Occurrence Of Ischemic Events Research Articles

Triptan use and risk of cardiovascular events: a nested-case-control study from the French health system database

The use of triptans (5-HT agonists) in the treatment of migraine is associated with a potential increasing risk of cardiovascular events and raises the question of the relationship between overuse and the occurrence of ischemic events. The aim of this study was to examine the association between the intensity of triptan use and occurrence of an cardiac event. Using the reimbursed drug prescription database of the National French Health Insurance System in the Midi-Pyrenees area, we identified subjects receiving at least one triptan in the second semester of 2002. From this population, we selected new users and retrieved all reimbursed care data up to 31 December 2003. We estimated the patterns of triptan exposure by calculating the number of defined daily doses (DDD) received per 30-day period. Another reimbursed health care database was used to identify as cases of cardiac outcomes those patients receiving care for the management of a possible heart ischemic event. Each case was randomly matched on age and gender with four controls free of any cardiovascular event before the index date. A conditional logistic regression was performed to assess the relationship between cardiac outcomes and exposure to triptans in the 30 days before the index date. The cohort of new users of triptans included 8625 subjects, 4414 (51.18%) of whom received only one dispensation for triptans during the follow-up period (median duration: 427 days). For the remaining subjects, the peak of triptans delivery was </=8 DDD for 14.68% of the cohort, between 9 and 14 DDD for 22.17%, between 15 and 29 for 10.04% and >/=30 DDD for 1.92%. Fifty-seven users (0.66%) presented a cardiac history and 1388 patients (16.09%) had cardiovascular risk factors. We identified 155 incident cases of cardiac outcomes during the follow-up and compared these to 620 matched controls. Cases were older and presented more frequently with cardiac history or cardiovascular risk factors than the other users of triptans. The distribution exposure to triptans did not significantly differ between cases and controls with an odds ratio for an exposure </=8 DDD in the last 30 days of 0.74 [95% CI (0.31-1.77)] and that for an exposure >8 DDD equal to 1.14 [95% CI (0.58-2.27)]. The proportion of patients showing an overuse of triptans (more than 15 DDD for 30 days) reached 12% in this cohort of new users of triptans. However, we did not find any relationship between the overuse of triptans and cardiac outcomes. This study also shows that some patients with cardiovascular risk factors are actually treated by triptans. These patients are more likely to present a cardiac outcome potentially related to an ischemic event after the introduction of triptan.

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Drive-Through Angioplasty

In this issue of Circulation , Bertrand et al1 report the results of the Early Discharge after Transradial Stenting of Coronary Arteries (EASY) Study. After receiving a standard bolus of abciximab and undergoing a successful and uncomplicated transradial stent placement, 1005 patients were randomized to a traditional strategy with overnight hospitalization or early discharge after 4 to 6 hours. All patients received aspirin, clopidogrel, and a bolus dose of abciximab before their procedure. Those in the traditional strategy group also received a 12-hour abciximab infusion, whereas those in the early discharge group did not. The goal of the EASY study was to show that stent implantation by the radial approach with only a bolus of abciximab and then early discharge was not inferior to the traditional strategy in terms of effectiveness and safety. The primary composite end point was the 30-day incidence of death, any myocardial infarction, unplanned revascularization, major bleeding, repeat hospitalization, access-site complications, or severe thrombocytopenia. On the basis of their data, the authors concluded that the abbreviated abciximab therapy with same-day discharge was clinically not inferior to the traditional strategy after uncomplicated stent placement. Article p 2636 With healthcare costs increasing, strategies to limit expenditures are popular and deserve careful examination. Accepted cardiology practice has moved toward dramatically shortened hospital stays for diagnostic coronary angiography and percutaneous coronary intervention (PCI) as well as many other procedures. The present study suggests that many patients who undergo PCI could be managed safely as outpatients. Substantial accomplishments in the practice of PCI have resulted in the excellent success and safety of the procedure we now observe, but are we ready for routine outpatient PCI? The use of radial artery access has been well described in the literature. Despite studies demonstrating the feasibility, safety, and acceptance by patients of this …

Prasugrel

Clinical trials have demonstrated the superior clinical efficacy of dual antiplatelet therapy with a thienopyridine (a P2Y12 receptor blocker) and aspirin (COX-1 inhibitor) in patients undergoing stenting as well as patients with acute coronary syndromes. However, clopidogrel treatment is associated with a wide response variability and non-responsiveness in selected patients. The latter phenomenon is linked to the occurrence of recurrent ischaemic events including stent thrombosis in the recent studies. Prasugrel is a new thienopyridine derivative that produces more potent platelet inhibition and a rapid onset of action that is associated with irreversible P2Y12 receptor blockade. The latter properties of prasugrel may provide a superior alternative to clopidogrel, with less response variability and a decreased prevalence of non-responsiveness.

Drug Insight: clopidogrel nonresponsiveness

Platelet reactivity to agonists and subsequent activation are important factors that affect the development of atherothrombosis and resultant ischemic events. Pharmacologic intervention with clopidogrel and aspirin during acute coronary syndromes and percutaneous coronary intervention is considered the gold standard for attenuating platelet activation and aggregation. Despite significant benefits reported with dual antiplatelet treatment in major clinical trials, the occurrence of adverse ischemic events, including stent thrombosis, remains a serious clinical problem. Nonresponsiveness, also called resistance, to current clopidogrel regimens might play a part in the occurrence of ischemic events. Various mechanisms have been implicated in nonresponsiveness to clopidogrel, including variability in intestinal absorption and hepatic conversion to the active metabolite, drug-drug interactions and receptor polymorphisms. Increased loading and maintenance doses and the use of new and more-potent P2Y12-receptor blockers might overcome the phenomenon of clopidogrel nonresponsiveness. The aim of this article is to provide a comprehensive and current review of clopidogrel response variability and nonresponsiveness.

Hyperviscosity as a Possible Risk Factor for Cerebral Ischemic Complications in Atrial Fibrillation Patients

Recent studies have suggested that hyperviscosity is frequent in patients with atrial fibrillation (AF). The aims of this study were to evaluate if hemorheologic alterations play a role in the occurrence of cerebral ischemic events in patients with AF and to explore a possible association between inflammation and hyperviscosity in these patients. Sixty-two patients with AF with a history of >or=1 cerebral ischemic event and 94 patients with AF without cerebral ischemic events were studied. A control population included 130 age- and gender-matched healthy volunteers. Hemorheologic variables (whole-blood viscosity, plasma viscosity, the erythrocyte deformability index, and hematocrit), fibrinogen, and high-sensitivity C-reactive protein levels were assayed. An alteration in whole blood viscosity at 94.5 seconds(-1) and the erythrocyte deformability index were found more frequently in patients with previous ischemic events on univariate and multivariate analyses (odds ratio 3.19, p=0.023 and odds ratio 4.26, p=0.002, respectively) adjusted for age, gender, hypertension, diabetes, history of coronary artery disease, left ventricular dysfunction, smoking habit, dyslipidemia, hematocrit, fibrinogen, high-sensitivity C-reactive protein, and hemorheologic parameters. These results should stimulate prospective studies on the role of hemorheologic alterations in the occurrence of cerebral ischemic complications in patients with AF.

Silent microemboli related to diagnostic cerebral angiography: a matter of operator’s experience and patient’s disease

The aim of the present investigation was to elucidate in a large consecutive patient cohort whether the level of training has an effect on the number of microemboli detected by diffusion-weighted imaging (DWI) and which additional risk factors can be identified. A total of 107 consecutive patients in whom a diagnostic cerebral angiography had been performed were prospectively investigated with DWI; 51 angiographies were performed by experienced neuroradiologists, 56 by neuroradiologists in training. In 12 patients (11.1%), a total of 17 new lesions without any clinically overt neurological symptoms were identified. Of these, 12 patients, 11 (91.7%) with 16 lesions were investigated by junior neuroradiologists. In 11 of 12 patients with DWI abnormalities (91.7%), risk factors could be identified (atherosclerotic vessel wall disease, vasculitis, hypercoagulable states). Experienced neuroradiologists performed 21 of 48 angiographies (43.8%) on patients with the above-mentioned risk factors, whereas junior neuroradiologists performed 27 angiographies in this subgroup (46.2%). The rate of diffusion abnormalities in patients with risk factors was 11/48 (22.9%) - considerably higher than in patients without risk factors (1/59; 1.7%). The level of experience and the nature of the underlying disease are predictors of the occurrence of cerebral ischemic events following neuroangiography. Alternative diagnostic modalities should be employed in patients who are investigated for diseases with the highest risk of angiographic complications (i.e., vasculitis, and arteriosclerotic vessel wall disease). If diagnostic angiography remains necessary in these patients, the highest level of practitioner training is necessary to ensure good patient outcome.

Pharmaceutical Interventions to Influence Arteriogenesis: New Concepts to Treat Ischemic Heart Disease

Despite the technical progress in interventional techniques to overcome the harmful effects of ischemic heart disease there is still an urgent need for alternative, pharmaceutical treatment modalities. Exogenous stimulation of vessel growth, i.e. vasculogenesis, angiogenesis or arteriogenesis serves as a promising strategy to restore blood flow to the jeopardized tissue regions downstream of arterial stenosis or occlusion. While vasculogenesis is defined as the arrangement of angioblasts during prenatal development creating the first vascular network, angiogenesis and arteriogenesis refer to important adaptive mechanisms in the adult organism. Angiogenesis, neo-formation of capillaries, is a key process in many different physiological and pathophysiological events where improvement of microvascular function and tissue nutrition is needed (e.g. wound healing, tumor growth). In contrast to this capillary sprouting, the term arteriogenesis refers to the development of large caliber collateral arteries. Under conditions of increasing shear stress, anastomoses between interconnected perfusion territories can undergo adaptive enlargement, developing into a functional network of collateral arteries, natural bypasses able to maintain sufficient blood flow and compensating for the gradual occlusion of a large artery (e.g. in the coronary circulation). However, in most cases arteriogenesis does not proceed as fast as the stenosis progresses and infarction and tissue necrosis results. A well-developed collateral network is an important protective factor for the occurrence of ischemic events and therefore pharmaceutical acceleration and stimulation of arteriogenesis in patients represents an eminent aim for the future. This review focuses on the basic mechanisms of arteriogenesis, the recent progresses in translating these insights into the clinical situation and the problems yet to be solved.

Anticoagulation Intensity and Stroke During Warfarin-Use in Atrial Fibrillation Patients

HomeStrokeVol. 37, No. 2Anticoagulation Intensity and Stroke During Warfarin-Use in Atrial Fibrillation Patients Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessLetterPDF/EPUBAnticoagulation Intensity and Stroke During Warfarin-Use in Atrial Fibrillation Patients Robert G. Hart Robert G. HartRobert G. Hart University of Texas Health Science Center, Department of Medicine (Neurology), San Antonio, TX Search for more papers by this author Originally published5 Jan 2006https://doi.org/10.1161/01.STR.0000199633.41324.36Stroke. 2006;37:334–335Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 5, 2006: Previous Version 1 To the Editor:The interesting study by Poli and colleagues examined risk factors for ischemic stroke during anticoagulation of atrial fibrillation patients.1 For the 21 patients with ischemic events, it would be of interest to know the mean of the last “routine” INR before the ischemic event and the mean of the INR recorded nearest to/at the time of stroke to compare with the means of INRs during total follow-up of these 21 patients and of the mean INR for 343 patients without ischemic events. These data may shed additional light on the potential contribution of anticoagulation intensity to ischemic events in this setting.1 Poli D, Antonucci E, Cecchi E, Marcucci R, Liotta AA, Cellai AP, Lenti M, Gensini GF, Abbate R, Prisco D. Culprit factors for the failure of well-conducted warfarin therapy to prevent ischemic events in patients with atrial fibrillation. The role of homocysteine. Stroke. 2005; 36: 2159–2163.LinkGoogle ScholarstrokeahaStrokeStrokeStroke0039-24991524-4628Lippincott Williams & WilkinsResponse:Poli Daniela and Prisco Domenico01022006We thank Dr Hart for his interest in our study and for his questions aiming at clarifying our data. The mean INR of the 343 patients without ischemic events was 2.5±0.19, and the mean INR of the 21 patients who experienced an ischemic event during follow-up was 2.5±0.16, a difference not statistically significant. The mean INR related to the ischemic event (obtained at the time of the event or during the preceding 8 days) was 2.1±0.58, statistically lower in comparison to both the mean INR of this group and the mean INR of all the other patients (P=0.002). Fifteen patients had the INR related to the event ≥1.8. The last mean routine INR recorded before the event was 2.34±0.56, not different with respect to both the mean INR value in this group and the mean INR of all the other patients (P=0.1).To evaluate if the occurrence of ischemic events could be related to a long period of under-anticoagulation, we have calculated the mean INR of the 3 months preceding the event. It was 2.5±0.7, a figure not different from the mean INR of all the patients.In our opinion, these data confirm that the reduced INR related to the event is only one of the risk factors for the occurrence of ischemic complications during OAT. In fact, 15 out of 21 patients had an INR ≥1.8 at the time of the event. In addition, patients without ischemic events during OAT had been exposed to the risk of a poor anticoagulation for a time similar to patients with ischemic events. Actually, the time spent below the intended therapeutic range was not different between the 2 groups. Oral anticoagulant therapy has an intrinsic variability of response so that even an optimized management cannot avoid significant periods of time with INR <2.The use of this treatment on a growing population makes this goal more and more difficult to obtain, further underscoring the need for a specifically devoted management. Together with the continuous efforts to ameliorate the quality of anticoagulation, the identification of other risk factors could help to reduce adverse events in nonvalvular atrial fibrillation patients. Previous Back to top Next FiguresReferencesRelatedDetails February 2006Vol 37, Issue 2 Advertisement Article InformationMetrics https://doi.org/10.1161/01.STR.0000199633.41324.36PMID: 16397176 Originally publishedJanuary 5, 2006 PDF download Advertisement

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HomeStrokeVol. 37, No. 2Anticoagulation Intensity and Stroke During Warfarin-Use in Atrial Fibrillation Patients Free AccessLetterPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyRedditDiggEmail Jump toFree AccessLetterPDF/EPUBAnticoagulation Intensity and Stroke During Warfarin-Use in Atrial Fibrillation Patients Robert G. HartMD Robert G. HartRobert G. Hart University of Texas Health Science Center, Department of Medicine (Neurology), San Antonio, TX Search for more papers by this author Originally published5 Jan 2006https://doi.org/10.1161/01.STR.0000199633.41324.36Stroke. 2006;37:334–335Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 5, 2006: Previous Version 1 To the Editor:The interesting study by Poli and colleagues examined risk factors for ischemic stroke during anticoagulation of atrial fibrillation patients.1 For the 21 patients with ischemic events, it would be of interest to know the mean of the last “routine” INR before the ischemic event and the mean of the INR recorded nearest to/at the time of stroke to compare with the means of INRs during total follow-up of these 21 patients and of the mean INR for 343 patients without ischemic events. These data may shed additional light on the potential contribution of anticoagulation intensity to ischemic events in this setting.1 Poli D, Antonucci E, Cecchi E, Marcucci R, Liotta AA, Cellai AP, Lenti M, Gensini GF, Abbate R, Prisco D. Culprit factors for the failure of well-conducted warfarin therapy to prevent ischemic events in patients with atrial fibrillation. The role of homocysteine. Stroke. 2005; 36: 2159–2163.LinkGoogle ScholarstrokeahaStrokeStrokeStroke0039-24991524-4628Lippincott Williams & WilkinsResponse:Poli Daniela and Prisco Domenico01022006We thank Dr Hart for his interest in our study and for his questions aiming at clarifying our data. The mean INR of the 343 patients without ischemic events was 2.5±0.19, and the mean INR of the 21 patients who experienced an ischemic event during follow-up was 2.5±0.16, a difference not statistically significant. The mean INR related to the ischemic event (obtained at the time of the event or during the preceding 8 days) was 2.1±0.58, statistically lower in comparison to both the mean INR of this group and the mean INR of all the other patients (P=0.002). Fifteen patients had the INR related to the event ≥1.8. The last mean routine INR recorded before the event was 2.34±0.56, not different with respect to both the mean INR value in this group and the mean INR of all the other patients (P=0.1).To evaluate if the occurrence of ischemic events could be related to a long period of under-anticoagulation, we have calculated the mean INR of the 3 months preceding the event. It was 2.5±0.7, a figure not different from the mean INR of all the patients.In our opinion, these data confirm that the reduced INR related to the event is only one of the risk factors for the occurrence of ischemic complications during OAT. In fact, 15 out of 21 patients had an INR ≥1.8 at the time of the event. In addition, patients without ischemic events during OAT had been exposed to the risk of a poor anticoagulation for a time similar to patients with ischemic events. Actually, the time spent below the intended therapeutic range was not different between the 2 groups. Oral anticoagulant therapy has an intrinsic variability of response so that even an optimized management cannot avoid significant periods of time with INR <2.The use of this treatment on a growing population makes this goal more and more difficult to obtain, further underscoring the need for a specifically devoted management. Together with the continuous efforts to ameliorate the quality of anticoagulation, the identification of other risk factors could help to reduce adverse events in nonvalvular atrial fibrillation patients. Previous Back to top Next FiguresReferencesRelatedDetails February 2006Vol 37, Issue 2Article InformationMetrics Download: 112 https://doi.org/10.1161/01.STR.0000199633.41324.36PMID: 16397176 Originally publishedJanuary 5, 2006 PDF download

Chronic Chlamydia pneumoniae infection in patients with symptomatic atherothrombosis

The aim of the present study was to search for an association between chronic Chlamydia pneumoniae infection, indicated by elevated antibody titers against the pathogen, atherothrombosis and the occurrence of arterial ischemic events. We studied 52 patients presenting at baseline with at least one symptomatic episode of atherothrombosis. A screening for fasting blood glucose and a lipid profile was performed on all patients who had no known history of diabetes or hypercholesterolemia. The prevalence of IgG and IgA anti-C. pneumoniae antibodies at baseline was 90% (95% CI: 79-97) and 81% (67-90), respectively. Forty-two of the 52 patients (81%) experienced a new arterial ischemic event after a mean follow-up of 9 years [heart: 19 (37%); brain: 12 (23%); lower limbs: 8 (15%); and other: 13 (25%)]. Occurrence of a new arterial ischemic event was related to age (p=0.003), sex (p=0.009), and tobacco smoking (p=0.06). Prevalences of IgA and IgG anti-C. pneumoniae were significantly higher in patients with atherothrombosis at baseline than that in controls. Our study confirmed the links between C. pneumoniae and atherothrombosis. However, neither IgA nor IgG antibodies for C. pneumoniae was a significant predictive factor for new ischemic arterial events in patients with atherothrombosis.

Platelet Reactivity in Patients and Recurrent Events Post-Stenting: Results of the PREPARE POST-STENTING Study

We investigated the relation of high ex vivo platelet reactivity, rapid fibrin generation, and high thrombin-induced clot strength to postdischarge ischemic events in patients undergoing percutaneous coronary intervention (PCI). High platelet reactivity and rapid fibrin generation may affect the incidence of ischemic events after PCI. However, limited data is available to link these ex vivo markers to the occurrence of events. We measured platelet reactivity to adenosine diphosphate (ADP) by light transmittance aggregometry (LTA) in patients undergoing PCI (n = 192). Clot strength, a measure of thrombin-induced fibrin and platelet interactions, and the time to initial fibrin generation, a marker of thrombin activity, were measured by thrombelastography. The relation of these measurements to ischemic event occurrence was prospectively examined over six months. A total of 100% and 84% of patients were on aspirin and clopidogrel therapy, respectively, at the time of the initial event. Posttreatment ADP-induced aggregation by LTA (63 +/- 12% vs. 56 +/- 15%, p = 0.02) and clot strength (MA) were higher (74 +/- 5 mm vs. 65 +/- 4 mm, p < 0.001) and time to initial fibrin generation was shorter (4.3 +/- 1.3 min vs. 5.9 +/- 1.5 min, p < 0.001) in patients with events (n = 38). The event rates in the highest quartiles of LTA and MA were 32% and 58%, respectively. High platelet reactivity and clot strength, and rapid fibrin formation are novel risk factors for ischemic events after PCI. Clot strength is more predictive than ADP-induced platelet aggregation and may explain the occurrence of events despite treatment with cyclooxygenase-1 and P2Y12 inhibitors.

Stent-assisted arterial reconstruction of traumatic extracranial carotid dissections

Objectives: Dissection of the internal carotid artery is a well-recognized complication of craniocervical trauma with potentially grave neurological outcome in patients with significant ischemic symptoms. Traditional anticoagulation therapy may not be applicable, since anticoagulation is contraindicated in multiple trauma or penetrating injuries. In these circumstances, rapid stenting followed by antiplatelet therapy may be performed.Methods: Patients with angiographically proven traumatic carotid artery dissection were prospectively selected for endovascular stenting according to clinical and radiological criteria. Essentially, patients with hemodynamic significant hemispheric hypoperfusion (as indicated by angiography or perfusion MRI), or in whom anticoagulant therapy failed clinically, or anticoagulation was contraindicated, were considered at high risk for stroke and were selected for stenting. Twelve patients were selected for stenting.Results: In seven patients, multiple stents were implanted. Endovascular treatment reduced mean dissection stenosis from mean 65±33% (range, 10–100%) to mean 7±9% (range, 20–0%). In a mean clinical follow-up of 11.5±6.3 months (range 3–24 months), eight patients improved and four remained stable, and none of the patients had a TIA or stroke. Doppler U/S studies did not detect any signs of de novo in-stent stenosis in any of the patients at a mean follow-up time of 9.2±6.4 months.Conclusions: In selected cases of traumatic dissections of the carotid artery, endovascular stent-assisted angioplasty may immediately restore the integrity of the vessel lumen, even of acutely occluded arteries. This approach efficiently prevented the occurrence of new ischemic events, without additional anticoagulation.

Plasma cystatin-C and development of coronary heart disease: The PRIME Study

The pathogenesis of ischemic coronary events involves degradation of the extracellular matrix in atherosclerotic lesions. The cysteine protease inhibitor cystatin-C may be involved in this phenomenon. The association of plasma cystatin-C with the incidence of myocardial infarction—coronary death and angina, was examined in a nested case–control (two controls per case) design within the prospective cohort study (Prospective Epidemiological Study of Myocardial Infarction (PRIME Study)) which included 9758 men aged 50–59 years who were free of coronary heart disease (CHD) on entry and followed for a 5-year period. Three hundred and thirteen participants suffered myocardial infarction or coronary death ( n = 159) or angina pectoris ( n = 154) during follow-up. Cystatin-C was positively correlated with body mass index (BMI), low-density lipoprotein (LDL)-cholesterol, triglycerides and several inflammatory markers such as fibrinogen ( r = 0.18), C-reactive protein (CRP) ( r = 0.24), interleukin-6 (=0.20), tumor necrosis factor-α (TNFα) ( r = 0.27) and two TNFα receptors: TNFR1A ( r = 0.43) and TNFR1B ( r = 0.41); and negatively with high-density lipoprotein (HDL)-cholesterol ( r = −0.25). After adjustment for traditional risk factors (age, diabetes, smoking, hypertension, BMI, triglycerides, LDL- and HDL-cholesterol), cystatin-C was significantly associated with the occurrence of the first ischemic coronary event. However, this association was no longer significant when CRP was included in the analysis. A decrease in glomerular filtration rate did not explain higher cystatin-C in cases than in controls. Cystatin-C appears to participate in the inflammatory phenomenon observed in the atherosclerotic process. Cystatin-C is not a more predictive risk marker of CHD than CRP or interleukin-6, but could be useful in detecting moderate chronic renal disease.

Endovascular Stent-Assisted Angioplasty in the Management of Traumatic Internal Carotid Artery Dissections

The prognosis of traumatic dissection of the internal carotid artery is worse than for spontaneous dissections. Rapid stenting followed by antiplatelet therapy may prevent complications when anticoagulation therapy is not applicable. Patients with angiographically proven traumatic carotid artery dissection and hemodynamic significant hemispheric hypoperfusion, or in whom anticoagulant therapy was either contraindicated or failed clinically, were regarded as being at high risk for stroke and were selected for stenting. Ten patients with traumatic dissection underwent stenting. Endovascular treatment reduced mean dissection stenosis from 69% to 8%. During a mean clinical follow-up time of 16 months, none had additional transient ischemic attacks or stroke. Doppler ultrasound studies did not detect any signs of de novo in-stent stenosis. In selected cases of traumatic carotid artery dissections, endovascular stent-assisted angioplasty immediately restored the integrity of the vessel lumen and prevented efficiently the occurrence of new ischemic events, without additional anticoagulation.

Tratamiento endovascular de la enfermedad carotídea. Situación actual, aspectos técnicos y capacitación profesional

The aim of this study was to carry out a review of the state of the art in the endovascular treatment of carotid disease, taking into account the findings currently available, its indications, the technical aspects linked to the intervention as well as those related to the occupational training of the specialists involved in performing the technique.Surgical treatment of carotid artery disease can be of benefit to symptomatic patients with stenoses above 70% and to subgroups of patients with symptomatic stenoses between 50-69%. The benefit of carotid endarterectomy in asymptomatic patients is the object of a great deal of controversy that is concerned with the reduction in risk that is obtained and also the large number of patients to be treated in order to prevent the occurrence of ischaemic events. The endovascular treatment of carotid disease comes to the fore, then, as an alternative to surgical treatment. At the present time, a number of randomised multicentre studies are being conducted that will allow the two techniques to be compared in homogeneous groups of patients. Preliminary data nevertheless seem to suggest that this technique offers a number of benefits, especially in groups of subjects with a high surgical risk, and thus they could allow the indications for revascularisation to be extended. We analyse the technical and medical aspects linked to this procedure, the findings from studies carried out to date, its indications and the occupational training of the specialists involved in performing the technique.The endovascular treatment of carotid disease constitutes an alternative to surgical treatment in specifically selected patients. The potential increase in its indications is conditioned by the results from the multicentre studies currently being carried out.

Hyperhomocysteinemia and vitamin B 6 deficiency: New risk markers for nonvalvular atrial fibrillation?

Background A recent “ex-vivo” study showed that nonvalvular atrial fibrillation (NVAF) is associated with enhanced activity of metalloproteinases at the atrial level, and in animal models homocysteine (Hcy) is able to activate metalloproteinases. The aim of this case-control study was to investigate the association of total Hcy plasma levels, vitamin status (folate, vitamin B 6, and vitamin B 12), and methylenetetrahydrofolate reductase C677T and CBS 844ins68 polymorphisms with NVAF. Furthermore, the role of these variables in the occurrence of ischemic events was investigated. Methods We studied 310 NVAF patients on oral anticoagulant treatment (168 patients with previous ischemic events and 142 without) and 310 controls. Results Hyperhomocysteinemia (highest quartile) and vitamin B 6 deficiency (lowest quartile) were independently associated with NVAF after multivariate analysis (Hcy: odds ratio [OR] 6.40, 95% CI 3.29–12.46; vitamin B 6: OR 3.02, 95% CI 1.02–8.95). A significant correlation was found between Hcy levels and left atrial diameter ( r = 0.46; P < .001). As shown by multivariate analysis, elevated Hcy levels were an independent risk factor for ischemic complications during NVAF (OR 2.66, 95% CI 1.15–6.20). Conclusions This study demonstrates a significant association of both elevated Hcy levels and low vitamin B 6 levels with the presence of NVAF; in addition, it confirms the role of Hcy as a risk factor for ischemic events during NVAF.

Residual dissection of the brachiocephalic arteries: Significance, management, and long-term outcome

Objectives Residual dissection of the brachiocephalic arteries after operations for acute type A dissection is considered a benign condition that does not expose patients to late neurologic events. This retrospective study, conducted on an outpatient clinic basis between June 1995 and May 2003, had the objectives of evaluating the consequences of residual dissection of the brachiocephalic arteries, investigating the long-term outcomes of patients with this condition, and illustrating our approach to the condition. Methods Forty-two of 137 patients with spontaneous aortic dissection were identified as having residual dissection of the brachiocephalic arteries. There were 30 men and 12 women, with median age of 64.8 years. Patients were followed for a median time of 3.17 years (25th-75th percentile, 1.43-4.40 years; maximum, 7.5 years). The main outcome was the occurrence of cerebral ischemic events (transient ischemic attack or stroke) or death. The functional consequences of brachiocephalic artery dissection were studied by using duplex scanning and transcranial Doppler ultrasonography. Results Twenty-four focal neurologic complications occurred in 13 of 42 patients (incidence, 30.9%); major strokes occurred in 6 patients, and none were fatal. Minor strokes occurred in 12 patients. In all patients the damaged territory was dependent on a dissected artery. Kaplan-Meier (90-months) freedom from focal neurologic events was 55.7% (95% confidence interval, 33.7%-72.9%). Mean time of freedom from focal neurologic events was 64.5 months (95% confidence interval, 53.1-75.9 months). Positive transcranial Doppler monitoring for microembolic signals was 24.1%, and patients with clinical symptoms had higher microembolic signal counts than did those without symptoms (8.4/h vs 1.9/h, P < .001). Reduced cerebrovascular reactivity to hypercapnia, calculated by using the breath-holding index values, was associated with severely impaired brachiocephalic artery perfusion. The multivariable model for predictors of late stroke (minor and major) included the following variables: microembolic signal count (1 signal/h increase; relative risk, 1.27 [95% CI, 1.12-1.77]), breath-holding index (0.10 increase; relative risk, 0.91 [95% CI, 0.87-0.94]), and the presence of at least one carotid axis with a thrombosed false channel (relative risk, 0.82 [95% CI, 0.64-0.93]). Sixteen operations were performed in 12 patients to relieve residual dissection. Conclusions These results suggest an increased risk of ischemic events ipsilateral to the dissected arteries. Strict follow-up and identification of subjects at risk implies the exact knowledge of vessel anatomy and perfusion status. Ultrasonographic transcranial Doppler examination plays an important role in the clinical work-up of these patients.

Prognostic value of rest myocardial perfusion imaging in patients with chest pain and negative troponin I

Background: Rest myocardial perfusion imaging (RMPI) in the evaluation of patients with chest pain has been shown to provide diagnostic information, but may also provide prognostic data. The aim of this study was to find the relationship between RMPI results and the occurrence of cardiac ischemic events (death, myocardial infarction or myocardial revascularization) over a ninety-day period in patients with chest pain and with negative troponin I. Methods: Patients (pts) without a prior myocardial infarction, admitted for chest pain in the emergency department, were studied by RMPI. Troponin I was assessed before RMPI and four hours later. Patients with values of troponin considered positive for myocardial injury (> 0,20ng/ml) were excluded. Tomographic perfusion images were acquired after the injection of 15mCi of 99mTc-tetrofosmin and analyzed using a 17 segment scoring system.The summed rest score was expressed as a percentage of the maximal possible score (% summed rest perfusion score SRPS). Regarding the result of the exam, 2 groups were established: I - %SRPS ≤ 15%; II > 15%. Ischemic events were: death, myocardial infarction and myocardial revascularization over a 90-day period. Statistical analysis was performed using Kaplan-Meier survival curves and the Logrank test. Results: Fifty-nine pts were enrolled, 41 pts were included in group I (69,5%), 18 in group II (30,5%).The cardiac events were: 8 revascularizations and 1 death (17,6%). Two pts from group I (4,9%) and 7 pts from group II (38,9%) had a cardiac event. Using the Logrank test with a Mantel-Cox analysis a p = 0,0007 was found. Conclusion: In this study a relationship was found between the occurrence of cardiac events and the extent of rest perfusion defects. RMPI in patients with chest pain and negative troponin I could be used for risk stratification regarding the underlying ischemic heart disease. Logrank p = 0,

Sympatho-modulatory therapies in perioperative medicine

With increasing life expectancy and improved surgical technology an ever-larger number of elderly patients with cardiovascular disease, or significant cardiovascular risk factors will undergo major surgery. More than 5% of an unselected surgical population undergoing non-cardiac surgery will suffer from perioperative cardiovascular complications including myocardial infarction and cardiac death. The incidence of adverse cardiac events may even reach 30% in high-risk patients undergoing vascular surgery causing a substantial financial burden of perioperative health care costs. 59 Thus, all therapeutic measures should be undertaken to reach the challenging goal of a lower incidence of perioperative cardiovascular complications. Gaining control over sympathetic nervous system activity, that is blunting the adrenergic response to the surgical trauma, traditionally represents an important aspect of anaesthetic practice. 21 Anaesthesiology has been regarded as the ‘practice of autonomic nervous system medicine’. While variable and moderate changes in sympathetic nervous system activity function as a servo-control mechanism and are even required to maintain and optimize cardiac performance, undue liberation of excitotoxic substances such as catecholamines and inflammatory cytokines, particularly during emergence from anaesthesia and the painful postoperative period, facilitates the occurrence of cardiovascular complications. 83 84 At this point, the life-supporting adrenergic drive (‘fight-or-flight-response’) turns into a potentially hazardous life-threatening maladaptation. In support of this concept, the beneficial effects of antiadrenergic treatment regimens in perioperative medicine have been confirmed, in observational studies, metaanalyses 55 1 66 and randomized controlled clinical trials. 43 54 59 63 80 84 However, the seemingly established concept of ‘sympatholysis’ as an effective cardioprotective treatment modality needs considerable refinement in the light of the many new experimental and clinical findings. The parlance of ‘sympatholytic’ protection erroneously equates annihilation of any type of adrenergic stimulation with cardioprotection and should be replaced by ‘sympathomodulatory’protection. The present review summarizes findings from large-scale heart failure trials and discusses basic and clinical aspects of individual sympatho-modulatory therapies, as currently used in perioperative medicine, including b-adrenergic antagonism, a2-agonism, and regional anaesthetic techniques. For limitation of space, reviews will often be cited where further references to the primary literature may be found.