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Modification To Acs Coronary Guiding

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Last Updated: 02 July 2021

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General | Latest Info

Atheromatous plaque sometimes becomes unstable or inflame, causing it to rupture or split, exposing thrombogenic material, which activate platelets and coagulation cascade and produce Acute thrombus. Platelet activation involves conformational change in membrane glycoprotein IIb / IIIa receptors, allowing cross-linking of platelets. Even atheromas causing minimal obstruction can rupture and result in thrombosis; in > 50 % of cases, pre-event stenosis is < 40 %. Thus, although the severity of Stenosis helps predict symptoms, it does not always predict acute thrombotic events. The Resultant thrombus abruptly interferes with blood flow to parts of the myocardium. Spontaneous thrombolysis occurs in about two thirds of patients; 24 hours later, thrombotic obstruction is found in only about 30 %. However, in virtually all cases, obstruction lasts long enough to cause varying degrees of tissue necrosis. Ischemic tissue has impaired contractility and relaxation, resulting in hypokinetic or akinetic segments; these segments may expand or bulge during systole. The Size of the affected area determines effects, which range from minimal to mild heart failure to cardiogenic shock; usually, large parts of the myocardium must be ischemic to cause significant Myocardial Dysfunction. Some degree of heart failure occurs in about two thirds of hospitalized Patients With Acute Myocardial Infarction. It is term ischemic cardiomyopathy if low cardiac output and heart failure persist. Ischemia involving papillary muscle may lead to mitral valve regurgitation. Dysfunctional wall motion can allow mural thrombus formation. Electrical Dysfunction can be significant in any form of Acute Coronary Syndrome. Ischemic and necrotic cells are incapable of normal electrical activity, resulting in various ECG changes, arrhythmias, and conduction disturbances.-T abnormalities of ischemia include-segment depression, T-WAVE inversion,-segment Elevation, and peak T waves in hyperacute phase of Infarction. Conduction disturbances can reflect damage to the sinus node, atrioventricular node, or specialized conduction tissues. Most changes are transient; some are permanent. Symptoms of Acute Coronary syndromes depend somewhat on the extent and location of obstruction and are quite variable. Painful stimuli from Thoracic organs, including the heart, can cause discomfort describe AS pressure, tearing, gas with urge to eructate, indigestion, burning, aching, stabbing, and sometimes sharp needle-like pain. Many patients deny they are having pain and insist it is merely discomfort. Except when the infarction is massive, recognizing the amount of ischemia by symptoms alone is difficult. Acute Coronary syndromes should be considered in men > 30 years and women > 40 years whose main symptom is chest pain or discomfort. Pain must be differentiated from pain of pneumonia, pulmonary embolism, pericarditis, rib fracture, costochondral separation, esophageal spasm, Acute aortic dissection, renal calculus, splenic Infarction, or various abdominal disorders. In patients with previously diagnosed hiatus hernia, peptic ulcer, or gallbladder disorder, clinicians must be wary of attributing new symptoms to these disorders. Pathologic Q waves are not necessary for diagnosis. ECG must be read carefully because-segment elevation may be subtle, particularly in inferior leads; sometimes readers ' attention is mistakenly focused on leads with-segment depression.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Overview

ACS results from sudden imbalance of myocardial oxygen demand and supply, most typically secondary to obstruction of blood flow in the coronary artery. 2 Obstruction may occur through rupture or erosion of vulnerable, lipid-laden, atherosclerotic plaque with fibrous cap that partially or completely occludes coronary artery. 2 3 Disruption of fibrous cap stimulates thrombogenesis. 2 3 Thrombus formation and vasospasm of coronary artery reduce blood flow and cause ischemic chest pain, classic symptom of ACS. 2 3 pressure-like chest pain often radiates to the left arm, neck, or jaw. 3 Accompanying symptoms may include dyspnea, sweating, cool or clammy skin, nausea, vomiting, and unexplained fatigue. 3 median age of ACS diagnosis in the US is 68 years.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Symptoms

Signs and symptoms of Acute Coronary syndrome usually begin abruptly. They include: Chest pain or discomfort, often described as aching, pressure, tightness or burning pain spreading from chest to shoulders, arms, upper abdomen, back, neck or jaw Nausea or vomiting Indigestion Shortness of breath sudden, heavy sweating, lightheadedness, dizziness or fainting, Unusual or unexplained fatigue, feeling restless or apprehensive Chest Pain or discomfort is most common symptom. However, signs and symptoms may vary significantly depending on your age, sex and other medical conditions. You're more likely to have signs and symptoms without chest pain or discomfort if you're woman, older adult or have diabetes.


Prognosis

Despite their smaller coronary vessels and higher risk profile, women with STEMI appear to respond just as well as men to Primary PCI and stenting, according to the Optical Coherence Tomography Assessment of Gender Diversity in Primary Angioplasty study. OCTAVIA, which was designed to examine gender differences at time of Primary PCI, includes 140 STEMI patients at 14 Italian centers, matched by age and risk factors, who receive everolimus-eluting stent. On initial OCT, no differences by gender were found in the proportion of ruptured or eroded plaques, thus suggesting that the pathophysiology of STEMI is nearly identical in men and women. On repeat OCT at nine months, intended to assess stent healing, more than 90 % of both men and women had fully covered stent struts. Although OCTAVIA was not power for clinical end points, no significant differences in death, reinfarction, stroke, stent thrombosis, or target vessel reintervention were evident at one year.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Causes

Careful and focused history taking and physical examination are essential both to assessing the likelihood that presenting illness is ACS and to determining risk of adverse outcome. Although patients typically describe stable Angina as deep, poorly localized chest or arm discomfort that is exacerbated by activity or emotional stress and relieved by rest, nitroglycerin, or both, discomfort associated with UA is more severe, occurs at rest, and is usually described as frank pain. Often located in substernal region, pain or pressure frequently radiate to the neck, jaw, leave shoulder, and leave arm. Some patients may present with symptoms other than chest discomfort; such anginal equivalent symptoms include dyspnea, nausea and vomiting, diaphoresis, and unexplained fatigue. 46 Atypical presentations are more common among women and elderly people. Rarely, syncope may be presenting symptom of ACS. Pain that is sharp, stabbing or pleuritic, reproducible with palpation or with movement, or able to be localized at the tip of 1 finger is usually not ischemic. Chest pain that resolved with administration of sublingual nitroglycerin in ED setting is not predictive of ACS. The 5 most important history-related factors that help identify Ischemia due to CAD, ranked in order of importance, are the nature of anginal symptoms, history of CAD, male sex, older age, and number of traditional risk factors present. 47 48 Traditional cardiac risk factors have actually been found to be weak predictors of likelihood of Acute Ischemia, 49 although their presence relates to poor outcomes for patients with established ACS. Primary goals of physical examination are to identify any precipitating causes of Myocardial Ischemia and to assess hemodynamic consequences of acute ischemic event. Physical examination findings that indicate large area of Ischemia and high risk include diaphoresis; pale, cool skin; sinus tachycardia; third or fourth heart sound; basilar rales; and hypotension. Physical examination may also provide clues that can help in determining differential diagnosis. For example, unequal pulses or murmur of aortic regurgitation indicate possible aortic dissection, whereas pericardial friction rub suggests Acute pericarditis. Cardiac biomarkers should be measured for all patients who present with chest discomfort or other symptoms suggestive of ACS. Measurements of cardiac-specific troponins T and I allow for highly accurate, sensitive, and specific determination of Myocardial injury in the context of ischemic symptoms; These troponins have replaced CK-MB as the preferred marker for detection of Myocardial necrosis. However, troponin measurements have some drawbacks. Troponin levels usually do not increase until at least 6 hours after onset of symptoms; therefore, negative result obtained within this period should prompt repetition of assay 8 to 12 hours after onset of symptoms. Because troponin levels remain elevated for a prolonged period after Myocardial necrosis, their usefulness in detecting Recurrent Myocardial damage is limit. However, they are helpful in detecting Myocardial damage in patients who present For Assessment several days after onset of symptoms.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Diagnosis

The term Acute Coronary syndrome refers to any group of clinical symptoms compatible with Acute Myocardial Ischemia and covers spectrum of clinical conditions ranging from Unstable Angina To NonST-segment Elevation Myocardial Infarction To-segment Elevation Myocardial Infarction. Unstable Angina and NSTEMI are closely related conditions: their pathophysiologic origins and clinical presentations are similar, but they differ in severity. Diagnosis Of NSTEMI can be made when Ischemia is sufficiently severe to cause Myocardial damage that results in release of biomarker of Myocardial necrosis into circulation. In contrast, patient is considered to have experienced UA if no such biomarker can be detected in bloodstream hours after initial onset of Ischemic chest pain. Unstable Angina exhibits 1 or more of 3 principal presentations: rest Angina, new-onset severe Angina, and crescendo pattern of occurrence. Each year in the United States, approximately 1. 36 million hospitalizations are required for ACS, Of which 0. 81 million are for Myocardial Infarction and the remainder are for UA. Roughly two-thirds of patients with MI have NSTEMI; rest have STEMI. 1 ACC = American College Of Cardiology; ACE = angiotensin-converting enzyme; ACS = Acute Coronary syndrome; ADP = adenosine diphosphate; AHA = American Heart Association; BNP = B-type natriuretic peptide; CABG = Coronary artery bypass grafting; CAD = Coronary artery disease; CHF = congestive Heart failure; CI = confidence interval; CK-MB = muscle and brain fraction Of creatine kinase; CRP = C-reactive protein; CURE = Clopidogrel in Unstable Angina To Prevent Recurrent Events; ECG = electrocardiography; ED = emergency department; GP = glycoprotein; HR = hazard ratio; IV = intravenous; LDL = low-density lipoprotein; LMWH = lowmolecular-weight heparin; LV = left ventricular; MI = Myocardial Infarction; NSTEMI = NonST-segment Elevation MI; PCI = percutaneous Coronary intervention; STEMI =-segment Elevation MI; TIMI = Thrombolysis in Myocardial Infarction; UA = Unstable Angina; UFH = unfractionated heparin timing Of release Of various biomarkers After Acute Myocardial Infarction. Biomarkers are plot showing multiples of cutoff For AMI over time. The Dash horizontal line shows the upper limit of normal. The earliest rising biomarkers are myoglobin and creatine kinase isoforms. Muscle and brain fraction of CK rises to a peak of 2 to 5 times ULN and typically returns to normal range within 2 to 3 D after AMI. Cardiac-specific troponins show small elevations above ULN in small infarctions but rise to 20 to 50 times ULN in the setting of large infarctions. Troponin levels may stay elevated above ULN to 7 D or more after AMI. Adapt from Mayo Clinic Cardiology: Concise Textbook, 3 ED. 58 long-term antithrombotic therapy at hospital discharge After Unstable Angina / NonST-segment Elevation Myocardial Infarction. LOE = level of evidence. For patients allergic to aspirin, use Clopidogrel alone indefinitely, or try aspirin desensitization. B For patients allergic to Clopidogrel, use ticlopidine, 250 mg by mouth twice daily.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Treatment

PLATelet aggregation involves GP IIb / IIIa, Receptor linked to fibrinogen or von Willebrand factor. Intravenous GP IIb / IIIa Receptor antagonists have been extensively tested in patients with ACS and in meta-analysis of all major randomise trials, the absolute risk reduction for death or MI at 30 days was 1 %. 18 absolute Treatment benefit was largest in high risk patientsin particular, those with evidence of troponin release or those undergoing Acute PCI. 18 Among those without troponin elevation or without PCI, no significant benefits were observed with GP IIb / IIIa Administration. The CREDO trial has helped to resolve the question of whether Clopidogrel plus GP IIb / IIIa Receptor antagonists may be required in patients undergoing PCI. Approximately half of patients receive GP IIb / IIIa antagonists and two thirds had present with ACS. The frequency of MI, stroke, or death At one year was reduced with Clopidogrel from 11. 5 % to 8. 5 %, with similar risk ratios in the presence or absence of GP IIb / IIIa inhibitors. However, in lower risk patients both of PLATelet antagonists may not be require: ISAR-REACT trial do not show additional benefits for abciximab in presence of background Treatment of Aspirin and Clopidogrel. There is no evidence to support use of oral GP IIb / IIIa antagonists following ACS. Partial or transient inhibition of IIb / IIIa Receptor may upregulate PLATelet activation, and composite of trials of oral GP IIb / IIIa inhibitors suggest increased risk of death. In summary, Aspirin remains the cornerstone of antiplatelet Treatment in patients with ACS. Robust evidence supports use of Clopidogrel in patients presenting with non-elevation ACS and extensive evidence supports use of intravenous GP IIb / IIIa inhibitors in high risk patients with ACS, especially those undergoing Acute PCI.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Lifestyle and home remedies

The present study demonstrates the following key points: confidence levels in lifestyle modification were different across various risk factors for patients with CAD and patients had low confidence in their blood pressure and cholesterol control, diet regulation, Body Weight maintenance and routine exercise; low confidence in overall lifestyle modification was associated with male sex and lower education level and there was substantial gap between recognition of and action towards Heart attack. Much of existing research on lifestyle modification has focused on single behaviours, for example, smoking cessation. However, level of accomplishment regarding lifestyle modification can vary among main modifiable risk factors, including alcohol restriction, dyslipidaemia, obesity, physical inactivity, hypertension and diabetes. The strength of this study IS that we quantified patient confidence levels based on patient behaviour towards several risk factors for CAD that could be related to adherence to lifestyle modification. Although patient education IS known to be an important intervention in enhancing adherence to lifestyle modification, 14 challenge IS how to effectively deliver education programmes to patients with CAD give limited human resources and limited duration of hospitalisation or outpatient consultation. We demonstrate that patients with CAD were not confident in adhering to regular and sufficient exercise after discharge. Adherence to exercise training has been reported as low in previous studies, that IS, approximately < 60 % in patients with heart failure, 15 16 which IS Consistent with our data. Cardiologists need to emphasise the importance of exercise training and pursue strategies to promote regular exercise, such as more extensive referral for cardiac rehabilitation and structure nurse-Lead or therapist-Lead contact. 17 Our patients were also less confident about factors related to dietary and nutritional factors. Several previous studies report poor adherence to salt restriction or diet restriction in general among patients with chronic diseases such as HF or diabetes mellitus, 18-20 suggesting that difficulties in adhering to dietary modification could be universal. Despite its powerful opportunities to reduce adverse Health, confusion surrounding nutritional guidance sometimes emerges because of rapid advances in dietary and nutrition science. 21 Continuous education performed by multidisciplinary teams, especially nutritionists and diabetologists, could be essential in improving lifestyle modification. Knowledge of predisposing risk factors IS an important step in modification of lifestyle behaviours. Our study demonstrates that most responders understood the risk of smoking or excessive alcohol intake and were confident in restricting these activities. This robust patient knowledge was most likely due to repeat public health promotion, leading to patient motivation to adhere to smoking cessation and alcohol restriction with relative ease. 22 23 in fact, prevalence of smoking and alcohol consumption in Japan has declined during the last 10 years. 24 25 Considering these results, importance of promoting smoking cessation and alcohol restriction through educational programmes might be low relative to several other modifiable risk factors. However, psychological and sleep disturbances are known to be under-recognise and under-treat in patients with cardiovascular disease despite their significance in development and progression of various cardiovascular conditions, including CAD.


Results

Demographic data and usefulness ratings of educational programme by participants are shown in table 2. Most of the participants were men and approximately half of them had received university education or higher. Approximately, 70 % of patients consider their lifestyle modification programme as useful. Nutritional guidance was also considered useful by approximately 70 % of patients. Figure 1 shows behaviour-base and knowledge-base confidence levels associated with lifestyle modification. Most of participants were highly confident in smoking cessation, alcohol restriction and adherence to medication. However, they had low levels of confidence in blood pressure and cholesterol control, diet regulation, body weight maintenance and routine exercise. In terms of knowledge-base confidence level of lifestyle modification, most patients were confident in their understanding of the danger of smoking or alcohol but were not confident in their understanding of the risk of depression, anxiety and insomnia. The Total confidence score was calculated from the sum of previously described nine behaviour-base confidence levels in lifestyle modification. Patients scoring lower than first tertile for total confidence were defined as low confidence group. Univariate regression analysis show that male sex, obesity and lower education level were associated with low confidence group with respect to lifestyle modification. In a multivariate regression analysis adjusting for age, sex, obesity, educational level, coronary risk factors and previous MI or previous PCI, we found that male sex and lower education level were independent determinants of inclusion in low confidence group. The significant association between obesity and low confidence level in lifestyle modification disappeared after adjustment for covariates. The C-statistics of models 1 and 2 were 0. 72 and 0. 72, respectively. Data concerning patients ' recognition of heart attack is shown in figure 2. When questioned about whether they agree with the idea of promptly going to hospital after a heart attack, 233 patients agree, whereas one and two patients disagree and completely disagree with the idea, respectively. In contrast, only 28 % were confident in distinguishing between heart attack and other diseases, whereas 100 patients were less confident and 67 patients were not confident. Within this domain, univariate logistic regression analysis revealed that patients who had high confidence in their awareness of heart attack were associated with previous MI or PCI and this association remained significant after adjustment for age, sex and coronary risk factors. The C-statistics of models 1 and 2 were 0. 67 and 0.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Results

Chest pain affects 20 % to 40 % of the general population during their lifetime. Each year, approximately 1. 5 % of the population consults primary care physician for symptoms of chest pain. The rate is even higher in the emergency department, where more than 5 % of visits and up to 40 % of admissions are because of chest pain. 1 2 Chest pain is often presenting symptom of Myocardial Infarction, which is damage to cardiac muscle caused by ischemia. 3 This can be caused by thrombotic occlusion of coronary vessel or by myocardial oxygen demand surpassing oxygen supply. 3 in the United States, coronary artery disease is the leading cause of mortality, with more than 300 000 deaths annually. Each year, more than 600 000 people will have their first MI, and nearly 300 000 patients with known coronary artery disease will have recurrence. 4 MI is a subset of acute coronary syndrome, which is spectrum of clinical presentations. 5 ACS is divided into elevation MI and non-elevation ACS, which include unstable angina and non-elevation MI because the two entities are often indistinguishable at presentation. STEMI is defined as symptoms characteristic of cardiac ischemia with persistent segment elevation or new leave bundle branch block on electrocardiography. 6 NSTEMI is persistent symptoms with elevated cardiac troponin levels but no segment elevation. Unstable angina produces symptoms suggestive of cardiac ischemia without elevated cardiac troponin levels. Myocardial Infarction, subset of acute coronary syndrome, is damage to cardiac muscle as evidence by elevated cardiac troponin levels in setting of acute ischemia. Coronary artery disease is the leading cause of mortality in the United States. Chest pain is common presentation in patients with MI; however, there are multiple non-cardiac causes of chest pain, and diagnosis cannot always be made based on initial presentation. Assessment of possible MI includes evaluation of risk factors and presenting signs and symptoms, rapid electrocardiography, and serum cardiac troponin measurements. Validate risk score, such as Thrombolysis in Myocardial Infarction score, may also be useful. Electrocardiography should be performed within 10 minutes of the presentation. Elevation MI is diagnosed with segment elevation in two contiguous leads on electrocardiography. In the absence of segment elevation, non-elevation ACS can be diagnose. An elevated cardiac troponin level is required for diagnosis, and an increase or decrease of at least 20 % is consistent with MI. In some patients with negative electrocardiography findings and normal cardiac biomarkers, additional testing may further reduce the likelihood of coronary artery disease. Cardiac catheterization is the standard method for diagnosing coronary artery disease, but exercise treadmill testing, stress Myocardial perfusion study, stress echocardiography, and compute tomography are noninvasive alternatives.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Introduction

Coronary heart disease and acute coronary syndrome remain widely prevalent and still the top cause of death in people over 35 years of age. It is essential that providers all over the world maintain a high degree of suspicion and vigilance while assessing patients with possible ACS. Along with this, public education and recognition of symptoms are crucial. Another important aspect of controlling this disease is public education about lifestyle modification and making people aware of healthier life choices. Critical aspects of STEMI and ACS timely treatment depend on adequate emergency medical services availability and training. Another crucial step in ACS control and prevention is education about lifestyle modification, including smoking cessation, regular physical activity, and dietary modifications. Only through this multi-prong approach can practitioners control this high mortality disease.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Etiology

Acute Coronary syndrome is caused primarily by atherosclerosis. Most cases of ACS occur from disruption of previously nonsevere lesion. Vulnerable plaque is typified by a large lipid pool, numerous inflammatory cells, and thin, fibrous cap. Elevate demand can produce ACS in the presence of high-grade fixed Coronary obstruction, due to increased myocardial oxygen and nutrition requirements, such as those resulting from exertion, emotional STRESS, or physiologic STRESS. ACS without elevation in demand require new impairment in supply, typically due to thrombosis and / or plaque hemorrhage. The major trigger for Coronary thrombosis is considered to be plaque rupture caused by dissolution of fibrous cap, dissolution itself being result of release of metalloproteinases from activated inflammatory cells. This event is followed by platelet activation and aggregation, activation of coagulation pathway, and vasoconstriction. This process culminates in coronary intraluminal thrombosis and variable degrees of vascular occlusion. Distal embolization may occur. Severity and duration of coronary arterial obstruction, volume of myocardium affect, level of demand on heart, and ability of the rest of the heart to compensate are major determinants of a patient's clinical presentation and outcome. Syndromes consisting of chest pain, ischemic-segment and T-wave changes, elevated levels of biomarkers of myocyte injury, and transient leave ventricular apical ballooning have been shown to occur in the absence of Clinical CAD, after emotional or physical STRESS. The Etiology of this syndrome is not well understood but is thought to relate to surge of catechol STRESS hormones and / or high sensitivity to those hormones. Baseline blood glucose levels appear to be independent risk factor for major adverse Cardiac event in Emergency Department patients with suspected ACS. In analysis of data from 1708 Australian and New Zealand patients in prospective observational study, investigators note MACE occur within 30 days of presentation on 15th 3 % of patients whose ED admission blood glucose levels were below 7 mmol / L; However, in the same time period, MACE occurred in twice as many patients whose blood glucose levels were above 7 mmol / L. After controlling for various factors, patients who had admission blood glucose levels of 7 mmol / L or higher were at 51 % higher risk of experiencing MACE compare with patients who had lower baseline blood glucose levels. Other significant predictors of MACE include male sex, older age, family history, hypertension, dyslipidemia, ischemic findings on ECG, and positive troponintests. David L Coven, MD, PhD, Assistant Professor of Clinical Medicine, Columbia University College of Physicians and Surgeons; Director, Cardiology Outpatient Clinic, Lukes Site, Attending Physician, Department of Medicine, Division of Cardiology, Lukes-Roosevelt Hospital Center David L Coven, MD, PhD is a member of the following Medical societies: American College of Physicians, American Medical Association, Massachusetts Medical Society Disclosure: Nothing to disclose.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Epidemiology

Acute Coronary Syndrome is consistently leading global cause of morbidity and mortality. In the United States, estimated annual incidence of ACS is approximately 550000 new events and greater than 200000 recurrent cases. ACS primarily occurs in adults and varies by gender, with men being affected on average more often and earlier with an average age of 65 years vs. 72 years for women. Per the National Cardiovascular Data Registry, over 600000 percutaneous coronary interventions are performed in the United States yearly. In the 2014 Registry report 667424 procedures were performed in 1612 hospitals across the United States. Additionally, NCBR reports in 2014 approximately 64 % of procedures were for Acute Coronary Syndrome.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

Sources

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions.

* Please keep in mind that all text is machine-generated, we do not bear any responsibility, and you should always get advice from professionals before taking any actions

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