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Biomedical subjects

Michael Haude

Publications and source records attributed to Michael Haude.

At least 19 recordsLinked to original sources
PubMed2005

[Coronary stents. From a simple idea to a medical high-tech device].

BACKGROUND: Coronary stents were introduced in clinical cardiology in the middle of the 1980s, as balloon angioplasty was associated with a high incidence of acute vessel closure and restenosis. EVOLUTION OF CORONARY STENTS: However, primarily designed to counteract elastic recoil after angioplasty, initial results were complicated by acute and subacute stent thrombosis. With the introduction of drugs effectively inhibiting platelet aggregation like ticlopidine and clopidogrel, stent could exhibit its superiority in comparison to angioplasty. Although the incidence of restenosis could be decreased significantly by coronary stents, restenosis remained a major drawback of this interventional technique. Several modifications of stent design and stent material had been tested, but without a real breakthrough. The introduction of active stent coating with anti-inflammatory and antiproliferative drugs marks a milestone in the development of this technology. With this approach the restenosis problem could be, even though not solved, but essentially mitigated. Current developments address bioabsorbable materials to make stents compatible with new upcoming noninvasive imaging techniques. CONCLUSION: Introduced 20 years ago as a simple wire mesh, modified by new designs and materials, and coated by highly effective drugs, coronary stents have advanced to medical high-tech devices in interventional cardiology.

Adult↗
PubMed2005

Diagnostic discrimination between graft-related and non-graft-related perioperative myocardial infarction with cardiac troponin I after coronary artery bypass surgery.

AIMS: The rise of markers for myocardial injury indicates early graft-related or non-graft-related perioperative myocardial infarction (PMI) after coronary artery bypass grafting (CABG). A diagnostic discrimination between these two situations may enable adequate therapeutic measures, limiting myocardial damage, and improving outcome. METHODS AND RESULTS: In a prospective study, 94 among 3308 consecutive CABG patients underwent acute reangiography because of evidence of PMI. Of these 94 patients, 56 had graft-related PMI (group 1), 38 patients had non-graft-related PMI (group 2), and 95 patients without evidence of PMI and angiographically patent grafts served as control (group 3). Cardiac troponin I (cTnI), creatine kinase (CK), and its MB fraction were determined. CTnI, but not CK/CK-MB levels were significantly higher in group 1 than in groups 2 and 3 at 12 and 24 h after aortic unclamping (P<0.0001). Receiver operating characteristic and multivariable logistic regression analyses indicated cTnI as the best discriminator between PMI 'in general' and 'inherent' release of cTnI after CABG with a cut-off value of 10.5 ng/mL and between graft-related and non-graft-related PMI with a cut-off value of 35.5 ng/mL. CONCLUSION: Perioperative cTnI elevation after CABG separates among patients with graft-related, non-graft-related, and without PMI, however, not earlier than 12 h after surgery.

Aged↗
PubMed2005

[Clinical and pharmacological testing of patients with pulmonary hypertension for treatment decision].

Pulmonary arterial hypertension (PAH) is a rare and rapidly progressing disease characterized by an increase in pulmonary resistance, which, if untreated, inevitably progresses to right ventricular heart failure and death. New treatment options were developed in the last 10 years. Endothelin receptor antagonists (ERAs) and prostanoids are an effective treatment with a better survival. Phosphodiesterase inhibitors (PDIs) are of a great interest, and first results in the treatment of patients are promising. PDIs are different in pulmonary selectivity and half-life.Right heart catheterization is the "gold standard" in the diagnosis of pulmonary hypertension. Direct classification of the pulmonary hypertension is feasible, and the effects of the drugs are directly measurable. The results of right heart catheterization are comparable for inhalative and oral drugs. New generations of drugs resulted in special testing protocols. Furthermore, individual concepts of therapy can be developed.

Antihypertensive Agents↗
PubMed2005

Preinfarction angina: no interference of coronary microembolization with acute ischemic preconditioning.

Transient episodes of angina preceding acute myocardial infarction may both, protect the myocardium by ischemic preconditioning or damage it when associated with coronary microembolization. We now studied the potential loss of ischemic preconditioning with coronary microembolization. Anesthetized pigs (group 1; n=8) were subjected to 90 min sustained low-flow ischemia. Group 2 (n=8) was subjected to coronary microembolization (i.e. microspheres; 42 microm slashed circle; 3000 per ml min-1 inflow) 35 min before sustained ischemia. In group 3, coronary microembolization was followed 10 min later by one cycle of ischemic preconditioning (10 min ischemia/15 min reperfusion) before subsequent sustained ischemia. Infarct size was determined after 2 h reperfusion by triphenyl tetrazolium chloride staining. Infarct size after sustained ischemia alone (group 1) was 19.4+/-3.4% of the area at risk (mean+/-S.E.M.). With coronary microembolization before sustained ischemia (group 2) infarct size was only slightly larger (23.6+/-4.6%, ns). In group 3 with microembolization followed by ischemic preconditioning, infarct size was reduced to 12.7+/-3.0% (P<0.05 vs. group 2). The relationships between infarct size and transmural blood flow in groups 1 and 3 were not different, giving the impression that ischemic preconditioning failed to protect microembolized myocardium. However, additional coronary microembolization shifted the relationship between infarct size and blood flow upwards to a larger infarct size at any given blood flow. Thus when comparing the relationship of group 3 to its true control (group 2), it was shifted downwards (P<0.05; analysis of covariance (ANCOVA)) indicating persistent protection of microembolized myocardium by ischemic preconditioning. Coronary microembolization induces additional infarction when superimposed on sustained ischemia but does not interfere with the endogenous protection by ischemic preconditioning.

Adenosine↗
PubMed2005

Overview of contemporary reperfusion strategies in acute ST-elevation myocardial infarction.

The rupture of an atherosclerotic plaque in an epicardial coronary artery with subsequent occlusive coronary thrombosis has been established as the decisive event in the pathogenesis of an acute coronary syndrome, which encompasses the clinical entities of unstable angina, non-ST- and ST-elevation myocardial infarction. This article focuses on contemporary treatment strategies for patients with acute ST-elevation myocardial infarction and reviews the role of pharmacologic thrombolysis and mechanical reperfusion by percutaneous transluminal approaches. Statements of the latest guidelines for the treatment of ST-elevation myocardial infarction are included, as well as some recently distributed information not covered by the guideline publications. Finally, some future perspectives for the treatment of acute ST-elevation myocardial infarction are outlined.

Angioplasty, Balloon, Coronary↗
PubMed2004

Determinants of coronary blood flow in humans: quantification by intracoronary Doppler and ultrasound.

The direct determinants of coronary flow are lumen area and blood flow velocity; however, the precise mechanisms that control these factors are not fully understood. The aim of the present study was to assess by which mechanisms lumen area and coronary flow velocity interact with hemodynamic and morphometric factors, thereby influencing coronary flow. Intracoronary Doppler and ultrasound measurements were performed in 28 patients without coronary lumen irregularities. Flow velocity and lumen cross-sectional area were measured in the proximal segments of all three coronary arteries. Global lumen cross-sectional area and global flow were obtained by adding up the values of all three coronary arteries. Left ventricular mass was assessed by echocardiography. Stress-mass-heart rate and pressure-rate products reflecting myocardial oxygen demand were calculated. Global coronary flow increased during adenosine-induced hyperemia from 197 +/- 72 to 637 +/- 204 ml/min (P < 0.001). Global coronary flow closely correlated with the stress-mass-heart rate product (r = 0.62; P < 0.001). Looking at the two constituents of flow separately, global coronary cross-sectional area was closely related to left ventricular muscle mass (r = 0.61; P < 0.001), whereas mean coronary flow velocity at rest showed a strong linear relation with the pressure-rate product (r = 0.64; P < 0.001). There was no interaction between cross-sectional area and blood flow velocity in any of the coronary vessels. Coronary lumen size and flow velocity, the two determinants of coronary flow, are principally determined by different physiological factors. Long-term flow adaptation is achieved by an increase in coronary lumen size, whereas short-term myocardial oxygen requirements are met by changes in resting flow velocity.

Blood Flow Velocity↗
PubMed2004

Coronary microembolization does not induce acute preconditioning against infarction in pigs-the role of adenosine.

OBJECTIVE: After coronary microembolization (ME) adenosine is released from ischemic areas of the microembolized myocardium. This adenosine dilates vessels in adjacent nonembolized myocardium and increases coronary blood flow. For ischemic preconditioning (IP) to protect the myocardium against infarction, an increase in the interstitial adenosine concentration (iADO) prior to the subsequent ischemia/reperfusion is necessary. We hypothesized that the adenosine release after ME is sufficient to increase iADO and protect the myocardium against infarction from subsequent ischemia/reperfusion. We have therefore compared myocardial protection by either coronary microembolization or ischemic preconditioning prior to ischemia/reperfusion. METHODS: In anesthetized pigs, the left anterior descending (LAD) was cannulated and perfused from an extracorporeal circuit. In 11 pigs, sustained ischemia was induced by 85% inflow reduction for 90 min (controls). Two other groups of pigs were subjected either to IP (n = 8; 10-min ischemia/15-min reperfusion) or coronary ME (n = 9; i.c. microspheres; 42 microm Ø; 3000 x ml(-1) x min inflow) prior to sustained ischemia. Coronary venous adenosine concentration (vADO) and iADO (microdialysis) were measured. Infarct size was determined after 2-h reperfusion by triphenyl tetrazolium chloride staining. RESULTS: In pigs subjected to IP, infarct size was reduced to 2.6 +/- 1.1% (mean +/- S.E.M.) vs. 17.0 +/- 3.2% in controls. iADO was increased from 2.4 +/- 1.3 to 13.1 +/- 5.8 micromol x l(-1) during the reperfusion following IP. In pigs subjected to ME, at 10 min after ME, coronary blood flow (38.6 +/- 3.6 to 53.6 +/- 4.3 ml x min(-1)) and vADO (0.25 +/- 0.04 to 0.48 +/- 0.07 micromol x l(-1)) were increased. However, iADO (2.0 +/- 0.5 at baseline vs. 2.3 +/- 0.6 micromol x l(-1) at 10 min after ME) did not increase. Infarct size induced by sustained ischemia following ME (22.5 +/- 5.2%) was above that of controls for any given subendocardial blood flow. CONCLUSION: ME released adenosine into the vasculature and increased coronary blood flow. The failure of iADO to increase with ME possibly explains the lack of protection against infarction after ME.

Adenosine↗
PubMed2004

Spectrum of remodeling behavior observed with serial long-term (>/=12 months) follow-up intravascular ultrasound studies in left main coronary arteries.

Most intravascular ultrasound (IVUS) studies of arterial remodeling in native coronary arteries reported a remodeling index obtained at a single time point. We analyzed serial IVUS examinations, including the vessel cross-sectional area changes (remodeling behavior), of 60 hemodynamically nonstenotic left main lesions (baseline vs 18.4 +/- 9.4 months follow-up). Lumen reduction resulted from vessel reduction (sometimes despite plaque + media decrease), plaque + media increase (with or without vessel increase), or both. The percent annual changes in lumen area correlated strongly with changes in vessel (r = 0.84), but not with changes in plaque + media area. Plaques were classified as group A lesions, reflecting positive remodeling behavior (vessel changes >0), or group B lesions, reflecting negative (or intermediate) remodeling behavior (vessel changes <==0). Both groups did not differ significantly in demographics, laboratory data, and medications. Group A lesions (n = 40) more often showed plaque + media increase than group B lesions (32 of 40 [80%] vs 9 of 20 [45%]; p = 0.02). Group A lesions had, on average, mild annual lumen increase despite mild plaque + media increase, i.e, overcompensation of remodeling for plaque + media increase (vessel increase greater than plaque + media area increase, 19 of 40 [47%]). Conversely, group B lesions (n = 20) showed a significant lumen area reduction (-2.8 +/- 2.6 mm(2)/year) as a result of a decrease in vessel area only. Thus, serial long-term reduction of lumen size may result from vessel shrinkage (sometimes despite plaque decrease), plaque increase (with or without vessel increase), or both; overall, only the remodeling behavior has a significant relation to lumen changes. More than 30% of lesions show a negative remodeling behavior, which shows no relation to patient characteristics or initial plaque burden.

Aged↗
PubMed2004

Glucocorticoid treatment prevents progressive myocardial dysfunction resulting from experimental coronary microembolization.

BACKGROUND: The frequency and importance of microembolization in patients with acute coronary syndromes and during coronary interventions have recently been appreciated. Experimental microembolization induces immediate ischemic dysfunction, which recovers within minutes. Subsequently, progressive contractile dysfunction develops over several hours and is not associated with reduced regional myocardial blood flow (perfusion-contraction mismatch) but rather with a local inflammatory reaction. We have now studied the effect of antiinflammatory glucocorticoid treatment on this progressive contractile dysfunction. METHODS AND RESULTS: Microembolization was induced by injecting microspheres (42-microm diameter) into the left circumflex coronary artery. Anesthetized dogs were followed up for 8 hours and received placebo (n=7) or methylprednisolone 30 mg/kg IV either 30 minutes before (n=7) or 30 minutes after (n=5) microembolization. In addition, chronically instrumented dogs received either placebo (n=4) or methylprednisolone (n=4) 30 minutes after microembolization and were followed up for 1 week. In acute placebo dogs, posterior systolic wall thickening was decreased from 20.0+/-2.1% (mean+/-SEM) at baseline to 5.8+/-0.6% at 8 hours after microembolization. Methylprednisolone prevented the progressive myocardial dysfunction. Increased leukocyte infiltration in the embolized myocardium was prevented only when methylprednisolone was given before microembolization. In chronic placebo dogs, progressive dysfunction recovered from 5.0+/-0.7% at 4 to 6 hours after microembolization back to baseline (19.1+/-1.6%) within 5 days. Again, methylprednisolone prevented the progressive myocardial dysfunction. CONCLUSIONS: Methylprednisolone, even when given after microembolization, prevents progressive contractile dysfunction.

Animals↗
PubMed2004

[Coronary microembolization: perfusion-contraction mismatch secondary to myocardial inflammation].

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not necessarily lead to thrombotic occlusion of a coronary artery and subsequent myocardial infarction. Milder forms may result in the embolization of atherosclerotic and/or thrombotic debris into the coronary microcirculation. The characteristic consequences of coronary microembolization are arrhythmias, microinfarcts, and a reduced coronary reserve. Experimental studies revealed that an inflammatory reaction is causally involved in the progressive contractile dysfunction following coronary microembolization. Thus, anti-inflammatory treatment appears as a promising strategy to protect patients from the consequences of coronary microembolization.

Animals↗
PubMed2004

Coronary microembolization.

Atherosclerotic plaque rupture is a key event in the pathogenesis of acute coronary syndromes and during coronary interventions. Atherosclerotic plaque rupture does not always result in complete thrombotic occlusion of the entire epicardial coronary artery with subsequent acute myocardial infarction, but may in milder forms result in the embolization of atherosclerotic and thrombotic debris into the coronary microcirculation. This review summarizes the available morphological evidence for coronary microembolization in patients who died from coronary artery disease, most notably from sudden death. Then the experimental pathophysiology of coronary microembolization in animal models of acute coronary syndromes is detailed. Finally, the review presents the available clinical evidence for coronary microembolization in patients, highlights its key features--arrhythmias, contractile dysfunction, microinfarcts and reduced coronary reserve--, compares these features to those of the experimental model and addresses its prevention by mechanical protection devices and glycoprotein IIb/IIIa antagonism.

Animals↗
PubMed2004

The EchoMap System: online integration of intracoronary ultrasound and Doppler images into angiographic images during cardiac catheterization. Influence on radiation exposure and procedure parameters.

The EchoMap system allows online integration of intravascular ultrasound (IVUS) and intracoronary Doppler (ICD) images into angiographic images during catheterization, providing exact localization of the IVUS transducer and the ICD wire tip position. Although this is a major advance, the use of the system could lead to more angiographic documentation sequences and enhanced radiation exposure. We investigated the influence of system use on radiation and procedure parameters. During a 22-month period, 794 patients underwent coronary angiography with simultaneous performance of IVUS and/or ICD. The EchoMap system was applied in 392 patients ("EchoMap group"), the remaining 402 patients formed the "No-EchoMap group." Multivariate regression analysis showed no independent association between the use of EchoMap and fluoroscopy time (14.7 +/- 8.5 minutes in the EchoMap group vs 14.5 +/- 10 minutes in the No-EchoMap group, P = NS) or dose area product (7589 +/- 4916 in the EchoMap group vs 7031 +/- 5434 cGy x cm(2), P = NS). EchoMap use was significantly associated with a moderate increase in contrast media amount (392 +/- 162 in the EchoMap vs 356 +/- 155 mL in the No-EchoMap group, P = 0.001). In conclusion, the use of the EchoMap system had no significant influence on radiation exposure during cardiac catheterization, whereas it was associated with a moderate increase in contrast media amount.

Cardiac Catheterization↗
PubMed2004

Identification of syndrome X using intravascular ultrasound imaging and Doppler flow mapping.

BACKGROUND: The purpose of this study was to assess the morphological changes and physiological function of coronary arteries in patients presenting with chest pain but having normal coronary angiograms, using intravascular ultrasound imaging (IVUS) and intracoronary Doppler (ICD) flow measurements, in order to elucidate the mechanism of syndrome X. METHODS: A total of 126 patients [67 males, 59 females, mean age (53.1 +/- 13.0) years] who experienced chest pain but had normal coronary angiograms were included in this study. ICD flow measurements of the left anterior descending coronary artery (LAD) were performed using a Cardiometrics FloMap II system. Coronary flow velocity reserve (CFVR) was defined as the ratio of the average peak velocity during hyperemia to that at baseline, induced by an intracoronary bolus injection of 18 microg adenosine. A 3.2F or 2.9 F 30 MHz mechanical rotating ultrasound catheter (CVIS, Boston Scientific) or a 3.0 F 20 MHz electronic ultrasound catheter (Endosonics) was used for IVUS. RESULTS: The mean CFVR value of the LAD was 2.71 +/- 0.74. Reduction of CFVR (< 3.0) was found in 82 of 126 (65.1%) patients. IVUS images of the LAD were available for 109 patients. Plaque formation was detected in 76/109 (69.7%) patients. Based on the presence or absence of plaque formation as well as the reduction or non-reduction of CFVR, patients were divided into four groups: Group I (n = 10), normal IVUS findings and normal CFVR; Group II (n = 23), normal IVUS findings with reduction in CFVR; Group III (n = 29), IVUS evidence of plaque formation but normal CFVR; and Group IV (n = 47), IVUS evidence of plaque formation with reduction in CFVR. CONCLUSION: This study shows the important clinical value of a combination of IVUS and ICD in diagnosing patients with angiographically normal coronary arteries. Only 10% of patients studied (Group I) were found to be truly free of coronary disease, while 20% of patients (Group II) would be diagnosed as suffering from syndrome X.

Adult↗
PubMed2004

Impact of gender on femoral access complications secondary to application of a collagen-based vascular closure device.

BACKGROUND: Vascular complications at the femoral access site continue to be a significant problem after cardiac catheterization procedures. It was the aim of the present study to assess the impact of gender on the incidence of severe femoral access complications following the application of a collagen-based vascular closure device after transfemoral catheterization procedures. METHODS: A total of 1,294 consecutive patients (977 male, 317 female) underwent closure of femoral access sites with 8F collagen-based vascular closure devices (Angioseal) immediately after diagnostic or interventional coronary catheterization procedures, independently of the coagulation status. All patients were closely monitored for the occurrence of complications during the following 24 hours. RESULTS: Between male and female patients, there was no difference in the technical performance of the device with successful deployment being achieved in 96.7% and 95.9%, respectively (p=0.60). Severe access complications were found to be significantly higher in female versus male patients (1.6% vs. 0.2%; Odds ratio 7.7, 95% confidence interval 1.5-40.1; p=0.015), although similar accomplishment of an immediate hemostasis was seen in 92.8% and 92.4% of male and female patients (p=0.98). CONCLUSION: Women show a significantly increased risk of developing severe femoral access complications secondary to the application of a collagen-based vascular closure device, although the overall incidence of these complications is relatively low. We speculate that the increased risk in women may be related to smaller arterial dimensions, which could be evaluated by femoral angiography prior to deployment of a closure device.

Adult↗
PubMed2003

A randomized trial of polytetrafluoroethylene-membrane-covered stents compared with conventional stents in aortocoronary saphenous vein grafts.

We compared a conventional stent (Jostent Flex, Jomed GmbH, Rangendingen, Germany) with a polytetrafluoroethylene (PTFE)-membrane-covered stent (Jostent Stentgraft) in patients undergoing intervention of a stenosis in an obstructed vein graft. The use of stents improved results of percutaneous revascularization of obstructed vein grafts, but did not demonstrate the reduced elevated restenosis rate. In addition, long-term clinical event rate is still high compared with intervention in native vessels. Observational studies suggested that stents covered with a PTFE membrane might be associated with a low complication and restenosis rate in venous bypass grafts. This prospective multicenter study included a total of 211 patients who were randomly assigned to receive either a Flex stent or Stentgraft. The primary end point was binary restenosis rate at six months by core lab quantitative coronary angiography. Acute success and procedural events were comparable between the two groups. Restenosis rate was not significantly different between the Flex (20%) and the Stentgraft (29%) groups (p = 0.15), although there was a nonsignificant trend toward a higher late occlusion rate in the Stentgraft group (7% vs. 16%, p = 0.069) at follow-up. Likewise, after a mean observation period of 14 months, cumulative event rates (death, myocardial infarction, or target lesion revascularization) were comparable in the two groups (31% vs. 31%, p = 0.93). This controlled trial does not indicate a superiority of the PTFE-membrane-covered Stentgraft compared with a conventional stent with respect to acute results, restenosis, or clinical event rates.

Aged↗
PubMed2003

Preintervention arterial remodeling affects vessel stretch and plaque extrusion during coronary stent deployment as demonstrated by three-dimensional intravascular ultrasound.

The mechanisms of lumen enlargement during stent implantation may be significantly affected by arterial remodeling. To assess effects of lesion remodeling, we performed 3-dimensional intravascular ultrasound (IVUS) analyses in 55 coronary lesions before and after deployment of balloon-expandable stents. Standard quantitative analysis was performed, and arterial remodeling was assessed by the remodeling index (target site divided by mean of proximal and distal reference segment vessel areas), which classified lesions into group A (remodeling index < or =1, negative or intermediate remodeling, n = 40) or group B (remodeling index >1, positive remodeling, n = 15) lesions. Characteristics of the 55 patients and the interventional procedures were similar in the 2 groups. IVUS demonstrated that stenting resulted in increased lumen and vessel dimensions and in a reduced plaque size (p < or =0.001 each) in both group A and group B lesions. The extent of lumen increase inside the stents was almost identical, but resulted from different mechanisms: (1) vessel stretch was greater in group A (p <0.002 at minimum lumen site); (2) plaque compression (or embolization) tended to be greater in group B (p = 0.05, along entire stented segment); (3) plaque redistribution within the stent was observed in both groups (p <0.005 both); and (4) significant (p <0.01) plaque extrusion into the distal reference segment was found in group B only. Thus, the remodeling pattern of coronary lesions has a significant impact on the mechanisms of lumen enlargement during stent deployment. Lesions with positive remodeling show more plaque extrusion into the distal reference and less stent-induced vessel stretch than those with negative remodeling.

Aged↗
PubMed2003

Impact of moderate lesion calcium on mechanisms of coronary stenting as assessed with three-dimensional intravascular ultrasound in vivo.

Axial plaque redistribution is an important mechanism of lumen enlargement after stenting of noncalcified lesions. To assess effects of lesion calcification on mechanisms of coronary stenting, we analyzed 55 lesions with noncircumferential calcification with 3-dimensional intravascular ultrasound (IVUS) (standard qualitative and quantitative analyses) before and after implantation of balloon-expandable stents. Thirty-two plaques (58%) showed arcs of calcium <120 degrees of vessel circumference (group A), whereas 23 lesions (42%) contained arcs of calcium > or =120 degrees of vessel circumference (group B). In the entire cohort of 55 lesions, as well as groups A and B, which were studied separately, both single-slice IVUS analysis (performed at minimum lumen site before intervention) and mean stented segment IVUS analysis showed an increase in lumen and vessel area and a decrease in plaque area (p <0.001). The magnitude of lumen and vessel increase and of plaque decrease was similar in both groups. Group A lesions showed significant plaque extrusion into the distal reference segment that was not observed in group B (increase in plaque area of 1.3 +/- 1.9 vs 0.1 +/- 2.0 mm(2), p <0.04). Stenting did not alter plaque area of the proximal reference segment in either group. In addition, there was an increase in vessel area of the distal reference of both groups, indicating that stent-induced vessel expansion observed within the lesion also affected the distal reference. Thus, longitudinal plaque redistribution and vessel expansion contribute to increased lumen dimensions during stenting of lesions with varying amounts of calcium; however, marked plaque extrusion was found only in lesions with a calcium arc of <120 degrees.

Aged↗