The patient was a 48-year-old man admitted to the coronary care unit complaining of substernal chest pain. During the 4 months preceding admission, he noted chest pain radiating to his neck and jaw during exercise or emotional upsets. The pain dissipated when he discontinued the activity or relaxed. The results of his physical examination were essentially normal except for a systolic murmur heard best at the apex of the precordium and radiating into the left axilla.
Routine laboratory work
Within normal limits (WNL)
Cardiac enzyme studies
Creatine phosphokinase (CPK), p. 167
235 units/L (normal: 55–170 units/L)
CPK-MB, p. 171
12 ng/mL (normal: 0–3 ng/mL)
Lactic dehydrogenase (LDH), p. 293
120 units/L (normal: 90–200 units/L)
Serum aspartate aminotransferase (AST), p. 107
24 International units/L (normal: 5–40 International units/L)
Troponins, p. 451
Echocardiography, p. 820
Hypokinetic portion of the lateral left ventricle
Electrocardiography (EKG), p. 485
Evidence of left ventricular hypertrophy
Chest x-ray study, p. 956
Exercise stress test, p. 481
Positive: pain reproduced; ST segment depression noted on EKG (normal: negative)
Echocardiography, p. 820
Normal ventricular wall motion
Transesophageal echocardiography (TEE), p. 840
Mitral regurgitation, dilated left atrium
Lipoproteins, p. 304
29 mg/dL (normal: >45 mg/dL)
189 mg/dL (normal: 60–180 mg/dL)
12 mg/dL (normal: 7–32 mg/dL)
Homocysteine, p. 269
C-reactive protein (CRP), p. 165
Cardiac catheterization, p. 950
All WNL except:
Left ventricular systolic pressure
140 mm Hg (normal: 90–140 mm Hg)
Aortic systolic pressure
130 mm Hg (normal: 90–140 mm Hg)
Ventricular-aortic pressure gradient
5 mm Hg (normal: 0)
Left ventricular function
3.5 L/min (normal: 3–6 L/min)
End diastolic volume (EDV)
60 mL/m2 (normal: 50–90 mL/m2)
End systolic volume (ESV)
22 mL/m2 (normal: 25 mL/m2)
Stroke volume (SV)
38 mL/m2 (SV = EDV − ESV)
0.63 (normal: 0.67 ± 0.07)
Mitral regurgitation present, normal muscle function (normal: normal ventricle)
Analysis of O2 gas content, p. 98
No shunting (normal: no shunting)
Coronary angiography (coronary cineangiography), p. 950
90% narrowing of left coronary artery (normal: no narrowing)
Cardiac radio-nuclear scanning, p. 733
Scans normal showed localized area of decreased perfusion and poor muscle function in the myocardium during exercise
Cholesterol, p. 138
502 mg/dL (normal: <200 mg/dL)
Triglycerides, p. 447
198 mg/dL (normal: 40–150 mg/dL)
Cardiac radio-nuclear scanning, EKG, and studies ruled out the possibility of MI. Troponins and serial cardiac enzyme indicated cardiac ischemia. Stress testing and a nucleotide scan indicated that the patient was having exercise-related myocardial ischemia (angina). Echocardiography indicated that the heart muscle at the site of ischemia was functioning poorly. Transesophageal echocardiography indicated that the patient had mitral regurgitation. Cardiac catheterization with cineventriculography demonstrated near-normal ventricular function, and coronary angiography indicated significant narrowing of the left coronary artery. Mitral regurgitation was also seen. The patient’s angina was then thought to be caused by the coronary artery disease. Open heart surgery was performed. The patient’s mitral valve was replaced with a prosthesis, and an aortocoronary artery bypass graft was performed. Postoperatively, he had a large pericardial effusion. This diminished his heart function. He underwent pericardiocentesis, and his function improved. Because his serum lipids study showed type IIa hyperlipidemia, a low-cholesterol diet and cholesterol-lowering agents were prescribed. The other cardiac risk factors did indicate increased risk for coronary heart disease. Six months later he was asymptomatic and jogging 3 miles per day.
1. Based on the ratio of cholesterol to HDL, what is the patient’s risk for coronary heart disease?
2. If these blood tests were drawn 1 year ago, what treatment would have been indicated?
3. Could surgery have been avoided?
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