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Acute Ischemia (acute + ischemia)
Selected AbstractsOccurrence of "J Waves" in 12-Lead ECG as a Marker of Acute Ischemia and Their Cellular BasisPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2007SHINDE RITUPARNA M.D. The "J wave" (also referred to as "the Osborn wave,""the J deflection," or "the camel's hump") is a distinctive deflection occurring at the QRS-ST junction. In 1953, Dr. John Osborn described the "J wave" as an "injury current" resulting in ventricular fibrillation during experimental hypothermia. Although "J Wave" is supposed to be pathognomonic of hypothermia, it is seen in a host of other conditions such as hypercalcemia, brain injury, subarachnoid hemorrhage, cardiopulmonary arrest from over sedation, the Brugada syndrome, vasospastic angina, and idiopathic ventricular fibrillation. However, there is paucity of literature data as regards to ischemic etiology of "J Wave." In this article, we present a case where "J waves" were probably induced by ischemia. We also discuss the mechanism of ischemia-induced "J wave" accentuation and its prognostic implications. [source] Continuous Coronary Sinus Perfusion Reverses Ongoing Myocardial Damage in Acute IschemiaARTIFICIAL ORGANS, Issue 10 2009Francesco Onorati Abstract Acute cardiogenic shock or cardiac arrest (CS/CA) before cardiopulmonary bypass (CPB) installation are life-threatening events in acute coronary syndromes. We evaluated whether continuous retrograde warm-blood perfusion (CRWBP) before aortic cross-clamping (ACC), with immediate CPB installation may improve hospital results in these dreadful events. Hospital outcome of 18 coronary artery bypass grafting (CABG) (Group A) with CS/CA before CPB, with immediate CPB installation and CRWBP, has been compared with 24 CABG (Group B) with CS/CA undergoing only immediate CPB installation. No differences have been detected in the mean time to establish CPB (P = 0.655). Electrocardiography normalized in a significantly higher number of CRWBP (P = 0.0001). Group B showed longer CPB (116.2 ± 21.2 min vs. 157.8 ± 32.4; P = 0.0001) and postoperative intra-aortic balloon pumping time course (36.2 ± 5.9 h vs. 77.8 ± 13.2; P = 0.0001). CRWBP reduced postoperative acute myocardial infarction (P = 0.004) and damage (P = 0.033), death (P = 0.026), and need for high inotropic support (0% vs. 37.5%; P = 0.003). Troponin I was significantly lower in Group A (P = 0.013 from coronary sinus; P , 0.0001 at 12, 24, and 48 h postoperatively; P = 0.008 at 72 h), never reaching values suggestive of acute myocardial infarction. Group A had also lower lactate release from aortic declamping to 48 h postoperatively (P , 0.0001). CRWBP improved postoperative left ventricular ejection fraction (EF) (P = 0.017) and wall motion score index (P = 0.041), whereas Group B showed a significant worsening of EF (P = 0.0001) and wall motion score index (P = 0.002). Patients in Group A had shorter intubation time (P = 0.0001), intensive therapy unit (ITU) stay (P = 0.001), and hospital stay (P = 0.0001). CRWBP reverses myocardial damage in patients with CS/CA during acute coronary syndromes, adding a straightforward benefit to hospital survival. [source] 2112: AO imaging of acute macular diseasesACTA OPHTHALMOLOGICA, Issue 2010M PAQUES Purpose To show clinical cases of acute macular diseases and their follow-up by adaptive optics flood imaging. Methods Cases of acute retinal ischemia, of acute macular neuroretinopathy, of photic injury and of poppers-related retinopathy have been observed by a prototypic adaptive optics flood imaging (ImagineEye corporation). Images from follow-up examinations have been registered in order to obtain retinal monitoring at the single photoreceptor level. Iamges were compared to high resolution OCT scans. Results Precise extension and progression/regression of lesions could be documented in all cases. Acute macular neuroretinopathy showed residual cones persisting within an area devoid of any detectable cone. Minute progression and regression of lesions could be documented. Acute ischemia of the inner retina due to central retinal vein occlusion resulted in focal masking of the cone mosaic. The cone mosaic reappeared during follow-up. Photic injury showed no changes over a 1 year follow-up. Images of poppers-related retinopathy showed partial improvement over time. Conclusion Adaptive optics flood imaging allows documentation of the extension and progression of acute maculopathies of various origins. [source] Heterogeneous Regional Endocardial Repolarization is Associated with Increased Risk for Ischemia-Dependent Ventricular Fibrillation after Myocardial InfarctionJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 8 2003Michael H. Swann M.SC. Introduction: The aim of this study was to investigate whether the characteristics of endocardial ventricular repolarization are associated with differential risk for sudden death. Prolonged surface QT interval is associated with increased arrhythmic risk after myocardial infarction (MI), but the underlying mechanism of QT prolongation and its relation to lethal arrhythmias are unclear. Methods and Results: Ventricular fibrillation (VF) risk was assessed in 12 dogs 1 month after anterior MI during an exercise test coupled with brief circumflex coronary occlusion. Susceptible dogs (n = 5) developed VF during the brief ischemic episode, whereas resistant dogs did not (n = 7). Surface QT interval was measured at rest. Endocardial electroanatomic catheter maps of left ventricular repolarization were obtained in four unique regions identified by echocardiography and compared between groups. Compared to resistant dogs, susceptible dogs were characterized by prolonged surface QT intervals (240 ± 10 msec vs 222 ± 7 msec, P = 0.04). In addition, they had lower baroreflex sensitivity (9.7 ± 1.5 msec/mmHg vs 28 ± 9.8 msec/mmHg, P < 0.01) and a tachycardic response to acute ischemia suggesting higher propensity for stronger sympathetic reflexes. Surface QT interval prolongation in susceptible dogs was due to a marked heterogeneity of endocardial left ventricular repolarization (239 ± 42 msec, basal anterior wall vs 197 ± 35, lateral wall; P < 0.001). Resistant animals had no regional differences in endocardial repolarization. Conclusion: Sympathetic activation following MI not only produces adverse structural remodeling but also contributes to adverse electrophysiologic remodeling resulting in heterogeneous ventricular repolarization and in a myocardial substrate conducive to lethal reentrant arrhythmias. (J Cardiovasc Electrophysiol, Vol. 14, pp. 873-879, August 2003) [source] Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary DiseasePACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 1p2 2003DALIA GIEDRIMIENE GIEDRIMIENE, D., et al.: Effects of Ischemia on Repolarization in Patients with Single and Multivessel Coronary Disease. To evaluate if QT dispersion (QTd) may be affected by the number of obstructed coronary arteries (CAs) in patients with acute myocardial infarction (MI) and undergoing angioplasty, and to evaluate if QTd may be affected by ejection function of the heart. The infarct related CA was identified by coronary angiography in 141 patients (97 men, mean age61.6 ± 12.9years) with acute MI undergoing percutaneous angioplasty. Successful reperfusion was defined as TIMI III flow with <20% residual stenosis. QTd, calculated by subtracting the shortest from the longest QT interval on 12-lead electrocardiograms, was examined immediately before and after angioplasty, at 24 hours, and 3 days after angioplasty. Successful reperfusion was achieved in 98 (69.5%) patients. Prolonged QTd at baseline was found in all patients with ischemia. A trend toward a decrease in QTd was observed immediately after angioplasty and at 24 hours, and a significant decrease at 3 days in patients with successful reperfusion regardless of the number of occluded CAs. There was no change in QTd found in patients with no reperfusion. An increase in QTd was observed in patients with acute ischemia due to single or multivessel disease. (PACE 2003; 26[Pt. II]:390,393) [source] Effect of Underlying Heart Disease on the Frequency Content of Ventricular Fibrillation in the Dog HeartPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 2 2000JASON T. JACOBSON Although prior studies have examined the frequency content of heal electro-gram characteristics during fibrillation, little is know about the effects of underlying heart disease on these parameters. This study was designed to compare the frequency content of local electrograms during VF in canine models of acute ischemia, subacute infarction, and chronic myocardial infarction (MI) to those in control animals to test the hypothesis that underlying heart disease can alter the basic characteristics of VF. VF was induced using burst pacing in three groups of mongrel dogs. Five dogs were evaluated 8 weeks after LAD occlusion MI, five were evaluated 5 days after experimental MI, and 5 had VF induced before (control) and immediately after LAD occlusion (ischemia). During VF, unipolar electrograms were recorded from 112 sites on the anterior LV and electrograms were evaluated 15 and 30 seconds after VF initiation in each group. Electrograms were analyzed by fast Fourier transform. No significant time dependent changes in VF characteristics were noted. The peak frequency was highest in control animals and 8-week MI, intermediate in 5-day MI, and lowest in acute ischemia (P < 0.01 for pairwise comparisons). In contrast, the fractional of energy within a bandwidth of 25% peak amplitude was highest in acute ischemia, (P < 0.001) and similar in the other three groups. Infarction decreased total energy by approximately 50%. In conclusion, the pressure of ischemia or infarction alters the frequency content of VF in a complex fashion. In addition to decreasing the peak frequency, the shape of the power spectral curve is altered in models of structural heart disease. These results suggest that the electrophysiological changes produced by infarction or ischemia alter the structural organization of ventricular fibrillation. [source] Influence of Genetic Variation in the C-Reactive Protein Gene on the Inflammatory Response During and After Acute Coronary IschemiaANNALS OF HUMAN GENETICS, Issue 6 2006J. Suk Danik Summary The aim of this research was to assess whether common genetic variants within the C-reactive protein gene (CRP) are related to the degree of acute rise in plasma C-reactive protein (CRP) levels following an acute coronary syndrome (ACS). While polymorphisms within CRP are associated with basal CRP levels in healthy men and women, less is known about the relationship of such genetic variants and the degree of CRP rise during and after acute ischemia. Plasma CRP is associated with increased rates of recurrent coronary events. We evaluated seven common genetic variants within CRP and assessed their relationship to the degree of rise in CRP levels immediately following an acute coronary syndrome in 1827 European American patients. Variants in the putative promoter region, ,757T > C and ,286C > T > A, were associated with the highest CRP elevations after ACS. Patients with two copies of the A allele of SNP ,286C > T > A had median CRP values of 76.6 mg/L, compared to 11.1 mg/L in patients with no copies of the rare variant (p-value <0.0001), post ACS. The lowest CRP values were found for patients with minor alleles of the exonic 1059G > C and the 3,untranslated region 1846G > A SNPs. For example, patients homozygous for the minor allele of 1059G > C had 71% lower median CRP values than those homozygous for the major allele [3.5 vs 12.0 mg/L, p < 0.0001]. These trends persisted in the chronic stable phase after ischemia had resolved, and after adjustment for infarct size by peak creatinine kinase levels and clinical status by Killip class. Assessment of CRP genetic variants identified patients with higher and lower CRP elevation after acute coronary syndrome. [source] Hemodynamic Changes in a Model of Chronic Heart Failure Induced by Multiple Sequential Coronary Microembolization in SheepARTIFICIAL ORGANS, Issue 11 2009Jan Dieter Schmitto Abstract Although a large variety of animal models for acute ischemia and acute heart failure exist, valuable models for studies on the effect of ventricular assist devices in chronic heart failure are scarce. We established a stable and reproducible animal model of chronic heart failure in sheep and aimed to investigate the hemodynamic changes of this animal model of chronic heart failure in sheep. In five sheep (n = 5, 77 ± 2 kg), chronic heart failure was induced under flouroscopic guidance by multiple sequential microembolization through bolus injection of polysterol microspheres (90 µm, n = 25.000) into the left main coronary artery. Coronary microembolization (CME) was repeated up to three times in 2 to 3-week intervals until animals started to develop stable signs of heart failure. During each operation, hemodynamic monitoring was performed through implantation of central venous catheter (central venous pressure [CVP]), arterial pressure line (mean arterial pressure [MAP]), implantation of a right heart catheter {Swan-Ganz catheter (mean pulmonary arterial pressure [PAPmean])}, pulmonary capillary wedge pressure (PCWP), and cardiac output [CO]) as well as pre- and postoperative clinical investigations. All animals were followed for 3 months after first microembolization and then sacrificed for histological examination. All animals developed clinical signs of heart failure as indicated by increased heart rate (HR) at rest (68 ± 4 bpm [base] to 93 ± 5 bpm [3 mo][P < 0.05]), increased respiratory rate (RR) at rest (28 ± 5 [base] to 38 ± 7 [3 mo][P < 0.05]), and increased body weight 77 ± 2 kg to 81 ± 2 kg (P < 0.05) due to pleural effusion, peripheral edema, and ascites. Hemodynamic signs of heart failure were revealed as indicated by increase of HR, RR, CVP, PAP, and PCWP as well as a decrease of CO, stroke volume, and MAP 3 months after the first CME. Multiple sequential intracoronary microembolization can effectively induce myocardial dysfunction with clinical and hemodynamic signs of chronic ischemic cardiomyopathy. The present model may be suitable in experimental work on heart failure and left ventricular assist devices, for example, for studying the impact of mechanical unloading, mechanisms of recovery, and reverse remodeling. [source] Selective Neuronal Vulnerability Following Mild Focal Brain Ischemia in the MouseBRAIN PATHOLOGY, Issue 4 2003Juri Katchanov The evolution of cellular damage over time and the selective vulnerability of different neuronal subtypes was characterized in the striatum following 30-minute middle cerebral artery occlusion and reperfusion in the mouse. Using autoradiography we found an increase in the density of [3H]PK11195 binding sites,likely reflecting microglial activation,in the lesion border at 3 days and in the whole striatum from 10 days to 6 weeks. This was accompanied by a distinct loss of [3H]flumazenil and [3H]CGP39653 binding sites from 10 days up to 6 weeks reflecting neuronal loss. Brain ischemia resulted in a substantial loss of medium spiny projection neurons as seen at three days by Nissl staining, TUNEL and immunocytochemistry using antibodies against microtubule-associated protein (MAP2), NeuN, (,-opioid receptors, substance P, Lenkephalin, neurokinin B, choline acetyltransferase, parvalbumin, calretinin and somatostatin. Both patch and matrix compartments were involved in ischemic damage. In contrast, the numbers of cholinergic, GABAergic, and somatostatin-containing interneurons in the ischemic striatum were not different from those in the contralateral hemisphere at 3 and 14 days. A low density of glutamate receptors, the ability to sequester calcium by calcium-binding proteins and other hitherto unidentified factors may explain this relative resistance of interneurons to acute ischemia. [source] Nationwide study of the outcome of popliteal artery aneurysms treated surgicallyBRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 8 2007H. Ravn Background: The aim was to study the epidemiology and outcomes of popliteal artery aneurysm (PA) treated surgically. Methods: Among 110 000 procedures registered prospectively in the Swedish Vascular Registry (Swedvasc), there were 717 primary operations for PA among 571 patients. Patient records were reviewed and data validated against other registries. Results: The median age of the patients was 71 years; 5·8 per cent were women. Among 264 legs treated urgently, 235 had acute ischemia and 24 had rupture. Of patients with unilateral PA, 28·1 per cent had an aortic aneurysm, 8·4 per cent an iliac aneurysm and 9·4 per cent a femoral aneurysm. Extra-popliteal aneurysms were more common when the PAs were bilateral (P = 0·004). The rate of limb loss within 1 year of operation was 8·8 per cent; 12·0 per cent for symptomatic and 1·8 per cent for asymptomatic limbs (P < 0·001). Risk factors for amputation were symptomatic disease, poor run-off, urgent treatment, age over 70 years, prosthetic graft and no preoperative thrombolysis when the ischaemia was acute. Amputation rates decreased over time (P = 0·003). Crude survival was 91·4 per cent at 1 year and 70·0 per cent at 5 years. Conclusion: Multiple aneurysm disease was common when PAs were bilateral. Preoperative thrombolysis of acute thrombosis and the use of vein grafts for bypass improved outcome. Copyright © 2007 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source] Postsystolic thickening detected by doppler myocardial imaging: A marker of viability or ischemia in patients with myocardial infarctionCLINICAL CARDIOLOGY, Issue 1 2004Jae-Kwan Song M.D. Abstract Background: Postsystolic thickening (PST) of ischemic myocardial segments has been reported to account for the characteristic heterogeneity or regional asynchrony of myocardial wall motion during acute ischemia. Hypothesis: Postsystolic thickening detected by Doppler myocardial imaging (DMI) could be a useful clinical index of myocardial viability or peri-infarction viability in patients with myocardial infarction (MI). Methods: Doppler myocardial imaging was recorded at each stage of a standard dobutamine stress echocardiogram (DSE) in 20 patients (16 male, 60 ± 13 years) with an MI in the territory of the left anterior descending artery. Myocardial velocity data were measured in the interventricular septum and apical inferior segment of the MI territory. Postsystolic thickening was identified if the absolute velocity of PST was higher than peak systolic velocity in the presence of either a resting PST > 2.0 cm/s or if PST doubled at low-dose dobutamine infusion. Results: Doppler myocardial imaging data could be analyzed in 38 ischemic segments (95%), and PST was observed in 21 segments (55%), including 3 segments showing PST only at low-dose dobutamine infusion. There was no significant difference of baseline wall motion score index (2.1 ± 0.3 vs. 2.1 ± 0.6, p = 0.77) orpeak systolic velocity (1.1 ± 1.1 vs. 1.9 ± 2.0 cm/s, p = 0.05) between segments with and without PST. Peri-infarction ischemia or viability during DSE was more frequently observed in segments with PST than in those without (86 vs. 24%, p < 0.05). The sensitivity and specificity of P ST for prediction of peri-infarction viability or ischemia was 82 and 81%, respectively. Conclusions: Postsystolic thickening in the infarct territory detected by DMI is closely related with peri-infarction ischemia or viability at DSE. [source] Computed Tomography Coronary Angiography for Rapid Disposition of Low-risk Emergency Department Patients with Chest Pain SyndromesACADEMIC EMERGENCY MEDICINE, Issue 2 2007Judd E. Hollander MD Background Patients with recent normal cardiac catheterization are at low risk for complications of ischemic chest pain. Computed tomography (CT) coronary angiography has high correlation with cardiac catheterization for detection of coronary stenosis. Therefore, the investigators' emergency department (ED) incorporated CT coronary angiography into the evaluation of low-risk patients with chest pain. Objectives To report on the 30-day cardiovascular event rates of the first 54 patients evaluated by this strategy. Methods Low-risk chest pain patients (Thrombolysis In Myocardial Infarction [TIMI] score of 2 or less) without acute ischemia on an electrocardiogram had CT coronary angiography performed in the ED. If the CT coronary angiography was negative, the patient was discharged home. The main outcomes were death and myocardial infarction within 30 days of ED discharge, as determined by telephone follow up and record review. Data are presented as percentage frequency of occurrence with 95% confidence intervals (CIs). Results Of the 54 patients evaluated, after CT coronary angiography, 46 patients (85%) were immediately released from the ED, and none had cardiovascular complications within 30 days. Eight patients were admitted after CT coronary angiography: one had >70% stenosis, five patients had 50%,69% stenosis, and two had 0,49% stenosis. Three patients had further noninvasive testing; one had reversible ischemia, and catheterization confirmed the results of CT coronary angiography. All patients were followed for 30 days, and none (0; 95% CI = 0 to 6.6%) had an adverse event during index hospitalization or at 30-day follow up. Conclusions When used in the clinical setting for the evaluation of ED patients with low-risk chest pain, CT coronary angiography may safely allow rapid discharge of patients with negative studies. Further study to conclusively determine the safety and cost effectiveness of this approach is warranted. [source] | ||||||||||