Acute coronary syndromes: the American epidemic continues.
Explore the source record for details and available documents.
Angina, Unstable↗
Biomedical subjects
F M Sheridan
Publications and source records attributed to F M Sheridan.
Medical management of acute ST elevation myocardial infarction.
Advances have occurred rapidly in how the patient who presents with acute ST elevation myocardial infarction is managed. Nevertheless, due to availability and effectiveness, medical therapy continues to be the mainstay of treatment. Several drugs are of proven efficacy in decreasing myocardial loss and mortality. Thrombolytics, antiplatelets, and anticoagulants combine to decrease the thrombus overlying the active plaque and thus increase blood flow to the infarcting myocardium. Beta blockers, nitrates, and angiotensin converting enzyme inhibitors diminish myocardial oxygen consumption and have been shown to decrease morbidity and mortality. Supportive therapies provide patient comfort and aid survival until definitive therapies are instituted. However, as advanced as treatments become, none are effective unless patients are educated to seek help quickly and emergency response systems are efficient. Health care providers must ensure patient education and prompt medical response in communities so that medical regimens can be as effective as possible.
Adrenergic beta-Antagonists↗
Interventional therapy for acute myocardial infarction.
Percutaneous transluminal coronary angioplasty has proven to be more effective and safer than thrombolytic therapy for the treatment of acute ST elevation myocardial infarction. Coronary intervention decreases early mortality and the incidence of intracerebral hemorrhage when performed by an experienced interventional team in a timely fashion. After failed fibrinolytic therapy for myocardial infarction, percutaneous transluminal coronary angioplasty is indicated for signs of ischemia and is very effective in restoring vessel patency and reducing mortality when used as a rescue procedure. The glycoprotein IIb-IIIa inhibitors improve outcomes in percutaneous transluminal coronary angioplasty, particularly in patients undergoing stent placement. Percutaneous interventional therapy in acute myocardial infarction is particularly beneficial in patients with cardiogenic shock and effective for saphenous vein graft occlusions, patients with diabetes mellitus, and in the elderly. New devices and drugs are currently being tested for acute myocardial infarction and provide hope for even better interventional therapies in the near future.
Angioplasty, Balloon, Coronary↗
It is more than just the heart for the American Heart Association: new interventions in the vascular tree.
Explore the source record for details and available documents.
American Heart Association↗
Carotid stenting: a technology in evolution.
Interest in stenting lesions involving the carotid artery bifurcation has grown during the past 10 years. Techniques first utilized by Theron and Mathias in Europe and Roubin and colleagues in the United States have evolved to where the technique has been extensively refined and its safety and efficacy firmly established. The only prospective randomized study comparing carotid stenting with carotid endarterectomy, CAVATAS (Carotid and Vertebral Artery Transluminal Angioplasty Stenting), showed similar safety profiles and long-term results for both techniques. A large scale NIH-sponsored trial is now in progress, CREST (Carotid Revascularization Endarterectomy versus Stent Trial), but the results are 5-6 years away. In the interim, one approach toward instituting a carotid stent program is described.
Angioplasty↗
Percutaneous interventional approaches to diseases of the aorta.
Diseases of the aorta are prevalent in the Western world. Pathophysiology is influenced by hypertension, atherosclerosis, and genetic factors. The rupture of an aortic aneurysm or the dissection of a hematoma into the aortic wall causes significant mortality in this country. Physicians have long wrestled with therapies to prevent this fatal natural history. It was not until the surgical insertion of aortic grafts in the 20th century that effective therapy was developed. However, surgical mortality and morbidity still remain quite significant in the higher risk population in which these procedures often must be performed. During the 1990s, techniques and devices have been developed which allow placement of endovascular grafts into the aorta percutaneously, without traditional surgery. Two recently FDA-approved devices require a team approach for optimal deployment and care. In the initial experience, these endovascular devices appear to offer the promise of effective treatment with low procedural complications.
Angioplasty, Balloon↗
Coronary interventions approaching the year 2000.
Interventional cardiology is only 22 years old, but its successes at the end of this century stand heavily on the shoulders of innovative pioneers who labored earlier in the century. Balloon angioplasty gradually developed and eventually achieved great success in treating America's greatest health risk, coronary artery disease, through the 1980s. Both mortality benefit and symptom improvement have been demonstrated for coronary angioplasty, making it one of the most frequently performed procedures in the world today. In an effort to overcome acute complications and late restenosis, atherectomy devices and stents became useful tools over the past decade. As the generation of baby boomers begins to swell the ranks of the middle aged and elderly in the early 21st century, it is with great hope that molecular biology and the continued development of the technology of interventional cardiology will allow even greater successes in decreasing death and disability from ischemic heart disease.
Angioplasty, Balloon, Coronary↗
Getting to the heart of a hidden epidemic--the American Heart Association's dedication to women.
Explore the source record for details and available documents.
Aged↗
Making the diagnosis in women with coronary artery disease.
It can be difficult to make a timely and proper diagnosis in women who have coronary artery disease. The erroneous impression by physicians and the community that fewer women than men experience this disease plays a role. Timing of presentation and the spectrum of symptoms in women are somewhat different than in men. Once heart disease enters into the differential diagnosis, the choice of evaluation methods becomes a challenge. The variety of exercise or pharmacologic stress tests with decisions concerning the addition of nuclear techniques or echocardiography makes it important to understand the benefits and shortfallings of each modality. Pre-test probability of disease, the baseline ECG, accuracy, and expertise available all should be considered. Sometimes, technologies such as MRI, CT, or PET are useful. Whatever choice is made, it is vital to appreciate the high mortality and morbidity of coronary artery disease in women. Making prudent decisions to uncover their disease as early as possible allows appropriate treatment and risk factor modification.
Adult↗
Cardiovascular research support by the American Heart Association in Louisiana.
The American Heart Association (AHA) was founded in 1924 by a group of physician-scientists to promote the exchange of research ideas in an era when the treatment of heart disease was extremely frustrating. The organization has evolved to include education and community service in its mission, but the support and promotion of quality research has remained at the AHA's core. Research support by the AHA has been responsible for major advances in cardiovascular medicine, including the development of diuretics, pacemakers, artificial heart valves, defibrillators, cardiopulmonary resuscitation, hypercholesterolemia therapy, and artificial surfactant. Working to ensure the efficient distribution of funds, the AHA has distributed nearly $1.4 billion in support of quality research for graduate and medical students, post-doctoral fellows, and beginning and established investigators. Such support has assisted in the career development of four Nobel Prize winners. While cardiovascular disease remains America's leading cause of death, the activities of the AHA continue to support advances in its diagnosis and treatment.
American Heart Association↗
Leukocyte adhesion to the coronary microvasculature during ischemia and reperfusion in an in vivo canine model.
BACKGROUND: Prompt reperfusion of ischemic myocardium or myocardium that is in the process of becoming infarcted is a cornerstone of current therapy for coronary artery disease. Paradoxically, experimental evidence suggests that cardiac damage may be caused by the reperfusion itself. Leukocyte attachment to the coronary vascular endothelium during reperfusion may be an initiating step in this detrimental process. Leukocyte adhesion to microvascular endothelium has never been demonstrated directly in a cardiac model of ischemia and reperfusion. METHODS AND RESULTS: Fluorescent videomicroscopy through a special "floating" objective that allows a series of lenses to move in unison with the beating dog heart was used on the left ventricular surface of open-chest dogs. Epicardial microvessels (25 to 130 microm), in focus throughout the cardiac cycle, were recorded after infusion of acridine orange (to fluorescently label leukocytes) during either 1 hour of ischemia followed by 2 hours of reperfusion, 3 hours of ischemia, or 3 hours of no ischemia. The amount of net fluorescence recorded along microvessel walls, which represented leukocyte accumulation, significantly increased in dogs during reperfusion (n = 8) compared with the same time period in the animals that were kept ischemic (n=5) (21.0 +/- 3.8 versus 10.9 +/- 4.5 gray scale; P = .0001). The rapid increase in fluorescence during reperfusion was also significantly different from values in the same group during the preceding period of ischemia (21.0 +/- 3.8 versus 5.1 +/- 2.1 gray scale; P =.0001), whereas no significant increase was seen over the same time periods in the animals that remained ischemic throughout the protocol. CONCLUSIONS: Reperfusion, compared with ischemia alone, promotes the rapid accumulation of leukocytes in the coronary microvasculature of dogs.
Animals↗
Management of chronic ischemic heart disease.
Explore the source record for details and available documents.
Female↗
Percutaneous interventions for ischemic heart disease.
In the United States, when necessary due to symptoms or prognosis, percutaneous coronary interventions are performed on patients with ischemic heart disease more frequently than is coronary artery bypass surgery. A wide array of options are available to the interventional cardiologist. Improvements over the 17 years that coronary balloon angioplasty has been performed have kept it the primary therapy. It is currently used safely and effectively in the majority of patients. The problems of abrupt closure, restenosis, and inadequate results in some complex lesions have spurred the development of intracoronary stents, coronary atherectomy and ablation devices, and coronary excimer lasers. Metallic stents perform well in large vessels to treat abrupt closures and to reduce restenosis, but confer a risk of hemorrhage. Specific complexities of lesion characteristics determine the effective use of atherectomy/ablation devices and lasers. Future technologic improvements anticipate even better treatments for patients with coronary artery disease.
Angioplasty, Balloon, Coronary↗
The vasoactive effect of serotonin on canine coronary arteries after ischemia and reperfusion.
BACKGROUND: Reperfusion of the ischemic myocardium is a cornerstone of current therapy for acute coronary syndromes. Experiments show that reperfusion is associated with injury to the coronary artery. Such injury may manifest as augmented vasospasm or impaired vasodilation, and in this study we assessed whether such coronary responses to serotonin do occur. METHODS: Left anterior descending arteries (LAD) were occluded in 12 open-chested dogs for 1 h, then reperfused for 1 h. Vasoreactivity to serotonin was measured in isolated rings from the LAD and circumflex arteries (Cx), both at basal resting tension and after preconstriction with U-46619. Endothelium was removed in half of the rings. RESULTS: In the basal state, LAD rings displayed increased initial constriction and decreased dilation in response to serotonin (maximum dilation: LAD, -4.5 +/- 1.7% versus Cx, -7.6 +/- 1.4%, P < 0.05). With endothelium removed, peak constrictions of the LAD and Cx were significantly augmented, and LAD dilations remained slightly impaired compared with the Cx. After U-46619, dilation in response to serotonin was impaired in the LAD compared with Cx rings (maximum dilation: LAD, -18.3 +/- 11.4% versus Cx, -44.0 +/- 8.4 LAD, P < 0.05). Endothelium removal diminished, but did not abolish, this relationship. De-endothelialized Cx, but not LAD, rings displayed slightly impaired dilations in response to serotonin compared with their respective controls. CONCLUSIONS: After ischemia-reperfusion, coronary arteries respond to serotonin with enhanced constriction and impaired dilation. Changes in both the endothelium and the smooth muscle may determine these responses to serotonin.
15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
Coronary vascular injury due to ischemia-reperfusion is reduced by pentoxifylline.
Myocardial ischemia and reperfusion cause coronary vascular injury involving both the large epicardial arteries and the microcirculation. Although the mechanisms are unclear, leukocytes appear to play an important role. Since the methylxanthine derivative pentoxifylline (PTX) decreases neutrophil activity in vitro, we hypothesized that it might diminish coronary vascular injury due to ischemia and reperfusion. We investigated the effects of PTX on coronary microvascular and epicardial artery injury in open chest, anesthetized dogs undergoing moderate (60 min) or more prolonged (90 min) ischemia due to left anterior descending coronary artery occlusion followed by 60 min of reperfusion. As an index of microvascular injury, we assessed regional permeability with a dual radioisotope protein leak index (PLI) method. Both ischemic periods with reperfusion increased the PLI of severely ischemic (flow less than or equal to 20/ml/min/100 g) myocardium by 2.5- and 3-fold, respectively, compared to nonischemic (flow greater than or equal to 100 ml/min/100 g) myocardium. Treated dogs received PTX (20 mg/kg bolus plus 0.1 mg/kg/min infusion) before ischemia. PTX reduced the increase in the PLI by 40% after 60 min of ischemia (PLI = 5.87 +/- 0.48 vs. 4.10 +/- 0.52 untreated vs. PTX-treated; P less than .05), and by 25% after 90 min of ischemia (6.84 +/- 0.49 vs. 4.84 +/- 0.42; P less than .05). The amount of protein leak was inversely related to ischemic blood flow, and the magnitude of this relationship was significantly reduced in PTX-treated animals. In arterial rings from untreated dogs exposed to 90 min of ischemia followed by reperfusion, there was impaired relaxation to ADP and acetylcholine, but not to sodium nitroprusside.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
A rationale for the use of percutaneous transluminal angioplasty in the setting of acute myocardial infarction.
Rapid reperfusion of infarcting myocardium has become a cornerstone of modern medical care. The role of percutaneous transluminal coronary angioplasty (PTCA) in this treatment of acute myocardial infarction is not clear. PTCA is effective in the early hours of MI as primary reperfusion therapy, in lieu of thrombolysis. Arterial patency using this strategy is excellent with low complication rates, and this therapy is comparable and may be superior to thrombolysis when myocardial performance and recurrent ischemia are considered. PTCA is the treatment of choice for the patient in whom thrombolysis is contraindicated, or who develops cardiogenic shock. The role of angioplasty as secondary therapy for myocardial infarction after pharmacologic thrombolysis and reperfusion is controversial. The evidence is clear that immediate PTCA after successful thrombolysis is not warranted. The decision for elective angioplasty after successful or unsuccessful thrombolysis should probably be judged on a case to case basis.
Angioplasty, Balloon, Coronary↗
Effects of phorbol esters on canine coronary artery constriction and dilation in vitro.
The influence of protein kinase C (PKC) activation on canine coronary vasoreactivity was assessed in vitro. Activation of PKC by phorbol 12,13-dibutyrate (PDBu) or phorbol 12-myristate 13-acetate (PMA) caused slow sustained constriction of isolated coronary artery rings. PDBu was a more potent and efficacious constrictor than PMA (169 +/- 21 vs. 81 +/- 7% of maximum KCl constriction). Constriction to PDBu was reduced slightly by deendothelialization and by meclofenamate. Pretreatment with threshold concentrations of PDBu increased constriction to serotonin from 3 +/- 1 to 48 +/- 4% of maximum KCl constriction whether or not the endothelium was present but had no effect on response to the thromboxane analogue U-46619. In addition, in arteries constricted with PDBu, dilations to ADP, thrombin, acetylcholine, and sodium nitroprusside were impaired when compared with arteries constricted with U-46619. These results suggest that activation of PKC in coronary arteries 1) produces potent constriction mediated only in small part by the endothelium and by cyclooxygenase products, 2) potentiates markedly the constrictor response to serotonin by an endothelium-independent mechanism, and 3) attenuates both endothelium-dependent and endothelium-independent vasodilation.
6-Ketoprostaglandin F1 alpha↗
Role of leukocytes in coronary vascular endothelial injury due to ischemia and reperfusion.
A possible cause of the coronary endothelial injury that occurs with ischemia and reperfusion is the local accumulation of leukocytes during these events. To investigate the role of leukocytes in coronary endothelial injury, we tested the effect of leukocyte removal by filtering on coronary endothelial function in a canine model of regional myocardial ischemia and reperfusion. Blood was supplied to the left anterior descending and circumflex arteries of anesthetized dogs via an extracorporeal circulation. A 60-minute left anterior descending occlusion was followed by 120 minutes of reperfusion either with (n = 6) or without (n = 6) leukocyte filters in the extracorporeal circuit. Regional myocardial blood flow was measured with radiolabeled microspheres. Radiolabeled autologous transferrin (113mIn) and erythrocytes (99mTc) were given intravenously during reperfusion for assessment of microvascular permeability. Left anterior descending and circumflex coronary artery rings were assessed in vitro for endothelium-dependent dilation to acetylcholine, ADP, and thrombin. In unfiltered dogs, ischemia and reperfusion increased the protein leak index of ischemic myocardium 2.3-fold compared with that of nonischemic myocardium (2.3 +/- 0.5 to 5.2 +/- 1.6, p less than 0.05). In filtered dogs, there was no difference in the protein leak index of nonischemic versus ischemic myocardium (1.5 +/- 0.4 versus 1.9 +/- 0.5, p = NS). There was impaired left anterior descending coronary artery relaxation (versus circumflex) in response to endothelium-dependent vasodilators in vitro. However, relaxation was not consistently improved by leukocyte filtering. We conclude that leukocytes are responsible for the endothelial injury secondary to ischemia and reperfusion in the coronary microvasculature but have little or no effect on the endothelial injury in epicardial coronary arteries.
Acetylcholine↗