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Click here to go to the American Heart Association's in-depth review of the Third Universal Definition of Myocardial Infarction.

SERUM MARKERS OF ACUTE MYOCARDIAL INFARCTION

In recent years, the increasing sensitivity and accuracy of measurement of serum markers in acute MI have made them the gold standard for diagnosis of this problem. Serum markers for acute MI, ideally, are substances which are not normally present in the bloodstream, are released by dying myocardial cells, and which are not found elsewhere in the body. The troponin markers cTnT and cTnI are considered the best of these, although the previously discovered creatine kinase MB isoenzyme (CK-MB) continues to be useful.

The troponins (cTnT and cTnI) are contained in the cells of the myocardium, and are chemically distinct(DNA) from their counterparts in non-cardiac muscle. The troponins generally are first detectable 2 to 4 hours after the onset of acute MI, are maximally sensitive at 8 to 12 hours, peak at 10 to 24 hours, and persist for 5 to 14 days. Troponins are both more specific for myocardial injury than CK-MB, and also more sensitive. Even small acute Mis can cause a many fold increase in troponin levels.

One disadvantage to the troponins is that, due to their prolonged elevation and persistent serum levels, recurrent MIs, or extension of the affected myocardial area after the initial injury may be difficult to detect.

The MB isoenzyme of creatine kinase (CK-MB) is more specific to myocardial injury than total serum levels of CK, however, the specificity is improved by calculation of an MB/total CK ratio. However, even with ratio calculation, CK-MB is not as specific as either Troponin marker for myocardial injury. As a result, CK-MB is primarily used to confirm acute MI with an already positive Troponin level in a unclear clinical situation, to look for evidence of re-infarction during the days after initial MI, or when Troponin measurement is not available.

It is important to note that the finding of an elevated level of either Troponins or CK-MB does not identify the underlying cause of myocardial infarction.

CK-MB increases within 3 to 4 hours after the onset of acute MI, is maximally sensitive within 8 to 12 hours, peaks at 12 to 24 hours, and returns to normal in 2 to 4 days.

Other lab testing

A complete blood count, platelet count, coagulation studies (partial thromboplastin time - APTT, prothrombin time – PT), serum glucose, kidney function and electrolytes, and lipid panel should all be performed upon admission to hospital. Typically, the white blood cell count rises within a few hours of acute MI and persists for 3-4 days. Coagulation studies are useful particularly iffibrinolytic (clot “busting”) therapy is contemplated.

MYOCARDIAL INFARCTION: PRESENTING SYMPTOMS

The most common presenting symptom of myocardial infarction is chest pain. Classically, the location of the pain is described as being behind the breastbone, and may be described as a feeling of heaviness, squeezing, band-like, crushing or burning in quality, However, the location of the pain may vary considerably, being present in the left chest, the right chest, or all across the chest.Highly localized sharp or stabbing pain is not characteristic.

Radiation of the chest pain is typically to the left arm, but may also radiate to the right arm, both arms, into the neck jaw or teeth,upper abdomen (epigastrium) or between the shoulder blades. Pain noted below the umbilicus of the abdomen or above the jaw is not characteristic of acute MI.Chest pain which is aggravated or reproduced by external pressure on the chest by the examiner is not characteristic.

Additional symptoms may include one or more of the following: nausea, vomiting, profuse sweating (diaphoresis), cardiac palpitations (perception of abnormal heartbeat), vomiting, lightheadedness, restlessness, weakness, or anxiety.

Chest pain related to coronary ischemia without MI is known as angina. The chest pain of angina is typically of lesser severity and shorter duration than that of acute MI.Ischemic related chest pain that lasts 20-30 minutes or more must be considered to be caused by acute MI until proven otherwise.

Approximately 20% of acute myocardial infarctionsare completely asymptomatic (symptom-free), and may first be discovered as old events on routine EKGs performed for other purposes.

MYOCARDIAL INFARCTION: PHYSICAL EXAMINATION

Physical examination may be completely normal during acute MI. There are no specific physical signs which will make the diagnosis. Blood pressure may be elevated, normal or low. Pulse may be reduced, normal or elevated. Mis involving the anterior (front) wall of the left ventricle are often associated with increased blood pressure (hypertension) and fast pulse (tachycardia). MIs involving the inferior (lower) wall of the left ventricle may result in abnormally slow pulse (bradycardia) and low blood pressure (hypotension). Abnormal cardiac rhythms manifested by irregular palpable pulses may be present and often indicate a highly critical situation.An S4 gallop sound may be heard when listening to the heart with the stethoscope (the S4 sound occurs just at the end of the relaxation or diastole phase of the ventricles, and is a sound caused by blood being squirted into an abnormal left ventricle by the left atrium). Signs of cardiac failure such as pulmonary (lung) congestion with the presence of audible rales (crepitations) at the lung bases, marked shortness of breath, and distended neck veins should be sought.

MYOCARDIAL INFARCTION: ELECTROCARDIOGRAM

An electrocardiogram (EKG) should be obtained in all cases of suspected MI. While an EKG is neither 100% sensitive nor 100% specific for MI, it is easily performed and without risk, and is very often of great value in determining the next step in treatment. and evaluation.

The earliest EKG finding during MI is elevation of the ST segments in the leads recording signals from the area of infarction (Fig 2 ) . ST segment elevation usually begins to occur within minutes of the onset of infarction, increases in degree over several hours, and may persist for up to 2 weeks after infarction. ST elevation may persist beyond 2 weeks in anterior wall MI, and may indicate a large area of abnormal ventricular wall motion (akinesis, dyskinesis) or ventricular aneurysm (a weakened area of the ventricular wall which tends to move paradoxically with contraction). The presence of ST segment depression in some leads with ST elevation in opposing leads (reciprocal changes) may indicate larger areas of infarction and are associated with a worse prognosis although such patients may benefit more greatly from interventions aimed at restoring coronary flow (recanalization).

As ST segment changes regress, T waves in leads with ST elevation become inverted and Q waves develop (Fig 3) . These Q waves may become a permanent EKG feature in anterior wall infarctions, but may resolve in inferior wall infarctions.

Successful efforts at reestablishing coronary artery flow (recanalization) hasten the evolution of EKG changes, with ST changes resolving in minutes or hours instead of days or weeks.

ST segment elevation on EKG may occur in some non-MI disease states, particularly acute pericarditis. In such cases, it is critical to make the correct diagnosis, as fibrinolytic therapy (clot ‘busting’) is contraindicated in pericarditis, and may lead to severe complications.

FIGURE 1 - NORMAL EKG PATTERN

FIGURE 2 - ST SEGMENT ELEVATION DURING ACUTE MYOCARDIAL INFARCTION

FIGURE 3 - Q WAVES ACUTE MYOCARDIAL INFARCTION

12 lead ekg in acute myocardial infarction (click to enlarge)

MYOCARDIAL INFARCTION: IMAGING STUDIES

While measurement of Troponin biomarkers are currently considered the most importantfinding in the diagnosis of acute myocardial infarction, imaging studies can provide very useful supplemental information.

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James Ferrell Sunday 6 October 2013

Like Dan above I hear the lyrics as being related to the death of Paul’s mother.

It’s a beautiful song. But the big revelation to me when it came out was Paul’s guitar playing on the tuned down Martin. It’s such a great natural idiosyncratic strumming style and every time he reverts to it (e.g.Heart of the Country, Here Today) it really affects me.

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BILLY SHEARS Monday 7 October 2013

Nothing Paul did while in Wings compares to this song. Wings produced mostly sappy gobbly-de-gook . Paul was what – 23 – 24 years old when he wrote this masterpiece? The PID folks can certainly use this song as evidence that that master is no longer with us.

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Water Falls Thursday 5 March 2015

I couldnt disagree more with this entire comment. Wings was a fantastic band with a catalogue of great songs that I dare say would have been just as beloved if part of the Beatles catalogue. You sound like a nutcase PIDer or a Lennonista bitter that John isn’t still around to show us all what’s what or just a plain old Paul hater! Paul McCartney is ICONIC in his status as a LIVING Legend which he has earned through hard work, brilliant songwriting and music, scaling many genres, beautiful singing. He is beloved the world over by many fans and admirers, of all ages, and races. You may not like it, you don’t have to, but he is and that is that. Deal with it!

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Johan Cavalli Friday 14 February 2014

Important to know. 1. the idea with strings was George Martin´s idea, not McCartney´s. Without the strings, the song would never been that success. 2. The melody was inspired by Lennon´s Do You Want to Know a Secret? The same upclimbing melody.

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Ray Sunday 9 March 2014

Do you have a source for your second claim? I really don’t have the same impression.

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Robert Wednesday 5 October 2016

Of course you would make this (point number 2 above) claim. In your opinion John Lennon WAS The Beatles and Paul, George and Ringo were merely his sidemen. You,sir, couldn’t be more wrong.

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stpaul Thursday 29 June 2017

Paul has said many times the song came to him in a dream and when he awoke with it he thought it was an old standard. This directly contradicts your second claim, does it not?

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