Single-step atrial thrombus exclusion and internal cardioversion of atrial fibrillation via a transesophageal echocardiography probe.
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Animals↗
Biomedical subjects
Peter Hanrath
Publications and source records attributed to Peter Hanrath.
Statin treatment after onset of sepsis in a murine model improves survival.
BACKGROUND: HMG-CoA-reductase inhibitors have been shown to exhibit pronounced immunomodulatory effects independent of lipid lowering. We have recently demonstrated that pretreatment with simvastatin profoundly improves survival in a cecal ligation and perforation (CLP) model of sepsis. Here, we studied whether treatment with simvastatin after onset of sepsis-induced hemodynamic alterations is beneficial and whether prolonged survival can also be achieved with other statins. METHODS AND RESULTS: Mice were rendered septic by CLP. At 6 hours after sepsis induction, when profound hemodynamic alterations were manifest, treatment with atorvastatin, fluvastatin, pravastatin, simvastatin, or placebo was initiated. Except for fluvastatin (27+/-2.3 hours), survival time was extended from 23+/-1.2 hours for placebo-treated mice to 37+/-3.6 hours for simvastatin-treated, to 40+/-4.2 hours for atorvastatin-treated, and to 39+/-3.9 hours for pravastatin-treated mice. This profound improvement is based on the preservation of cardiac function and hemodynamic status in statin-treated animals, both of which are severely impaired in untreated CLP mice. As underlying mechanisms, improved susceptibility to endothelial nitric oxide synthase stimulation and reduced endothelial adhesion of leukocytes could be demonstrated after statin treatment. CONCLUSIONS: Well established in the treatment of lipid disorders and coronary artery disease, statins harbor the additional and novel potential of effective sepsis treatment. This benefit extends to several but not all statins tested.
Animals↗
Prognostic relevance of atrial fibrillation in patients with chronic heart failure on long-term treatment with beta-blockers: results from COMET.
AIMS: Atrial fibrillation is common in patients with chronic heart failure (CHF). We analysed the risk associated with atrial fibrillation in a large cohort of patients with chronic heart failure all treated with a beta-blocker. METHODS AND RESULTS: In COMET, 3029 patients with CHF were randomized to carvedilol or metoprolol tartrate and followed for a mean of 58 months. We analysed the prognostic relevance on other outcomes of atrial fibrillation on the baseline electrocardiogram compared with no atrial fibrillation and the impact of new onset atrial fibrillation during follow-up. A multivariate analysis was performed using a Cox regression model where 10 baseline covariates were entered together with study treatment allocation. Six hundred patients (19.8%) had atrial fibrillation at baseline. These patients were older (65 vs. 61 years), included more men (88 vs.78%), had more severe symptoms [higher New York Heart Association (NYHA) class] and a longer duration of heart failure (all P<0.0001). Atrial fibrillation was associated with significantly increased mortality [relative risk (RR) 1.29: 95% CI 1.12-1.48; P<0.0001], higher all-cause death or hospitalization (RR 1.25: CI 1.13-1.38), and cardiovascular death or hospitalization for worsening heart failure (RR 1.34: CI 1.20-1.52), both P<0.0001. By multivariable analysis, atrial fibrillation no longer independently predicted mortality. Beneficial effects on mortality by carvedilol remained significant (RR 0.836: CI 0.74-0.94; P=0.0042). New onset atrial fibrillation during follow-up (n=580) was associated with significant increased risk for subsequent death in a time-dependent analysis (RR 1.90: CI 1.54-2.35; P<0.0001) regardless of treatment allocation and changes in NYHA class. CONCLUSION: In CHF, atrial fibrillation significantly increases the risk for death and heart failure hospitalization, but is not an independent risk factor for mortality after adjusting for other predictors of prognosis. Treatment with carvedilol compared with metoprolol offers additional benefits among patients with atrial fibrillation. Onset of new atrial fibrillation in patients on long-term beta-blocker therapy is associated with significant increased subsequent risk of mortality and morbidity.
Adrenergic beta-Antagonists↗
Transplantation of human umbilical vein endothelial cells improves left ventricular function in a rat model of myocardial infarction.
INTRODUCTION: Although cell-based therapy after myocardial infarction (MI) may be beneficial in improving cardiac dysfunction, the underlying mechanisms remain to be clarified. Since human umbilical vein endothelial cells (HUVEC) harbor the potential for transdifferentiation, we studied the functional effects of HUVEC transplantation in a rat model of MI. METHODS AND RESULTS: HUVEC labeled with BrdU or medium alone were injected into the infarcted area and its margin 4 weeks after ligation of the left coronary artery in cyclosporine-treated rats. BrdU(+) signals could be detected in the area of MI at two weeks and two months after injection only in hearts transplanted with HUVEC. While no signs of transdifferentiation into cardiomyocytes were evident, staining for the rat macrophage marker ED-1, adjacent to or colocalized with BrdU(+) signals, revealed an in.ltration with macrophages and implied the phagocytosis of injected HUVEC. In the vicinity of BrdU(+) signals, the density of CD31(+) microvessels was significantly increased in HUVEC-transplanted as compared to medium-treated hearts after two months. HUVEC transplantation led to improved contractility as assessed by echocardiography and to higher coronary flow rates as well as to improved response to volume strain and catecholamine stress in Langendorff perfused hearts. CONCLUSIONS: After MI, transplanted HUVEC persist in the host myocardium and trigger an infiltration with macrophages. The ensuing increase in neovascularization and improvement in global left ventricular function may be attributable to the associated inflammatory response.
Animals↗
Sirolimus- and paclitaxel-eluting stents in comparison with balloon angioplasty for treatment of in-stent restenosis.
This study evaluated the acute and follow-up effectiveness of sirolimus-eluting stents (SESs) and nonpolymer-based paclitaxel-eluting stents (PESs) in comparison will balloon angioplasty for treatment of complex in-stent restenosis (ISR) lesions. Drug-eluting stents have been demonstrated to be highly effective for treatment of de novo lesions. The use of drug-eluting stents for treatment of complex ISR is less well defined. Eighty one lesions with in-stent restenosis (lesion length < 30 mm in a native coronary artery) were treated with either PTCA alone (n = 26 lesions in 25 patients), PES (n = 27 lesions in 24 patients; Achieve, Cook; 3,1 mug paclitaxel/mm(2) nonpolymer-based coating), SES (n = 28 lesions in 28 patients; Cypher, Cordis; 140 mug sirolimus/cm(2) metal surface area). Nine-month MACE rates were 32%, 8%, and 14% (all due to repeated revascularization procedures, except one death in the SES group) in the PTCA, PES, and SES group, respectively. Postintervention minimal lumen diameter in stent was significantly greater in the SES and the PES group in comparison with the PTCA group (2.37 +/- 0.26, 2.54 +/- 0.42, 1.78 +/- 0.23 mm; P < 0.001). At 6-month angiographic follow-up, late loss in stent was 0.77 +/- 0.45, 0.43 +/- 0.53, and 0.29 +/- 0.52 mm for the PTCA, PES, and SES group, respectively (P = 0.005). In-lesion restenosis rate was 61% for the PTCA group, 20% for the PES group, and 13% for the SES group (P = 0.042). The implantation of SES as well as nonpolymer PES proved to be effective for treatment of ISR. The combination of improved acute gain and reduced late loss results in a significantly improved angiographic follow-up result in comparison with PTCA.
Aged↗
Effect of cardiac resynchronization therapy on sleep quality, quality of life, and symptomatic depression in patients with chronic heart failure and Cheyne-Stokes respiration.
Patients with heart failure (HF) often suffer from sleep-related breathing disorders (SRBD) like Cheyne-Stokes respiration (CSR). Cardiac resynchronization therapy (CRT) improves myocardial function and exercise capacity in patients with HF and conduction disturbances. As CRT has been shown to reduce CSR in patients with HF, it is not clear whether CRT improves quality of life and symptomatic depression by improvement of apnea/hypopnea index (AHI) and sleep quality. Forty-two HF patients with conduction disturbance before CRT were screened for CSR and evaluated for sleep quality [Pittsburgh Sleep Quality Index (PSQI)], quality of life score [36-item short form (SF-36)], depression, and exercise capacity (VO2 peak) and ejection fraction (EF). Eighteen patients (three females, age 61+/-10, body mass index 24+/-4 kg m(-2), EF 24+/-4%, QRS complex duration 156+/-32 ms) presented CSR with an AHI of 18+/-8 (11 CSR, 7 mixed). Fourteen patients showed no SRBD (PSQI<5,AHI<5). All patients received CRT and were reevaluated after 18+/-7 weeks. CSR worsen quality of life in seven of eight terms compared to patients without SRBD. Symptomatic depressive symptoms (Beck Depression Inventory>10) were only present in patients with CSR. CRT results in improvement of peak VO2 and EF. There was no difference between patients with CSR and without SRBD on exercise capacity or EF under CRT, whereas CRT led to a significant decrease in AHI (18+/-8 to 3+/-2, p<0.0001), PSQI (18+/-4 to 6+/-3, p=0.0007), with reduction of depression score (12+/-3 to 4.8+/-3, p=0.004). In patients with HF, CSR is associated with symptomatic depressive syndromes and impaired quality of life. CRT reduced CSR with improvement of sleep quality and symptomatic depression.
Cardiac Pacing, Artificial↗
Effects of metoprolol and carvedilol on cause-specific mortality and morbidity in patients with chronic heart failure--COMET.
BACKGROUND: Beta-blockers with different receptor bindings reduce mortality in patients with chronic heart failure. We compared the effects of the beta1-blocker metoprolol tartrate and the beta1-, beta2-, and alpha1-blocker carvedilol. METHODS: In a randomized double-blind design, 3029 patients with chronic congestive heart failure requiring diuretic therapy and with left ventricular dysfunction were randomized to treatment with carvedilol (n = 1511) or metoprolol tartrate (n = 1518) and titrated to target doses of 25 mg of carvedilol twice daily or 50 mg of metoprolol tartrate twice daily. The main outcome measures were total mortality and the combination of mortality or hospitalization for any cause. Secondary end points were cardiovascular death, combinations of morbidity and mortality, New York Heart Association class, worsening of heart failure, hospitalizations, and discontinuation of study therapy. RESULTS: A total of 512 and 600 patients in the carvedilol group and metoprolol group, respectively, died (hazard ratio [HR] 0.83, 95% CI 0.74-0.93, P = .0017). Cardiovascular death was reduced by carvedilol (HR 0.80, 95% CI 0.70-0.90, P = .0004). There were fewer sudden deaths and deaths caused by circulatory failure or by stroke in the carvedilol group. There was no difference in all-cause hospitalizations or in worsening heart failure between treatment groups. The incidence of fatal or nonfatal acute myocardial infarction was significantly lower in the carvedilol group (HR 0.71, 95% CI 0.52-0.97, P = .03). Discontinuations of study therapy were similar in the 2 groups. CONCLUSION: Compared with metoprolol tartrate, carvedilol reduced cardiovascular mortality, sudden death, death caused by circulatory failure, death caused by stroke, as well as fatal and nonfatal myocardial infarctions.
Adrenergic beta-Antagonists↗
Targeted pharmacological reversal of electrical remodeling after cardioversion--rationale and design of the Flecainide Short-Long (Flec-SL) trial.
Persistent atrial fibrillation (AF) causes relevant mortality and cardiovascular and noncardiovascular morbidity. Therefore, maintenance of sinus rhythm is an important clinical goal, especially when the patient is symptomatic, despite the fact that current treatment strategies are not sufficient to completely prevent recurrent AF. In addition to underlying atrial disease that predisposes to AF, AF in itself induces structural and electrical adaptations ("electrical remodeling" and "structural remodeling"). Underlying disease processes and parts of structural remodeling are not always reversible. Electrical remodeling, in contrast, is reversed by a few weeks of maintenance of sinus rhythm under experimental conditions. This corresponds to the period when most of the recurrent episodes of AF occur after cardioversion. Antiarrhythmic drugs that prolong the atrial action potential can assist in the prevention of recurrent AF by promoting the reversal of electrical remodeling. Such drugs, which are currently used over long periods after cardioversion, may only be needed until the physiological action potential duration is restored, for example, during the first few weeks after cardioversion of persistent AF. This treatment concept that we call "targeted pharmacological reversal of electrical remodeling" would limit both cost and drug-induced side effects of antiarrhythmic drug therapy after cardioversion. The Flec-SL trial, ISECTN62728743, therefore tests the main hypothesis that targeted pharmacological reversal of electrical remodeling by short-term antiarrhythmic drug therapy for 4 weeks after cardioversion is not inferior to standard long-term antiarrhythmic drug therapy for the prevention of recurrent AF after cardioversion in a parallel group, randomized, multicenter, open, blinded end point analysis design. Based on its effectiveness and pharmacokinetic profile, flecainide is used to test the study hypothesis. The trial uses daily transtelephonic electrocardiographic monitoring for all patients and will be conducted within the German Atrial Fibrillation Competence NETwork (AFNET) to facilitate inclusion of patients from electrophysiologically oriented cardiology centers, ordinary hospitals, and office-based physicians.
Anti-Arrhythmia Agents↗
Strain rate analysis allows detection of differences in diastolic function between viable and nonviable myocardial segments.
Analysis of diastolic function for assessment of myocardial viability has not been evaluated. Strain rate (SR) analysis allows quantitative segmental analysis of myocardial function and has been used during dobutamine stimulation for assessment of systolic functional reserve. In 37 patients with ischemic left ventricular dysfunction diastolic function was evaluated at rest and during low-dose dobutamine stimulation (10 mug/kg/min) using SR imaging and related to F18-fluorodeoxyglucose positron emission tomography. Analysis of peak early (E waves) and late (A waves) diastolic myocardial SR was performed using apical views. In all, 317 segments had normal function at rest by 2-dimensional echocardiography. A total of 192 segments with dyssynergy at rest were classified by positron emission tomography as viable in 94 cases and nonviable in 98 cases. Dys-synergic segments had lower E and A waves SR compared with normal contracting segments. There were no significant differences in peak E and A waves SR at rest between dys-synergic viable and nonviable segments. With dobutamine stimulation peak E waves SR increased significantly for viable segments (0.89 +/- 0.51-1.06 +/- 0.51 L/s, P < .01) whereas it was unchanged for nonviable segments (0.77 +/- 0.49-0.78 +/- 0.48 L/s, P = .835). Peak A waves SR increased for viable (0.71 +/- 0.55-1.00 +/- 0.56 L/s, P < .01) and nonviable (0.57 +/- 0.47-0.71 +/- 0.58 L/s, P = .023) segments. However, during dobutamine stimulation peak A waves SR was larger ( P < .001) for viable than for nonviable segments. In conclusion, normal contracting segments at rest have higher E and A waves SR compared with dys-synergic segments. Dys-synergic viable myocardial segments demonstrate an increase in E and A waves SR with dobutamine stimulation whereas nonviable segments are less responsive to dobutamine.
Analysis of Variance↗
Impact of sleep-related breathing disorders on health-related quality of life in patients with chronic heart failure.
BACKGROUND: Quality of life in patients with chronic heart failure (HF) is often severely compromised. Sleep-related breathing disorders (SRBD) like Cheyne-Stokes Respiration (CSR) or obstructive sleep apnea (OSAS) are often observed in patients with severe HF resulting in fragmentation of sleep, excessive daytime sleepiness and an increased mortality. While an apnea/hypopnea-index (AHI) >30/h represents an independent predictor of poor prognosis, clinical relevance of even minor SRBD with an AHI <30/h remains unclear with respect to quality of life, exercise capacity or depression rate. METHODS: Sixty-nine consecutive ambulatory patients with stable HF (NYHA II-III, EF 25%) underwent two night polygraphies with a six-channel ambulatory recording. Spiroergometry was performed, and patients were examined for sleep quality (PSQI), depressed mood (BDI) and health-related quality of life (SF-36). The data were compared to 10 age-matched healthy controls and 11 patients with OSAS (AHI 14-29/h) not suffering from HF. RESULTS: Fifty-one patients completed follow up. 52% were positively diagnosed for SRBD (AHI 16-30/h: 12 patients CSR, 5 patients OSAS, 9 patients mixed); 25 patients (48%) showed no relevant SRBD. Patients with HF and SRBD had lower quality of life than patients without SRBD and HF. The severity of SRBD as indicated by the AHI significantly correlated with quality of life measures: Bodily pain, physical functioning and social functioning showed largest impairment in patients with HF and SRBD. Furthermore, elevated depression rates in correlation to the AHI were only observed in patients with SRBD similar to patients with OSAS without HF. CONCLUSION: Even minor SRBD in patients with HF independently influence quality of life and correlate with estimation of depression and sleep disturbances.
Adult↗
CD14 gene -260 C/T polymorphism is associated with chronic heart failure.
BACKGROUND: Patients with chronic heart failure (CHF) show inflammatory changes and elevated plasma levels of TNFalpha and endotoxins. However, the role of the CD14 C(-260)T polymorphism in patients with CHF is unclear. Therefore, we sought to determine whether the C=>T promoter polymorphism (position -260) of the CD 14 gene is associated with a higher risk for the development of CHF. METHODS: We studied 100 patients with CHF (mean age 62+/-3 years, LVEF 28+/-8%) and 100 healthy controls (59+/-10 years, p=NS; LVEF 60+/-4%, p<0.05). CD14 genotyping was performed using a PCR-RFLP technique. RESULTS: Among CHF patients, the frequency of the T allele was lower (38% vs. 48%, p<0.05) and the frequency of the C allele higher (62 % vs. 52 %, p<0.05) than among controls. The distribution of CD14 genotypes in healthy controls was as follows: CC 32%, CT 40%, and TT 28%. Among CHF patients, the TT genotype was significantly underrepresented compared to controls: CC 38%, CT 48%, and TT 14% (p<0.05). CONCLUSIONS: The C -260T polymorphism of CD14 seems to influence the susceptibility for the development of CHF. The T allele is less frequent among CHF patients than among controls. The TT genotype could be a new genetic protective factor against the development of CHF.
Journal Article↗
Use of fractional flow reserve versus stress perfusion scintigraphy in stent restenosis.
BACKGROUND: Fractional flow reserve (FFR) is a valid surrogate for hemodynamic significance in stenotic native coronary arteries. The aim of this study was to examine the value of FFR compared to stress perfusion myocardial scintigraphy (SPMS) in patients with coronary stent restenosis. METHODS: We studied 42 patients, aged 62+/-10 years, with stent restenosis 5.3+/-1.6 months after coronary stent implantation. All patients had a single coronary lesion of intermediate severity (diameter stenosis 40-70%). FFR measurement, SPMS, and quantitative angiography of the stent stenosis were performed in all patients. RESULTS: The mean percentage in stent diameter stenosis was 53+/-9%. FFR was 0.77+/-0.15. In 20 patients FFR was below 0.75. Nineteen patients had reversible perfusion defects in SPMS. FFR showed good diagnostic accuracy for the detection of reversible perfusion defects in SPMS (AUROC 0.86, 95% CI 0.74-0.98). The percentage of agreement of SPMS and FFR was 88%, with the best cutoff value of 0.75 for FFR. CONCLUSIONS: A FFR value of 0.75 is not only valid for diagnosing significant native coronary stenosis, but also for stent restenosis. Thus, FFR measurement should be taken into account when making decisions regarding patients with stent restenosis.
Journal Article↗
Urotensin II in patients with chronic heart failure.
BACKGROUND: Human Urotensin II (hU-II) is the most potent vasoconstrictor known to date. HU-II receptors are predominant in the human heart and arterial vessels, suggesting hU-II to be of importance as a cardiovascular mediator. METHODS: We studied 32 consecutive patients (60+/-12 years) with chronic heart failure (CHF) and 10 control subjects (54+/-12 years, n.s.) with cardiopulmonary exercise testing. Blood samples for the measurement of plasma hU-II and big-endothelin-1 (big-ET1) were obtained at rest and at peak exercise. RESULTS: Peak VO(2) was significantly higher in controls than in CHF patients (19.8+/-3.8 vs. 14.7+/-3.6 ml min(-1) kg(-1), P<0.001). Big-ET1 levels were increased in CHF compared to controls at rest (2.8+/-1.8 vs. 1.7+/-0.1 fmol/ml, P<0.01) and at peak exercise (2.7+/-1.7 vs. 1.6+/-0.2 fmol/ml, P<0.005). HU-II concentrations were comparable in patients with CHF and controls at rest (2990+/-1104 vs. 3290+/-508 pg/ml, n.s.) and peak exercise (3063+/-1185 vs. 3213+/-1188 pg/ml, n.s.). Resting hU-II levels demonstrated no correlation with peak VO(2) in controls or CHF patients. CONCLUSIONS: The measurement of circulating plasma levels of hU-II does not seem to be very helpful in studying the effects of hU-II in human cardiovascular regulation. A local paracrine or autocrine mediator effect of hU-II in CHF is possible.
Aged↗
Administration of vascular endothelial growth factor adjunctive to fetal cardiomyocyte transplantation and improvement of cardiac function in the rat model.
BACKGROUND: The functional impact of cellular transplantation and the potential role of the addition of angiogenic factors for survival of engrafts remain controversial. METHODS: Vascular endothelial growth factor (VEGF) (25 ng/mL) was added to cultured fetal cardiomyocytes labeled with bromodeoxyuridine (BrDU), which was injected into the border zones of myocardial infarction 4 weeks after coronary occlusion in rat hearts. Group 1 (n = 12) received cells plus VEGF protein (100 ng), group 2 (n = 12) received cells without VEGF, group 3 (n = 10) received VEGF without cells, and group 4 (n = 12) received pure culture medium. Cardiac function was then assessed by transthoracic two-dimensional echocardiography and Langendorff perfusion system. In situ hybridization for Y chromosomes of transplanted cells, detection of BrDU-labeled cells, and platelet/endothelial cell adhesion molecule-1 (PECAM-1) staining for endothelial cells was performed. RESULTS: Echocardiography revealed smaller end-diastolic left ventricular dimensions in transplanted hearts in group 1 (0.83 +/- 0.13 cm 4 weeks after coronary occlusion before transplantation and 0.69 +/- 0.14 cm 2 months after transplantation, P < .05) and in group 2 (0.88 +/- 0.09 cm after coronary occlusion before transplantation and 0.76 +/- 0.08 cm 2 months after transplant), and increases in fractional shortening (34.2% +/- 8.53% before transplant and 45.3% +/- 10.9% after [P < .05] in group 1; 26.9% +/- 6.02% before transplant and 37.15% +/-8.08% after [P < .005] in group 2), whereas groups 3 and 4 showed a decrease in fractional shortening. Transplanted hearts developed higher pressures at rest (group 1, 96.8 +/- 20.8 mm Hg; group 2, 98.6 +/- 21.9 mm Hg) compared with controls (group 4, 70.9 +/- 25 mm Hg) (P < .05) and during inotropic stimulation (group 1, 111 +/- 19.5 mm Hg and group 2, 113.3 +/- 32.6 vs group 4, 80.7 +/- 31.6 mm Hg, P < .05). Histologic analysis demonstrated the presence of transplanted cells in border zones of infarcted host myocardium with neovascularization in all transplanted hearts. CONCLUSION: Transplantation of fetal cardiomyocytes results in improvement of left ventricular function. The addition of VEGF does not contribute to further improvement of left ventricular function and angiogenesis in the present model.
Animals↗
Clinical significance of fractional flow reserve for evaluation of functional lesion severity in stent restenosis and native coronary arteries.
OBJECTIVE: Fractional flow reserve (FFR) is a valid surrogate for hemodynamic significance in stenotic native coronary arteries, but its validity in patients with coronary stent restenosis is unknown. DESIGN: Prospective. SETTING: University hospital. PATIENTS: We studied 42 patients (mean age +/- 1 SD, 62 +/- 10 years) with stent restenosis and 57 patients (mean age, 61 +/- 12 years) with a native coronary lesion. All patients demonstrated a single coronary lesion of intermediate severity (stenosis diameter, 40 to 70%). Determination of FFR and quantitative angiography of the stenosis were performed. RESULTS: Stenosis diameter was comparable in both groups (native, 52 +/- 11%; stent, 52 +/- 9%; not significant [NS]). FFR was lower in stent restenosis (0.77 +/- 0.15 vs 0.82 +/- 0.12, p < 0.05) and more often pathologic with an FFR < 0.75 (48% vs 26%, p < 0.05) compared to native coronary stenosis. However, the area under the receiver operating characteristic curve for native stenosis was 0.82 (95% confidence interval [CI], 0.71 to 0.94) and for stent restenosis was 0.84 (95% CI, 0.71 to 0.97; NS). In patients with an FFR > 0.75, there was no adverse coronary event that was related to the stented lesion in the subsequent 6 months. CONCLUSIONS: The threshold of stenosis diameter of coronary lesions for pathologic FFR measurement (FFR < 0.75) is similar for stent restenosis and native coronary stenosis. Thus, FFR measurement seems to be applicable for decision making in patients with stent restenosis.
Aged↗
Intravascular ultrasonic comparative analysis of degree of intimal hyperplasia produced by four different stents in the coronary arteries.
Intravascular ultrasound studies were performed at angiographic follow-up on 121 native coronary lesions treated with 1 bare metal stent (n = 50), high-dose dexamethasone-eluting stents (n = 18), non-polymer-based paclitaxel-eluting stents (n = 18), or sirolimus-eluting stents (n = 35). Paclitaxel- and sirolimus-eluting stents reduced mean intimal hyperplasia thickness compared with bare metal stents by 49% and 90% (p = 0.048 and p <0.001), respectively, whereas mean intimal hyperplasia thickness treated with dexamethasone-eluting stents was similar to those lesions treated with bare metal stents.
Coronary Restenosis↗
Prognostic value of endocardial electromechanical mapping in patients with left ventricular dysfunction undergoing percutaneous coronary intervention.
Endocardial electromechanical mapping (EEM) has been proposed as a method for myocardial viability assessment. However, the impact of EEM data on clinical outcome has not been studied before. We sought to assess the prognostic value of EEM in patients with left ventricular (LV) dysfunction undergoing percutaneous coronary intervention (PCI). Seventy-five patients with coronary artery disease and LV dysfunction (angiographic LV ejection fraction [EF] 49 +/- 15%) underwent LV EEM for myocardial viability assessment before coronary revascularization. EEM parameters included mean unipolar electrographic amplitude, mean local shortening, LV volumes, LVEF, number of regions with electrographic amplitudes <7.5 mV, number of electromechanical mismatch, and match regions. Cardiac death, nonfatal myocardial infarction, nonfatal stroke, and acute heart failure requiring hospitalization were defined as clinical events. During a follow-up of 3.6 +/- 1.8 years, 20 clinical events occurred. Event-free survival after coronary revascularization was significantly better in patients with a mean unipolar electrographic amplitude of >/=9.5 mV than in patients with a mean unipolar electrographic amplitude of <9.5 mV (88% vs 57%; p <0.005). Cox regression analysis revealed angiographic LVEF, mean electrographic amplitude, number of regions with electrographic amplitudes <7.5 mV, number of electromechanical match regions, and EEM EF as univariate predictors of clinical events. In a multivariate analysis, angiographic LVEF <40% (hazard ratio 4.78, p <0.005) and mean electrographic amplitude <9.5 mV (hazard ratio 2.92, p <0.05) were independent predictors of clinical events. Thus, EEM provides prognostic information in patients with LV dysfunction undergoing coronary revascularization.
Aged↗
Evaluation of a high-dose dexamethasone-eluting stent.
This study evaluated the safety and efficacy of a dexamethasone-eluting stent with a special high dexamethasone-loading dose for treatment of de novo coronary lesions in 30 patients. Eight patients had in-stent restenosis (restenosis rate 31%) at 6-month follow-up, and the in-stent late lumen loss was 0.96 +/- 0.63 mm due to an average intimal hyperplasia area obstruction of 32 +/- 21%, indicating that high-dose dexamethasone-loaded stents do not significantly reduce neointimal proliferation.
Adult↗