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Age | Gender | Occupation | Working Diagnosis |
---|---|---|---|
63 Years | Male | Businessman | Acute Coronary Syndrome |
A 63-year-old man presented to the emergency room with recent-onset episodic chest discomfort described as “muscle ache.” The chest discomfort was radiating to the upper neck and both arms, associated with a tingling sensation. It was not reproducible or worsened on deep inspiration. He recently noticed dyspnea with minimal effort without any associated chest discomfort. However, he denied orthopnea, paroxysmal nocturnal dyspnea, pedal edema, and loss of consciousness.
A year previously, he was diagnosed with coronary artery disease, requiring a bare metal stent insertion for revascularization of 95% obstructive stenosis in the proximal left anterior descending coronary artery. His left ventricular ejection fraction (LVEF) was 38% at the time, and his electrocardiogram (ECG) revealed left bundle branch block (LBBB) morphology. His medical history included 9 months of chemotherapy for non-Hodgkin’s lymphoma. Approximately 4 years before the current visit, he was diagnosed with right cavernous meningioma, which was successfully treated with stereotactic radiation therapy without mantle radiation. During the same year, he was treated for benign prostatic hypertrophy with transurethral resection of prostate. He was being treated for depression, anxiety disorder, and hypothyroidism. The patient was married for 35 years and had two grown children. He reported stress at work, was a nonsmoker, and consumed alcohol socially. During the period of chemotherapy, he used marijuana. He had two sisters, who had cardiomyopathy of unclear cause. Both of his sisters died young, at 16 and 42 years of age. The patient’s niece was diagnosed with cardiomyopathy at the age of 38 and eventually needed cardiac transplantation.
The patient was taking levothyroxine 175 mcg daily, metoprolol 25 mg twice daily, bupropion 150 mg twice daily for depression, valsartan 160 mg daily, hydrochlorthiazide 12.5 mg daily, atorvastatin 40 mg daily, lorazepam 0.5 mg three times daily as needed for anxiety, zolpidem 5 mg daily at bedtime as needed for insomnia, and aspirin 325 mg daily.
The patient’s current symptoms were chest discomfort of 2 weeks, exertional dyspnea, and reduced exercise tolerance. On examination, he was overweight and not in any apparent distress and had a temperature of 36.8° C (98.2° F) and oxygen saturation of 99% on room air. The neurologic examination was nonfocal.
BP/HR: 147/80 mm Hg/54 bpm
Neck veins: No jugular venous distention
Lungs/chest: Exertional dyspnea, reduced exercise tolerance, respiratory rate of 18 breaths per minute, no crackles, rhonchi, or wheezes
Heart: Regular rate, normal heart sounds, 1/6 holosystolic murmur at the left sternal border, no pericardial rub or gallop
Abdomen: Soft, nontender, no evidence of pedal edema
Hemoglobin: 13.7 g/dL
Hematocrit: 38.4%
Total leukocyte count: 6200 cells/mm 3
Platelet count: 164 × 10 3 /µL
Sodium: 135 mmol/L
Potassium: 3.9 mmol/L
Chloride: 104 mmol/L
Creatinine: 1.2 mg/dL
Creatine kinase: 88 units/mL
Bicarbonate: 24 mmol/L
N-Terminal brain natriuretic peptide: 258 ng/mL
Blood urea nitrogen: 30 mmol/L
Creatine kinase–myocardial bound: 2.9%
Troponin I and T: Negative
The ECG showed sinus bradycardia at a rate of 55 bpm, first-degree atrioventricular block (PR interval of 210 ms), LBBB unchanged in contrast to ECG obtained 1 month earlier. The QRS duration was 164 ms. No ST-T changes suggestive of ischemia were noted ( Figure 38-1 ).
The posteroanterior and lateral radiographic views demonstrated poor inspiration, mild cardiomegaly, and no evidence of infiltrate or effusion ( Figure 38-2 ).
The patient’s chest discomfort and exertional dyspnea in the setting of prior coronary artery disease were concerning for acute coronary syndrome. It was reassuring that the initial myocardial markers were negative. Most important, the patient was not in acute heart failure.
The transthoracic echocardiogram showed normally functioning valves in mitral, aortic, tricuspid, and pulmonary positions. The left ventricle was diffusely hypokinetic with some regional variation, which was especially worse in the septum and apex. The LVEF diminished further to 32% in contrast to 38% 8 months previously.
The patient was admitted to the cardiac care unit. The serial cardiac enzyme examinations and ECGs showed no evidence of acute myocardial infarction.
The patient was able to complete a technetium-99m single-photon emission computed tomography (SPECT) myocardial perfusion scan. The exercise test was terminated because of the development of 2:1 atrioventricular block with hypotension. The SPECT perfusion imaging showed fixed perfusion defects in the anterior and septal segments. The left ventricle was dilated, demonstrating global systolic dysfunction.
Subsequently, coronary angiography was performed that showed no evidence of obstructive coronary artery disease. The proximal left anterior descending artery with a prior bare metal stent was patent. The right coronary artery, the left main coronary artery, and the left circumflex artery showed minor luminal irregularities. No obstructive lesions were present.
Cardiac magnetic resonance (CMR) with and without gadopentetate dimeglumine showed no evidence of myocardial edema. Delayed enhancement was seen in the subendocardial region of mid-anterior, anterolateral, and lateral apical segment consistent with scar. Scar extent was about 2% of left ventricular mass ( Figure 38-3 ).
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