Search PubMed⌕ Search

Biomedical subjects

K M Kent

Publications and source records attributed to K M Kent.

At least 109 records · Page 6Linked to original sources
PubMed1997

Serial intravascular ultrasound predictors of restenosis at the margins of Palmaz-Schatz stents.

To evaluate predictors of restenosis at margins of Palmaz-Schatz stents, intravascular ultrasound studies were performed after intervention and at follow-up (5.4 months) in 161 stented lesions. Of 301 stent margins, 77 (26%) were restenotic at follow-up (>50% late lumen loss). Intimal hyperplasia was greater for restenotic than for nonrestenotic stents margins. The dominant periprocedural predictor of stent margin restenosis was the plaque burden of the continuous reference segment.

Coronary Disease↗
PubMed1997

Contribution of inadequate arterial remodeling to the development of focal coronary artery stenoses. An intravascular ultrasound study.

BACKGROUND: Adaptive remodeling occurs to compensate for the accumulation of atherosclerotic plaque. Lumen reduction depends on the relative rates of plaque deposition and adaptive remodeling responses. Intravascular ultrasound permits detailed, high-quality, cross-sectional imaging of the coronary arteries in vivo. METHODS AND RESULTS: Preintervention intravascular ultrasound was used to study 603 focal, new, nonostial significant coronary artery stenoses in patients with chronic stable angina. Measurements of the target lesion of the external elastic membrane (EEM), lumen, and plaque plus media (P&M; P&M = EEM - Lumen) cross-sectional areas (CSAs) were compared with a proximal reference segment (most normal-looking cross section within 10 mm proximal to the lesion but distal to any side branch). Inadequate remodeling was defined as lesion/ reference EEM CSA that exceeded the upper limits of normal arterial tapering (lesion/reference EEM CSA ratio < or = 0.78 or a 21% reduction in EEM CSA per 10-mm length). Overall, the lesion/reference EEM CSA ratio was 1.00 +/- 0.22; 15% of lesions had inadequate remodeling, and 37% of the 603 lesions had less plaque than expected. This represented a lesion-specific response. The only predictor of inadequate remodeling was the arc of superficial lesion calcium. CONCLUSIONS: Inadequate remodeling is present in at least 15% of chronic, focal, new coronary arterial stenoses in patients with stable angina. The magnitude of arterial remodeling appears to be a lesion-specific response.

Adaptation, Physiological↗
PubMed1997

Increased restenosis in diabetes mellitus after coronary interventions is due to exaggerated intimal hyperplasia. A serial intravascular ultrasound study.

BACKGROUND: The increased risk of restenosis after catheter-based coronary interventions in diabetic patients has not been determined. Intravascular ultrasound (IVUS) has shown that the decrease in arterial area is responsible for most of the late lumen loss in nonstented lesions and that intimal hyperplasia is responsible for all of the late lumen loss in stented lesions. METHODS AND RESULTS: Serial (postintervention and follow-up at 5.6 +/- 3.3 months) IVUS was used to study 251 native coronary lesions in 241 patients; 63 patients had treated diabetes mellitus (oral hypoglycemic drugs or insulin). Interventional procedures included percutaneous transluminal coronary angioplasty, directional or rotational atherectomy, excimer laser angioplasty, or Palmaz-Schatz stents. The external elastic membrane (EEM), stent, and lumen areas were measured. The plaque+media (P+M) area in nonstented lesions was calculated as EEM minus lumen area, and the intimal hyperplasia (IH) area in stented lesions was calculated as stent minus lumen area. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen area. Nonstented lesions in diabetics and nondiabetics had a similar decrease in EEM cross-sectional area (CSA; 1.9 +/- 2.8 versus 1.8 +/- 4.2 mm2; P = .6350). However, nonstented lesions in diabetics had a greater increase in P+M CSA (1.3 +/- 2.8 versus 0.6 +/- 2.5 mm2, P = .0720), and the increase in P+M CSA contributed a greater percentage to the decrease in lumen CSA. In stented lesions, the decrease in lumen CSA (5.2 +/- 2.5 versus 2.0 +/- 2.3 mm2) and the increase in IH CSA (5.0 +/- 2.8 versus 1.8 +/- 2.0 mm2) were greater in diabetics than nondiabetics (P = .0009 and P = .0007, respectively). These findings were even more striking in (nonstented and stented) restenotic lesions. CONCLUSIONS: Serial IVUS analysis showed that the main reason for increased restenosis in diabetes mellitus was exaggerated intimal hyperplasia in both stented and nonstented lesions.

Aged↗
PubMed1997

The device with a name on it.

Conflict of interest is a significant problem in interventional cardiology that can potentially affect how data are presented and evaluated. Creative inventor clinicians and scientists should rely on investigators without conflict of interest to evaluate and report on new devices and outcomes.

Cardiology↗
PubMed1997

Influence of guiding catheter selection on the measurement of coronary flow reserve.

The impact of guiding catheter selection on the measurement of coronary flow reserve was assessed by injecting increasing doses of adenosine through 3 different catheters often used during coronary interventions. When guiding catheters with side holes were used, an approximate doubling of the adenosine dose was required to produce a coronary flow reserve response similar to a 12-micrograms dose of adenosine injected through guiding catheters without side holes.

Adenosine↗
PubMed1997

Continuous subcutaneous angiopeptin treatment significantly reduces neointimal hyperplasia in a porcine coronary in-stent restenosis model.

BACKGROUND: In-stent restenosis results primarily from neointimal hyperplasia. This study evaluated the efficacy and the optimal mode of administration of angiopeptin, a somatostatin analogue with antiproliferative activity, in a porcine coronary in-stent restenosis model. METHODS AND RESULTS: Forty pigs were randomly assigned to one of four groups (n = 10 per group): (1) controls receiving saline infusion at the site of stent implantation via a local delivery catheter, (2) local treatment group receiving one-time treatment (200 (micrograms angiopeptin) at the site of stent placement, (3) systemic treatment group receiving continuous angiopeptin over a 1-week period via a subcutaneous osmotic pump (200 micrograms/kg total dose) and (4) combined local and systemic treatment group. Then, one oversized Palmaz-Schatz stent (mean ratio of stent to artery diameters, 1.3:1) was implanted in the left anterior descending coronary artery. The degree of neointimal reaction was evaluated 4 weeks later by angiography (maximal percent diameter stenosis), intravascular ultrasound (total in-stent neointimal volume), and histology (maximal area stenosis). Systemic treatment produced the least neointimal hyperplasia and significantly reduced in-stent restenosis compared with the control group by all end points, despite similar degrees of injury. Angiography showed 25 +/- 17% versus 50 +/- 17% diameter stenosis in the systemic angiopeptin group versus the control group (P < .0001), intravascular ultrasound revealed 23 +/- 10 versus 58 +/- 27 mm3 neointimal volume in the systemic angiopeptin versus control group (P = .0002), and histology showed 41 +/- 16% versus 69 +/- 18% area stenosis (P = .0016) in the systemic angiopeptin versus control group. Plasma angiopeptin levels revealed rapid clearance (within 6 hours) after local therapy, whereas the levels persisted for up to 2 weeks in the systemic group. CONCLUSIONS: This study shows that continuous subcutaneous treatment with angiopeptin after stent implantation significantly reduces in-stent restenosis by inhibiting neointimal hyperplasia.

Animals↗
PubMed1997

Intravascular ultrasound insights into mechanisms of stenosis formation and restenosis.

Using intravascular ultrasound (IVUS), stenosis formation and restenosis (or late lumen loss following coronary angioplasty procedures) can be subdivided into two distinct underlying components: tissue accumulation and arterial remodeling. Arterial remodeling is defined as a change in total arterial cross-sectional area over time; it can be adaptive (an increase in arterial cross-sectional area as a compensatory response to plaque accumulation) or pathologic (a decrease in arterial cross-sectional area or chronic arterial shrinkage). Adaptive arterial remodeling can delay the development of coronary artery stenoses and prevent restenosis; pathologic remodeling can contribute to de novo lesion formation and has been shown to be the dominant mechanism of restenosis following coronary intervention. Serial IVUS studies have also been used to study the natural history of the restenosis process; adaptive remodeling occurs early (within 1 month) and pathologic remodeling occurs late (between 1 and 6 months) after intervention. The residual plaque burden postintervention acts as an amplifier in this process.

Animals↗
PubMed1997

Determinants and correlates of target lesion calcium in coronary artery disease: a clinical, angiographic and intravascular ultrasound study.

OBJECTIVES: This report used intravascular ultrasound and quantitative coronary angiography to explore the relation between lesion-associated calcium and risk factors, clinical presentation and angiographic severity of coronary artery stenoses. BACKGROUND: Coronary artery calcium is a marker for significant coronary atherosclerosis. Noninvasive procedures are being proposed as screening tests for coronary artery disease. Intravascular ultrasound identification of tissue calcium has been validated in vitro. METHODS: Independent chart review, preintervention intravascular ultrasound imaging and coronary angiography were used to study primary native vessel lesions in 1,442 patients. Target lesions and reference segments were evaluated according to previously published quantitative and qualitative methods. Results are presented as mean value +/- SD. RESULTS: Overall, 1,043 lesions contained target lesion calcium (72%); the arc of target lesion calcium was 110 +/- 109 degrees. Lesions with an ultrasound plaque burden > 0.75 or an angiographic diameter stenosis > 0.25 had a prevalence of calcium of at least 65%, with a mean arc > 100 degrees. Intermediate lesions had as much target lesion calcium as did angiographically severe lesions. Using multivariate linear regression analysis, patient age, stable (vs. unstable) angina and the intravascular ultrasound lesion site and reference segment plaque burden (but not the angiographic diameter stenosis) were the independent predictors of the arc of target lesion calcium (all p < 0.0001). CONCLUSIONS: Intravascular ultrasound analysis shows that coronary calcification correlates with plaque burden but not with degree of lumen compromise. Thus, the noninvasive detection of coronary calcium is predictive of future cardiac events, presumably because coronary calcification is a marker for overall atherosclerotic plaque burden. Coronary calcium increases with increasing patient age and is less common in unstable lesion subsets.

Adult↗
PubMed1997

Single-dose intramuscular administration of sustained-release Angiopeptin reduces neointimal hyperplasia in a porcine coronary in-stent restenosis model.

BACKGROUND: In-stent restenosis results primarily from neointimal hyperplasia. In a previous study we showed that continuous subcutaneous Angiopeptin infusion for 1 week significantly reduces neointimal hyperplasia in a porcine coronary overstretch in-stent restenosis model. The present study evaluated the relative efficacy of immediate-release and sustained-release Angiopeptin in the same model. METHODS: Thirty pigs (n = 10 in each group) were randomly assigned to three groups: controls receiving no Angiopeptin (Group 1); a sustained-release treatment group receiving one time intramuscular administration of 20 mg of Angiopeptin (Group 2); and a systemic treatment group receiving continuous Angiopeptin over a 1-week period via a subcutaneous osmotic pump (200 micrograms/kg total dose) (Group 3). One oversized Palmaz-Schatz stent (mean stent/artery = 1.25) was subsequently implanted in the left anterior descending coronary artery. The degree of neointimal reaction was evaluated 4 weeks later by angiography (maximal per cent diameter stenosis) and histology (maximal neointimal area corrected for injury score). RESULTS: A trend towards a reduction in diameter stenosis was observed by angiography, despite a similar degree of injury (25 +/- 17% in Group 1, 13 +/- 8% in Group 2, and 14 +/- 9% in Group 3; P = 0.072 by ANOVA). Histology demonstrated that both Angiopeptin treatment strategies significantly reduced in-stent neointimal area compared with the control group (1.65 +/- 0.97 mm2 in Group 1 versus 0.93 +/- 0.41 mm2 in Group 2 versus 0.85 +/- 0.28 mm2 in Group 3; P = 0.016 by ANOVA). Measurement of plasma Angiopeptin levels revealed comparable levels in both treatment groups, which persisted for up to 2 weeks. CONCLUSIONS: This study shows that single-dose intramuscular administration of sustained-release Angiopeptin reduces in-stent restenosis as effectively as the prolonged systemic treatment requiring a subcutaneous pump. Thus, a practical, effective, pharmacologic therapy for preventing in-stent restenosis may be available and should be evaluated in patients.

Animals↗
PubMed1996

Chronic arterial responses to stent implantation: a serial intravascular ultrasound analysis of Palmaz-Schatz stents in native coronary arteries.

OBJECTIVES: We used intravascular ultrasound (IVUS) imaging to evaluate the chronic vessel responses to Palmaz-Schatz stents. BACKGROUND: Palmaz-Schatz stents have been shown to inhibit early elastic recoil and late arterial remodeling while triggering neointimal hyperplasia. However, changes occurring in native vessels surrounding stent struts have not been well studied. METHODS: Postintervention and follow-up (mean [+/-SD] 5.4 +/- 3.8 months) serial IVUS imaging was performed in 25 stents without restenosis and 24 with in-stent restenosis. Intravascular ultrasound imaging using automatic transducer pullback at 0.5 mm/s allowed measurement at 1-mm axial increments of external elastic membrane (EEM), stent and lumen cross-sectional areas (CSAs) and calculation of peristent plaque plus media (P + M = EEM - stent) CSA, intrastent plaque (stent-lumen) CSA, arterial remodeling (delta EEM CSA), tissue growth outside the stent (delta P + M CSA) and tissue growth within the stent (delta stent-lumen CSA). Volumes were calculated using the Simpson rule. RESULTS: Mean EEM CSA increased significantly from 16.9 +/- 5.0 mm2 after intervention to 18.4 +/- 4.9 mm2 at follow-up (p < 0.0001), reflecting an increase in P + M CSA surrounding the stent (1.6 +/- 1.3 mm2). Greater tissue growth within the stent (2.4 +/- 2.2 mm2) correlated weakly, but directly with tissue growth surrounding the stent (r = 0.356, p = 0.0121). The ratio of peristent/intrastent tissue growth correlated weakly with arterial remodeling (r = 0.282, p = 0.0525). Restenotic stents had more tissue growth both within and surrounding the stent than did nonrestenotic stents. Volumetric measurements, which could be obtained in 15 lesions, showed similar results. CONCLUSIONS: After implantation there is a chronic increase in plaque mass both within and surrounding the stents. The increase in peristent plaque mass is associated with adaptive remodeling.

Aged↗
PubMed1996

Mechanisms and results of balloon angioplasty for the treatment of in-stent restenosis.

Restenosis within tubular slotted stents is secondary to intimal hyperplasia and is usually treated with percutaneous transluminal coronary angioplasty (PTCA). Sequential intravascular ultrasound (IVUS) was used to assess the mechanisms and results of PTCA for in-stent restenosis. Sixty-four restenotic Palmaz-Schatz stents were studied by IVUS imaging before and after PTCA. IVUS measurements of stent and lumen cross-sectional areas (CSAs) at 5 segments (proximal and distal stent edges, proximal and distal stent bodies, and the central articulation) were used to calculate intimal hyperplasia CSA (stent-lumen CSA). The results of the 5 segments were then averaged. Mean and minimum CSAs were compared before and after PTCA. Quantitative angiographic measurements showed a minimal lumen diameter increase from 1.05 +/- 0.63 mm (mean +/- 1 SD) before intervention to 2.77 +/- 0.51 mm after PTCA (p < 0.0001). Conversely, the diameter stenosis decreased from 63 +/- 19% to 18 +/- 12% (p < 0.0001). IVUS measurements showed a minimum lumen CSA increase from 2.3 +/- 1.3 mm2 to 6.1 +/- 2.2 mm2 (p < 0.0001) as a result of an increased minimum stent CSA (7.2 +/- 2.4 mm2 to 8.7 +/- 2.6 mm2, p < 0.0001) and a decreased intimal hyperplasia CSA within the stent (4.9 +/- 2.2 mm2 to 2.7 +/- 2.0 mm2, p < 0.0001). Of the total mean lumen enlargement, 56 +/- 28% was the result of additional stent expansion and 44 +/- 28% was the result of a decrease in neointimal tissue. The minimum lumen CSA after PTCA was significantly smaller than the minimum stent CSA before PTCA (presumably an accurate reflection of lumen dimensions immediately after stent implantation; p = 0.0002). The mechanism of PTCA for restenosis is a combination of additional stent expansion and tissue extrusion out of the stent; there is a relatively high residual stenosis (angiographic diameter stenosis of 18 +/- 12%).

Aged↗
PubMed1996

Patterns and mechanisms of in-stent restenosis. A serial intravascular ultrasound study.

BACKGROUND: Studies have suggested that restenosis within Palmaz-Schatz stents results from neointimal hyperplasia or chronic stent recoil and occurs more frequently at the articulation. METHODS AND RESULTS: Serial intravascular ultrasound (IVUS) was performed after intervention and at follow-up in 142 stents in 115 lesions. IVUS measurements (external elastic membrane [EEM], stent, and lumen cross-sectional areas [CSAs] and diameters) were performed, and plaque CSA (EEM lumen in reference segments and stent lumen in stented segments), late lumen loss (delta lumen), remodeling (delta EEM in reference segments and delta stent in stented segments), and tissue growth (delta plaque) were calculated. After intervention, the lumen tended to be smallest at the articulation because of tissue prolapse. At follow-up, tissue growth was uniformly distributed throughout the stent; the tendency for greater neointimal tissue accumulation at the central articulation reached statistical significance only when normalized for the smaller postintervention lumen CSA. In stented segments, late lumen area loss correlated strongly with tissue growth but only weakly with remodeling. Stents affected adjacent vessel segments; remodeling progressively increased and tissue growth progressively decreased at distances from the edge of the stent. These findings were similar in native arteries and saphenous vein grafts and in lesions treated with one or two stents. There was no difference in the postintervention or follow-up lumen (at the junction of the two stents) when overlapped were compared with nonoverlapped stents. CONCLUSIONS: Late lumen loss and in-stent restenosis were the result of neointimal tissue proliferation, which tended to be uniformly distributed over the length of the stent.

Aged↗
PubMed1996

Intravascular ultrasound to discern device-specific effects and mechanisms of restenosis.

Restenosis continues to be the "Achilles heel" of transcatheter interventions. While attempts to reduce restenosis by inhibiting cellular proliferation through pharmacologic or mechanical means have been unsuccessful, stents, which inhibit acute recoil and chronic remodeling, have been shown convincingly to reduce restenosis in 2 randomized clinical trials. Intravascular ultrasound (IVUS) allows transmural, tomographic imaging of coronary arteries in humans in vivo to subdivide restenosis into the two basic underlying components: tissue proliferation and arterial remodeling. In studies performed at the Washington Hospital Center, in nonstented lesions 73% of late lumen loss was due to arterial remodeling (a decrease in arterial, or external elastic membrane cross-sectional area) and 27% was due to tissue growth (an increase in plaque plus media cross-sectional area). These findings were confirmed by 2 other studies: the Optimal Atherectomy Restenosis Study (OARS) and the Serial Ultrasound analysis of REstenosis (SURE) Trial. IVUS was also used to study the mechanisms by which stents reduce restenosis. Stents created a larger final lumen cross-sectional area and, for all practical purposes, abolished arterial remodeling to offset a stent-related increase in neointimal tissue accumulation. Neointimal hyperplasia is solely responsible for in-stent restenosis and therefore appears to be a pure model for studying strategies to limit tissue proliferation.

Angioplasty, Balloon, Coronary↗
PubMed1996

Arterial remodeling after coronary angioplasty: a serial intravascular ultrasound study.

BACKGROUND: Restenosis occurs after 30% to 50% of transcatheter coronary procedures; however, the natural history and pathophysiology of restenosis are still incompletely understood. METHODS AND RESULTS: Serial (postintervention and follow-up) intravascular ultrasound imaging was used to study 212 native coronary lesions in 209 patients after percutaneous transluminal coronary angioplasty, directional coronary atherectomy, rotational atherectomy, or excimer laser angioplasty. The external elastic membrane (EEM) and lumen cross-sectional areas (CSA) were measured; plaque plus media (P+M) CSA was calculated as EEM minus lumen CSA. The anatomic slice selected for serial analysis had an axial location within the target lesion at the smallest follow-up lumen CSA. At follow-up, 73% of the decrease in lumen (from 6.6+/-2.5 to 4.0+/-3.7 mm2, P<.0001) was due to a decrease in EEM (from 20.1+/-6.4 to 18.2+/-6.4 mm2, P<.0001); 27% was due to an increase in P+M (from 13.5+/-5.5 to 14.2+/-5.4 mm2, P<.0001). Delta Lumen CSA correlated more strongly with delta EEM CSA (r=.751, P<.0001) than with delta P+M CSA (r=.284, P<.0001). Delta EEM was bidirectional; 47 lesions (22%) showed an increase in EEM. Despite a greater increase in P+M (1.5+/-2.5 versus 0.5+/-2.0 mm2, P=.0009), lesions exhibiting an increase in EEM had (1) no change in lumen (-0.1+/-3.3 versus 3.6+/-2.3 mm2, P<.0001), (2) a reduced restenosis rate (26% versus 62%, P<.0001), and (3) a 49% frequency of late lumen gain (versus 1%, P<.0001) compared with lesions with no increase in EEM. CONCLUSIONS: Restenosis appears to be determined primarily by the direction and magnitude of vessel wall remodeling (delta EEM). An increase in EEM is adaptive, whereas a decrease in EEM contributes to restenosis.

Aged↗
PubMed1996

In vivo validation of intravascular ultrasound length measurements using a motorized transducer pullback system.

Using sonoreflective endovascular targets of known length (stainless steel tubular slotted stents), we have validated in vivo the accuracy and reproducibility of intravascular ultrasound length measurements using a system incorporating motorized transducer pullback through a stationary imaging sheath. The correlation was r = 0.936, with a measurement error of only +/- 5.2%, minimal intraobserver variability, and variability of sequential measurements of only +/- 4.8%.

Aged↗
PubMed1996

Limitations of angiography in the assessment of plaque distribution in coronary artery disease: a systematic study of target lesion eccentricity in 1446 lesions.

BACKGROUND: Plaque distribution (eccentricity) may be a determinant of the success of transcatheter therapy, and certain devices may be better suited to treating severely eccentric lesions than others. However, no study has compared methods for assessing plaque distribution or systematically studied the validity of the angiographic assessment of plaque distribution. METHODS AND RESULTS: We studied 1446 native vessel target lesions in 1349 patients by intravascular ultrasound and coronary angiography. Angiographic and intravascular ultrasound criteria for lesion eccentricity were compared. Angiography showed that 795 of 1446 (55.0%) of target lesions were eccentric. When intravascular ultrasound was used, only 219 lesions (15.1%) had an arc of normal arterial wall within the lesion (equivalent to the pathological definition of lesion eccentricity). When an eccentricity index of >/= 3.0 was used, intravascular ultrasound classified 659 lesions (45.6%) as eccentric. The concordance rates of classification were only 47.7% (versus lesions containing an arc of normal arterial wall) and 53.8% (versus lesions with an ultrasound eccentricity index of >/= 3.0). More eccentric lesions had larger lumen cross-sectional areas, smaller plaque plus media and external elastic membrane cross-sectional areas, and smaller arcs of calcium, suggesting that they may represent less advanced atherosclerotic disease. CONCLUSIONS: There was significant discordance between angiography and ultrasound in assessing plaque distribution. Angiography appeared to detect lesion eccentricity more often than intravascular ultrasound. Furthermore, markedly eccentric lesions, in which there is an arc of normal vessel wall, were uncommon.

Coronary Angiography↗