Sudden Coronary Artery Occlusion Research Articles

Advancements in Interventional Techniques of Percutaneous Transluminal Coronary Angioplasty (PTCA) in Acute Myocardial Infraction

Andreas Gruentzig is the father of interventional cardiology performed the first PTCA procedure in Zurich, Switzerland (1977). Later, the developments of angioplasty were done by interventional radiologist Charles Dotter. Percutaneous Transluminal Coronary Angioplasty (PTCA) is a primary procedure used in the field of interventional cardiology to treat blocked or stenosed coronary arteries. The blockages occur because of the lipid –rich plaque within the arteries causing diminished blood flow to the myocardium. In acute myocardial infarction, there is plaque rupture with platelet aggregation, and acute thrombus formation, which results in a sudden occlusion of coronary artery. The patient present with acute chest heaviness, diaphoresis, and nausea, urgent PTCA is required to save the life of the patient in order to limit the myocardial damage.

The effect of door-to-balloon delay in primary percutaneous coronary intervention on clinical outcomes of STEMI: a systematic review and meta-analysis protocol

BackgroundAcute myocardial infarction (AMI) is a medical emergency in which sudden occlusion of coronary artery(ies) results in ischemia and necrosis of the cardiac tissues. Reperfusion therapies that aim at reopening the occluded artery remain the mainstay of treatment for AMI. Primary percutaneous coronary intervention (PCI), which enables the restoration of blood flow by reopening the occluded artery(ies) via a catheter with an inflatable balloon, is currently the preferred treatment for AMI with ST segment elevation (STEMI). The door-to-balloon (D2B) delay refers to the time interval counting from the arrival of a patient with STEMI at a hospital to the time of the balloon inflation (or stent deployment) that reopens the occluded artery(ies). Reducing this delay in primary PCI is thought to be an important strategy toward achieving better patient outcomes. Unfortunately, significant reduction of D2B delay in the USA over the last decade has not been shown to be associated with improved STEMI mortality. It has been suggested that the lack of impact could be due to the expanding use of primary PCI in STEMI as well as the survival cohort effect, leading to a shift toward a higher risk population receiving the procedure. Others have suggested that reduction in D2B delay may not be as impactful as expected, given that it only represents a small fraction of the total ischemic time. Although most existing evidence have pointed to the presence of a beneficial effect of shorter D2B delay, some inconsistencies however exist. This study aims to synthesize available evidence in order to answer the following questions: (1) what is the overall effect of D2B delay on clinical outcomes in patients with STEMI treated with primary PCI? (2) What factors explain the differences of the effect estimates among the studies? (3) What are the important strength and limitation of the existing body of evidence?MethodWe will search PubMed/MEDLINE, EMBASE, ClinicalTrials.gov, WHO International Clinical Trials Registry, CINAHL Database, and the Cochrane Library using a predefined search strategy. Other sources of literature will include proceedings from the European Society of Cardiology, the American College of Cardiology, the American Heart Association, the EUROPCR, and the ProQuest Dissertations and Theses Database. We will include data from observational studies (case-control and cohort study design) and randomized control trials (that have investigated the relationship of D2B time and clinical outcome(s) in an adult (older than 18) STEMI population). Mortality (cardiac related and all-cause) and incidence heart failure (HF) have been prioritized as the primary outcomes. All eligible studies will be assessed for risk of bias using the Risk Of Bias in Non-randomized Studies - of Interventions tool. The Grading of Recommendations, Assessment, and Evaluation (GRADE) framework will be used to report the quality of evidence and strength of recommendations. We will proceed to analyze the data quantitatively if the pre-specified conditions are satisfied.DiscussionRecent discussion on the negative findings of improved D2B delay over time being unrelated to better STEMI outcomes at the population level has reminded us of an important knowledge gap we have on this domain. This systematic review will serve to address some of these key questions not previously examined. Answers to these questions could clarify the controversies and offer empirical support for or against the suggested hypotheses.Systematic review registrationPROSPERO CRD42015026069Electronic supplementary materialThe online version of this article (doi:10.1186/s13643-016-0304-7) contains supplementary material, which is available to authorized users.

The Importance of Restoring the Adiponectin Signaling Pathway to Reduce Myocardial Reperfusion Injury in Diabetes.

The incidence of heart failure after an acute myocardial infarction (AMI) remains unacceptably high despite medical advances in the past several years (1). Therefore, the discovery of new drugs or strategies to reduce myocardial damage in patients with AMI is urgently warranted. This problem is exacerbated particularly in those affected by diabetes. Diabetes significantly reduces myocardial ischemic tolerance after a sudden coronary artery occlusion, thereby leading to increased ischemic and reperfusion (IR) injuries (2). During the past several years, ischemic postconditioning (IPo) has emerged as an efficient intervention to reduce reperfusion injury and infarct size in patients with AMI (3). It consists of very short repetitive episodes of IR applied at the immediate onset of reperfusion after a prolonged coronary artery occlusion. Unfortunately, previous experimental studies demonstrated that the beneficial effects of IPo are largely lost in the presence of diabetes, although the mechanisms underlying this phenomenon remain to be fully clarified (2). In their study in this issue of Diabetes , Li et al. (4) demonstrate that type 1 diabetes abrogates the beneficial effects of IPo through the disruption of adiponectin signaling. Adiponectin is an adipocytokine that regulates glucose and fatty acid metabolism, exerting antioxidant, anti-inflammatory, and pro-survival effects (5). Adiponectin is also synthetized and secreted by cardiomyocytes, protecting against myocardial IR injury (5,6). Li et al. demonstrate …

Protocolo diagnóstico-terapéutico del síndrome coronario agudo con elevación del ST en Urgencias

ST-segment myocardial infarction or acute coronary syndrome are caused by sudden coronary artery occlusion. Immediate electrocardiogram performance and activation of health system to get an early coronary reperfusion are key to the management of the patients. Decision between fibrinolysis or emergent catheterization has to take into account ischemia time, estimated delay in the transfer to a percutaneous coronary intervention capable centre, and patient characteristics.

Acute ST Elevated Myocardial Injury due to Coronary Thrombosis during Thoracic Endovascular Aortic Repair in Patient with Protein S Deficiency.

A 71-year-old woman who had suffered from pulmonary thromboembolism with deep vein thrombosis for 12 years presented the hospital with a huge thoracic aortic aneurysm. During thoracic endovascular therapy, she had a sudden coronary artery occlusion without having organized stenosis or plaque rupture even under the dual antiplatelet treatment and heparinization. She turned out to be having a protein S deficiency. A procedure related thrombotic adverse event in patient with protein S deficiency is very rare, so we report a case with literature review.

Modulación del sistema betaadrenérgico durante el infarto agudo de miocardio: justificación para un nuevo ensayo clínico

Acute myocardial infarction is caused by sudden coronary artery occlusion. Persistent ischemia results in necrosis of the myocardial tissue supplied by the occluded vessel. It has recently been shown that the final size of the infarct is a major predictor of future clinical events, and is, therefore, used as a surrogate outcome in clinical trials. Moreover, it has become clear that the duration of ischemia in the main determinant of the success of myocardial salvage (i.e. of non-necrotic at-risk myocardium). In addition to minimizing the time between symptom onset and reperfusion, there is considerable interest in finding therapies that can further limit the size of the infarction (i.e. cardioprotective therapies) and they are the focus of numerous clinical studies. Oral β-blockade within the first few hours of an AMI is a class-IA indication in clinical practice guidelines. However, early intravenous β-blockade, even before coronary artery reperfusion, is not routinely recommended. Preclinical research has demonstrated that the selectiveβ1-blocker metoprolol is able to reduce the infarct size only when administered before coronary artery reperfusion, which indicates that its cardioprotective properties are secondary to its ability to reduce reperfusion injury. In addition, retrospective studies of AMI suggest that starting intravenous β-blockade early has clinical benefits (i.e. lower mortality and better recovery of left ventricular contractility) in patients without contraindications. Our general hypothesis is that early administration of metoprolol (i.e. intravenously before reperfusion) results in smaller infarcts than administering the drug orally after reperfusion. The Effect of METOprolol in CARDioproteCtioN during an acute myocardial InfarCtion (METOCARD-CNIC) trial will test this hypothesis in patients with ST-segment elevation AMI.

736 Automated classification of wall motion abnormalities by analysis of left ventricular endocardial contour motion patterns

Background: Previous studies have shown that transmural myocardial ischemia caused by sudden epicardial coronary artery occlusion determines a typical sequence of events characterized, in order, by left ventricular wall motion abnormalities, ST segment modifications and, only at the end, angina. In this study, we investigate if this typical ischemic cascade presents with the same modalities also during subendocardial ischemia induced by dipyridamole infusion. Patients and Methods: A total of 41 patients (63±9 years; 12 women) with chronic stable angina and angiographically documented coronary artery disease (1-vessel: 14 [34%]; 2-vessel: 8 [19%]; 3-vessel: 19 [46%]) underwent dipyridamole stress echocardiography (total dose: 0,84 mg/kg iv). Cardiac images were acquired by a 2.5 MHZ probe connected to a Toshiba set, Power Vision 8000. Results: During test, 39 patients (95%) had left ventricular wall motion abnormalities, 31 patients (75%) had ST segment depression and 32 patients (78%) had angina. The first manifestation of ischemia was left ventricular wall motion abnormalities in 7 patients (17%), ST segment depression in 16 patients (39%) and angina in 9 patients (22%). When considering only the 21 patients who developed all three manifestations of ischemia during dipyridamole stress echocardiography, left ventricular wall motion abnormalities were the first manifestation of ischemia (alone or in association with ST segment depression or angina) in 5 patients (24%), ST segment depression was the first manifestation of ischemia (alone or in association with left ventricular wall motion abnormalities or angina) in 14 patients (66%) and angina was the first manifestation of ischemia (alone or in association with left ventricular wall motion abnormalities or ST segment depression) in 8 patients (38%). Conclusion: Our data indicate that dipyridamole induced subendocardial ischemia results in a very variable sequence of events, which doesn’t seem to reproduce the typical ischemic cascade described after sudden coronary artery occlusion. The heterogeneity of the response among patients likely depends on a variable association of interindividual differences in the extension of ischemia, in the sensitivity of cardiac neuronal algogenic receptors and in the adenosine-mediated effects of dipyridamole on cardiac perception of pain and on electrophysiological characteristics of myocardial cells. 735 Cultural evolution of digital description of coronary artery disease severity potential of inducing myocardial ischemia during exercise stress echocardiography.

Quantification of the passive mechanical properties of the resting platelet.

Sudden coronary artery occlusion is one of the leading causes of death. Several in vitro models have been used to study the relationship between hemodynamic forces and platelet function. However, very few in vivo studies exist that fully explore this relationship due to the lack of rheologic data for the platelet. For this purpose, micropipette aspiration techniques were used in the present study to determine the mechanical properties of platelets. The data were analyzed by two mathematical models: (1) an erythrocyte-type membrane model which yielded a platelet shear modulus of 0.03+/-0.01 dyn cm[-1] (mean+/-SD) and a viscous modulus of 0.12+/-0.04 dyn s cm[-1]. (2) An endothelial-type cell model which approximated the platelet Young's modulus to be 1.7+/-0.6 x 10(3) dyn cm(-2) with a viscous modulus of 1.0+/-0.5 x 10(4) dyn s cm(-2). The endothelial-type cell model more accurately describes the mechanics occurring at the micropipette tip and permits more appropriate assumptions to be made in quantifying the rheologic properties of a platelet. Results from this study can be integrated into numerical models of blood flow in stenosed coronary arteries to elucidate the impact of local hemodynamics on platelets and thrombus formation in coronary artery disease.

Effects of acute coronary artery occlusion on the coronary microcirculation

The exact microvascular site of coronary vasodilation after coronary artery occlusion has not been clearly established. We sought to determine 1) the microvascular site of recruitable vasodilator reserve after a critical stenosis as assessed by adenosine and EDTA, 2) the coronary microvascular site responsible for vasodilatation after total coronary artery occlusion, and 3) the microvascular site for recruitable vasodilator reserve after coronary artery occlusion as assessed by adenosine and EDTA. Hemodynamics and coronary epicardial microvascular diameter were measured in 33 dogs by means of intravital epiillumination microscopy at control conditions, during a critical stenosis, or 30, 60, and 120 min following coronary artery occlusion. To evaluate the site of pharmacologically recruitable vasodilator reserve, EDTA or adenosine was suffused onto the epicardial surface. After a critical stenosis EDTA dilated all sizes of microvessels, whereas adenosine only dilated small microvessels (less than 150 microns). After coronary artery occlusion there was vasodilation that was inversely proportional to the control microvascular diameter. Coronary microvascular diameter did not change during 2 h after coronary artery occlusion. In addition, intravenous or topically applied adenosine or topically applied EDTA had no additional effect on the coronary arteriolar diameter. We concluded that in response to sudden coronary artery occlusion, the coronary microvascular dilation was inversely related to the control microvascular diameter, and in contrast to the response after a critical stenosis, there was no pharmacologically recruitable vasodilator reserve to adenosine or EDTA following acute coronary artery occlusion.

Management of complicated coronary angioplasty by intracoronary urokinase and immediate re‐angioplasty

Percutaneous transluminal coronary angioplasty was complicated by acute coronary occlusion, dissection of the arterial wall, or angiographic evidence of intraluminal thrombosis in 33 high-risk patients from 153 consecutive angioplasty procedures (21.5%). Ten patients (group I) were managed with nitroglycerin (0.2 to 0.4 mg i.c.) and repeated attempts at mechanical guide wire recanalization or dilation, but they did not receive thrombolytic therapy. In the remaining 23 patients (group II), intracoronary urokinase (100,000 to 360,000 U.I.) was administered over 15-20 min after onset of coronary occlusion or thrombosis and continued during attempts at repeated dilation of the stenosis. The incidence of sudden coronary artery occlusion was 70% in group I patients and 52% in group II. The angiographic evidence of thrombus formation was observed in a higher, but not significant, proportion of group II patients (65%) as compared with group I (30%). The incidence of intimal tearing or dissection was similar in the two groups of patients (40 vs. 34.7%). The overall final success rate of the complicated angioplasty series was 48% (6/33). However, the success rate was lower (10%) in group I than in group II patients (10 vs. 65%; P less than 0.005), and the frequency of emergency coronary artery bypass grafting was lower in group II patients (13 vs. 60%; P = 0.01), suggesting that thrombolytic therapy with urokinase may be effective in the management of acute coronary occlusion and thromboembolic complications of coronary angioplasty.

Determination of Serum Myoglobin Level After Death in the Diagnosis of Sudden Coronary Artery Occlusion

Serum myoglobin was determined by radioimmunoassay in 20 cases of sudden and unexpected death resulting from acute coronary occlusion. There was consistent elevation of myoglobin 2 h after death, with peaking at 3 h. No comparable elevation of serum myoglobin level was noted in patients who had succumbed to pulmonary embolism, ruptured aortic aneurysm, or subarachnoid or intracerebral hemorrhage. Thus, determination of serum myoglobin seems useful in confirming or establishing acute coronary occlusion as the cause of sudden and unexpected death.