Acute Coronary Syndrome

A 49-year-old man is evaluated in the emergency department for chest discomfort accompanied by nausea and dyspnea that began 2 hours ago. On physical examination, blood pressure is 109/78 mm Hg and heart rate is 88/min. There is no jugular venous distention and no carotid bruits. The lungs are clear. Cardiac examination shows a normal S1 and S2 and no gallops, rubs, or murmurs. The troponin level is 6 ng/mL (normal <0.5 ng/mL). Electrocardiogram shows a 1-mV ST elevation in leads II, III, and aVF.

He is treated with enoxaparin, aspirin, metoprolol, and glycoprotein receptor blockers and is taken to the cardiac catheterization laboratory. A stent is placed in a subtotally occluded right coronary artery. A follow-up echocardiogram shows normal wall motion, normal valve function, and a normal ejection fraction. By day 4, he has no complications and is prepared to be discharged.

In addition to aspirin, clopidogrel, and metoprolol, which of the following medications should be given at discharge?
A Atorvastatin
B Gemfibrozil
C Niacin
D Warfarin

Key Point
In patients with an acute coronary syndrome, statin therapy is indicated regardless of the serum cholesterol level.

Answer and Critique (Correct Answer = A)

This patient has survived a small inferior wall myocardial infarction and was successfully treated with a stent. At discharge, he should receive aspirin, metoprolol, clopidogrel for at least 180 days, and a statin regardless of his serum cholesterol level. In patients with coronary artery disease, especially those presenting with symptoms and those undergoing revascularization by either stenting or bypass graft surgery, statin therapy reduces late cardiovascular events despite having minimal or no effect on the angiographic appearance of the coronary arteries.

The PROVE IT-TIMI 22 study compared a moderate-dose statin (pravastatin, 40 mg/d) with a high-dose statin (atorvastatin, 80 mg/d) in patients hospitalized for acute coronary syndrome. The median LDL cholesterol levels achieved were 95 mg/dL by the pravastatin group and 62 mg/dL for the atorvastatin group. Those receiving atorvastatin had a 16% reduction in the composite endpoint of death from any cause, myocardial infarction, unstable angina requiring rehospitalization, coronary artery revascularization, and stroke during 2 years of follow-up. These results showed evidence of benefit from early aggressive LDL cholesterol lowering with high-dose atorvastatin.

Warfarin is not indicated after ST-elevation myocardial infarction treated by stenting unless there is another indication such as atrial fibrillation, deep venous thrombosis, or intracardiac thrombus.

Niacin for hypertriglyceridemia may be needed, but at this time the triglyceride values are not reported and may be falsely elevated early in the course of ST-elevation myocardial infarction. The first line of treatment would be statins even for normal LDL cholesterol levels in patients with documented coronary artery disease. The combination of statins with a fibrate (e.g., gemfibrozil) is attractive for patients who have both high cholesterol and triglyceride levels or for those who continue to have elevated triglyceride levels after reaching their LDL cholesterol target on statin therapy. However, in this patient, the best initial choice is a statin.
Bibliography

1. Ray KK, Cannon CP, Ganz P. Beyond lipid lowering: What have we learned about the benefits of statins from the acute coronary syndromes trials? Am J Cardiol. 2006;98:18P-25P. Epub 2006 Sep 29. [PMID: 17126675]

Acute Coronary Syndrome: Coronary Vasospasm

Acute Coronary Syndrome: Coronary Vasospasm

Description

Ø Spontaneous episodes of chest pain due to coronary artery vasospasm in absence of increase in myocardial oxygen demand in either normal or diseased coronary vessels

Ø Also known as Prinzmetal angina or variant angina

Ø Most common in younger patients and men

Ø Occurs in patients without other cardiac risk factors

Ø Risk factors:

o Smoking

o Hyperinsulinemia

o Insulin resistance

Ø Associated with minimal coronary artery disease:

o Usually has normal coronary angiogram

Etiology

• Abnormal vasodilator function in coronary arteries
• Focal coronary artery vasospasm
• Often adjacent to or at the site of fixed stenoses
• Unopposed alpha sympathetic stimulation
• Sympathetic stimulation by endogenous hormones may cause vasoconstriction
• Hypersensitivity of coronary arteries due to mediators of vasoconstriction
• May or may not be associated with a fixed coronary lesion

Diagnosis

Signs and Symptoms

• Chest pain:
• Retrosternal
• Radiates to neck, jaw, left shoulder, or arm
• Occurs at rest
• Palpitations
• Presyncope or syncope
• Associated with migraine headaches and Raynaud disease in a minority of patients
• May occur during cold weather or stress
• May be prolonged in duration compared to typical angina
• May be elicited by hyperventilation
• May be relieved by exercise
• Circadian pattern, most commonly in early morning

Tests

ECG:

• Transient ST-segment elevation is characteristic
• May be followed by ST depression or T-wave inversion
• May have associated arrhythmia during coronary spasm
• Heart block with right coronary artery spasm
• Ventricular tachycardia with LAD spasm

Lab

• CK-MB and troponin I or T
• Toxicologic screen:
• Helpful if cocaine is suspected as etiology of chest pain

Imaging

• Chest radiograph:
• May be helpful to rule out other etiologies such as pneumonia, pneumothorax, or aortic dissection
• Thallium scintigraphy may be useful to localize area of spasm

Diagnostic Procedures/Surgery

• Exercise stress testing:
• Helpful only if there are underlying fixed stenoses
• Coronary angiography:
• Mild atherosclerosis is often the norm
• Provocative test with ergonovine, acetylcholine, or hyperventilation will induce coronary spasm

Differential Diagnosis

• Angina pectoris
• Anxiety and panic disorders
• Aortic dissection
• Esophageal rupture
• Esophageal spasm
• Esophagitis
• Gastroesophageal reflux
• Mitral valve prolapse
• Musculoskeletal chest pain
• Myocardial infarction
• Peptic ulcer disease
• Pericarditis
• Pneumothorax
• Pulmonary embolism

Treatment

Pre Hospital

Treat as any other acute coronary syndrome

Initial Stabilization

• IV access
• Oxygen
• Cardiac monitoring
• Vital signs and oxygen saturation

ED Treatment

• All patients with chest pain in which cardiac ischemia is a consideration should receive an aspirin upon arrival to the ED:
• Possibility of actually increasing severity of episodes in Prinzmetal angina due to inhibiting biosynthesis of naturally-occurring coronary vasodilator prostacyclin
• Nitroglycerin should then be administered and is appropriate to help relieve both ischemic and vasospastic chest pain.
• A trial of calcium-channel blockers is indicated if clinical history is consistent with coronary vasospasm
• Heparin and beta-blockers are not helpful:
• Beta-blockers may actually be detrimental due to unopposed alpha-mediated vasoconstriction.

Medication (Drugs)

• Aspirin: 325 mg PO
• Diltiazem: 30-60 mg PO
• Nitroglycerin, either:
• 0.4 mg sublingual
• 10-20 mcg/min IV, titrating to effect
• 1-2 inches of nitropaste
• Verapamil: 40-80 mg PO

Follow-Up

Disposition

Admission Criteria

• New-onset chest pain
• Rest chest pain (by definition most patients with coronary vasospasm)
• Accelerated chest symptoms

Discharge Criteria

Stable (chronic chest pain)

References

1. Braunwald E. Unstable angina: an etiologic approach to management [editorial]. Circulation. 1998;98:2219-2222.
2. Crea F, Kaski JC, Maseri A. Key references on coronary artery spasm. Circulation. 1994;89:2442-2446.
3. Gersh BJ, Braunwald E, Bonow RO. Chronic coronary artery disease. In: Braunwald E, ed. Heart disease: a textbook of cardiovascular disease. 6th ed. Philadelphia: WB Saunders, 2001;1324-1328.
4. Mayer S, Hillis LD. Prinzmetal's variant angina. Clin Cardiol. 1998;21:243-246.
5. Orford JL. Coronary artery vasospasm. Med J. 2001;2:111.
6. Prinzmetal M, Kennamer R, Merliss R. A variant form of angina pectoris. Am J Med. 1959;27:375-388.
Codes
ICD9-CM

413.1