I am trying to find out who collects the data for when they do a study on Acute Myocardial Infarction?
Where can I find information on Acute Myocardial Infarction? I want to know who takes the responsibility to collect data for the studies made to make possible improvement. Who will be collecting the data? I am just curious I've ask several people but they don't have an anwer. Could you direct me where I can find such information?
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The AMA collects the data from state agencies. The system works as long as the doctors do their part. (
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does anyone know how painful a myocardial infarction is?
My Mother died from myocardial infarction. I was told there was no pain, but I am not sure I believe that.
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A myocardial infarction is the death of heart muscle cells that have been deprived of blood flow by a blocked artery. How much pain was involved depended on her specific heart condition. For some such a death is truly painless. In cases of sudden heart death the individual becomes unconscious so quickly they feel no pain and death is within minutes after that. My uncle worked in his small vegetable garden one morning for a couple of hours on a bright sunny, relatively cool day in late August. He came in got a drink of water then sat in his chair and died. No warning, no pain, he never uttered a sound. It was as if he just went to sleep. It was found that he had suffered a so called "massive heart attack" caused by blocked coronary arteries. The only way anyone could know if your mom suffered was to have been present at the time and witnessed her passing. I hope for her sake there was no pain. My mom died several years ago from an enlarged heart. She became unconscious and then just stopped breathing. I am sorry for your loss. (
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How does LBBB make diagnosing myocardial infarction more difficult?
If someone could explain in reasonably simple terms please. Also other than the "william morrow" method are there any set differences which will aid in differentiating LBBB from RBBB.
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If a person has LBBB it can make it more difficult to make an infarct diagnosis based on an ECG alone. This is because the baseline ST segments and T waves are often shifted in a discordant direction which can confuse an AMI diagnosis. Usually an infarct diagnosis isn't made on an ECG alone. If there is doubt, the Sgarbossa criteria (see here http://www.ncbi.nlm.nih.gov/pubmed/8559200?dopt=Abstract ) can be used, although studies show that electrocardiographic criteria are poor predictors of AMI in LBBB situations and suggested that all patients suspected of AMI with LBBB should be considered for thrombolysis regardless. Of course, enzyme studies should always be done.
And the william marrow is the mnemonic I use. It's 'W'on V1 and 'M' + V6 which are specific for LBBB because in V1 it is usually in 'W' pattern, while in V6 it tends to be M. Remember, when LBBB is present, the septum depolarizes from R to L, not from L to R. This means the first ECG change produced in LBBB is a loss of the normal septal r wave in lead V1 + the normal septal q wave in lead V6. There is also a wide QRS complex because the total time for LV depolarization is prolonged in LBBB. (
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How long can you live after being diagnosed with Acute Myocardial Infarction?
If you have a Family History of Heart Disease, and you are a Smoker with High Cholesterol, how long can you live, if you make positive Changes? Will I definitive get a Heart Disease down the Road? Since I got the Diagnose,Iam terrified. Need Info
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Well, how long a person lives after a heart attack (acute MI) varies hugely depending on how much of the heart muscle (myocardium) was damaged and died off during the event; some people die instantly whereas some are able to go back to living fairly normal lives.
I would definitely recommend you make some positive lifestyle changes. Smoking is an absolutely terrible thing to do to your body (hearing that a patient smokes makes any doctor cringe) and it's especially bad when you've got a high chance of heart disease. However, if you make some changes now you can certainly improve your health and hopefully avoid heart disease. Talk to your doctor and work out a plan to stop smoking, eat a little better (high cholesterol is also a very poor risk factor for heart disease), and get some more exercise.
It's definitely not too late - good luck! (
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Why is pain felt in a myocardial infarction?
I think it would be either because there is not enough oxygen being delivered, or narrowing of the arteries. Can someone help me out with the answer to this question?
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1. The heart is working far harder than in healthy times, trying to push though the extreme narrowing or occlusion. It is a muscle, not so different than other muscles in your body.
2. Tissue is dying, because oxygen levels are low. This is painful. (
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What are the first things to ask a post myocardial infarction patient before exercise prescription?
Thanks!
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A lot of people are referred to a cardiac rehab-type exercise program where they can be monitored closely. Ask your doc if there is one available in your area.
If not, ask what activities can be done safely. Walking is a good place to start, gradually increasing intensity as tolerated.
Good luck, hope this is somewhat helpful. (
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What are the different protocol used for myocardial infarction?
This may help you:
This is the first of five articles on myocardial infarction
Preview: The average time that elapses from a patient's first awareness of heart attack symptoms to start-up of specific reperfusion therapy is currently 4 hours. The National Heart Attack Alert Program wants to see this time reduced to 2 hours. Such dispatch would surely benefit patients, because when it comes to thrombolytic therapy, the sooner the better. Dr Ryan summarizes the new recommendations for handling patients with acute myocardial infarction rapidly and efficiently, from the 911 call and transport to the emergency department, through the important first 24 hours of hospitalization, to hospital discharge and long-term management.
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The American College of Cardiology and the American Heart Association recently updated the guidelines for managing acute myocardial infarction, which are intended for physicians, nurses, and allied healthcare personnel who attend to patients with suspected or established infarction. The guidelines are published in their entirety in the Journal of the American College of Cardiology (November 1996) (1) and include specific recommendations on 35 separate treatment aspects. Each series of recommendations regarding indications for a diagnostic procedure, a particular therapy, or an intervention are classified as class I, II, or III (table 1) according to the weight of evidence and the degree of agreement that such therapy or intervention is beneficial, useful, and effective.
Table 1. Ranking of evidence indicating a diagnostic procedure, therapy, or intervention for acute myocardial infarction.
Class I: Evidence or agreement that a procedure or treatment is beneficial, useful, and effective
Class II: Conflicting evidence or divergent opinions regarding usefulness or efficacy of a procedure or treatment
IIa: Weight of evidence or opinion favors usefulness or efficacy
IIb: Usefulness or efficacy less well established
Class III: Evidence or agreement that a procedure or treatment is not useful and may be harmful
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This synopsis provides an overview of managing a routine case of acute myocardial infarction. For more complex cases with complications, readers should see the full text of the guidelines (see box below).
Prehospital issues
Perhaps the newest and most important message to be found in the updated acute myocardial infarction guidelines relates to the fact that of the 900,000 people in the United States who experience acute myocardial infarction each year, about 20% die before reaching the hospital and 30% die within 30 days. Accordingly, much emphasis is given to the prehospital phase of management.
The National Heart, Lung, and Blood Institute's National Heart Attack Alert Program divides management into four parts: (1) patient awareness of symptoms, (2) transportation, (3) hospital admission, and (4) reperfusion time (1). These four parts take the patient from onset of symptoms to start-up of specific reperfusion therapy, which currently averages 4 hours. The objective of the National Heart Attack Alert Program is to reduce this time by 50%. Such a reduction requires that all physicians provide specific detailed information on signs and symptoms of a heart attack to persons at risk (eg, those with hypertension, diabetes) during routine office visits.
All physicians should take a role in assisting their communities in establishing state-of-the-art 911 emergency systems and in designing and adhering to written protocols regarding triage of patients entering the emergency department with suspected acute myocardial infarction. Since early-phase deaths are nearly all arrhythmic in origin, there is an urgent need to provide the necessary protection with antiarrhythmic medications and defibrillators as soon as possible.
Initial recognition and emergency department management
Every emergency department should be organized for immediate triage so that on entry, patients suspected of having acute myocardial infarction are sent to an area where specific evaluation can be accomplished promptly. All other patients should be directed to another area of the emergency department, where con ditions can be handled according to priority of need.
Initial evaluation
Initial evaluation of acute myocardial infarction should be accomplished within 10 minutes of the patient's arrival in the emergency department and should include thoughtful history taking conducted without haste. A 12-lead electrocardiogram (ECG) should be performed concurrently with this evaluation.
The object of history taking is to further classify the patient's status according to likelihood of infarction. The following classification should be used: (1) definitely myocardial infarction, (2) probably myocardial infarction, (3) probably not myocardial infarction, and (4) definitely not myocardial infarction. Eliminating such commonly used categories as "possible myocardial infarction" or "rule out myocardial infarction" forces the interviewing physician to make a mental commitment to the actual diagnosis. This commitment sharpens the focus and is worth making before ECG results are reviewed.
Physical examination should be targeted to exclude the well-known mimics of acute myocardial infarction: aortic dissection, acute pericarditis, spontaneous pneumothorax, and acute pulmonary embolism.
An ECG showing ST-segment elevation (> 0.1 mV) in contiguous leads provides strong evidence of thrombotic coronary artery occlusion. Patients with this finding are candidates for immediate reperfusion therapy, with either thrombolytic therapy or primary percutaneous transluminal coronary angioplasty (PTCA). Patients with symptoms consistent with acute myocardial infarction and left bundle branch block should be treated similarly to patients with ST-segment elevation.
In contrast, patients without ST-segment elevation, no matter how strong the indications from history taking, should not receive thrombolytic therapy. Recent data suggest that patients with ST-segment depression exclusively may have a worse outcome if they receive thrombolytic therapy, and benefits of primary PTCA in these patients are uncertain (2).
Recommendations are that patients undergoing prompt evaluation in the emergency department for suspected myocardial infarction immediately receive the following (table 2):
Oxygen by nasal prongs
Sublingual nitroglycerin (unless systolic blood pressure <90 mm Hg or heart rate <50 or >100 beats per minute)
Adequate analgesia with morphine sulfate or meperidine hydrochloride
Aspirin (160 to 325 mg, orally)
Table 2. Recommendations for initial emergency department management of suspected myocardial infarction
Initial evaluation with electrocardiography in <10 min
Oxygen by nasal prongs, establishment of IV access, continual electrocardiography
Sublingual nitroglycerin (unless systolic blood pressure
<90 mm Hg or heart rate <50 or >100 beats per min)
Analgesia (morphine sulfate or meperidine hydrochloride)
Aspirin (160-325 mg po)
Measurement of lipid, electrolyte, magnesium, enzyme levels
Thrombolysis or percutaneous transluminal coronary angioplasty if ST segment elevated >0.1 mV or left bundle branch block present (door-to-needle time <30 min or door-to-dilatation time <60 min)
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Thrombolytic therapy
The second important message of the current guidelines is the emphasis on use of thrombolytic therapy in all myocardial infarction patients who have ST-segment elevation. Compared with standard medical therapy, use of thrombolytic agents exerts a highly significant 21% proportional reduction in 35-day mortality. This figure corresponds to an overall reduction of 21 deaths per 1,000 patients treated and is based on data from more than 10 large, randomized trials that enrolled more than 1,000 patients (3).
A powerful time dependent effect on mortality has also been observed in administration of thrombolytic agents. The greatest benefit occurs when these agents are started within 3 hours of onset of symptoms, although definite benefit is still observed when they are begun within 12 hours (table 3). An estimated 35 lives are saved per 1,000 patients treated when thrombolysis is started in the first hour of symptom onset, compared with 16 lives saved per 1,000 patients treated within 7 to 12 hours of symptom onset.
Table 3. Recommendations for use of thrombolytic therapy in acute myocardial infarction
Class I
ST segment elevated >0.1 mV in two or more leads,
time to therapy <12 hr, age <75
Bundle branch block and history suggesting acute
myocardial infarction
Class IIa
ST segment elevated, age >75
Class IIb
ST segment elevated, time to therapy >12-24 hr
Systolic blood pressure >180 mm Hg and/or diastolic
blood pressure >110 mm Hg at presentation
Class III
ST-segment depression only
ST-segment elevation, time to therapy >24 hr, no pain
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Another point that is emphasized in the current guidelines is that thrombolysis is of benefit regardless of the patient's age and sex, the presence of comorbid conditions (eg, diabetes), or a history of myocardial infarction. Benefit is greater in the setting of anterior myocardial infarction, low blood pressure (systolic pressure <100 mm Hg), or high heart rate (>100 beats per minute). Benefit is less with inferior myocardial infarction, except for the subgroup with associated right ventricular infarction (ST-segment elevation RV-4) or anterior-segment depression.
The third important message of the guidelines is wider use of thrombolytic agents and universal use of aspirin. The Second International Study of Infarct Survival (4) found that aspirin in daily doses of 160 to 325 mg resulted in a reduction in 35-day mortality equal to the reduction brought about with use of streptokinase. Thus, if a patient has an absolute contraindication (table 4) or a relative contraindication (table 5) to thrombolytic therapy, aspirin should be promptly administered. This holds true for all patients with acute myocardial infarction, regardless of ST-segment change. Use of ticlopidine hydrochloride can be considered in patients who are intolerant of aspirin.
Table 4. Absolute contraindications to use of thrombolytic therapy in acute myocardial infarction
Active internal bleeding
Suspected aortic dissection
Known intracranial neoplasm
Previous hemorrhagic stroke at any time; other strokes or cerebrovascular events within 1 yr
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Alternative PTCA
Although there are a few randomized, controlled trials which taken together might suggest that primary PTCA is more effective than thrombolytic therapy (5-7), the committee compiling the new guidelines does not agree. Rather, they recommend that primary PTCA be performed as an alternative to thrombolytic therapy, provided it can be accomplished in a timely fashion by persons skilled in the procedure and supported by experienced personnel. Since less than 20% of US hospitals have the capability to perform primary PTCA, it is unlikely to ever become the primary method of treatment for acute myocardial infarction. The committee also expresses concern that a policy of routine primary PTCA might result in unacceptable delays in achieving reperfusion in a substantial number of cases, because thrombolytic therapy must be withheld to perform primary PTCA.
Table 5. Relative contraindications to use of thrombolytic therapy in acute myocardial infarction
Severe uncontrolled hypertension on presentation (blood pressure >180/110 mm Hg)
History of chronic severe hypertension
History of cerebrovascular accident or other intracerebral disease
Recent trauma (within 2-4 wk) or major surgery (<3 wk)
Traumatic or prolonged (>10 min) cardiopulmonary resuscitation
Noncompressible vascular punctures
Recent (within 2-4 wk) internal bleeding
For use of streptokinase or anistreplase: prior exposure or allergic reaction (use tissue plasminogen activator)
Known bleeding diathesis or current use of anticoagulant (International Normalized Ratio >2-3)
Pregnancy
Active peptic ulcer
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Once reperfusion therapy is chosen, the patient should be hospitalized and subsequent management undertaken, regardless of initial ECG findings.
Hospital management in the first 24 hours
Since death from acute myocardial infarction often occurs during the first 24 hours, patients should receive continuous ECG monitoring once they are hos pitalized. In addition, the diagnosis of acute myocardial infarction should be confirmed with serial ECGs and measurements of serum cardiac markers of myo cyte necrosis (eg, creatine kinase isoenzymes, cardiac-specific troponin T or I). During the first 12 hours, liberal use of analgesics to minimize pain is recommended. Bed rest is also recommended for this period, but not for longer, because of the deleterious effects of deconditioning caused by prolonged bed rest.
Not widely appreciated is the recommendation that a lipid profile be ordered on admission along with other routine blood tests. Lipid measurements are considered valid for purposes of subsequent therapy and risk stratification up to about 8 hours after admis sion for acute myocardial infarction. Thereafter, the stability of the lipid measurements declines, and results of testing are not reliable for another 2 months.
Prophylactic use of antiarrhythmic agents in the first 24 hours of hospitalization is not recommended, as it once was. Routine use of lidocaine hydrochloride has been shown to be associated with increased mortality from cardiac arrest, even though the degree of ventricular ectopy was decreased (8).
In patients who have already received aspirin, use of heparin has no proven benefit in survival. Therefore, heparin is recommended only for patients who have a large or anterior myocardial infarction, a left ventricular mural thrombus seen on echocardiography, or a history of embolic stroke.
In patients who received thrombolytic therapy, subsequent administration of heparin is based more on current practice than on evidence. The decision depends on whether the patient received a nonspecific thrombolytic agent (eg, streptokinase, urokinase), for which only subcutaneous heparin (7,500 U twice daily) is recommended, or a more clot-specific agent (eg, alteplase). In patients who received alteplase, intravenous heparin is recommended for the subsequent 48 hours; however, there are no firm data to prove this method is of benefit.
Aspirin, beta-adrenoceptor blocking agents, and angiotensin-converting enzyme (ACE) inhibitors should be given to all patients daily for an indefinite period. ACE inhibitors are intended primarily for patients with accompanying congestive heart failure, an ejection fraction below 0.40, or an anterior infarction. Use of ACE inhibitors should be maintained for at least the first 6 weeks in all acute myocardial infarction patients, after which time the decision of whether to continue use can be made with greater accuracy.
Intravenous nitroglycerin is given customarily for the first 48 hours. In the absence of continuing pain, congestive heart failure, or hypertension, this therapy can usually be discontinued at the end of this period.
Use of calcium channel blockers has not been shown to reduce mortality in patients with acute myocardial infarction, and in certain patients with cardiovascular disease, this method appears to be harmful. Therefore, the committee believes that "these agents are still used too frequently in patients with acute myocardial infarction." Recommendations are that verapamil hydrochloride or diltiazem hydrochloride be given only to patients in whom beta blockers are ineffective or contraindicated (ie, those with bronchospastic disease). They should be used for relief of ongoing ischemia or control of a rapid ventricular response (atrial fibrillation) in the absence of congestive heart failure, left ventricular dysfunction, or atrioventricular block.
Hospital management after the first 24 hours
Regardless of whether they receive thrombolytic therapy, patients with spontaneous myocardial ischemia or ischemia that is provoked days to weeks after acute myocardial infarction ordinarily should undergo elective angiographic evaluation with subsequent consideration of percutaneous or surgical revascularization. There is considerable variability in use of coronary angiography and catheter interventions among survivors of uncomplicated acute myocardial infarction who have preserved left ventricular systolic function. Although some practitioners routinely perform angiography and PTCA during the days after acute myocardial infarction in virtually all patients, available data suggest that such a strategy does not salvage myocardium, nor does it reduce the incidence of reinfarction or death. Accordingly, coronary angiography and subsequent revascularization should be reserved for survivors of acute myocardial infarction who have preserved left ventricular systolic function and spontaneous or provoked ischemia.
Patients with recurrent chest pain that is believed to be the result of pericarditis should receive high-dose aspirin therapy (650 mg every 4 to 6 hours).(9) Recurrent chest discomfort that is thought to be caused by myocardial ischemia should be treated with intravenous nitroglycerin, analgesics, and antithrombotic medications (aspirin, heparin). Subsequent coronary angiography with revascularization should be considered in these patients. Patients with congestive heart failure should receive a diuretic (usually intravenous furosemide) and an afterload-reducing agent. For patients in cardiogenic shock, insertion of an intraaortic balloon pump and emergency coronary angiography followed by PTCA or coronary artery bypass graft surgery should be considered (10).
Atrial fibrillation is often a manifestation of extensive left ventricular systolic dysfunction in patients with acute myocardial infarction. If its occurrence causes hemodynamic compromise or ongoing ischemia, direct-current cardioversion should be performed. In the absence of these signs, beta blockers or digitalis should be given to slow the ventricular response. Episodes of ventricular fibrillation should be treated with immediate direct-current countershock; the same is true for episodes of monomorphic ventricular tachycardia associated with angina, pulmonary congestion, or hypotension. Symptomaticsinus bradycardia or atrioventricular block warrants administration of atropine sulfate.
Temporary pacing should be performed in patients with any of the following:
Sinus bradycardia unresponsive to drug therapy
Mobitz type II second-degree atrioventricular block
Third-degree heart block
Bilateral bundle branch block
Newly acquired bundle branch block
Right or left bundle branch block in conjunction with first-degree atrioventricular block
Immediate surgical intervention is often required when PTCA is unsuccessful and patients have persistent chest pain or hemodynamic instability. Patients known to have a mechanical abnormality leading to severe pulmonary congestion or hypotension, such as papillary muscle rupture (with resultant mitral regurgitation) or ventricular septal defect, are candidates for immediate emergency surgery.
Preparation for hospital discharge
Patients who had a complicated clinical course during the early days of infarction are at high risk and should undergo coronary arteriography to identify candidates for revascularization. Patients without clinical complications after infarction are generally at low risk for subsequent events. Low-risk patients can safely defer the customary submaximal limited stress test before discharge in favor of a symptom-limited stress test, which may be more informative, 3 weeks after discharge (11).
Patients who can achieve at least five metabolic equivalents should be treated medically. If there are signs of severe ischemia at a low level of exercise (eg, marked ST-segment change, inability to complete stage 1 testing) or if blood pressure falls during exercise, coronary arteriography should be performed.
The committee points out that the positive predictive value of virtually all noninvasive tests has declined as late prognosis has improved, particularly in those relatively highly selected patients who have received reperfusion therapy. The paradigm for the future will be a new database that examines the cost-effectiveness and incremental value of noninvasive testing among lower-risk patients who have received reperfusion therapy.
Long-term management
For an indefinite period after acute myocardial infarction, patients should continue to receive aspirin, a beta blocker, and a selected dose of an ACE inhibitor. Patients should be instructed on achieving an ideal weight and educated about a diet low in saturated fat and cholesterol. Those with a low density lipoprotein cholesterol measurement higher than 130 mg/dL despite diet should be given drug therapy, with a goal of reducing the level to less than 100 mg/dL. Smoking cessation is essential. Additionally, patients should be encouraged to participate in a formal rehabilitation program and ultimately plan to engage in 20 minutes of exercise at the level of brisk walking at least three times a week.
Summary
The recently published "ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction" stress three major points: (1) The prehospital phase, from onset of symptoms to definitive therapy in the emergency department, must be shortened by 50% if the estimated 30% mortality rate from myocardial infarction is to be reduced. (2) More widespread use of thrombolytic agents is warranted because of the demonstrated benefit to survival. Benefits from thrombolytic agents are extremely time-dependent: The sooner this therapy is given, the better the outcome. (3) Daily use of aspirin (160 to 325 mg) for an indefinite period is perhaps the single most important therapy in acute myocardial infarction patients. For those who are completely intolerant of aspirin, alternative therapy with ticlopidine should be considered. PGM
This article was adapted, with permission of the American College of Cardiology and the American Heart Association, from "ACC/AHA Guidelines for the Management of Patients With Acute Myocardial Infarction" by the Committee on Management of Acute Myocardial Infarction, Journal of the American College of Cardiology 1996;28 (
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A person that has suffered a myocardial infarction has an altered ECG trace. Which of the following changes co
The Q wave on the ECG becomes deeper.
The S-T segment is elevated.
Inversion of the T wave.
Dysrhythmias
All of the above.
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All of the above. A lot determines of what section of the heart is infarcting. You can have a non q wave MI, ST elevation exists as well as ST depression, dysrythmias occur from the damaged heart tissue as well as electrolyte imbalances. (
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what food recipe for a patient suffering from Myocardial Infarction, easy to prepare?
please give me ingredients and procedures
COMMON INGREDIENTS PLEASE. i'm from the philippines.
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for people with myocardial infarction, the bulk of most meals should be starch-based foods (such as cereals, wholegrain bread, potatoes, rice, pasta), plus fruit and vegetables.
not much fatty food such as fatty meats, cheeses, full-cream milk, fried food, butter, etc. Use low fat, mono-, or poly-unsaturated spreads.
Eat oil-rich fish. If you eat meat it is best to eat lean meat or poultry such as chicken.
If you do fry, choose a vegetable oil such as sunflower, rapeseed or olive oil.
bearing these in mind, pretty much any healthy dish is ok so it really depends on what you would like to cook! what about trying a simple pasta dish?? wholewheat past with a homemade sauce (tomato, basil and chicken would make a good sauce!) or else you could try mackeral with garlic and lemon, served with boiled potatoes and veg. (
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What is the difference between angina pectoris and myocardial infarction?
angina pectoris is the chest pain located in the retrosternal area, that can or not be caused by exercise, and can or not calm with rest (that depends if the angina is stable or unstable)
angina can be a cause by myocadial infarction, or just because of ischemia of the muscle.-
infartion is the death by necrosis of the heart cells, cause by the lack of oxygen.- (
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