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
(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
Troponins, p. 451 18 ng/mL
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 WNL
Exercise stress test, p. 481 Positive: pain reproduced, ST segment depression noted
on EKG (normal: negative)
Echocardiography, p. 820 Normal ventricular wall motion
(TEE), p. 840
Mitral regurgitation, dilated left atrium
Lipoproteins, p. 304
HDL 29 mg/dL (normal: >45 mg/dL)
LDL 189 mg/dL (normal: 60–180 mg/dL)
VLDL 12 mg/dL (normal: 7–32 mg/dL)
Homocysteine, p. 269 16 mol/L
C-reactive protein (CRP), p. 165 22 mg/dL
Cardiac catheterization, p. 950 All WNL except:
Left ventricular systolic
140 mm Hg (normal: 90–140 mm Hg)
Aortic systolic pressure 130 mm Hg (normal: 90–140 mm Hg)
5 mm Hg (normal: 0)
Left ventricular function
Cardiac output 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)
Ejection fraction 0.63 (normal: 0.67 ± 0.07)
Cineventriculography 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
Cardiac radionuclear scanning, p.
Scans normal showed localized area of decreased
perfusion and poor muscle function in the myocardium
Cholesterol, p. 138 502 mg/dL (normal: <200 mg/dL)
Triglycerides, p. 447 198 mg/dL (normal: 40–150 mg/dL)
Cardiac radionuclear 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.
Critical Thinking Questions
1. Based on the ratio of cholesterol to HDL, what is the patient’s risk for coronary heart
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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