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Michael Haude

Publications and source records attributed to Michael Haude.

At least 19 recordsLinked to original sources
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↗
PubMed2003

Heparin-coated stent placement for the treatment of stenoses in small coronary arteries of symptomatic patients.

BACKGROUND: The role of stents, especially of heparin-coated stents for the treatment of stenoses in small coronary arteries, is still unclear. Therefore, we performed this prospective, randomized trial to evaluate the angiographic and clinical outcome after treatment of stenoses in small coronary arteries (2.0 to 2.6 mm) of symptomatic patients. METHODS AND RESULTS: We randomly assigned 588 patients to angioplasty (n=195), bare stenting (n=196), or heparin-coated stenting (n=197). The primary end point was minimal lumen diameter (MLD) at 6 months. With comparable baseline parameters, the two stent arms showed a larger postinterventional MLD, larger acute gain, and smaller residual percent diameter stenosis, although a residual stenosis of 12+/-16% was achieved in the angioplasty arm, including a 27% crossover rate to stenting. Eighty percent of patients had follow-up angiography, which documented a borderline significantly larger MLD and smaller percent diameter stenosis for the two stent groups (1.34+/-0.48 mm and 42+/-20% after angioplasty, 1.47+/-0.48 mm and 36+/-20% after bare stenting, and 1.45+/-0.54 mm and 38+/-23% after heparin-coated stenting; P=0.049 and P=0.038, respectively), but restenosis rates were not different (32%, 25%, and 30%). Thrombotic events occurred in 1.0% after angioplasty and 0.5% after bare or heparin-coated stenting. Survival without myocardial infarction or target vessel revascularization at 250 days was 84.6% (angioplasty), 88.3% (bare stenting), and 88.3% (heparin-coated stenting; log-rank P=0.39). CONCLUSION: Compared with angioplasty with provisional stenting, bare and heparin-coated stenting confer superior angiographic results and a nonsignificant 24% reduction in clinical events, with no difference between bare and heparin-coated stenting in the treatment of stenoses in small coronary arteries.

Angioplasty, Balloon, Coronary↗
PubMed2003

Catheter-based coronary bypass: a development update.

Catheter-based coronary bypass has evolved since its origin in 1995. We present a status update of one version of catheter-based bypass, percutaneous in situ coronary venous arterialization (PICVA), its successes and failures, and the many questions and challenges that remain. Initial clinical experience with PICVA demonstrated promising mitigation of angina in no-option patients, but was complicated by a relatively low procedural completion rate and a high incidence of MACE. A great deal was learned in these initial cases. The system of devices is currently undergoing significant modification, and further clinical study is underway.

Cardiac Catheterization↗
PubMed2003

Percutaneous suture-mediated closure of femoral access sites deployed through the procedure sheath: initial clinical experience with a novel vascular closure device.

The objective of this study was to assess the initial safety and feasibility of a novel suture-mediated device for closure of femoral access sites immediately after diagnostic or interventional cardiac catheterization. In a prospective study, 150 patients (mean age, 61.5 years; 109 male) underwent femoral access closure with a novel suture closure device (Superstitch, Sutura) immediately after diagnostic (n = 106) or interventional (n = 44) catheterization procedures, independently of the coagulation status. All patients were monitored for 24 hr after the procedure. The closure device was successfully deployed in 92% of patients. Immediate hemostasis was achieved in 77% of patients with no differences between patients undergoing diagnostic catheterization or coronary interventions (79% vs. 73%; P = 0.659). After 2 min of additional light manual compression, hemostasis was achieved in 92% of patients. There was one major complication requiring vascular surgery (0.7%). The novel suture closure device is a safe and effective device that allows for immediate closure of femoral puncture sites after both diagnostic and interventional procedures with a low rate of major complications.

Aged↗