Progression Of Infarction Research Articles

227 Infarct size in a rat model of acute myocardial infarction is reduced by interleukin-6 trans-signalling blockade using sgp130fc but not an anti-il-6r monoclonal antibody

IntroductionInterleukin-6 (IL-6) is elevated during acute myocardial infarction (AMI) particularly after reperfusion with primary percutaneous coronary intervention (PPCI). Higher circulating levels of IL-6 and its soluble receptor (sIL-6R) are associated...

The effect of C-reactive protein deposition on myocardium with ischaemia-reperfusion injury in rats.

We evaluated the effect of monomeric C-reactive protein (CRP) deposition on areas at risk (AAR) of myocardium with ischaemia-reperfusion injury. Myocardial ischaemia-reperfusion injury model was produced by ligation of the left anterior descending coronary artery for 45 min followed by 45 min of reperfusion using female Sprague-Dawley rats. Tissue from non-ischaemic areas, areas at risk and infarct areas determined by Evans blue and 2,3,5-triphenyltetrazolium chloride staining was obtained from the sham group, the ischaemia-reperfusion injury without C-reactive protein (CRP) injection group (I/R only group), and the ischaemia-reperfusion injury with CRP injection group (I/R + CRP group). We assessed the effect of CRP injection on infarct size, CRP deposition, CRP and IL-6 mRNA expression, the third component of complement (C3) immunodeposition and mitochondrial structural remodelling with apoptosis by quantitative RT-PCR analyses, immunohistochemistry, direct immunofluorescence, electron microscopy and Terminal deoxynucleotide transferase dUTP Nick End Labelling assay, respectively. All images were analysed using an automated morphology tool. The infarct area significantly increased in the I/R + CRP group compared to the I/R only group. The anti CRP antibody confirmed that CRP deposition occurred in both the infarct and area at risk (AAR) of the I/R + CRP group. The myocardium did not exhibit CRP mRNA expression, and the CRP treatment group showed a tendency for IL-6 to increase without statistical significance. Activated C3, apoptosis and mitochondrial destruction increased on AAR and infarct area in the I/R + CRP group. These results strongly suggest the active participation of the deposition of CRP on AAR in the progression of myocardial infarction following ischaemia-reperfusion injury, accompanied by complement activation and mitochondrial change.

Ultrasound targeted microbubbles destruction-mediated the Ang1 gene transfection improves left ventricular mechanical synchrony during the progression of myocardial infarction in canines

Objective To evaluate the left ventricular synchrony after myocardial infarction (MI) by ultrasound targeted microbubbles destruction (UTMD)-mediated angiogenin 1 (Ang1) gene transfection in canine. Methods Twenty-one dogs were divided into three groups (n=7 in each group): ①control group (healthy dogs); ②MI group (MI dogs without treatment); ③UTMD group (MI dogs with UTMD treatment). One month later, the size and systolic function of heart were measured by echocardiography. The synchronization parameters derived from two dimensional-speckle tracking imaging(2D-STI) included the standard deviation and maximum difference of time to peak strain for all left ventricular segments (Tls-SD, Trs-SD, Tcs-SD, Tls-Dif, Trs-Dif and Tcs-Dif). CD31 and α-SMA were applied for quantifying capillary and arteriolar density. The Ang1, SERCA2a and PLB protein were detected by Western blotting. Results ①One month later, the conventional ultrasonic parameters were compared among three groups, the LVEDD, LVESD and E/e′ increased and LVEF, e′ and E/A reduced in MI group than those in control group, all of them partially recovered in UTMD group than those in MI group, but were still lower than those in control group (P 0.05); ③The immunohistochemistry showed the higher blood vessel density in UTMD group than that in MI group(P<0.05); ④The relative quantity of Ang1 was significantly higher in UTMD group. The relative quantity of SERCA2a protein was lower in MI group than that in control group, increased in UTMD group, the trend of PLB was contrary to it. The differences were statistically significant (all P<0.05). Conclusions The UTMD-mediated Ang1 gene transfection can promote angiogenesis after MI, reverse left ventricular remodeling and improve left ventricular synchrony. The myocardial synchrony may be related to the expression of calcium ions key protein SERCA2a and PLB. Key words: Sonication; Transfection; Myocardial infarction; Synchrony; Speckle tracking imaging

The role of phenylephrine in patients with small deep subcortical infarct and progressive weakness

Background and purposeAlthough progression of small deep subcortical infarct (PSDI) comprises 12% to 36% of all small deep subcortical infarcts, the therapy for progression is not clear. This study investigated whether induced-hypertension therapy using phenylephrine is a useful therapy for PSDI. MethodsA group of 2427 consecutive patients, diagnosed with stroke at a tertiary hospital over a period of 4years was reviewed retrospectively. We analyzed patients with small deep subcortical infarct using clinical, laboratory, and pulse wave velocity (PWV). PSDI is defined as one or more increase in the motor score according to the NIHSS. Good outcome was designated as a modified Rankin scale of 0 to 2 at discharge. ResultsAmong all 662 patients who had a small deep subcortical infarct, 66 patients experienced motor progression (9.97%). The induced-hypertension therapy group (n=25) received phenylephrine, and the conventional group (n=41) received anticoagulation therapy such as heparin, volume expansion, or both. Although there were no significant differences in baseline clinical and laboratory findings, the PSDI group showed a significantly more frequent decrease in blood pressure at progression (P<0.0001) and higher PWV (P=0.001). The phenylephrine group (vs the conventional group) had a lower NIHSS score (P=0.036) and good outcome at discharge (P=0.004). In multiple regression analysis, PWV (OR, 1.004 per 1-cm/s increase; 95% CI, 1.001–1.008; P=0.018) was an independent predictor of good outcome in the phenylephrine group. A side effect of phenylephrine treatment was dysuria (n=1). ConclusionsThe present study suggests that vascular stiffness can be not only a predictor for PSDI but also a predictor of motor improvement after induced-hypertension therapy using phenylephrine in lacunar stroke.

Comparison of ultrastructural and nanomechanical signature of platelets from acute myocardial infarction and platelet activation

Acute myocardial infarction (AMI) initiation and progression follow complex molecular and structural changes in the nanoarchitecture of platelets. However, it remains poorly understood how the transformation from health to AMI alters the ultrastructural and biomechanical properties of platelets within the platelet activation microenvironment. Here, we show using an atomic force microscope (AFM) that platelet samples, including living human platelets from the healthy and AMI patient, activated platelets from collagen-stimulated model, show distinct ultrastructural imaging and stiffness profiles. Correlative morphology obtained on AMI platelets and collagen-activated platelets display distinct pseudopodia structure and nanoclusters on membrane. In contrast to normal platelets, AMI platelets have a stiffer distribution resulting from complicated pathogenesis, with a prominent high-stiffness peak representative of platelet activation using AFM-based force spectroscopy. Similar findings are seen in specific stages of platelet activation in collagen-stimulated model. Further evidence obtained from different force measurement region with activated platelets shows that platelet migration is correlated to the more elasticity of pseudopodia while high stiffness at the center region. Overall, ultrastructural and nanomechanical profiling by AFM provides quantitative indicators in the clinical diagnostics of AMI with mechanobiological significance.

Abstract TP6: Factors Influencing Infarct Progression During Ischemic Stroke Patients Transfer: Collaterals Lost is Brain Lost

Introduction: When transferred from a referring hospital (RH) to a thrombectomy capable stroke center (TCSC), patients with initially favorable imaging profile (ASPECT score ≥6) often demonstrate infarct progression significant enough to make them ineligible at arrival. We sought to determine the clinical and imaging factors associated with this phenomenon in transferred ischemic stroke patients. Methods: We identified adult stroke patients transferred from one of 30 RH between 2010 and 2016 for which (1) a RH computed tomography (CT) and (2) a CT Angiography (CTA) at arrival were available for review. ASPECT scores were evaluated by 2 raters. The adequacy of leptomeningeal collateral flow was rated as none/poor, decreased, adequate or augmented per the Maas et al (Stroke 2009), modified scale. ASPECTS decay was defined as an ASPECT initial score ≥6 worsening between RH and TCSC CTs to a score &lt;6. Results: A total of 330 patients were included in the analysis (mean age 70.2 ± 14.2, 43.3% females). Univariable subgroup analyses showed that patients with ASPECTs decay were more likely to be females (55% vs 40%, p=0.02), not on anticoagulants (4% vs 15%, p=0.01), and with higher initial NIHSS (Median [IQR] 19 [15.3-22] vs 11 [6-17], p&lt;0.001), hyperdense vessel sign on initial CT (71% vs 26%, p&lt;0.001) and poor collaterals on CTA (72% vs 19%, p&lt;0.001). In multivariable models, higher NIHSS, lower baseline ASPECTs, CTA evidence of a proximal occlusion, and none/poor collaterals were strong predictors of ASPECTs decay, with collateral status demonstrating the highest odds ratio (aOR 10.3, 95%CI: [4.1-29], p&lt;0.001). Similar results were found after stratification by vessel occlusion level. Conclusion: In ischemic stroke patients transferred for thrombectomy, poor collateral flow, stroke severity and proximal vascular occlusion, but not time interval, are the main determinants of ASPECTs decay.

Interleukin-6 is increased in plasma and cerebrospinal fluid of community-dwelling domestic dogs with acute ischaemic stroke.

Inflammatory cytokines are potential modulators of infarct progression in acute ischaemic stroke, and are therefore possible targets for future treatment strategies. Cytokine studies in animal models of surgically induced stroke may, however, be influenced by the fact that the surgical intervention itself contributes towards the cytokine response. Community-dwelling domestic dogs suffer from spontaneous ischaemic stroke, and therefore, offer the opportunity to study the cytokine response in a noninvasive set-up. The aims of this study were to investigate cytokine concentrations in plasma and cerebrospinal fluid (CSF) in dogs with acute ischaemic stroke and to search for correlations between infarct volume and cytokine concentrations. Blood and CSF were collected from dogs less than 72 h after a spontaneous ischaemic stroke. Infarct volumes were estimated on MRIs. Interleukin (IL)-2, IL-6, IL-8, IL-10 and tumour necrosis factor in the plasma, CSF and brain homogenates were measured using a canine-specific multiplex immunoassay. IL-6 was significantly increased in plasma (P=0.04) and CSF (P=0.04) in stroke dogs compared with healthy controls. The concentrations of other cytokines, such as tumour necrosis factor and IL-2, were unchanged. Plasma IL-8 levels correlated significantly with infarct volume (Spearman’s r=0.8, P=0.013). The findings showed increased concentrations of IL-6 in the plasma and CSF of dogs with acute ischaemic stroke comparable to humans. We believe that dogs with spontaneous stroke offer a unique, noninvasive means of studying the inflammatory processes that accompany stroke while reducing confounds that are unavoidable in experimental models.

LEPR q223r gene polymorphism in patients having coronary heart disease with postinfarction cardiosclerosis and type 2 diabetes

Aim. To determine the prevalence of mononucleotide leptin receptor gene LEPR Q223R polymorphism in patients having coronary heart disease (CHD) with postinfarction cardiosclerosis depending on type 2 diabetes comorbidity.Materials and methods. 147 patients having stable CHD with postinfarction cardiosclerosis (100% male), the average age of 52, were examined. In 64 (43.5%) patients CHD combined with type 2 diabetes. The CHD diagnosis was established by АНА/АСС (2014) and ESC (2013) recommendations. LEPR Q223R (Gln223Arg, rs1137101) gene polymorphism was determined using allele-specific polymerase chain reaction in real time.Results and discussion. In the group of patients having CHD with postinfarction cardiosclerosis (Podillya region inhabitants) the frequency of LEPR Q223R gene genotypes was as follows: QQ – 25.2 %, QR – 42.4 %, RR – 32.7 %. The frequency of R allele in patients having CHD was significantly higher than in the practically healthy group, and was 53.7 to 41.3% (χ2=4.72, р=0.03). Сomorbidity chances significantly increase in R allele carriers (OR=1.58, 95 % СІ 0.99-2.53), while Q allele carrier state have a protective value (OR=0.63, 95 % СІ 0.40-1.01). RR genotype associated with CHD earlier debut, higher frequency of Q- myocardial infarction (OR=4.3; 95 % СІ 1.51-12.5) and heart failure progression (OR=3.60; 95 % СІ 1.67-7.77).Conclusion. RR genotype LEPR Q223R gene carrier state is a potential unmodified factor that accelerates development and increases the severity of CHD, associated with type 2 diabetes, in males

SIGNIFICANCE OF LABORATORY PARAMETERS IN PROGNOSIS OF OUTCOMES OF ACUTE MYOCARDIAL INFARCTION

The study objective is to validate a mathematical model for prognosis of progression of the acute period of myocardial infarction. Materials and methods . We examined 135 patients with acute Q-wave myocardial infarction of the left ventricle aged between 34 and 88 years (mean age 66, standard deviation 12 years), among them 64 women and 71 men. For prognosis of the outcome of the acute period of myocardial infarction we used an approach based on intellectual data analysis (data mining) in combination with mathematical methods based on decision trees. Results. Using decision tree algorithms, we singled out laboratory parameters (attributes) which were subsequently used as input. Adequacy of classification of these attributes was determined by a contingency table. Accuracy of the obtained calculation results was 95.56 % demonstrating good agreement between the model and observed data. In a decision tree visualization, the most significant 8 laboratory parameters were determined. Significance of NO 2 metabolite was 24.9 %, triglycerides – 16.7 %, urea – 14.8 %, erythrocytes – 11.2 %, alanine aminotransferase – 9.4 %, very low density lipoproteins – 9.4 %, creatinine – 8.5 %, prothrombin index – 5.1 %. In the Rules tab, only rules 4 and 9 can be used with confidence, because their confidence level approaches 100 %, and effect cost for the fact of death was 33.59 % and 32.03 %, respectively. Conclusion. Using a decision tree algorithm, we determined prognostically significant factors for progression of acute myocardial infarction. The following set of parameters predicts unfavorable outcome (death) with 95.56 % accuracy: NO 2 &lt; level 22.755 mmol/l, triglycerides ≥ 1.565 mmol/l, erythrocytes &lt; 4.91 M/uL, alanine aminotransferase &lt; 1.23 mmol/l, urea &lt; 7.05 mmol/l, very low-density lipoproteins &lt; 0.965 mmol/l, creatinine ≥ 91.55 µmol/l, NO 2 level ≥ 22.755 mmol/l predicts a favorable outcome with 95.56 % accuracy.

Serum SH3BP5-specific Antibody Level is a Biomarker of Atherosclerosis

Abstract Background: The discovery and development of novel biomarkers that could facilitate early diagnosis and thus prevent the progression of atherosclerosis-related diabetes mellitus (DM), cerebral infarction (CI), and cardiovascular disease (CVD) has garnered much research interest. Notably, recent reports have described a number of highly sensitive antibody markers. In this study, we aimed to identify additional antibody markers that would facilitate screening. Methods: The amplified luminescent proximity homogeneous assay (AlphaLISA) method, which incorporates glutathione- or streptavidin-donor beads and anti-human-IgG-acceptor beads, was used to evaluate serum antibody levels in serum samples. The protein array method was used for the initial screening, and peptide arrays were used to identify epitope sites. Results: The protein array identified SH3 domain-binding protein 5 (SH3BP5) as a target antigen of serum IgG antibodies in the sera of patients with atherosclerosis. We prepared recombinant glutathione S-transferase (GST)- fused SH3BP5 protein. Peptide arrays revealed that the epitope site recognized by serum antibodies is located within amino acids 161–174 of SH3BP5. AlphaLISA revealed significantly higher serum antibody levels against both the SH3BP5 protein and peptide in patients with DM, acute-phase CI, transient ischemic attack, CVD or chronic kidney disease (CKD), than in healthy donors. Furthermore, areas under the receiver operating characteristic curves of these antibodies were higher in patients with CKD and DM than in other patients. Spearman correlation analysis revealed associations between the serum antibody levels against SH3BP5 peptide and artery stenosis, hypertension, and smoking. Conclusions: The serum anti-SH3BP5 antibody marker appears to be useful for estimating the progress of atherosclerosis and may discriminate atherosclerosis associated with hypertension and/or habitual smoking.

Role of the Cysteinyl Leukotrienes in the Pathogenesis and Progression of Cardiovascular Diseases.

Cysteinyl leukotrienes (CysLTs) are potent lipid inflammatory mediators synthesized from arachidonic acid, through the 5-lipoxygenase (5-LO) pathway. Owing to their properties, CysLTs play a crucial role in the pathogenesis of inflammation; therefore, CysLT modifiers as synthesis inhibitors or receptor antagonists, central in asthma management, may become a potential target for the treatment of other inflammatory diseases such as the cardiovascular disorders. 5-LO pathway activation and increased expression of its mediators and receptors are found in cardiovascular diseases. Moreover, the cardioprotective effects observed by using CysLT modifiers are promising and contribute to elucidate the link between CysLTs and cardiovascular disease. The aim of this review is to summarize the state of present research about the role of the CysLTs in the pathogenesis and progression of atherosclerosis and myocardial infarction.

Recent Advances in Understanding Audiovestibular Loss of a Vascular Cause.

Acute audiovestibular loss is characterized by abrupt onset of prolonged (lasting days) vertigo and hearing loss. Acute ischemic stroke in the distribution of the anterior inferior cerebellar artery (AICA) is known to be the leading cause of acute audiovestibular loss. So far, eight subgroups of AICA territory infarction have been identified according to the patterns of audiovestibular dysfunctions, among which the most common pattern is the combined loss of auditory and vestibular functions. Unlike inner ear dysfunction of a viral cause, which can commonly present as an isolated vestibular (i.e., vestibular neuritis) or cochlear loss (i.e., sudden deafness), labyrinthine dysfunction of a vascular cause rarely results in isolated loss of vestibular or auditory function. As audiovestibular loss may precede the central symptoms or signs of an ischemic stroke in the posterior circulation, early diagnosis and proper management of audiovestiubular loss may provide a window to prevent the progression of infarction to larger areas of the posterior circulation. A clinician should consider the possibility that acute audiovestibular loss may herald impending AICA territory infarction, especially when patients have basilar artery occlusive disease close to the origin of the AICA on brain MRA. This review aims to highlight the recent advances in understanding audiovestibular loss of a vascular cause and to address its clinical significance.

Is management of hyperglycaemia in acute phase stroke still a dilemma?

Close monitoring of blood glucose levels during the immediate post-acute stroke phase is of great clinical value, as there is evidence that the risk of neurological deterioration is associated with both hyper- and hypoglycaemia. The aim of this review paper is to summarise the evidence on post-stroke blood glucose management and its impact on clinical outcomes, during the early post-acute stage. Post-stroke hyperglycaemia has been associated with increased cerebral oedema, haemorrhagic transformation, lower likelihood of recanalisation and deteriorating neurological state. Thus, hyperglycaemia during an acute stroke may result in poorer clinical outcomes, infarct progression, poor functional recovery and increased mortality rates. Although hypoglycaemia may also lead to poorer outcomes via further brain injury, it can be readily reversed by glucose administration. In most patients, the goal of regular treatment is euglycaemia and for acute-stroke patients, a reasonable approach is to target control of glucose level at 100-150mg/dL. Both hypoglycaemia and hyperglycaemia may lead to further brain injury and clinical deterioration; that is the reason these conditions should be avoided after stroke. Yet, when correcting hyperglycaemia, great care should be taken not to switch the patient into hypoglycaemia, and subsequently aggressive insulin administration treatment should be avoided. Early identification and prompt management of hyperglycaemia, especially in acute ischaemic stroke, is recommended. Although the appropriate level of blood glucose during acute stroke is still debated, a reasonable approach is to keep the patient in a mildly hyperglycaemic state, rather than risking hypoglycaemia, using continuous glucose monitoring.

Atrial fibrillation, progression of coronary atherosclerosis and myocardial infarction.

Background Despite atrial fibrillation representing an established risk factor for stroke, the association between atrial fibrillation and both progression of coronary atherosclerosis and major adverse cardiovascular events is not well characterized. We assessed the serial measures of coronary atheroma burden and cardiovascular outcomes in patients with and without atrial fibrillation. Methods Data were analyzed from nine clinical trials involving 4966 patients with coronary artery disease undergoing serial intravascular ultrasonography at 18-24 month intervals to assess changes in percent atheroma volume (PAV). Using a propensity weighted analysis, and following adjustment for baseline variables, patients with ( n = 190) or without ( n = 4776) atrial fibrillation were compared with regard to coronary plaque volume and major adverse cardiovascular events (death, myocardial infarction, and stroke). Results Atrial fibrillation patients demonstrated lower baseline PAV (36.0 ± 8.9 vs. 38.1 ± 8.9%, p = 0.002) and less PAV progression (-0.07 ± 0.34 vs. + 0.23 ± 0.34%, p = 0.001) compared with the non-atrial fibrillation group. Multivariable analysis revealed atrial fibrillation to independently predict both myocardial infarction [HR, 2.41 (1.74,3.35), p<0.001] 2.41 (1.74, 3.35), p < 0.00) and major adverse cardiovascular events [HR, 2.2, (1.66, 2.92), p<0.001] 2.20 (1.66, 2.92), p < 0.001]. Kaplan-Meier analysis showed that atrial fibrillation compared with non-atrial fibrillation patients had a significantly higher two-year cumulative incidence of overall major adverse cardiovascular events (4.4 vs. 2.0%, log-rank p = 0.02) and myocardial infarction (3.3 vs. 1.5%, log-rank p = 0.05). Conclusions The presence of atrial fibrillation independently associates with a heightened risk of myocardial infarction despite a lower baseline burden and progression rate of coronary atheroma. Further studies are necessary to define the pathogenesis of myocardial infarction in the setting of atrial fibrillation.

Carotid stenting versus endarterectomy in the same patient: A “direct” comparison

The aim of this study was to evaluate outcomes and feasibility of carotid artery stenting versus carotid endarterectomy, both procedures performed in the same patient. Forty-five subjects (33 males, 70 ± 7 years) underwent carotid endarterectomy or carotid artery stenting, the counter procedure on the contralateral carotid performed after a variable period. We evaluated the post-procedural percentage of carotid stenosis at 30, 180 days and one-year follow-up, and the occurrence of acute myocardial infarction, New York Heart Association class progression, stroke, death, cardiovascular death, angina, transient ischemic attack and renal failure. Carotid artery stenting treatment reduced the degree of re-stenosis after 180 days equally to carotid endarterectomy procedure (difference: 0.033%, P = 0.285). No statistically significant differences were observed according to the occurrence of acute myocardial infarction and New York Heart Association class progression, revealing odds ratio (OR) equal to 0.182 ( P = 0.361) for acute myocardial infarction and 0.303 ( P = 0.434) for New York Heart Association class progression. Carotid endarterectomy confirms its efficacy in carotid revascularization, but carotid artery stenting constitutes a good alternative when the procedures are selected based on patient-specific risk factors.

La gangrène cutanée thrombotique : une manifestation extradigestive rare de la rectocolite hémorragique

Thrombotic cutaneous gangrene is a rare extra-intestinal manifestation of ulcerative colitis with a severe prognosis. A 35-year-old woman with a 7-year history of ulcerative colitis presented with extensive ecchymotic lesions that began a few hours earlier. On examination, she was febrile with multiple necrotic lesions. Skin biopsy showed multiple microthrombi in the dermal vessels. A diagnosis of thrombotic cutaneous gangrene was established. The patient was treated with heparin and systemic corticosteroids. The majority of cutaneous lesions showed improvement after 1month. Thrombophlebitis of the left lower limb occurred subsequently. Thrombotic cutaneous gangrene is attributed to microvascular thrombosis, which arises from the hypercoagulability observed in ulcerative colitis. Complete blood and coagulation tests must be performed and early anticoagulation with heparin must be considered in order to prevent the progression of cutaneous infarction.

TMEM16F-Mediated Platelet Membrane Phospholipid Scrambling Is Critical for Hemostasis and Thrombosis but not Thromboinflammation in Mice-Brief Report.

It is known that both platelets and coagulation strongly influence infarct progression after ischemic stroke, but the mechanisms and their interplay are unknown. Our aim was to assess the contribution of the procoagulant platelet surface, and thus platelet-driven thrombin generation, to the progression of thromboinflammation in the ischemic brain. We present the characterization of a novel platelet and megakaryocyte-specific TMEM16F (anoctamin 6) knockout mouse. Reflecting Scott syndrome, platelets from the knockout mouse had a significant reduction in procoagulant characteristics that altered thrombin and fibrin generation kinetics. In addition, knockout mice showed significant defects in hemostasis and arterial thrombus formation. However, infarct volumes in a model of ischemic stroke were comparable with wild-type mice. Platelet TMEM16F activity contributes significantly to hemostasis and thrombosis but not cerebral thromboinflammation. These results highlight another key difference between the roles of platelets and coagulation in these processes.

Impact of Initial Diffusion-Weighted Imaging Lesion Growth Rate on the Success of Endovascular Reperfusion Therapy.

Initial diffusion-weighted imaging lesion growth rate (IGR) assessed by diffusion-weighted imaging lesion volume divided by the delay from onset to magnetic resonance imaging offers an estimate of early brain infarction progression. We investigated the impact of IGR on the rate of favorable outcome according to the occurrence of a successful endovascular revascularization within 6 hours after onset in patients experiencing an acute brain infarction complicating internal carotid artery terminus/middle cerebral artery M1 occlusion. The primary study end point was a favorable outcome defined by a modified Rankin Scale score of ≤2, 90 days after onset. A Thrombolysis in Cerebral Infarction score 2b/3 defined a successful recanalization. A total of 166 patients were included. Median IGR was 7 mL/h (interquartile range, 2-26). Sixty-eight patients (41%) experienced a favorable outcome. After adjustment on age, systolic blood pressure, vessel site occlusion, National Institutes of Health Stroke Scale, and antithrombotic medication, increase in IGR was associated with a decreased occurrence of favorable outcome with an odds ratio per SD increase of 0.60 (95% confidence interval, 0.38-0.94; P=0.03). A successful recanalization was achieved among 56% of the patients after a median delay of 251 minutes (interquartile range, 211-291 minutes). Increasing IGR was associated with a decreased favorable outcome only when a successful recanalization was not achieved (adjusted odds ratio, 0.32; 95% confidence interval, 0.12-0.85; P=0.02). Proximal internal carotid artery/M1 occlusion did result into a wide range of IGR within 6 hours after onset. Increasing IGR was associated with a lower rate of favorable outcome after endovascular treatment overall and when a successful recanalization was not achieved.

Multiterritory Atherosclerosis and Carotid Intima-Media Thickness as Cardiovascular Risk Predictors After Percutaneous Angioplasty of Symptomatic Subclavian Artery Stenosis.

To identify independent predictors of cardiovascular events among patients with subclavian artery stenosis. Two hundred eighteen consecutive patients with subclavian artery stenosis referred to angioplasty were examined for coexistent coronary, renal, or lower extremity artery stenosis of 50% or greater. Initial carotid intima-media thickness and internal carotid artery (ICA) stenosis were assessed. Intima-media thickness was reassessed in 108 randomly chosen patients to evaluate the change over time. The incidence of cardiovascular death, myocardial infarction (MI), ischemic stroke, and symptomatic lesion progression was recorded. The patients included 116 men and 102 women (mean age ± SD, 62.1 ± 8.4 years). Isolated subclavian artery stenosis and involvement of 1, 2, and 3 or 4 other territories with stenosis of 50% or greater were found in 46 (21.1%), 83 (38.1%), 55 (25.2%), and 34 (15.6%) patients, respectively. Internal carotid artery stenosis of 50% or greater (relative risk [RR], 1.54; 95% confidence interval [CI], 1.39-1.70; P < .001) and initial intima-media thickness (RR, 1.16; 95% CI, 1.05-1.28; P = .005) were identified as independent markers of multiterritory atherosclerosis. The optimal intima-media thickness cutoff for atherosclerosis extent was 1.3 mm (sensitivity, 75.6%; specificity, 76.1%). During follow-up of 57 ± 35 months, cardiovascular death, MI, and ischemic stroke occurred in 29 patients (13.3%). Those patients had significantly higher intima-media thickness progression (+0.199 ± 0.57 versus +0.008 ± 0.26 mm; P = .039) and more widespread initial atherosclerosis (mean territories, 1.8 ± 1.1 versus 1.3 ± 1.1; P = .042). Independent predictors of cardiovascular death, MI, ischemic stroke, and lesion progression were coronary artery disease (RR, 1.32; 95% CI, 1.10-1.58; P = .003) and intima-media thickness progression (RR, 1.22; 95% CI, 1.02-1.46; P = .033; sensitivity, 75.0%; specificity, 61.8%). In patients with symptomatic subclavian artery stenosis, baseline carotid intima-media thickness and ICA stenosis of 50% or greater are associated with multiterritory atherosclerosis, whereas intima-media thickness progression is associated with the risk of cardiovascular events.

Increased arterial pulsatility and progression of single subcortical infarction.

We investigated the association of clinical, laboratory, sonographic and imaging parameters, in the progression of single subcortical infarctions. Consecutive 169 patients with lacunar (n = 89) and striatocapsular infarctions (n = 80) in the middle cerebral artery (MCA) territory with nonstenotic MCAs were recruited and examined for stroke progression. The pulsatility index (PI) was measured by transcranial Doppler from ipsilateral M1. The striatocapsular infarction group exhibited more stroke progression. The patients with progressive lacunar infarctions had more diabetes, higher HbA1c levels, and higher initial National Institutes of Health Stroke Scale (NIHSS) scores, and the patients with progressive striatocapsular infarctions had more hypertension, higher cholesterol levels, and higher NIHSS scores. The MCA PI was higher in the lacunar infarction patients with progression (0.99 ± 0.19 vs. 0.90 ± 0.14, p = 0.048), while the striatocapsular infarction patients did not differ according to progression. From a multivariate analysis, higher MCA PI were independently associated with lacunar infarction progression (by 0.1 increase, OR 1.51; 95% CI 1.06-2.15; p = 0.024). Higher pulsatility was associated with progression in lacunar infarction. PI measured by transcranial Doppler sonography might reflect downstream arterial resistance and vascular/paravascular perfusion status and be a possible indicator of stroke progression. • Higher pulsatility index was observed in progression group of lacunar infarction patients. • Higher pulsatility index seemed to be associated with progression in lacunar infarction patients. • Differences in the factors associated with stroke progression suggest different underlying pathophysiologies.