Myocardial ischemia is usually due to atherosclerotic plaque, which reduces the blood supply to part of the myocardium. original plates of blood flow sufficient to meet the demand of the myocardium. When demand increases infarction, the areas of reduction becomes clinically significant angina and precipitate. Angina that is reproduced by exercise, eating, and / or stress and subsequently relieved by rest and without recent change in the frequency or severity of the activity that produces symptoms of the angina chronic stable chest. Over time, exposing patches may thicken and fractures, a thrombogenic surface on which platelet thrombus forms and collected. the patient may notice a change in the symptoms of cardiac ischemia with a change in scope or duration of symptoms. this condition is called unstable angina.
Patients with STEMI is a high risk of coronary thrombosis occluding the infarct artery. angiographic evidence of coronary thrombus formation can be seen in more than 90% of STEMI, but only 1% of stable angina pectoris, and about 35-75% of patients with unstable angina or NSTEMI. However, it is always evolving STEMI-Q-wave myocardial infarction (MI) and NSTEMI patients may develop Q waves
The excess mortality from coronary heart disease is mainly due to rupture and thrombosis of atherosclerotic plaque. Inflammation plays a crucial role in the destabilization of plaque and is widely used in coronary and peripheral vascular disease. Systemic inflammatory factors, thrombotic and hemodynamic relevant for the solution. Evidence that platelets contribute to the promotion of inflammation and thrombosis. A new theory on inflammation cytokine imbalance is by train, giving an opportunity for intervention.
A less common cause of angina pectoris is dynamic obstruction, which can be caused by an intense spasm of a segment of an epicardial artery (Prinzmetal). Coronary vasospasm is a frequent complication in patients with connective tissue diseases. Other causes include arterial inflammation and secondary unstable angina. arterial inflammation can be caused by or related to infection. secondary unstable angina occurs when the cause of precipitation is extrinsic to the coronary arterial bed, such as fever, tachycardia, hyperthyroidism, hypotension, anemia or hypoxemia. Most patients with secondary unstable angina have chronic stable angina and basic health.
Spontaneous and cocaine-related coronary artery dissection remains an unusual cause of ACS and should be included in the differential diagnosis, especially when a young woman or cocaine users are being evaluated. An early clinical suspicion of this disease is necessary for good results. cardiology consultation should be obtained in consideration for a percutaneous coronary intervention fast.
Although rare GBA, children and adults may result from the following (see myocardial infarction in children):
ACS can occur with Marfan syndrome, Kawasaki disease, Takayasu disease, or cystic medial necrosis with dilation of the aortic root aneurysm formation and dissection in the coronary artery.
Anomalous origin of left coronary artery from the pulmonary artery may occur as sudden unexplained death of the newborn.
Acute coronary ostial stenosis may occur after repair of large blood vessels in the neonatal period.
Outstanding in the left coronary artery origin of the right sinus of Valsalva can cause ACS, especially under stress.
Traumatic myocardial infarction can occur in patients of all ages.
accelerated atherosclerosis occurs in patients undergoing cardiac transplantation, recipients of immunosuppressive therapy.
ACS can occur with progeria.
Whatever the cause of unstable angina is the result of the sustained ischemia MI.
Although the exact incidence of ACS is difficult to determine the output data show that 1,680,000 hospital discharges for ACS occurred only in 2001.
In Britain, the annual incidence of angina pectoris is estimated at 1.1 cases per 1000 men and 0.5 cases per 1000 women aged 31-70 years. in Sweden, the chest pain of ischemic origin is estimated to affect 5% of all men aged 50-57 years. in industrialized countries, the annual incidence of unstable angina about 6 cases per 10,000 inhabitants.
Mortality and morbidity
When the only treatment for angina pectoris and nitroglycerin has been the limitation of activity, patients newly diagnosed with angina had a 40% incidence of myocardial infarction and a mortality rate of 17% in 3 months. A recent survey shows that mortality by 30 days of the AEC has decreased as the treatment is improved, a statistically significant reduction of 47% over the 30-day mortality among newly diagnosed ACS from 1987 to 2000. this decrease in mortality due to aspirin, glycoprotein (GP) IIb / IIIa and coronary revascularization interventions or medical care.
The clinical features associated with poor prognosis are advanced age, male gender, prior MI, diabetes, hypertension, and multiple vessel disease or left main stem.
The incidence is higher among men, all patients under 70 years. the reason is that the cardioprotective effect of estrogen in women. at 15 years of accident postmenopausal angina occurs with equal frequency in both sexes. Proof that women are more often coronary events without typical symptoms, which may explain the frequent failure to diagnose first ACS in women.
ACS is becoming increasingly common with age. among people aged 40-70 years, ACS diagnosed more often in men than in women. among people aged 70 years, men and women are affected almost equally.
Usually, angina is a symptom of myocardial oxygen deficiency, which appears in some circumstances, the increased oxygen consumption. it is usually described as pressure or heaviness in the chest, repeated activities or conditions that increase myocardial oxygen consumption.
Not all patients experiencing chest pain. some present only with the neck, jaw, ear, arm, or epigastric discomfort.
Other symptoms such as shortness of breath or extreme weakness, can represent anginal equivalents.
A patient may present to the emergency room due to a change in the pattern or severity of symptoms. A new case of angina pectoris is more difficult to diagnose because symptoms are often vague and similar to those caused by other conditions (eg, indigestion, anxiety).
Patients may have no pain and can not complain about the brevity of episodic breathing, weakness, dizziness, sweating, nausea or vomiting.
Patients may complain of the following:
The pain is usually described as pressure, squeezing, or burning sensation in the chest region and may radiate to the neck, shoulders, jaw, back, upper abdomen, or both arms
dyspnea on exertion that resolves at rest or pain
Diaphoresis sympathetic discharge
Nausea by vagal stimulation
Decreased exercise tolerance
Patients with diabetes and elderly patients are more likely to be atypical presentations, and offer only vague complaints such as weakness, shortness of breath, dizziness and nausea.
It involves breakthrough pain that lasts 5.15 minutes
Caused by an effort
Relieved by rest or nitroglycerin
Unstable angina: patients have an increased risk of adverse cardiovascular events such as heart attack or death. Three different clinical forms exist, as follows:
New onset angina of effort
Angina pectoris with increasing frequency or duration, or refractory to nitroglycerin
Angina at rest
angina (Prinzmetal angina)
occurs primarily at rest
Powered by smoking
Presumably due to coronary vasospasm
The elderly and people with diabetes can have very subtle presentations and may complain of fatigue, fainting, or weakness. the elderly may also have mental status are changed. People already suffering from disorders of consciousness or dementia may have no recollection of the last symptoms and perhaps no complaints.
Half of all cases of ACS are clinically silent because they do not cause the classic symptoms described above, and not be recognized by the patient. Maintain a high index of suspicion of ACS in particular when women evaluate, in diabetic patients, older patients, patients with dementia and those with a history of heart failure.
The physical findings are often normal. if the chest pain is ongoing, the patient usually lies quietly in bed and may appear anxious, sweating and pallor.
High blood pressure can precipitate angina or high levels of catecholamines, which reflects the anxiety caused by an external stimulus or sympathomimetics.
Hypotension indicates ventricular dysfunction due to myocardial ischemia, acute myocardial infarction or valvular dysfunction.
third heart sound (S3) may be present.
A new murmur may be due to papillary dysfunction.
Rales is a lung examination may suggest left ventricular (LV) dysfunction or mitral regurgitation.
Presence of a fourth heart sound (S4) is a common finding in patients with poor ventricular compliance by a pre-existing ischemic heart disease or hypertension.
atherosclerotic plaque is the main cause. Coronary vasospasm is less common.
Other causes of angina are:
ventricular hypertrophy due to hypertension, valvular disease or cardiomyopathy
embolic occlusion of coronary arteries
Hypoxia, as a carbon monoxide poisoning or acute pulmonary disease
Cocaine and amphetamine, which increases myocardial oxygen demand and may cause vasospasm
underlying coronary disease, which can be unmasked by severe anemia
Infection of epicardial arteries
Coronary artery dissection
Risk factors for the ACS should be documented and include:
Diabetes mellitus (DM)
Prior cerebrovascular accident (CVA) – These patients constitute 7.5% of patients with ACS and have high risk characteristics.
Consumption of methamphetamine
Stress at Work
connective tissue diseases
In general, patients with chest pain flown must be operated under the assumption that the pain is ischemic. prehospital interventions should be guided by the nature of the complaint to the factors present, the individual risk, and associated symptoms (eg difficulty breathing, hemodynamic instability, the appearance of ectopy). Airway, breathing and circulation should be evaluated promptly with institution of CPR, ACLS-guided interventions, or other measures, as indicated for unstable patients.
ACS spectrum concept is a useful framework for developing therapeutic strategies. antithrombin therapy and antiplatelet therapy should be administered to all patients with ACS irrespective of the presence or absence of ST-segment elevation. Patients with persistent ST segment elevation are candidates for reperfusion therapy (either pharmacological or catheter-based) to restore power quickly in the artery occluded infarct epicardial. Patients without ST elevation are not candidates for immediate pharmacological reperfusion, but should receive anti-ischemic and PCI, if applicable. the time is myocardium is a saying do not forget that the survival has been shown to correlate with time to reperfusion in patients with acute myocardial infarction. Many centers set goals and routinely record, door-to-ECG, door-to-needle (thrombolysis) or access door to disease (for patients receiving PCI) both as a measure of quality care.
Rathore and colleagues found that delayed primary percutaneous coronary intervention after a heart patient with ST-elevation myocardial infarction (STEMI) arrives at the hospital is associated with more mortality.9 in a prospective cohort study of 43,801 patients included the American College of Cardiology Cardiovascular Data Registry, 2005-2006, plus door-to-balloon times were associated with higher risk-adjusted mortality in the hospital, a continuous non-linear (30 min = 3%, 60 min = 3.5%, 4.3% = 90 min, 120 min = 5.6%, 150% = 7 min, 180 min = 8.4%, P
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