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Coronary Occlusion (coronary + occlusion)
Kinds of Coronary Occlusion Selected AbstractsHYPERBARIC OXYGENATION APPLIED IMMEDIATELY AFTER CORONARY OCCLUSION REDUCES MYOCARDIAL NECROSIS AND ACUTE MORTALITY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2009Leonardo Dos Santos SUMMARY 1Because in ischaemia there is a critical lack of O2, it has been reasoned that increasing O2 delivery to the ischaemic myocardium could serve as adjunctive therapy for acute myocardial infarction (MI). Accordingly, in the present study, the effect of early hyperbaric oxygenation (HBO) on mortality and MI size after coronary occlusion was examined in rats. 2After coronary occlusion, male Wistar rats were randomly assigned to receive either HBO for 1 h in a hyperbaric chamber (100% O2 at 253 kPa; n = 106) or ambient O2 as the control (n = 111). The extent of myocardial necrosis was assessed (triphenyltetrazolium) immediately after treatment in the HBO (n = 50) and control (n = 47) groups. The remaining rats were evaluated 24 h after occlusion to enable calculation of MI size and mortality. 3Immediately after therapy, the size of the MI was significantly greater in the control group compared with that in the HBO group (40 ± 3 vs 27 ± 2% of the left ventricle (LV), respectively; P < 0.001). The 24 h mortality of control rats was higher than that of HBO rats (34 vs 16%, respectively; P = 0.02). Control rats that survived 24 h had a larger MI than did HBO rats that survived 24 h (40 ± 4 vs 29 ± 3% of the LV, respectively; P = 0.005). Furthermore, large necrotic areas (> 40% of the LV) were more frequent in control than HBO rats (55 vs 27% of infarcted hearts, respectively; P = 0.01). There was less pulmonary congestion observed in HBO rats compared with control rats. 4In conclusion, early therapy with HBO during the onset of an acute ischaemic event decreases the necrotic area and reduces acute mortality. These data support further investigation of HBO as an adjuvant therapy for acute MI. [source] Emergency Off-Pump Coronary Artery Bypass (OPCAB) for Left Main Coronary Occlusion Using Rapid Aorto-Coronary PerfusionJOURNAL OF CARDIAC SURGERY, Issue 6 2002Paul Kerr D.O. LAD grafted with sapenous vein and immediate aorto-coronary perfusion. Circumflex grafted and patient taken to ICU. Patient discharged on POD #6 after echo shows normal ventricular with no wall motion abnormality. [source] Successful Pediatric Stenting of a Nonthrombotic Coronary Occlusion as a Complication of Radiofrequency Catheter AblationPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 6 2001GUNNAR G. STROBEL STROBEL, G.G., et al.: Successful Pediatric Stenting of a Nonthrombotic Coronary Occlusion as a Complication of Radiofrequency Catheter Ablation. This is a case of a right coronary artery occlusion complicating a RF catheter ablation of a posteroseptal accessory connection in an 8-year-old boy. After multiple balloon angioplasty attempts in the occluded vessel, only transient patency was achieved. The occlusion was successfully treated with placement of an intracoronary stent. [source] Sequence of Electrocardiographic and Acoustic Cardiographic Changes and Angina during Coronary Occlusion and Reperfusion in Patients Undergoing Percutaneous Coronary InterventionANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009A.N.P., Eunyoung Lee R.N., Ph.D. Background: Previous studies have suggested that ventricular function may be impaired without or prior to electrocardiographic changes or angina during ischemia. Understanding of temporal sequence of electrical and functional ischemic events may improve the detection of myocardial ischemia. Methods: A prospective study was performed in 21 subjects undergoing percutaneous coronary intervention (PCI) who had both ST amplitude changes >2 standard deviations above baseline on 12-lead electrocardiography (ECG), and new or increased third or fourth heart sound (S3 or S4) intensity measured by computerized acoustic cardiography. The sequence of the onset and resolution of these signs of ischemia were examined following coronary balloon inflation and deflation. Results: Electrocardiographic ST amplitude and diastolic heart sound changes occurred contemporaneously, shortly after coronary occlusion (mean onset from balloon inflation; ST changes, 21 ± 17 seconds; S4, 25 ± 26 seconds; S3, 45 ± 43 seconds). In 40% of patients, a new or increased S3 or S4 developed earlier than ST changes. Anginal symptoms occurred in only 2 of the 21 subjects during ischemia with a mean onset time of 68 seconds. ST-segment changes resolved earliest (33 seconds after balloon deflation) while diastolic heart sounds (89 ± 146 seconds) and angina (586 ± 653 seconds) resolved later. Conclusion: A new or intensified S3 and/or S4 occurred contemporaneously with electrocardiographic changes during ischemia. These diastolic heart sounds persisted longer than ST changes following coronary reperfusion. Acoustic cardiographic assessment of diastolic heart sounds may aid in the early detection of myocardial ischemia, particularly in those patients with an uninterpretable ECG. [source] The Challenges of Chronic Total Coronary Occlusions: An Old Problem in a New PerspectiveJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2004DAVID E. KANDZARI M.D. In spite of the remarkable technological innovation and improved outcomes with percutaneous coronary revascularization, chronic coronary artery total occlusions remain a familiar source of procedural frustration and clinical uncertainty. However, considering the recent development of catheter-based technologies specific for chronic total occlusion (CTO) recanalization and the potential for drug-eluting stents to reduce restenosis and reocclusion, this challenging lesion subset is now recognized as the last formidable barrier to percutaneous revascularization success. Further, consistent observations from more recent clinical trials support successful CTO revascularization to avoid subsequent adverse cardiac events and improve long-term overall survival. This review of total coronary occlusions provides an overview of CTO pathophysiology, describes the procedural and clinical outcomes associated with CTO revascularization, and presents future directions for clinical investigation. [source] Immediate and Long-Term Outcome of Recanalization of Chronic Total Coronary OcclusionsJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2002FEDERICO PISCIONE M.D. Eighty-three consecutive patients with 85 coronary total occlusions undergoing coronary angioplasty were retrospectively studied. Patients were divided into two groups according to the occlusion age that was<30 days (subacute total occlusion [STO]: 25 patients; range 1,30 days) or>30 days (chronic total occlusion [CTO]: 58 patients; range 3,144 months). All procedures were carried out using a hydrophilic guidewire. Clinical success, consisting of crossing the lesion, balloon dilatation, stent deployment without complication, was 96% in STO and 81% in CTO. Multiple stepwise logistic regression analysis identified a family history of coronary artery disease (CAD), left anterior descending and right coronary artery occlusions as independent predictors of a successful procedure. No major events occurred during or immediately after the angioplasty. After a mean follow-up of 24 ± 2 months, no difference was found in survival or freedom from myocardial infarction or target vessel revascularization among the STO and CTO patients. Successful recanalization by using a hydrophilic guidewire was achieved in a high percentage of chronic total occlusions with a low incidence of complications and a satisfactory late clinical outcome. Family history of CAD and occlusion of left anterior descending or right coronary arteries are independent predictors of procedural success. [source] Effects of trimetazidine, a partial inhibitor of fatty acid oxidation, on ventricular function and survival after myocardial infarction and reperfusion in the ratFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 4 2010Frederic Mouquet Abstract Trimetazidine (TMZ), a partial inhibitor of fatty acid oxidation, has been effective in treating chronic angina, but its effects on the development of post-myocardial infarction (MI) left ventricular remodeling are not defined. In this study, we tested whether chronic pre-MI administration of TMZ would be beneficial during and after acute MI. Two-hundred male Wistar rats were studied in four groups: sham + TMZ diet (n = 20), sham + control diet (n = 20), MI + TMZ diet (n = 80), and MI + control diet (n = 80) splitted into one short-term and one long-term experiments. Sham surgery consisted of a thoracotomy without coronary ligation. MI was induced by coronary occlusion followed by reperfusion. Left ventricle (LV) function and remodeling were assessed by serial echocardiography throughout a 24-week post-MI period. LV remodeling was also assessed by quantitative histological analysis of post-MI scar formation at 24 weeks post-MI. During the short-term experiment, 10/80 rats died after MI, with no difference between groups (MI + control = 7/40, MI + TMZ = 3/40, P = 0.3). In the long-term experiment, the deaths occurred irregularly over the 24 weeks with no difference between groups (MI + control = 16% mortality, MI + TMZ = 17%, P = 0.8). There was no difference between groups as regard to LV ejection fraction (MI + control = 36 ± 13%, MI + TMZ = 35 ± 13%, P = 0.6). In this experimental model, TMZ had no effects on the post-MI occurrence of LV dysfunction or remodeling. Further investigations are warranted to assess whether the partial inhibition of fatty acid oxidation may limit the ability of the heart to respond to acute severe stress. [source] Acute Effect of Cerivastatin on Cardiac Regional Ischemia in a Rat Model Mimicking Off-Pump Coronary SurgeryJOURNAL OF CARDIAC SURGERY, Issue 6 2005Koki Nakamura M.D. The aims of this study were to investigate the optimal duration of coronary occlusion for making reversible ischemia and to examine whether cerivastatin increases myocardial tolerance against prolonged coronary occlusion. Methods: Study 1,Male Sprague-Dawley rats (350 to 450 g) underwent temporary occlusion of either left anterior descending artery (LAD; for 3, 5, 7.5, 10, 12.5, 15, or 20 min) or circumflex artery (CX; for 5, 10, or 15 min). Study 2,Rats were divided into two groups, control and cerivastatin groups, which had 0.1 mg/kg cerivastatin intravenously after anesthesia. LAD was occluded for 10, 15, or 20 minutes. In the both studies, hearts were stained to determine the area at risk (AR) and infarcted (IF) area 24 hours after reperfusion. Results: In LAD occlusion, IF/AR increased in a time dependent manner: 4.5 ± 3.2%, 9.7 ± 5.2%, 17.2 ± 3.0%, 16.8 ± 2.7%, 23.9 ± 9.5% (p < 0.01 vs. 3 min), 62.4 ± 2.9% (p < 0.0001), and 63.4 ± 2.9% (p < 0.0001) at 3, 5, 7.5, 10, 12.5, 15, and 20 min, respectively. Also in CX, IF/AR increased with time: 14.3 ± 2.3%, 25.9 ± 2.1%, and 40.9 ± 6.2% (p < 0.001 vs. 5 min) at 5, 10, and 15 min, respectively. Cerivastatin significantly reduced IF/AR at 15 minutes (43.7 ± 6.2%) and at 20 minutes (44.6 ± 5.3%) compared to control (62.4 ± 2.9% and 60.6 ± 2.5%, respectively, p < 0.05). Conclusion: Cerivastatin increased myocardial tolerance after prolonged coronary occlusion over 10 minutes, which was considered to be the upper limit for creating a regional reversible ischemia in rats. [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] Relationship of Specific Electrogram Characteristics During Sinus Rhythm and Ventricular Pacing Determined by Adaptive Template Matching to the Location of Functional Reentrant Circuits that Cause Ventricular Tachycardia in the Infarcted Canine HeartJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 4 2000EDWARD J. CIACCIO Ph.D. Localization of Reentrant Circuits. Introduction: It would be advantageous, for ablation therapy, to localize reentrant circuits causing ventricular tachycardia by quantifying electrograms obtained during sinus rhythm (SR) or ventricular pacing (VP). In this study, adaptive template matching (ATM) was used to localize reentrant circuits by measuring dynamic electrogram shape using SR and VP data. Methods and Results: Four days after coronary occlusion, reentrant ventricular tachycardia was induced in the epicardial border zone of canine hearts by programmed electrical stimulation. Activation maps of circuits were constructed using electrograms recorded from a multichannel array to ascertain block line location. Electrogram recordings obtained during SR/AP then were used for ATM analysis. A template electrogram was matched with electrograms on subsequent cycles by weighting amplitude, vertical shift, duration, and phase lag for optimal overlap. Sites of largest cycle-to-cycle variance in the optimal ATM weights were found to be adjacent to block lines bounding the central isthmus during reentry (mean 61.1% during SR; 63.9% during VP). The distance between the mean center of mass of the ten highest ATM variance peaks and the narrowest isthmus width was determined. For all VP data, the center of mass resided in the isthmus region ocurring during reentry. Conclusion: ATM high variance measured from SR/AP data localizes functional block lines forming during reentry. The center of mass of the high variance peaks localizes the narrowest width of the isthmus. Therefore, ATM methodology may guide ablation catheter position without resorting to reentry induction. [source] Metabolic responses in ischemic myocardium after inhalation of carbon monoxideACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2009K. AHLSTRÖM Background: To clarify the mechanisms of carbon monoxide (CO) tissue-protective effects, we studied energy metabolism in an animal model of acute coronary occlusion and pre-treatment with CO. Methods: In anesthetized pigs, a coronary snare and microdialysis probes were placed. CO (carboxyhemoglobin 5%) was inhaled for 200 min in test animals, followed by 40 min of coronary occlusion. Microdialysate was analyzed for lactate and glucose, and myocardial tissue samples were analyzed for adenosine tri-phosphate, adenosine di-phosphate, and adenosine mono-phosphate. Results: Lactate during coronary occlusion was approximately half as high in CO pre-treated animals and glucose levels decreased to a much lesser degree during ischemia. Energy charge was no different between groups. Conclusions: CO in the low-doses tested in this model results in a more favorable energy metabolic condition in that glycolysis is decreased in spite of maintained energy charge. Further work is warranted to clarify the possible mechanistic role of energy metabolism for CO protection. [source] Role of a Streamer-like Coronary Thrombus in the Genesis of Unstable AnginaJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 3 2010YASUMI UCHIDA M.D. Introduction: It is generally believed that the coronary occlusion occurs at the site of plaque disruption in acute coronary syndromes. An exceptional mechanism of coronary occlusion, namely a streamer-like thrombus (SLT) originating in a nonstenotic lesion extended distally to obstruct a just distal nondisrupted stenotic segment, was found by angioscopy in patients with unstable angina (UA). This study was carried out to examine the incidence of this phenomenon and its relationship to the subtypes of UA. Methods: The culprit coronary artery was investigated by angioscopy in successive 48 patients (mean ± SE age, 61.0 ± 2.3 years; 10 females and 38 males) with UA. Results: SLT originating in a nonstenotic lesion extended distally, and obstructed the just distal most stenotic segment (DMSS) by its tail in 11 patients (eight with class III and three with class II according to Braunwald's classification). Recurrent anginal attacks were observed in all. The nonstenotic lesion in which the SLT originated was a disrupted yellow plaque in most cases. The SLT was frequently red and yellow in a mosaic pattern, indicating a mixture of fresh thrombus and plaque debris. The plaques that constructed the DMSS were not disrupted. Angiographically, the SLT was not detectable and the entry of the DMSS showed a "tapering" configuration. Conclusions: Obstruction of the DMSS by the tail of SLT originating in a nonstenotic lesion is another mechanism of UA. Therefore, treatment of both the nonstenotic lesion and DMSS is needed to prevent recurrent thrombus formation and consequent reattacks. (J Interven Cardiol 2010;23:216,222) [source] Fluid therapy in acute myocardial infarction: evaluation of predictors of volume responsivenessACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 1 2009J. SNYGG Background: Static vascular filling pressures suffer from poor predictive power in identifying the volume-responsive heart. The use of dynamic arterial pressure variables, including pulse pressure variation (PPV) has instead been suggested to guide volume therapy. The aim of the present study was to evaluate the performance of several clinically applicable haemodynamic parameters to predict volume responsiveness in a pig closed chest model of acute left ventricular myocardial infarction. Methods: Fifteen anaesthetized, mechanically ventilated pigs were studied following acute left myocardial infarction by temporary coronary occlusion. Animals were instrumented to monitor central venous (CVP) and pulmonary artery occlusion (PAOP) pressures and arterial systolic variations (SPV) and PPV. Cardiac output (CO) was measured using the pulmonary artery catheter and by using the PiCCO® monitor also giving stroke volume variation (SVV). Variations in the velocity time integral by pulsed-wave Doppler echocardiography were determined in the left (,VTILV) and right (,VTIRV) ventricular outflow tracts. Consecutive boluses of 4 ml/kg hydroxyethyl starch were administered and volume responsiveness was defined as a 10% increase in CO. Results: Receiver,operator characteristics (ROC) demonstrated the largest area under the curve for ,VTIRV [0.81 (0.70,0.93)] followed by PPV [0.76 (0.64,0.88)] [mean (and 95% CI)]. SPV, ,VTILV and SVV did not change significantly during volume loading. CVP and PAOP increased but did not demonstrate significant ROC. Conclusion: PPV may be used to predict the response to volume administration in the setting of acute left ventricular myocardial infarction. [source] Feasibility of complementary spatial modulation of magnetization tagging in the rat heart after manganese injectionNMR IN BIOMEDICINE, Issue 1 2008J.-N. Hyacinthe Abstract It has been shown that manganese-enhanced MRI (MEMRI) can safely depict the myocardial area at risk in models of coronary occlusion,reperfusion for at least 2,h after reperfusion. To achieve this, a solution of MnCl2 is injected during coronary occlusion. In this model, the regional function quantification deficit of the stunning phase cannot be assessed before contrast injection using MR tagging. The relaxation effects of manganese (which remains in normal cardiac myocytes for several hours) may alter the tags by increasing tag fading and hence the quality of strain measurement. Therefore, we evaluated the feasibility of cardiac MR tagging after manganese injection in normal rats. Six normal Sprague,Dawley rats were imaged in vivo using complementary spatial modulation of magnetization (C-SPAMM) at 1.5,T, before and 15,min after intraperitoneal injection of MnCl2 solution (,17.5,µmol,kg,1). The contrast-to-noise ratio of the tag pattern increased significantly (P,<,0.001) after injection and remained comparable to the control scan in spite of the higher myocardial relaxation rate caused by the presence of manganese. The measurements of circumferential strain obtained from harmonic phase imaging analysis of the tagged images after MnCl2 injection did not differ significantly from the measurements before injection in the endocardial, mid-wall, and epicardial regions. In particular, the transmural strain gradient was preserved. Thus, our study suggests that MR tagging could be used in combination with MEMRI to study the acute phase of coronary artery disease. Copyright © 2007 John Wiley & Sons, Ltd. [source] Temporal Changes in the Endocardial ST Segment During the Evolution of Myocardial Infarction in DogsPACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 11 2002JONATHAN LESSICK LESSICK, J., et al.: Temporal Changes in the Endocardial ST Segment During the Evolution of Myocardial Infarction in Dogs. Acute coronary occlusion causes ST-segment elevation on the body surface ECG and on the epicardial electrogram in the territory supplied by that artery. The occurrence and significance of endocardial ST changes have not been studied. The NOGA electromechanical mapping was performed on eight anesthetized dogs at baseline, immediately after occlusion of the LAD, and again at 5 hours to assess regional changes in the ST segment. At 3 days and 4 weeks the ventricles were remapped for comparison. Regional unipolar ST-segment elevation was measured for each zone from NOGA maps at 0, 80, and 120 ms after the J point. ST segments rose immediately in the infarct zones, as demarcated by echocardiography, compared to remote zones, but by 3 days had dropped below, and at 4 weeks returned to baseline values. Immediately postocclusion, ST elevation at 120 ms best differentiated between normal versus abnormal echo scores (concordance = 0.80), probably by correcting for pressure induced ST elevation. In conclusion, acute endocardial ST-segment changes occur in the infarct zone in the dog, showing a distinctive temporal evolution. [source] Effect of intracellular lipid droplets on cytosolic Ca2+ and cell death during ischaemia,reperfusion injury in cardiomyocytesTHE JOURNAL OF PHYSIOLOGY, Issue 6 2009Ignasi Barba Lipid droplets (LD) consist of accumulations of triacylglycerols and have been proposed to be markers of ischaemic but viable tissue. Previous studies have described the presence of LD in myocardium surviving an acute coronary occlusion. We investigated whether LD may be protective against cell death secondary to ischaemia,reperfusion injury. The addition of oleate,bovine serum albumin complex to freshly isolated adult rat cardiomyocytes or to HL-1 cells resulted in the accumulation of intracellular LD detectable by fluorescence microscopy, flow cytometry and 1H-nuclear magnetic resonance spectroscopy. Simulated ischaemia,reperfusion of HL-1 cells (respiratory inhibition at pH 6.4 followed by 30 min of reperfusion) resulted in significant cell death (29.7 ± 2.6% of total lactate dehydrogenase release). However, cell death was significantly attenuated in cells containing LD (40% reduction in LDH release compared with control cells, P= 0.02). The magnitude of LD accumulation was inversely correlated (r2= 0.68, P= 0.0003) with cell death. The protection associated with intracellular LD was not a direct effect of the fatty acids used to induce their formation, because oleate added 30 min before ischaemia, during ischaemia or during reperfusion did not form LD and did not protect against cell death. Increasing the concentration of free oleate during reperfusion progressively decreased the protection afforded by LD. HL-1 cells labelled with fluo-4, a Ca2+ -sensitive fluorochrome, fluorescence within LD areas increased more throughout simulated ischaemia and reperfusion than in the cytosolic LD-free areas of the same cells. As a consequence, cells with LD showed less cytosolic Ca2+ overload than control cells. These results suggest that LD exert a protective effect during ischaemia,reperfusion by sequestering free fatty acids and Ca2+. [source] Sequence of Electrocardiographic and Acoustic Cardiographic Changes and Angina during Coronary Occlusion and Reperfusion in Patients Undergoing Percutaneous Coronary InterventionANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 2 2009A.N.P., Eunyoung Lee R.N., Ph.D. Background: Previous studies have suggested that ventricular function may be impaired without or prior to electrocardiographic changes or angina during ischemia. Understanding of temporal sequence of electrical and functional ischemic events may improve the detection of myocardial ischemia. Methods: A prospective study was performed in 21 subjects undergoing percutaneous coronary intervention (PCI) who had both ST amplitude changes >2 standard deviations above baseline on 12-lead electrocardiography (ECG), and new or increased third or fourth heart sound (S3 or S4) intensity measured by computerized acoustic cardiography. The sequence of the onset and resolution of these signs of ischemia were examined following coronary balloon inflation and deflation. Results: Electrocardiographic ST amplitude and diastolic heart sound changes occurred contemporaneously, shortly after coronary occlusion (mean onset from balloon inflation; ST changes, 21 ± 17 seconds; S4, 25 ± 26 seconds; S3, 45 ± 43 seconds). In 40% of patients, a new or increased S3 or S4 developed earlier than ST changes. Anginal symptoms occurred in only 2 of the 21 subjects during ischemia with a mean onset time of 68 seconds. ST-segment changes resolved earliest (33 seconds after balloon deflation) while diastolic heart sounds (89 ± 146 seconds) and angina (586 ± 653 seconds) resolved later. Conclusion: A new or intensified S3 and/or S4 occurred contemporaneously with electrocardiographic changes during ischemia. These diastolic heart sounds persisted longer than ST changes following coronary reperfusion. Acoustic cardiographic assessment of diastolic heart sounds may aid in the early detection of myocardial ischemia, particularly in those patients with an uninterpretable ECG. [source] Effects of Primary Percutaneous Coronary Intervention on P Wave DispersionANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 3 2005Turgay Celik M.D. Background: Several studies demonstrated that P wave dispersion (PWD) increased after coronary occlusion. The effect of primary percutaneous coronary intervention (PCI) on PWD needs to be elucidated. Methods: The study consisted of 125 patients with acute myocardial infarction (110 men, mean age 59.8 ± 7.8 years) undergoing primary PCI. The patients were divided into three groups according to thrombolysis in myocardial infarction myocardial perfusion grade (TMPG) after successful PCI. Groups 1 (n = 12), 2 (n = 9), and 3 (n = 104) included the patients with TMPG 0/1, 2, 3, respectively. Electrocardiograms were obtained before and approximately 66 ± 18 minutes after PCI. Results: PWD and Pmaximum after PCI were significantly lower than the preintervention values (P < 0.001 for both). When PWD and Pmaximum values after PCI were compared among groups, PWD and Pmaximum in groups 1 and 2 were found to be higher than those of group 3 (P < 0.001 for PWD and Pmaximum). Atrial fibrillation (AF) occurred in 14 patients. Pmaximum and PWD in patients with AF were higher compared to those of the patients without AF (P < 0.001 for both P wave parameters). Also more frequent AF attacks were observed in group 1 compared to group 3 (P < 0.001). Conclusions: PWD and Pmaximum after primary PCI were lower compared to the preintervention values. Prolonged PWD in patients with poor myocardial perfusion can contribute to increased mortality, and also it can can be combined with ST segment resolution to predict clinical reperfusion and might help in predicting AF. [source] Cardioprotection: spotlight on PKGBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2007M V Cohen Classical ischaemic preconditioning, delayed or second window preconditioning and postconditioning are forms of cardioprotection that are dependent on cell surface receptors, intracellular signalling molecules and kinases that ultimately block formation of the mitochondrial permeability transition. The latter is presumed to cause myocardial necrosis as well as apoptosis, so prevention of its formation upon resumption of perfusion after a prolonged coronary occlusion should be cardioprotective. In all of these forms of cardioprotection, formation of cGMP and activation of protein kinase G (PKG) are recognized to be key steps in the signal transduction pathway. Burley et al. highlight the roles of cGMP and PKG in their comprehensive review. They describe the basic biology of PKG and emphasize its compartmentalization, which may be responsible for the frustration induced by assays for PKG in whole cell lysates and for the spurious conclusions about the role of PKG in cardioprotection. This review will be useful to both the novice and the seasoned investigator. British Journal of Pharmacology (2007) 152, 833,834; doi:10.1038/sj.bjp.0707453; published online 17 September 2007 [source] Anti-apoptotic effect of benidipine, a long-lasting vasodilating calcium antagonist, in ischaemic/reperfused myocardial cellsBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Feng Gao Ischaemia/reperfusion causes intracellular calcium overloading in cardiac cells. Administration of calcium antagonists reduces myocardial infarct size. Recent in vitro studies have demonstrated that calcium plays a critical role in the signal transduction pathway leading to apoptosis. However, whether or not calcium antagonists may reduce myocardial apoptosis induced by ischaemia-reperfusion, and thus decrease myocardial infarction, has not been directly investigated. The present study investigated the effects of benidipine, an L-type calcium channel blocker, on myocardial infarct size, apoptosis, necrosis and cardiac functional recovery in rabbits subjected to myocardial ischaemia/reperfusion (MI/R, 45 min/240 min). Ten minutes prior to coronary occlusion, rabbits were treated with vehicle or benidipine (10 ,g kg,1 or 3 ,g kg,1, i.v.). In the vehicle-treated group, MI/R caused cardiomyocyte apoptosis as evidenced by DNA ladder formation and TUNEL positive nuclear staining (12.2±1.1%). Treatment with 10 ,g kg,1 benidipine lowered blood pressure, decreased myocardial apoptosis (6.2±0.8%, P<0.01 vs vehicle) and necrosis, reduced infarct size (20±2.3% vs 49±2.6%, P<0.01), and improved cardiac functional recovery after reperfusion. Administering benidipine at 3 ,g kg,1, a dose at which no haemodynamic effect was observed, also exerted significant anti-apoptosis effects, which were not significantly different from those observed with higher dose benidipine treatment. However, treatment with this low dose benidipine failed to reduce myocardial necrosis. These results demonstrate that benidipine, a calcium antagonist, exerts significant anti-apoptosis effects, which are independent of haemodynamic changes. Administration of benidipine at a higher dose produced favourable haemodynamic effects and provided additional protection against myocardial necrotic injury and further improved cardiac functional recovery. British Journal of Pharmacology (2001) 132, 869,878; doi:10.1038/sj.bjp.0703881 [source] HYPERBARIC OXYGENATION APPLIED IMMEDIATELY AFTER CORONARY OCCLUSION REDUCES MYOCARDIAL NECROSIS AND ACUTE MORTALITY IN RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 5-6 2009Leonardo Dos Santos SUMMARY 1Because in ischaemia there is a critical lack of O2, it has been reasoned that increasing O2 delivery to the ischaemic myocardium could serve as adjunctive therapy for acute myocardial infarction (MI). Accordingly, in the present study, the effect of early hyperbaric oxygenation (HBO) on mortality and MI size after coronary occlusion was examined in rats. 2After coronary occlusion, male Wistar rats were randomly assigned to receive either HBO for 1 h in a hyperbaric chamber (100% O2 at 253 kPa; n = 106) or ambient O2 as the control (n = 111). The extent of myocardial necrosis was assessed (triphenyltetrazolium) immediately after treatment in the HBO (n = 50) and control (n = 47) groups. The remaining rats were evaluated 24 h after occlusion to enable calculation of MI size and mortality. 3Immediately after therapy, the size of the MI was significantly greater in the control group compared with that in the HBO group (40 ± 3 vs 27 ± 2% of the left ventricle (LV), respectively; P < 0.001). The 24 h mortality of control rats was higher than that of HBO rats (34 vs 16%, respectively; P = 0.02). Control rats that survived 24 h had a larger MI than did HBO rats that survived 24 h (40 ± 4 vs 29 ± 3% of the LV, respectively; P = 0.005). Furthermore, large necrotic areas (> 40% of the LV) were more frequent in control than HBO rats (55 vs 27% of infarcted hearts, respectively; P = 0.01). There was less pulmonary congestion observed in HBO rats compared with control rats. 4In conclusion, early therapy with HBO during the onset of an acute ischaemic event decreases the necrotic area and reduces acute mortality. These data support further investigation of HBO as an adjuvant therapy for acute MI. [source] The Challenges of Chronic Total Coronary Occlusions: An Old Problem in a New PerspectiveJOURNAL OF INTERVENTIONAL CARDIOLOGY, Issue 4 2004DAVID E. KANDZARI M.D. In spite of the remarkable technological innovation and improved outcomes with percutaneous coronary revascularization, chronic coronary artery total occlusions remain a familiar source of procedural frustration and clinical uncertainty. However, considering the recent development of catheter-based technologies specific for chronic total occlusion (CTO) recanalization and the potential for drug-eluting stents to reduce restenosis and reocclusion, this challenging lesion subset is now recognized as the last formidable barrier to percutaneous revascularization success. Further, consistent observations from more recent clinical trials support successful CTO revascularization to avoid subsequent adverse cardiac events and improve long-term overall survival. This review of total coronary occlusions provides an overview of CTO pathophysiology, describes the procedural and clinical outcomes associated with CTO revascularization, and presents future directions for clinical investigation. [source] High-frequency vibration for the recanalization of guidewire refractory chronic total coronary occlusions,CATHETERIZATION AND CARDIOVASCULAR INTERVENTIONS, Issue 6 2008Klaus Tiroch MD Abstract Background: Recanalization of coronary chronic total occlusions (CTOs) remains a clinical challenge, particularly when standard guidewire attempts fail. Objectives: We sought to determine the safety and efficacy of a novel method that used high-frequency (20 kHz) vibration to fragment occlusive fibrous tissue and facilitate guidewire crossing into the distal vessel. Methods: A total of 125 patients with CTO, who failed at attempts of conventional guidewire recanalization after more than 5 min of fluoroscopy time, were enrolled in the study. The primary efficacy endpoint was the advancement of the CROSSERÔ catheter through the occlusion and attainment of coronary guidewire positioning in the distal coronary lumen. The primary safety endpoint was the occurrence of death, myocardial infarction, clinical perforation, or target vessel revascularization within the first 30 days. Results: The average fluoroscopy time while delivering the CROSSER catheter was 12.4 min. CROSSER-assisted guidewire recanalization was achieved in 76 (60.8%) procedures and a final diameter stenosis <50% was obtained in 68 (54.4%) of cases. Major adverse events occurred in 11 (8.8%) patients, lower than the predefined objective performance criteria. Angina frequency and quality of life were improved in patients with successful guidewire recanalization. Conclusions: We conclude that high-frequency vibration using the CROSSER catheter is a safe and effective therapy for patients with CTO, which are refractory to standard guidewire recanalization. © 2008 Wiley-Liss, Inc. [source] | ||||||||||||||||||||||