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Adverse Cardiovascular Events (adverse + cardiovascular_event)

Distribution by Scientific Domains
Medical Sciences100%

Kinds of Adverse Cardiovascular Events

  • major adverse cardiovascular event
    		•

    Selected Abstracts

    Cardiovascular Tolerability and Safety of Triptans: A Review of Clinical Data

    HEADACHE, Issue 2004
    David W. Dodick MD
    Triptans are not widely used in clinical practice despite their well-established efficacy, endorsement by the US Headache Consortium, and the demonstrable need to employ effective intervention to reduce migraine-associated disability. Although the relatively restricted use of triptans may be attributed to several factors, research suggests that prescribers' concerns about cardiovascular safety prominently figure in limiting their use. This article reviews clinical data,including results of clinical trials, postmarketing studies and surveillance, and pharmacodynamic studies,relevant to assessing the cardiovascular safety profile of the triptans. These data demonstrate that triptans are generally well tolerated. Chest symptoms occurring during use of triptans are usually nonserious and usually not attributed to ischemia. Incidence of triptan-associated serious cardiovascular adverse events in both clinical trials and clinical practice appears to be extremely low. When they do occur, serious cardiovascular events have most often been reported in patients at significant cardiovascular risk or in those with overt cardiovascular disease. Adverse cardiovascular events also have occurred, however, in patients without evidence of cardiovascular disease. Several lines of evidence suggest that nonischemic mechanisms are responsible for sumatriptan-associated chest symptoms, although the mechanism of chest symptoms has not been determined to date. Importantly, most of the clinical trials and clinical practice data on triptans are derived from patients without known cardiovascular disease. Therefore, the conclusions of this review cannot be extended to patients with cardiovascular disease. The cardiovascular safety profile of triptans favors their use in the absence of contraindications. [source]

    Volume Overload and Cardiorenal Syndromes

    CONGESTIVE HEART FAILURE, Issue 2010
    Claudio Ronco MD
    To include the vast array of interrelated derangements and to stress the bidirectional nature of the heart-kidney interactions, the classification of the cardiorenal syndrome today includes 5 subtypes whose terminology reflects their primary and secondary pathology, time frame, and the presence of concomitant cardiac and renal dysfunction. Cardiorenal syndromes (CRSs) are pathophysiologic disorders of the heart and kidneys whereby acute or chronic dysfunction of one organ may induce acute or chronic dysfunction of the other. Type 1 CRS reflects an abrupt worsening of cardiac function leading to acute kidney injury. Type 2 CRS describes chronic abnormalities in cardiac function causing progressive chronic kidney disease. Type 3 CRS consists in an abrupt worsening of renal function causing acute cardiac disorder. Type 4 CRS describes a state of chronic kidney disease contributing to decreased cardiac function, cardiac hypertrophy, and/or increased risk of adverse cardiovascular events. Type 5 CRS reflects a systemic condition (eg, sepsis) simultaneously causing both cardiac and renal dysfunction. Biomarkers can help characterize the subtypes of CRS as well as suggest the timing of treatment initiation and its likely effectiveness. The identification of patients and the pathophysiologic mechanisms underlying each syndrome subtype, including fluid overload or, in general, altered conditions of fluid status, can help physicians understand clinical derangements, provide the rationale for management strategies, and allow the design of future clinical trials with more accurate selection and stratification of the population under investigation. Congest Heart Fail. 2010;16(4)(suppl 1):Si,Siv. ©2010 Wiley Periodicals, Inc. [source]

    Cardiovascular risk factors and collateral artery formation

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2009
    D. De Groot
    Abstract Arterial lumen narrowing and vascular occlusion is the actual cause of morbidity and mortality in atherosclerotic disease. Collateral artery formation (arteriogenesis) refers to an active remodelling of non-functional vascular anastomoses to functional collateral arteries, capable to bypass the site of obstruction and preserve the tissue that is jeopardized by ischaemia. Hemodynamic forces such as shear stress and wall stress play a pivotal role in collateral artery formation, accompanied by the expression of various cytokines and invasion of circulating leucocytes. Arteriogenesis hence represents an important compensatory mechanism for atherosclerotic vessel occlusion. As arteriogenesis mostly occurs when lumen narrowing by atherosclerotic plaques takes place, presence of cardiovascular risk factors (e.g. hypertension, hypercholesterolaemia and diabetes) is highly likely. Risk factors for atherosclerotic disease affect collateral artery growth directly and indirectly by altering hemodynamic forces or influencing cellular function and proliferation. Adequate collateralization varies significantly among atherosclerotic patients, some profit from the presence of extensive collateral networks, whereas others do not. Cardiovascular risk factors could increase the risk of adverse cardiovascular events in certain patients because of the reduced protection through an alternative vascular network. Likewise, drugs primarily thought to control cardiovascular risk factors might contribute or counteract collateral artery growth. This review summarizes current knowledge on the influence of cardiovascular risk factors and the effects of cardiovascular medication on the development of collateral vessels in experimental and clinical studies. [source]

    Impact of body fat mass extent on cardiac autonomic alterations in women

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 8 2009
    J. Sztajzel
    Abstract Background, Obesity has been associated with significant abnormalities of the cardiac autonomic regulation. However, the precise impact of increasing body weight on cardiac autonomic function and the metabolic and hormonal contributors to these changes are presently unclear. The aim of our study was to explore in subjects with increasing values of body mass index (BMI) the alterations of cardiac autonomic function and to establish the potential role of various metabolic and hormonal contributors to these alterations. Materials and methods, We investigated time and frequency domain heart rate variability (HRV) parameters taken from 24-h Holter recordings, and several anthropometric, metabolic and hormonal parameters (plasma glucose, insulin, triglycerides, free fatty acids, leptin and adiponectin) in 68 normoglycaemic and normotensive women (mean age of 40 ± 3 years), subdivided according to their BMI into 15 normal body weight (controls), 15 overweight, 18 obese and 20 morbidly obese. Results, Heart rate was increased and HRV was decreased in the morbidly obese group as compared with controls. In overall population, a negative association linked body fat mass (FM) to HRV indices. None of the metabolic and hormonal parameters were significantly related to the HRV indices, after they were adjusted for the body FM. Conclusions, Morbidly obese, normoglycaemic and normotensive young women have increased HR and low HRV, indicating an abnormal cardiac autonomic function and representing a risk factor for adverse cardiovascular events. A decrease of HRV parameters is associated with a progressive increase of body FM. Other metabolic and hormonal factors, characterising obesity, do not show an independent influence on these HRV alterations. [source]

    Markers of eosinophilic inflammation and risk prediction in patients with coronary artery disease

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 4 2006
    C. Falcone
    Abstract Background, The eotaxin family comprises three distinct peptides (eotaxin, eotaxin-2 and eotaxin-3) which have been implicated in eosinophilic inflammation. In vitro and clinical studies suggest that eotaxins could play a role in vascular inflammation, but no data are available on their prognostic significance in patients with angiographically documented coronary artery disease (CAD). Materials and methods, Baseline plasma samples were obtained from 1014 patients with documented CAD. We tested the predictive effect of markers of eosinophilic inflammation and C-reactive protein (CRP) on death from cardiovascular causes and nonfatal myocardial infarction over a 2·7,4·1-year follow-up period. Results, Unexpectedly, lower eotaxin-3 concentrations were observed in patients with adverse cardiovascular events, whereas both eotaxin and eotaxin-2 showed no association with risk. After adjustment for most potential confounders, patients in the upper-quartile of eotaxin-3 levels had a 0·42 hazard-ratio (95% CI, 0·29,0·61, P < 0·001) for adverse events compared with subjects in the lower-quartile. The highest risk of future cardiovascular events was observed in subjects with combined elevation of CRP and reduction of eotaxin-3; 4·4 hazard-ratio (95% CI, 2·1,9·5, P < 0·001). Importantly, receiver-operating-characteristic curves analysis suggested a superior prognostic value of eotaxin-3 compared with CRP for predicting cardiac events in patients with CAD. Conclusions, Low levels of eotaxin-3 are an independent predictor of future adverse cardiovascular events in patients with CAD and may be useful for risk stratification. [source]

    Haem oxygenase-1 genotype and cardiovascular adverse events in patients with peripheral artery disease

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2005
    P. Dick
    Abstract Background, A functional GT dinucleotide length polymorphism in the haem oxygenase-1 (HO-1) gene promoter is thought to be involved in the pathogenesis of cardiovascular disease. Short (< 25) (GT)n repeats are suggested to facilitate enhanced HO-1 up-regulation in response to injury and confer potent anti-inflammatory and antioxidative effects. Materials and methods, We investigated the association between the HO-1 GT-polymorphism and cardiovascular outcome in 472 patients with advanced peripheral artery disease. Cardiovascular risk profile and DNA samples for determination of the HO-1 genotype (carrier vs. noncarrier of a short (GT)n repeat allele) were obtained at baseline, and patients were followed for median 21 months for the occurrence of coronary events (myocardial infarction, percutaneous coronary interventions and coronary artery bypass graft), cerebrovascular events (stroke or carotid revascularization) and all-cause mortality. Results, Coronary events occurred in 48 patients (9%), cerebrovascular events in 40 patients (9%) and 59 patients (13%) died. In total, 173 major adverse cardiovascular events (MACE) occurred in 133 patients (28%). Carriers of the short (GT)n repeat allele had a 0·46-fold reduced adjusted hazard ratio for coronary events (P = 0·016) as compared to noncarriers. No significant difference was found for cerebrovascular events, mortality and overall MACE. Conclusion, Apparently, the HO-1 genotype exerts potentially protective effects against coronary adverse events in patients with peripheral artery disease. Homozygous and heterozygous carriers of < 25 (GT)n repeats had lower rates of myocardial infarction, percutaneous coronary interventions and coronary bypass operations compared to patients with longer (GT)n repeats. [source]

    Development and Validation of a Risk Scoring Model to Predict Net Adverse Cardiovascular Outcomes after Primary Percutaneous Coronary Intervention in Patients Pretreated with 600 mg Clopidogrel: Rationale and Design of the RISK-PCI Study

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2009
    IGOR MRDOVIC M.D., Ph.D
    Background: No comprehensive primary PCI (pPCI) risk model to predict net adverse cardiovascular events (NACE) has been reported with the use of clopidogrel 600 mg, which is now considered the standard loading dose. The primary hypothesis of the RISK-PCI trial is that an accurate risk prediction may be achieved by using clinical, angiographic, and procedural variables available at the time of intervention. Methods: The present single-center, longitudinal, cohort study will include 1,750 consecutive patients with ST-elevation myocardial infarction (STEMI), undergoing pPCI after pretreatment with 300 mg aspirin and 600 mg clopidogrel. The primary end-points of the trial (NACE) include major adverse cardiovascular events (MACE) and major bleeding. A logistic regression model will be developed to predict 30-day and 1-year NACE after pPCI. A risk score derived from study set data will be validated using validation set data. Results: Until June 1, 2008, 1,166 patients have been enrolled. Thirty-day follow-up is available in 1,007 patients. Conclusions: The RISK-PCI study is designed to develop an accurate risk scoring system, using variables available at the time of intervention, to predict long-term adverse outcomes after pPCI. Trial Registration: Current Controlled Trials Register,ISRCTN83474650,http://www.controlled-trials.com/ISRCTN83474650). [source]

    Impact of Thienopyridine Administration Prior to Primary Stenting in Acute Myocardial Infarction

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2009
    LEROY E. RABBANI M.D.
    The impact of thienopyridine administration prior to primary stenting in acute myocardial infarction (AMI) has not been well studied. We therefore examined the database from the prospective, multicenter, controlled CADILLAC trial in which 1,036 patients were randomized to bare metal stenting with or without abciximab to determine whether patients who received a thienopyridine prior to bare metal stenting in AMI had superior clinical outcomes. Per operator discretion, 659 patients (63.6%; Th+) received either a 500 mg ticlopidine loading dose (n = 623) or a 300 mg clopidogrel loading dose (n = 40), while 377 patients (36.4%; Th-) received no thienopyridine prior to stent implantation. Baseline and procedural characteristics of the two groups, including abciximab use (52.5% vs 52.8%, P = 0.93) were well matched. Th+ compared to Th- patients had lower rates of core lab assessed TIMI 0/1 flow postprocedure (0.8% vs 2.7%, P = 0.01). Th+ compared to Th- patients also had significantly reduced in-hospital and 30-day rates of ischemic target vessel revascularization (TVR) (1.1% vs 3.2%, P = 0.01 and 1.5% vs 3.8%, P = 0.02, respectively) and major adverse cardiovascular events (MACE) (2.7% vs 5.8%, P = 0.01 and 4.0% vs 6.9%, P = 0.03, respectively), results that remained significant after covariate adjustment. In conclusion, in this large prospective, controlled trial, patients receiving a thienopyridine prior to primary stenting in AMI were less likely to have TIMI 0/1 flow postprocedure and experienced reduced in-hospital and 30-day rates of ischemic TVR and MACE compared to those not administered a thienopyridine prior to stent implantation. [source]

    Management of Multivessel Coronary Disease after ST Elevation Myocardial Infarction Treated by Primary Angioplasty

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2008
    Ph.D., STEFANO RIGATTIERI M.D.
    Background: Optimal treatment strategy of patients with ST elevation myocardial infarction (STEMI) and multivessel coronary artery disease (CAD) undergoing primary angioplasty is still unclear. Percutaneous coronary intervention (PCI) of non-culprit vessels simultaneously or soon after primary angioplasty is feasible and safe, but available data failed to consistently show a benefit in long-term clinical outcomes. Methods: We retrospectively compared in-hospital and long-term outcomes for patients with STEMI and multivessel CAD treated by primary angioplasty with (Group 1, n=64) or without (Group 2, n=46) early, staged PCI of other angiographically significant coronary lesions. In-hospital major adverse cardiovascular events (MACE) were defined as a composite of death, periprocedural myocardial infarction after staged, elective PCI, stroke, stent thrombosis, major bleeding, and vascular complications. MACE at follow-up were defined as a composite of death, stroke, stent thrombosis, any coronary revascularization, and re-hospitalization for acute coronary syndrome. Results: Group 1 patients underwent staged PCI 5.9 ± 3.5 days after primary angioplasty. The mean length of follow-up was 13 months (392 ± 236 days). The incidence of in-hospital MACE was 20.3% in Group 1 and 10.8% in Group 2 (P=0.186); the incidence of out of hospital MACE was 9.3% in Group 1 and 23.9% in Group 2 (P=0.037). In Group 1 in-hospital MACE were driven by periprocedural myocardial infarction after the elective procedure, which occurred in 15.6% of patients. Conclusions: Our data show that multivessel, staged PCI in STEMI patients is associated with a low incidence of adverse events at follow-up but with a higher incidence of in-hospital MACE, mainly driven by periprocedural myocardial infarction during the elective procedure. [source]

    Coronary Artery Bypass Surgery Versus Percutaneous Coronary Intervention with Drug-Eluting Stent Implantation in Patients with Multivessel Coronary Disease

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 1 2007
    ZHEN KUN YANG M.D.
    Background: Drug-eluting stents (DES) constitute a major breakthrough in restenosis prevention after percutaneous coronary intervention (PCI). This study compared the clinical outcomes of PCI using DES versus coronary artery bypass graft (CABG) in patients with multivessel coronary artery disease (MVD) in real-world. Methods: From January 2003 to December 2004, 466 consecutive patients with MVD underwent revascularization, 235 by PCI with DES and 231 by CABG. The study end-point was the incidence of major adverse cardiovascular events (MACEs) at the first 30 days after procedure and during follow-up. Results: Most preoperative characteristics were similar in the two groups, but left main disease (24.7% vs 2.6%, P<0.001) and three-vessel disease (65% vs 54%, P = 0.02) were more prevalent in CABG group. The number of coronary lesions was also greater in CABG group (3.7 ± 1.1 vs 3.3 ± 1.1, P<0.001). Despite higher early morbidity (3.9% vs 0.8%, P = 0.03) associated with CABG, there were no significant differences in composite MACEs at the first 30 days between the two groups. During follow-up (mean 25±8 months), the incidence of death, myocardial infarction, or cerebrovascular event was similar in both groups (PCI 6.3% vs CABG 5.6%, P = 0.84). However, bypass surgery still afforded a lower need for repeat revascularization (2.8% vs 10.4%, p = 0.001). Consequently, overall MACE rate (14.5% vs 7.9%, P = 0.03) remained higher after PCI. Conclusion: PCI with DES is a safe and feasible alternative to CABG for selected patients with MVD. The reintervention gap was further narrowed in the era of DES. Aside from restenosis, progression of disease needs to receive substantial emphasis. [source]

    Does Proximal Location of Culprit Lesion Confer Worse Prognosis in Patients Undergoing Primary Percutaneous Coronary Intervention for ST Elevation Myocardial Infarction?

    JOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2006
    KISHORE J. HARJAI M.D.
    ST segment elevation myocardial infarction (STEMI) from proximally located culprit lesion is associated with greater myocardium at jeopardy. In STEMI patients treated with thrombolytics, proximal culprit lesions are known to have worse prognosis. This relation has not been studied in patients undergoing primary percutaneous coronary intervention (PCI). In 3,535 STEMI patients with native coronary artery occlusion pooled from the primary angioplasty in myocardial infarction database, we compared in-hospital and 1-year outcomes between those with proximal (n = 1,606) versus nonproximal (n = 1,929) culprit lesions. Patients with proximal culprits were more likely to die and suffer major adverse cardiovascular events (MACE) during the index hospital stay (3.8% vs 2.2%, P = 0.006; 8.2% vs 5.8%, P = 0.0066, respectively) as well as during 1-year follow-up (6.9% vs 4.5%, P = 0.0013; 22% vs 17%, P = 0.003, respectively) compared to those with nonproximal culprits. After adjustment for baseline differences, proximal culprit was independently predictive of in-hospital death (adjusted odds ratio% 1.58, 95% confidence intervals, CI 1.05,2.40) and MACE (OR 1.41, CI 1.06,1.86), but not 1-year death or MACE. In addition, proximal culprit was independently associated with higher incidence of ventricular arrhythmias and sustained hypotension during the index hospitalization. The univariate impact of proximal culprit lesion on in-hospital death and MACE was comparable to other adverse angiographic characteristics, such as multivessel disease and poor initial thrombolysis in myocardial infarction flow, and greater than that of anterior wall STEMI. In conclusion, proximal location of the culprit lesion is a strong independent predictor of worse in-hospital outcomes in patients with STEMI undergoing primary PCI. [source]

    Influence of the Maximum Heart Rate Attained during Exercise Testing on Subsequent Heart Rate Recovery

    ANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 1 2010
    Sina Zaim M.D.
    Background: Abnormal heart rate recovery (HRR) following exercise testing has been shown to be a predictor for adverse cardiovascular events. The actual maximum heart rate (MHR) attained during the exercise test does not however have a distinct significance in traditional HRR assessment. The objective of this study was to investigate the role of MHR in HRR. Methods: This prospective study consisted of 164 patients (62% male, mean age 53.7 ± 11.7 years) who were referred for a symptom-limited standard Bruce Protocol treadmill exercise test, based on clinical indications. The patients were seated immediately at test completion and the heart rate (HR) recorded at one and two minutes postexercise. A normal HRR was defined as a HR drop of 18 beats per minute or more at the end of the first minute of recovery. The HRR profile of patients who reached ,85% of their maximum predicted heart rate (MPHR) during peak exercise were then compared to HRR profile of those who could not. Results: One hundred twelve patients (Group A) achieved a MHR , 85% of MPHR during peak exercise whereas 52 patients (Group B) did not. Chi-square analysis showed a higher incidence of normal HRR in Group A compared to Group B (p = 0.029). Analysis of variance with repeated measures showed that group A had a greater HRR at the first minute F1,162= 6.98, p = <0.01) but not the second minute (F1,162=1.83, p = .18) postexercise. Conclusion: There is a relation between the peak heart rate attained during exercise and the subsequent HRR. A low peak heart rate increases the likelihood of a less than normal HRR. Assessment of the entire heart-rate response seems warranted for more thorough risk-stratification. Ann Noninvasive Electrocardiol 2010;15(1):43,48 [source]

    Native chronic total occlusion recanalization after lower limb bypass graft occlusion: A series of nine cases,

    CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 2 2010
    FSCAI, Osami Kawarada MD
    Abstract Objective: The aim of the study was to report the clinical utility of native chronic total occlusion (CTO) recanalization as an endovascular strategy in lower limb bypass graft occlusion. Background: There is no consensus on the best approach for threatened limbs in patients with graft occlusion. Methods: The subjects were nine consecutive patients with limb-threatening ischemia after bypass graft occlusion. Native CTO recanalization was attempted endovascularly using conventional intraluminal and subintimal angioplasty techniques supported by stents. Results: The mean age of the bypass grafts was 6.7 ± 7.3 (range: 1,24) months and the mean number of previous lower limb bypass surgeries was 1.4 ± 0.5 (range: 1,2). Native CTO recanalization was performed in the iliofemoral (n = 2), iliac (n = 2), superficial femoral (n = 3), popliteal (n = 1), and popliteal-tibial (n = 1) arteries. Technical success was achieved in 89% (8/9) of cases without complications or major adverse cardiovascular events. The ankle-brachial index and skin perfusion pressure of the foot significantly increased after revascularization, with marked improvement of clinical symptoms (Rutherford class: 4.5 ± 1.1,0.9 ± 1.4, P < 0.001). Limb salvage was achieved in all successful recanalization cases during the mean follow-up time of 25 ± 20 months (range: 9,60). Conclusions: In this preliminary study, endovascular recanalization of native CTO showed satisfactory outcomes in patients with bypass graft occlusion. © 2010 Wiley-Liss, Inc. [source]

    Five-year clinical outcomes after coronary stenting of chronic total occlusion using sirolimus-eluting stents: Insights from the rapamycin-eluting stent evaluated at Rotterdam Cardiology Hospital,(Research) Registry,

    CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 7 2009
    Zhu Jun Shen MD
    Abstract Background: The use of drug eluting stents (DES) in patients with a successfully recanalized chronic total occlusion (CTO) has been associated with a significant decrease in the need for repeat revascularization, and a favorable short-term clinical outcome when compared with the use of bare metal stents (BMS). Our group, however, has previously reported similar rates of target lesion revascularisation (TLR) and major adverse cardiovascular events (MACE) at 3 years follow-up in patients with a successfully opened CTO who were treated with either a sirolimus eluting stent (SES) or a BMS. The objective of this report was to evaluate the outcomes of these patients at 5-years clinical follow-up. Methods and Results: A total of 140 (BMS 64, SES 76) patients with successfully opened CTOs were included. Seven patients died in the BMS group whilst nine patients died in the SES group (P = 0.90). Noncardiac death was the major component of all-cause mortality (11 noncardiac deaths vs. 5 cardiac). There were two and three myocardial infarctions (MI) in the BMS and SES group, respectively (P = 1.0). The composite of death and MI occurred in seven (10.9%) and eleven (14.5%) patients in the BMS and SES group, respectively (P = 0.53). Clinically driven TLR was performed in eight patients (12.5%) in the BMS group, and five (6.6%) in the SES group (P = 0.26). Non-TLR target vessel revascularization was performed in one patient in the BMS group, and four in the SES group (P = 0.37). The 5-year device-oriented cumulative MACE rate was 15.6% and 11.8% in the BMS and SES group, respectively (P = 0.56). Conclusion: In patients with a successfully treated CTO, clinical outcome after 5 years was similar between SES and BMS, however, clinically driven TLR was slightly higher in the BMS group. © 2009 Wiley-Liss, Inc. [source]

    Comparison of drug-eluting stents with bare metal stents in unselected patients with acute myocardial infarction

    CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 1 2007
    L. Iri Kupferwasser MD
    Abstract Objectives: The aim of this study was to compare the procedural characteristics and outcomes of patients with acute myocardial infarction treated with drug-eluting stents (DES) vs. bare metal stents (BMS). Background: DES have been shown to reduce the incidence of restenosis and target vessel revascularization (TVR) in clinical randomized studies when compared with BMS in patients undergoing elective percutaneous intervention. Limited data are available with the use of DES in patients with acute ST-segment elevation myocardial infarction. Methods: Two hundred and sixty-one consecutive patients who presented with myocardial infarction between 7/2001 and 8/2005 were studied. The procedural characteristics, 30-day and 12-month outcomes of 131 patients treated with DES were compared with 130 patients treated with BMS. Results: At 12-months follow-up DES therapy was associated with a substantial decrease in major adverse cardiovascular events (MACE) (HR 0.33; P =0.002), TVR (HR 0.19; P =0.002), and recurrent myocardial infarction (HR 0.23; P =0.051) vs. BMS therapy. Coronary interventions utilizing DES were characterized by a marked increase in the number of stent per target vessel (DES: 1.9 ± 0.9 vs. BMS: 1.38 ± 0.6, P < 0.0001), treatment of bifurcation (DES: 21% vs. BMS: 5%, P =0.0004), and multivessel intervention (DES: 22% vs. BMS: 8%, P =0.003). Conclusion: The routine use of DES in acute myocardial infarction is associated with reduced rates of MACE at 12 months vs BMS, despite a higher rate of complex procedures in the DES treated patients. In addition to its anti-restenosis effect, the improved outcome of patients treated with DES may be linked to a more complete revascularization in association with prolonged clopidogrel therapy. © 2007 Wiley-Liss, Inc. [source]

    Effects of pharmacological adrenergic and vagal modulation on fractal heart rate dynamics

    CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 5 2001
    Mikko P. Tulppo
    Breakdown of short-term fractal-like behaviour of HR indicates an increased risk for adverse cardiovascular events and mortality, but the pathophysiological background for altered fractal HR dynamics is not known. Our aim was to study the effects of pharmacological modulation of autonomic function on fractal correlation properties of heart rate (HR) variability in healthy subjects. Short-term fractal scaling exponent (,1) along with spectral components of HR variability were analysed during the following pharmacological interventions in healthy subjects: (i) noradrenaline (NE) infusion (n=22), (ii) NE infusion after phentolamine (PHE) (n=8), (iii) combined NE + adrenaline (EPI) infusion (n=12), (iv) vagal blockade with high dose of atropine (n=10), (v) and vagal activation by low dose of atropine (n=10). Then ,1 decreased progressively during the incremental doses of NE (from 0·85 ± 0·250 to 0.55 ± 0·23, P<0·0001). NE also decreased the average HR (P<0·001) and increased the high frequency spectral power (P<0·001). Vagal blockade with atropine increased the ,1 value (from 0·82 ± 0·22 to 1·24 ± 0·41, P<0·05). Combined NE + EPI infusion and vagal activation with a low dose atropine did not result in any changes in ,1, and ,-adrenergic blockade by PHE did not completely reverse the effects of NE on ,1. Increased levels of circulating NE result in reduction of short-term correlation properties of HR dynamics. The results suggest that coactivation of cardiac vagal outflow at the time of high levels of a circulating sympathetic transmitter explains the breakdown of fractal-like behaviour of human HR dynamics. [source]