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A Curious Case of Chest Pain

A 67-year-old man presented to the emergency department with chest pain, reporting
that he had felt well until 10 days before presentation, when nausea, nonbloody emesis,
bloating, and epigastric pain developed. At that time, he was evaluated at another
hospital, where the results of computed tomography (CT) of the abdomen and pelvis,
performed after the administration of intravenous contrast material, and laboratory
tests were normal except for an elevated platelet count (491,000 per cubic millimeter).
A presumptive diagnosis of gastroesophageal reflux was made, and omeprazole was
prescribed but provided no relief of symptoms. Over the course of several hours on the
day of presentation, heaviness of the chest developed on exertion and progressed to
pain at rest accompanied by diaphoresis and dyspnea. The pain was substernal and
nonradiating, and it did not change with a change in position or with food intake. The
patient rated the pain at 8 on a scale of 1 to 10, with 10 indicating the most severe pain.

The patient reported no fever, cough, or upper respiratory symptoms; no edema, redness,
or pain in the legs; and no weight change, diarrhea, jaundice, or joint pain. His
medical history included mild asthma and a hemicolectomy for dysplastic polyps
complicated by a ventral abdominal hernia. His medications included omeprazole,
inhaled glucocorticoids and bronchodilators, montelukast, and zolpidem as needed.
He had a remote smoking history of 20 pack-years, drank fewer than four alcoholic
beverages weekly, and reported no illicit drug use. The patient worked as a courier
and lived alone. He reported no known contacts with sick persons and no recent travel.
Owing to estrangement, his family history was unknown.

On examination, the patient was afebrile. The pulse was 125 beats per minute and regular, the blood pressure 84/62 mm Hg, the respiratory rate 22 breaths per minute, and the oxygen saturation
94% while he was breathing 6 liters of oxygen through a nasal cannula. The patient’s body-mass index (the weight in kilograms divided by the square of the height in meters) was 30. He appeared uncomfortable, pale, and diaphoretic, and he was using his accessory muscles to breathe. The jugular venous pressure was estimated at 18 cm of water. Cardiac examination revealed a regular tachycardia and a grade 2/6 holosystolic apical murmur, with no appreciable gallop, heave, or thrill. Examination of the lungs revealed rales at the left base. The abdomen was soft and nontender, without abdominojugular reflux. The liver
edge, which was palpable 4 cm below the costal margin, was not tender. The arms and legs were
cool and clammy, with no edema. Distal pulses were thready. There was no rash.

The hematocrit was 39.4%, the platelet count 465,000 per cubic millimeter, and the white-cell
count 12,730 per cubic millimeter, with a differential count of 83% neutrophils, 9% lymphocytes,
and 8% monocytes. The erythrocyte sedimentation rate was 40 mm per hour. The serum level of sodium was 130 mmol per liter, potassium 4.6 mmol per liter, chloride 97 mmol per liter, and bicarbonate 17 mmol per liter; levels of creatinine and urea were normal. The results of liverfunction tests were unremarkable. The lactic acid level was 2.8 mmol per liter (normal range, 0.5 to 2.2). The level of creatine kinase was 182 U per liter (normal range, 39 to 308), the creatine kinase MB (CK-MB) fraction 17.4 ng per milliliter (normal range, 0 to 6.6), troponin T 3.03 ng per milliliter (normal level, 0), N-terminal pro–B-type natriuretic peptide 40,843 pg per milliliter (normal range, 0 to 899), and C-reactive protein 64.5 mg per liter (normal range, 0 to 3.0).

An electrocardiogram (ECG) showed sinus tachycardia with premature atrial contractions, low
limb-lead voltage, left atrial enlargement, a vertical axis, septal Q waves, poor R-wave progression, and diffuse T-wave flattening (Fig. 1). A chest radiograph revealed mild cardiomegaly, small bilateral
pleural effusions, and mild-to-moderate pulmonary edema.

A transthoracic echocardiogram revealed mild left ventricular dilatation with mild concentric hypertrophy
and severely reduced global systolic function (ejection fraction, approximately 25%), with some regional variation (greater impairment of the anterolateral wall). The right ventricle was moderately dilated, with moderately reduced systolic function. There was moderate mitral regurgitation and mild-to-moderate tricuspid regurgitation. There was no pericardial effusion.

The patient underwent emergency coronary angiography for presumed non–ST-segment elevation
myocardial infarction. Angiography revealed a minor discrete lesion in the proximal left anterior descending coronary artery; the lesion obstructed 20% of the cross-sectional area of the artery. No other abnormalities were noted. Right heart catheterization confirmed elevated filling pressures (right atrial pressure, 15 mm Hg; pulmonarycapillary wedge pressure, 38 mm Hg) and low cardiac output (cardiac index, 2.0 liters per minute per square meter of body-surface area) despite intravenous administration of dopamine. During catheterization, the patient became progressively hypotensive, necessitating placement of an intraaortic balloon counterpulsation pump. Intubation was performed for worsening hypoxemia.

The patient underwent endomyocardial biopsy, and a transseptal continuous-flow PVAD was
placed to address the poor perfusion and ongoing hypotension. Filling pressures and cardiac output
improved substantially with PVAD support. Additional laboratory testing revealed a low serum iron level (30 μg per deciliter; normal range, 37 to 158) and reduced total iron-binding capacity (204 μg per deciliter; normal range, 220 to 460). The ferritin level was 6500 μg per liter (normal range, 20 to 400). Levels of thyrotropin, uric acid, carnitine, vitamin B12, and folate were normal. Antinuclear antibodies were not detected. Serum and urine toxicologic tests and serologic tests for the human immunodeficiency virus and Borrelia burgdorferi were negative.

Immunosuppressive therapy with intravenous methylprednisolone and cyclosporine was initiated,
and the patient was evaluated for heart transplantation and definitive mechanical support. Attempts to wean the patient from the PVAD were unsuccessful. On hospital day 5, fever developed and the white-cell count increased. A chest radiograph revealed new pulmonary infiltrates. The surgical risk associated with the introduction of definitive mechanical support was deemed too high, and the patient died from pneumonia.

http://www.nejm.org/doi/pdf/10.1056/NEJMcps1301819