placebo group (p50.45). We showed a significant interaction between treatment and C pneumoniae antibody titre (p50.038 for restenosis, p50.006 for revascularisation), favouring roxithromycin at high titres (adjusted odds ratios at a titre of 1/512 were 0.44 [0.19-1.06] and 0.32 [0.13-0.81], respectively). INTERPRETATION: Non-selective use of roxithromycin is inadequate for prevention of restenosis after coronary stenting. There is, however, a differential effect dependent on C pneumoniae titres. In patients with high titres, roxithromycin reduced the rate of restenosis.

Aged↗
PubMed2001

Incidence of thrombotic occlusion and major adverse cardiac events between two and four weeks after coronary stent placement: analysis of 5,678 patients with a four-week ticlopidine regimen.

OBJECTIVES: We attempted to make a comprehensive assessment of the risk of stent failure (death, myocardial infarction or angiographically documented occlusion), differentiating early (first and second weeks) and late (third and fourth weeks) events. BACKGROUND: The risk of stent failure decreases rapidly within the first week. It has been suggested that the risk rate for late events is close to 0% and that the thienopyridine regimen (ticlopidine or clopidogrel) could be safely reduced from four to two weeks, minimizing the risk of hematological complications. METHODS: We analyzed 5,678 patients with successful coronary stent placement and a four-week ticlopidine regimen. RESULTS: The rate of stent failure was 2.5% at four weeks, with 112 early (2.0%) and 30 late events (0.5%). Multivariate analysis identified different risk factors for early versus late events. While variables on stenosis severity and procedural results that can be influenced by the operator were identified as independent risk factors for early events (percent stenosis before and after the procedure, residual dissection, length of stented segment), more clinical variables were associated with late events (age, reduced left ventricular function, systemic hypertension as a protective factor). The late-event rate was <0.1% in the absence of these factors, but it was 2.5% with all three risk factors present. CONCLUSIONS: The risk of late stent failure is low with a four-week ticlopidine regimen. However, high-risk subgroups have a risk of 2.5%. As this rate is presumably higher if thienopyridines are discontinued after two weeks, these data suggest that a risk stratification to a two- or four-week regimen is preferable to a general reduction.

Aged↗
PubMed2001

Regulation of monocyte procoagulant activity in acute myocardial infarction: role of tissue factor and tissue factor pathway inhibitor-1.

In acute myocardial infarction (AMI), monocyte procoagulant activity is increased and may contribute to the risk for recurrence and other thrombotic events. This study sought to investigate the role tissue factor (TF) and tissue factor pathway inhibitor-1 (TFPI-1) in the regulation of monocyte procoagulant activity in AMI. Serial venous blood samples were obtained from 40 patients with AMI undergoing revascularization by stent placement. Twenty patients with elective stenting for stable angina served as control subjects. TF proteolytic activity was measured with spectrozyme factor Xa (FXa), TF and TFPI-1 surface expression on monocytes by flow cytometry, RNA expression in whole blood by reverse transcription-polymerase chain reaction, and concentrations of plasma prothrombin fragments F(1 + 2) by immunoassay. Forty-eight hours after AMI, an increase was found in TF RNA, followed by an increase in TF surface expression by 24% +/- 4% and in plasma concentration of F(1 + 2) by 103% +/- 17% (P <.05). These changes could not be attributed to the intervention because they did not occur in the control group. TFPI-1 RNA and binding to the monocyte surface remained unchanged. FXa generation by monocytes of patients with AMI increased 53.6% +/- 9% in the presence of polyclonal antibodies to TFPI-1, indicating that cell-associated TFPI-1 inhibits monocyte TF activity. The increased monocyte procoagulant activity in AMI was caused by an up-regulation of TF that was partially inhibited by surface-bound TFPI-1. Anticoagulant therapy by direct inhibition of TF activity may, thus, be particularly effective in AMI. (Blood. 2001;97:3721-3726)

Adult↗
PubMed2001

Intracoronary stenting and angiographic results: strut thickness effect on restenosis outcome (ISAR-STEREO) trial.

BACKGROUND: Increased thrombogenicity and smooth muscle cell proliferative response induced by the metal struts compromise the advantages of coronary stenting. The objective of this randomized, multicenter study was to assess whether a reduced strut thickness of coronary stents is associated with improved follow-up angiographic and clinical results. METHODS AND RESULTS: A total of 651 patients with coronary lesions situated in native vessels >2.8 mm in diameter were randomly assigned to receive 1 of 2 commercially available stents of comparable design but different thickness: 326 patients to the thin-strut stent (strut thickness of 50 microm) and 325 patients to the thick-strut stent (strut thickness of 140 microm). The primary end point was the angiographic restenosis (>/=50% diameter stenosis at follow-up angiography). Secondary end points were the incidence of reinterventions due to restenosis-induced ischemia and the combined rate of death and myocardial infarctions at 1 year. The incidence of angiographic restenosis was 15.0% in the thin-strut group and 25.8% in the thick-strut group (relative risk, 0.58; 95% CI, 0.39 to 0.87; P=0.003). Clinical restenosis was also significantly reduced, with a reintervention rate of 8.6% among thin-strut patients and 13.8% among thick-strut patients (relative risk, 0.62; 95% CI, 0.39 to 0.99; P=0.03). No difference was observed in the combined 1-year rate of death and myocardial infarction. CONCLUSIONS: The use of a thinner-strut device is associated with a significant reduction of angiographic and clinical restenosis after coronary artery stenting. These findings may have relevant implications for the currently most widely used percutaneous coronary intervention.

Aged↗
PubMed2001

Value of programmed ventricular stimulation for prophylactic internal cardioverter-defibrillator implantation in postinfarction patients preselected by noninvasive risk stratifiers.

OBJECTIVES: The aim of this prospective study was to evaluate the role of programmed ventricular stimulation (PVS) after noninvasive risk stratification to identify a subgroup of acute myocardial infarction (AMI) survivors considered at risk for ventricular arrhythmias and whether these patients could benefit from internal cardioverter-defibrillators (ICDs). BACKGROUND: The predictive value of noninvasive and invasive risk stratifiers after AMI has been questioned. The question of whether the group of patients with inducible monomorphic ventricular tachycardia (VT) after AMI could profit from ICD implantation is unanswered. METHODS: A consecutive series of 1,436 AMI survivors was screened noninvasively by Holter monitoring, heart rate variability, ventricular late potentials, and ejection fraction. A subgroup of 248 patients (17.3%) were identified as high-risk patients and scheduled for PVS. Due to the study design, 54 patients >75 years were excluded; thus, 194 patients were eligible for PVS. Triple extrastimuli at two paced cycle lengths (600 ms and 400 ms) were applied. RESULTS: In a subgroup of 98 (51%) high-risk patients, PVS was performed; 21 patients had an abnormal response, and in 20 patients an ICD was implanted. During a mean follow-up of 607 days the arrhythmic event rate (sudden cardiac death, symptomatic VT, cardiac arrest) was 33% with a positive electrophysiological test versus 2.6% (p < 0.0001) with a negative electrophysiological test. A subgroup of 96 high-risk patients declined electrophysiological study. In this nonconsent group, cardiac mortality (combined sudden and nonsudden) was significantly higher (log-rank chi-square 9.38, p = 0.0022, relative risk 4.7, 1.6 to 13.9) compared to the group guided by electrophysiological testing and consecutive ICD implantation. CONCLUSIONS: After a two-step risk stratification, PVS is helpful in selecting a subgroup of AMI survivors without spontaneous ventricular arrhythmias who benefit from prophylactic ICD implantation.

Defibrillators, Implantable↗
PubMed2001

Gene transfer of heterologous G protein-coupled receptors to cardiomyocytes: differential effects on contractility.

In heart failure, reduced cardiac contractility is accompanied by blunted cAMP responses to beta-adrenergic stimulation. Parathyroid hormone (PTH)-related peptide and arginine vasopressin are released from the myocardium in response to increased wall stress but do not stimulate contractility or adenylyl cyclase at physiological concentrations. To bypass the defective beta-adrenergic signaling cascade, recombinant P1 PTH/PTH-related peptide receptors (rPTH1-Rs) and V(2) vasopressin receptors (rV(2)-Rs), which are normally not expressed in the myocardium and which are both strongly coupled to adenylyl cyclase, and recombinant beta(2)-adrenergic receptors (rbeta(2)-ARs) were overexpressed in cardiomyocytes by viral gene transfer. The capacity of endogenous hormones to increase contractility via the heterologous, recombinant receptors was compared. Whereas V(2)-Rs are uniquely coupled to Gs, PTH1-Rs and beta(2)-ARs are also coupled to other G proteins. Gene transfer of rPTH1-Rs or rbeta(2)-ARs to adult cardiomyocytes resulted in maximally increased basal contractility, which could not be further stimulated by adding receptor agonists. Agonists at rPTH1-Rs induced increased cAMP formation and phospholipase C activity. In contrast, healthy or failing rV(2)-R-expressing cardiomyocytes showed unaltered basal contractility. Their contractility and cAMP formation increased only at agonist exposure, which did not activate phospholipase C. In summary, we found that gene transfer of PTH1-Rs to cardiomyocytes results in constitutive activity of the transgene, as does that of beta(2)-ARS: In the absence of receptor agonists, rPTH1-Rs and rbeta(2)-ARs increase basal contractility, coupling to 2 G proteins simultaneously. In contrast, rV(2)-Rs are uniquely coupled to Gs and are not constitutively active, retaining their property to be activated exclusively on agonist stimulation. Therefore, gene transfer of V(2)-Rs might be more suited to test the effects of cAMP-stimulating receptors in heart failure than that of PTH1-Rs or beta(2)-ARS:

Adenoviridae↗
PubMed2001

Prognostic value of an abnormal signal-averaged electrocardiogram in patients with nonischemic dilated cardiomyopathy.

The usefulness of an abnormal signal-averaged ECG (SAECG) for the risk stratification of patients with dilated cardiomyopathy was studied prospectively in 76 patients. Multiple analysis showed that an abnormal SAECG predicted cardiac mortality (p = 0.0046), sudden cardiac death, and the need for resuscitation (p = 0.003); however, it did not predict death from heart failure and heart transplantation.

Adult↗
PubMed2001

Gene expression profiling of human stent-induced neointima by cDNA array analysis of microscopic specimens retrieved by helix cutter atherectomy: Detection of FK506-binding protein 12 upregulation.

BACKGROUND: Restenosis due to neointima formation is the major limitation of stent-supported balloon angioplasty. Despite abundant animal data, molecular mechanisms of neointima formation have been investigated on only a limited basis in patients. This study sought to establish a method for profiling gene expression in human in-stent neointima and to identify differentially expressed genes that may serve as novel therapeutic targets. METHODS AND RESULTS: We retrieved tissue specimens from patients with symptomatic in-stent restenosis using a novel helix cutter atherectomy device. cDNA samples prepared from neointima (n=10) and, as a control, from the media of normal arteries (n=14) were amplified using a novel polymerase chain reaction protocol and hybridized to cDNA arrays. Immunohistochemistry characterized the atherectomy material as neointima. cDNA arrays readily identified differentially expressed genes. Some of the differentially expressed genes complied with expected gene expression patterns of neointima, including downregulation of desmin and upregulation of thrombospondin-1, cyclooxygenase-1, and the 70-kDa heat shock protein B. Additionally, we discovered previously unknown gene expression patterns, such as downregulation of mammary-derived growth inhibitor and upregulation of FK506-binding protein 12 (FKBP12). Upregulation of FKBP12 was confirmed at the protein level in neointimal smooth muscle cells. CONCLUSIONS: Gene expression patterns of human neointima retrieved by helix-cutter atherectomy can be reliably analyzed by cDNA array technology. This technique can identify therapeutic targets in patients, as exemplified by the findings regarding FKBP12. FKBP12 is the receptor for Rapamycin (sirolimus), which in animal models reduced neointima formation. Our study thus yields a rationale for the use of Rapamycin to prevent restenosis in patients.

Aged↗