A 45Year Old Man with Substantial Chest Pain

The Big Heart Disease Lie

How I Healed my Cardiovascular Disease

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Fred S. Apple

History of Current Presentation

The subject is a 45-year-old African-American male who presents with a chief complaint of "substantial chest pain" that radiated through his right arm and back. The pain awoke him from his sleep at approximately 3:30 am and was described as constant and as "8 out of 10." He also complained of nausea and shortness of breath. Over the past 2-3 months he stated that he had experienced similar symptoms that radiated through both arms. One month prior to admission, he visited his primary care internist, during which time his electrocardiogram (EKG) and x-rays were normal. A stress test was scheduled but the appointment was missed. On the morning of presentation, the patient took 1 aspirin (325 mg) within 30 minutes of awakening. The subject presents to the emergency department 1 hour [0430 h (4:30 am)] after onset of acute chest pain.

He had a past medical history of hypertension and takes both antihypertensive medication and aspirin daily. He is a smoker (20 years), and occasional drinker, and his father had a fatal myocardial infarction (MI) at the age of 72. At physical examination, temperature, pulse, and respiration were normal, blood pressure 200/40, O2 saturation (pulse oximetry) 92% on room air and 99% after receiving 100% oxygen. He was alert, awake, and oriented in moderate discomfort. His lungs were clear to auscultation bilaterally with no rales or wheezes. Heart rate and rhythm were regular without murmurs. Chest x-ray showed borderline cardiomegaly, without infiltrates.

At presentation, routine chemistries, CBC, and cardiac biomarkers were within normal limits. The EKG at presentation shows poor R-wave progression anteriorly, with an ST depression in lead III. Consultation with the attending cardiologist following a similar EKG repeated at 1 hour after presentation ruled out MI. The patient was managed medically with nitroglycerin sublingually (x3 doses), which improved his discomfort to the point where he was pain-free. His blood pressure improved (decreased) following medication. He was also given multiple doses of morphine sulfate for his right arm pain.

Given the history and current presentation, the patient was admitted to the cardiac short-stay unit, and monitored. He was given nitrogycerine and low-molecular-weight heparin (LMWH, enoxaparin). Repeat cardiac biomarkers were ordered for 4 and 8 hours after presentation. Four hours following presentation, the EKG showed inverted T waves, now with new Q waves in the anterior leads. Repeat measurements of biomarkers at 0845 h (8:45 am) showed elevated values for total CK, CKMB, and condiac troponin T(cTnT).

Day

Reference

Total CK U/L

CKMB, mg/L

cTnT, mg/L

Intervals

Time, h

60-300

<7.0

<0.01

EKG

1

0430

40

1.5

<0.01

ST depression

0845

405

88

3.2

Q wave

0930

Stent placement

1445

4850

950

31.5

2

0600

3225

505

24.2

1800

1258

245

18.1

The diagnosis of an evolving acute MI was made and the patient was immediately taken to the cardiac catheterization lab and a glycoprotein IIB IIIA inhibitor [ReoPro (abciximab)] was started. In the catherization lab (0930 h), the patient's 100% occluded left anterior descending (LAD) coronary artery was opened by angioplasty and a stent was placed, with successful reperfusion. His chest pain was relieved following the procedure, without recurrence. There were no signs of any congestive heart failure issues. His echocardiography (echo) study showed an ejection fraction of 48%.

In the hospital, the patient tolerated progressive ambulation without difficulty. He was discharged on day 4, on multiple medications, and scheduled for cardiac rehabilitation, medication assessment, and outpatient follow-up. Presently use of biomarkers such as cardiac troponin, BNP (B-type natriurtic peptide), or hsCRP are not routinely used for follow-up in post-MI patients for risk assessment, unless clinically indicated.

Definition of the Disease

Acute myocardial infarction (AMI) is defined as an imbalance between myocardial oxygen supply and demand resulting in injury and eventual death of myocytes. It is now thought that the migration of stem cells has the potential to replace at least some damaged myocytes. When the blood supply to the heart is interrupted, "gross necrosis" of the myocardium results. Necrosis is most often associated with a thrombotic occlusion superimposed on coronary atherosclerosis. The process of plaque rupture and thrombosis is one of the ways in which coronary atherosclerosis progresses and that we currently recognize only the more severe of these events. Total loss of coronary blood flow in a major coronary artery results in a clinical syndrome known as ST-segment elevation AMI (STEMI). Partial loss of coronary perfusion can also lead to necrosis as well, is generally less severe, and is known as non-ST-elevation myocardial infarction (NSTEMI). Other events of still lesser severity may be missed entirely and can range from stable to unstable angina.

Presenting Symptoms

The clinical history remains of substantial value in establishing a diagnosis. A prodromal history of angina can be found in 40-50% of patients with AMI; approximately one-third have symptoms 1 -4 weeks before hospitalization. In the remaining two-thirds, symptoms predate admission by a week or less, and one-third of these patients will have had symptoms for 24 hours or less.

The pain of AMI is variable in intensity; in most patients it is severe but rarely intolerable. The pain may be prolonged, up to 30 minutes. The discomfort is described as constricting, crushing, oppressing, or compressing; often the patient complains of something sitting on or squeezing the chest. Although usually described as a squeezing, choking, viselike, or heavy pain, it may also be characterized as a stabbing, knifelike, boring, or burning discomfort. The pain is usually retrosternal in location, spreading frequently to both sides of the chest, often favoring the left side and radiating down the left arm. In some instances, the pain of AMI may begin in the epigastrium and simulate a variety of abdominal disorders, which often causes MI to be misdiagnosed as indigestion. In other patients, the discomfort radiates to the shoulders, upper extremities, neck, and jaw. Older individuals, diabetics, and women often present without the typical pain. For example, less than 50% of those over age 80 who present with AMI will have chest discomfort. Sometimes, these patients will present with shortness of breath, fatigue, or even confusion. The pain of AMI may have disappeared by the time physicians first encounter the patient (or the patient reaches the hospital), or it may persist for a few hours.

Diagnostic Criteria

Previously, the diagnosis of AMI established by the World Health Organization in 1986 required at least two of the following criteria: a history of chest pain, evolutionary changes on the ECG, and/or serial elevations of cardiac markers. However, it was rare for a diagnosis of AMI to be made in the absence of biochemical evidence. A 2000 European Society of Cardiology/American College of Cardiology (ESC/ACC) consensus conference has codified the role of biomarkers, specifically cardiac troponin I or T, by advocating that the diagnosis be based on biomarkers of cardiac damage in the appropriate clinical situation.1-5 The criteria for diagnosis of an acute and established AMI are described in Table 1.1. The guidelines recognize the reality that neither the clinical presentation nor the ECG has adequate sensitivity and specificity for myocardial necrosis. This guideline does not suggest that all elevations of these biomarkers should elicit a diagnosis of AMI;

Table 1.1 Diagnosis of Myocardial Infarction

Acute MI: Either one of the following criteria satisfies the diagnosis for an acute, evolving, or recent MI:

1. Typical rise and gradual fall (cardiac troponin) or more rapid rise and fall (CK-MB) of biochemical markers of myocardial necrosis with at least one of the following:

a. Ischemic symptoms b. Development of pathological Q waves on ECG

c. ECG changes indicative of ischemia (ST-segment elevation or depression)

d. Coronary artery intervention (e.g., coronary angioplasty)

2. Pathological findings of an acute MI.

Established MI: Any one of the following criteria satisfies the diagnosis for established MI:

1. Development of new pathologic Q waves on serial ECGs. The patient may or may not remember previous symptoms. Biochemical markers of myocardial necrosis may have normalized, depending on the length of time that has passed since the infarct developed.

2. Pathological findings of a healed or healing MI.

Table 1.2 ESC/ACC Recommendations for Use of Cardiac Biomarkers for Detection of

Myocardial Injury and Myocardial Infarction

Increases in biomarkers of cardiac injury are indicative of injury to the myocardium, but not an ischemic mechanism of injury.

Cardiac troponins (I or T) are preferred markers for diagnosis of myocardial injury.

Increases in cardiac marker proteins reflect irreversible injury.

Improved quality control of troponin assays is essential.

Myocardial infarction is present when there is cardiac damage, as detected by marker proteins (an increase above the 99th percentile of the normal range) in a clinical setting consistent with myo-cardial ischemia.

For patients with an ischemic mechanism of injury, prognosis is related to the extent of troponin increases.

If an ischemic mechanism is unlikely, other etiologies for cardiac injury should be pursued.

Samples must be obtained at least 6-9 hours after the symptoms begin.

After PCI and CABG, the significance of marker elevations and patient care should be individualized.

only those associated with the appropriate clinical and/or ECG findings.6,7 When elevations that are not caused by an acute ischemia event, the clinician is obligated to search for another etiology for the elevation. The criteria suggested for use with these biomarkers by the Biochemistry Panel of the ESC/ ACC Committee is listed in Table 1.2.

The use of these new criteria has led to the NSTEMI diagnosis. The initial ECG used to have a sensitivity of about 50% for AMI. As the diagnosis of NSTEMI is made with greater and greater sensitivity, the frequency of STEMI among all AMI has decreased. Serial ECG tracings are helpful for STEMI but not for what now makes up almost 70% of AMIs, those with NSTEMI. The classic ECG changes of an STEMI are ST-segment elevation, which often evolves to the development of Q waves without intervention. Most NSTEMIs present with either ST segment depression, with or without T-wave changes; T-wave changes alone; or occasionally in the absence of any ECG findings. Those with ST-segment change have a substantially worse prognosis. There are many other clinical aspects that might suggest AMI as the etiology of a given biomarker elevation. For example, the finding of significant coronary obstructive lesions, especially in a pattern suggestive of recent plaque rupture, is highly suggestive. At times, a positive stress test with or without imaging may be necessary to help make the diagnosis. However, if the clinical situation is not suggestive, other sources for cardiac injury should be sought.

The term acute coronary syndrome (ACS) is increasingly used in the literature and encompasses all patients who present with unstable ischemic heart disease. If they have STE, they are called STEMI. If they do not have STE but have biochemical criteria for cardiac injury, they are called NSTEMI, few of whom develop ECG Q waves. Those who have unstable ischemia and do not manifest cardiac necrosis markers are designated patients with unstable angina (UA). Most of these syndromes occur in response to an acute event in the coronary artery when circulation to a region of the heart is obstructed. If the obstruction is high-grade and persists, then necrosis usually ensues. Since necrosis is known to take some time to develop, it is apparent that opening the blocked coronary artery in a timely fashion can often prevent death of myocardial tissue.

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