Diagnosis 2 of 3 criteria-ST-segment changes or new Q waves must be present on EKG, reported chest pain characteristic of AMI, and the must have abnormal elevation of cardiac enzymes.
Clinical evaluation 12 lead ECG, and cardiac troponin are the 3 pillars of diagnosis in ED.
Approximately one person has a myocardial infarction every 40 seconds, and more than 1 million coronary events occur each year, of which 1/3 are recurrent events.
Adults ages 75 years and older comprise only 6% of the population, but up to 40% of acute myocardial infarctions, 60% of AMI in deaths and 2/3 of all cardiovascular deaths in the United States.
High sensitivity cardiac troponin allows accurate rule out and rule in acute myocardial infarction within 1 hour in up to 75% of cases.
Coronary artery plaque rupture exposes blood to plaque, resulting in deposition and activation of platelets, inflammation of thrombi: complete thrombotic occlusion produces ST segment elevation myocardial infarction, whereas incomplete coronary bloodflow impairment results in unstable angina, or when biomarkers for myocardial. injury a present, a non-ST segment elevation myocardial infarction.
Presently, nearly 90% of patients hospitalized for an acute MI survive.
There has been a marked decrease in the incidence of AMI and decrease case fatality rate for patients hospitalized with AMI.
24-60% do not have EKG changes diagnostic of AMI at the time of admission to hospital.
Patients with AMI inappropriately sent home from an emergency department have approximately a two fold higher risk adjusted thirty-day mortality then for those patients hospitalized (Pope JH et al).
From an occlusive disease is recognized by ST segment elevation.
Approximately 1.1 million occur in the U.S. annually.
Approximately 800,000 Americans have a new MI each year, and approximately 470,000 have a recurrent MI.
Each year 7 million patients suffer an acute myocardial infarction worldwide.
Approximately one in five Medicare patients are readmitted to the hospital within 30 days after being discharged for in acute myocardial infarction.
Elderly patients represent approximately 30% of patients admitted with an acute MI.
Elderly patients with acute MI have a worse prognosis compared to younger patients.
In a large community based population, the incidence of myocardial infarction decreased after 2000, and the incidence of ST-segment elevation myocardial infarction decreased markedly after 1999 (Yeh, RW).
Reductions in short term case fatality from acute myocardial infarction from a decrease in ST-elevation myocardial infarction incidence and from a lower death rate after non-ST-segment elevation myocardial infarction (Yeh RW).
Overall incidence around 1-3 cases per 1000 person-years.
More than 100,000 women younger than 65 years of age have an acute MI each year in the U.S., and this represents 21% of all acute MI cases among women.
Is easier to diagnose in the presence of right bundle branch block than in left bundle branch block.
One third of patients do not have typical chest pain: particularly among those who present with atypical or subtle presentations, such as the elderly, women or those with diabetes.
90% of patients with AMI present with chest pain and or chest discomfort of some nature, however some patients present without typical chest pain.
Women with acute myocardial infarction more often present with atypical symptoms, resulting in more difficult diagnosis and treatment, and subsequent worse outcomes, with increased rates of readmission, reinfarction, and death.
Acute myocardial infarction: both sexes most often present with chest pain, but compared with men, women were more likely to present with pain between the shoulder blades, nausea or vomiting, and shortness of breath.
Pathophysiology reflects disruption of a coronary artery plaque followed by a coronary artery thrombosis.
Animal studies reveal a direct relationship between coronary occlusion and extent of myocardial necrosis with myocyte cell death beginning as early as 20 minutes after such occlusion with completion of the process by 6 hours.
Prompt reperfusion treatment can limit myocardial necrosis, and is the gold standard treatment for acute MI.
Size of infarction is a major determinant of risk of death and likelihood of developing heart failure.
High proportion-17-44% of patients have clinically unrecognized myocardial infarctions.
Prevalence and prognosis of unrecognized myocardial infarction in older patients with and without diabetes may be higher than previously suspected.
Subclinical coronary plaque rupture occurs frequently, especially in diabetic patients, which may be related to unrecognized myocardial infarction.
Prevalence of unrecognized myocardial infarction based on ECG, but ECG has limited sensitivity that varies with infarct location, and Q waves may resolve with time.
Cardiac magnetic resonance with late gadolinum enhancement is more sensitive than ECG for the detection of myocardial infarction.
In a study of older patients the prevalence of unrecognized MI by cardiac magnetic resonance was higher than the prevalence of recognized MI and was associated with increased mortality risk (Schelbert EB et al).
In the above study unrecognized MI by ECG prevalence was lower than that of recognized MI and was not associated with increased mortality risk.
Only 60% with myocardial infarction are older than 65 years of age, but they account for 80% of myocardial infarction related deaths.
Individuals with bundle-branch block have a high baseline mortality and receive the greatest incremental improvement in survival when given thrombolytic agents.
Both right and left bundle branch blocks associated with increased hospital mortality in the setting of an acute myocardial infarction.
Patients that have right or left bundle branch blocks at the time of acute myocardial infarction have lower ejection fractions and higher in patient and long-term mortality.
Patients who develop bundle branch blocks with acute myocardial infarction are older and more likely to have a history of coronary artery disease compared to patients without bundle branch blocks.
Hyperkalemia is common in patients hospitalized for acute myocardial infarction and is associated with marked increases in mortality even with mild elevations in potassium levels (Grodzinsky A et al).
Risk factors for unrecognized myocardial infarction include advanced age, female sex and absence of previous angina.
Patients with AMI with high heart rate at rest have higher mortality.
Women have a higher rate of misdiagnosis, more delayed diagnoses, a higher AMI mortality, and possibly less benefit from early revascularization.
The presence of anemia in acute myocardial infarction is associated with a worse prognosis.
Blood transfusions or a liberal blood transfusion strategy compared with no blood transfusions or a restricted blood transfusion strategy is associated with higher all cause mortality rates in patients with acute myocardial infarction (Chatterjee S et al).
In the above study liberal blood transfusion strategy was associated with a higher risk of subsequent myocardial infarction.
Risk of acute myocardial infarction following total hip or knee replacement was elevated during the first two weeks after the procedure (Lalmohamed A et al).
In the above study thee absolute six-week risk of acute myocardial infarction was 0.51% for hip replacement, and 0.21% for knee replacement.
Patients less than 50 years of age have lower morbidity and mortality after acute myocardial infarction.
Unemployment status, multiple job losses, and short periods without work are significant risk factors for acute cardiovascular events (Dupree M et al).
Risk of death associated with unrecognized myocardial infarction estimated to be similar to that of clinically recognized myocardial infarctions.
Sudden cardiac death due to ventricular tachyarrhythmias account for 20 to 50% of all deaths in patients with acute myocardial infarction.
Acute myocardial infarction is a pro-thrombotic state associated with left ventricular thrombus formation.
With the exception of beta blockers ant arrhythmic drugs do not reduce the risk of sudden death by tachyarrhythmias.
In a randomized trial patients with reduced left ventricular ejection fraction of less than 40%, a heart rate of 90 or more beats per minute on the first available EKG, nonsustained ventricular tachycardia with 150 or more beats per minute during Holter monitoring were randomly assigned to medical therapy or implantable cardioverter defibrillator: overall mortality was not reduced in the ICD group (Immediate Risk-Stratification Improves Survival trial (IRIS)).
Intravenous thrombolytic therapy lowers the early mortality rate by an estimated 20-30%.
Patients with an open infarcted artery after an acute myocardial infarction have better outcomes than patients whose arteries remain closed.
Women more likely to be misdiagnosed and more likely to die of their first infarction than men.
Recommended that aspirin be given on day 1 of AMI and continued indefinitely in all patients.
Clopidogrel is recommended as an alternative to aspirin when there is intolerance or contraindication to aspirin.
The WBC count measured within 24 hours of admission is a strong and independent indicator of in-hospital and 30-day mortality as well as in-hospital clinical events.
Thrombocytosis may predispose to AMI, and the incidence in patients with essential thrombocytosis is greater than 9%.
The development of thrombocytopenia associated with poorer clinical outcomes, with increased 30 day and 1 year mortality.
Thrombocytopenia in acute myocardial infarction is an independent predictor of bleeding, stroke, cardiogenic shock and death.
Triggers an inflammatory response with a release of proinflammatory cytokines with chemoattractant properties which contribute to neutrophil recruitment to the infarcted area.
Proinflammatory cytokines promote demargination of intravascular neutrophils and accelerates release of neutrophils by the bone marrow and activation of granulocytes, so that the early post MI period is associated with leucocytosis.
Neutrophil count at presentation of MI is strongly associated with adverse outcome.
Proinflammatory cytokines TNF, IL-I and IL-6 are increased in response to myocardial injury of MI.
IL-6 elevation after MI associated with increase LV end-diastolic volume and remodeling.
Chronic anemia that is present at the time of admission to the hospital and hospital acquired anemia in patients with anormal hemoglobin at the time of admission, are associated with greater mortality and worse health status in patients with AMI.
Hospital acquired anemia with acute MI may be secondary to bleeding, and impaired hematopoiesis from pre-existing and a non-modifiable factors such as inflammation, chronic renal disease, CHF.
Inflammation is plays a central role in the pathogenesis of atherosclerosis and acute coronary events.
30% reduction in 1-year mortality in patients with diabetes receiving insulin following myocardial infarction to maintain levels of blood glucose to below 210 mg/dL.
Only 0.9% triggered by sexual activity.
Physical exertion and anger account for 3-5% of acute myocardial infarctions.
Virtually all patients sustaining an acute myocardial infarction have underlying atherosclerosis a but less than half of such patients have prior symptomatology.
Recurrent acute myocardial infarction constitutes 30-50% of all deaths resulting from myocardial infarction.
Patients treated by high-volume admitting physicians are more likely to survive at 30 days and 1 year.
Higher exercise capacity at baseline after MI associated with lower risk of death.
Angioplasty restores normal blood flow in 80 to 95% of patients.
Cardiogenic shock represents the most ominous complication of AMI.
Mortality associated with cardiogenic shock about 60% when treated conservatively.
Complicated by shock associated with a mortality of 75% in patients not undergoing catheterization.
Complicated by shock associated with a mortality of 48% in those who undergo coronary artery bypass.
Complicated by shock associated with a mortality of 35% in those who undergo percutaneous coronary intervention with stenting.
Thrombolytic therapy restores normal blood flow in 50 to 70% of patients.
Estimated that improvement in care of patients with acute myocardial infarction accounts for about 15% of the overall decline in coronary artery mortality.
Low technology interventions-aspirin, beta-blockers, ACE inhibitors explain about 44% of the decline in 30-day mortality after and acute myocardial infarction.
High technology interventions, including thrombolysis, angioplasty explain approximately 32% of the decline in 30-day mortality after acute myocardial infarction.
The rates of death, nonfatal reinfarction and stroke are lower after primary angioplasty than after thrombolytic therapy.
Coronary stenting plus abciximab has a greater degree of myocardial savage and better clinical outcomes than does fibrinolysis with tissue plasminogen activator.
40%-50% of post-infarction deaths caused by ventricular tachyarrhythmias.
Ventricular septal rupture occurs in 1-4% of cases.
Rupture of the free wall on the left ventricle occurs in one to 4% of cases.
Ventricular rupture presents as acute or recurrent chest pain and is followed by electromechanical dissociation.
Ventricular rupture leads to pericardial effusion and may be associated with jugular venous distension, hypotension, pulsus paradoxus, and decreased intensity of heart sounds.
Reperfusion by thrombolytic treatment or primary angioplasty decreased the incidence of ventricular septal rupture.
Ventricular septal rupture usually occurs 3-7 days after myocardial infarction and it is associated with a holosytolic murmur, an S3 gallop and a thrill.
Left ventricular free wall rupture with tamponade occurs in 1-4% of myocardial infarctions and occurs 3-7 days after the event.
Left ventricular rupture associated with jugular venous distension and pulsus paradoxus.
Papillary muscle rupture occurs in about 1% of patients usually between 2 and 7 days after myocardial infarction.
Papillary muscle rupture associated with murmur of mitral regurgitation in 50% of cases.
The posterior papillary muscle ruptures more frequently than the anterior papillary muscle since the former is typically perfused by a single blood vessel from the right coronary artery or a tributary.
Right ventricle infarction carries the worst prognosis of any territorial subtype of MI (Assali AR et al).
Right ventricular infarction has a mortality of 10% by 30 days.
AV node is usually supplied by the right coronary artery and heart block is most common with inferiot wall infarction, with 4-10% having complete heart block
Nearly 50% of patients with AMI have normal cholesterol levels.
Incidence of associated stroke about 1.3%.
Higher mortality rate in women secondary to later arrival at hospital, less likely to be given aspirin acutely and less likely to be prescribed beta-blockers.
Beta blockers reduce all-clause mortality in patients with AMI with high heart rate, but not those with low heart rates.
In a study of 916,380 patients from the National Registry of Myocardial Infarction evaluating the hospital case fatality rate from June 1994 through December of 2006: there was a significant improvement in the hospital mortality after acute myocardial infarction in women, particularly younger ones, than men.
The higher mortality rates of younger women compared to men is narrowing.
Elevated troponim I results on admission predict a higher incidence of CHF, shock, death and primary angioplasty failure.
Myoglobin elevations occur in more than two thirds of patients with AMI at 3 hours and in nearly all patients by 6 hours after the onset of chest pain.
If myoglobin level does not increase within the first 3 to 6 hours after the onset of chest discomfort, an AMI has not occurred.
25% of patients wait >6 hours before seeking care.
C-reactive protein levels increase beginning 6 hours after the onset of ischemia in myocardial infarction and peaking at about 50 hours.
C-reactive protein values after myocardial infarction predict outcomes including death and congestive heart failure.
Patients with AMI treated by high-volume admitting physicians are mortality likely to survive at 30 days and 1 year.
CK-MB levels do not increase until 4 to 8 hours after the ischemic event, and they return to normal within 48-72 hours.
Historically it has been recommended that potassium levels should be maintained between 4.0-55 milliequivalents per liter in AMI patients.
In a retrospective study using the Cerner Health Facts database including 38,689 patients with biomarker confirmed AMI admitted to hospitals. Between January 2000 in December 2008: the lowest mortality was observed in patients with serum potassium levels between 3.5, and less than 4.5 mEq per liter compared with those who had a higher a lower potassium levels (Goyal A et al).
Glucose-insulin-potassium infusions in patients without congestive heart failure improve survival by reducing infarct size and decreasing ischemic cellular injury.
Infusion of glucose-insulin-potassium in the OASIS-6 and the CREATE-ECLA trials did not provide benefit in acute ST-segment elevation myocardial infarction (STEMI) and may increase early postinfarction deaths due to increases in glucose, potassium and fluid gains.
And increased fasting plasma glucose level is associated with a relatively higher risk of in-hospital mortality in men but not in women (Yang SW et al).
There is a U. shaped relationship between fasting plasma glucose levels and in-hospital and three-year mortality for acute myocardial infarction (Yang SW et al).
Smokers are 3 times more likely to have an MI, and persistent smoking after an acute MI carries a 50% higher chance of death in the firts two years.
Associated with increased free fatty acid levels because of lipolytic effects of catecholamines.
Observation studies of acute myocardial infarction and treatment with metformin is associated with lower peak CK levels, troponins and improve survival after STEMI in patients type 2 diabetes, compared with other anti-glycemic strategies.
Among patients without diabetes and who presented with a STEMI and undergo primary PCI, the use of metformin compared with placebo does not improve left ventricular ejection fraction after 4 months (Lexis CP et al.
Elevated free fatty acids cause myocardial membrane damage, arrhythmias, decreased cardiac function and metabolic changes which can be decreased by a glucose-insulin-potassium infusion.
The type of arrhythmias observed depends on its temporal relation to the myocardial infarction so during the acute phase ischemic associated metabolic changes may trigger ventricular fibrillation which accounts for half of sudden deaths.
Patients with left ventricular dysfunction congestive heart failure, or both, after acute myocardial infarction are at high risk for sudden death or cardiac arrest.
Advanced age an independent predictor of sot term morbidity and mortality in postinfarct patients.
Risk of sudden death highest in the early period after acute myocardial infarction and in patients with lowest ejection fraction and decreases significantly over time till it stabilizes at about 1 year.
Hospital mortality higher among patients admitted on weekends compared with those admitted on weekdays and there is a lower utilization of cardiac procedures as well.
Time between admission and performance of cardiac procedures is longer for patients admitted on weekends than for those admitted during weekdays.
Cardiac rehabilitation participation markedly reduces risk of readmission and death after incident myocardial infarction (Dunlay SM et al).
The routine use of oxygen therapy in patients with acute myocardial infarction with normal oxygen saturation levels shows no benefit on meta-analysis studies.
Factors associated with increased risk of re-hospitalization for patients with AMI include: older age, development of acute heart failure, and the presence of kidney disease, diabetes, and peripheral vascular disease.
Patients 75 years or older with acute myocardial infarction have a cognitive impairment present in 17% of patients and is associated with a higher mortality.