Case 7

Published on 02/03/2015 by admin

Filed under Internal Medicine

Last modified 22/04/2025

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Case 7

A 39-year-old woman with a history of hypertension, chronic renal failure (creatinine = 3.1), and remote cocaine abuse was admitted for evaluation of nonexertional dull chest pain. She had a normal coronary angiogram 4 years previously for similar symptoms.

Initial Diagnostic Evaluation

Laboratory data: troponin T = 0.375 ng/mL (normal < 0.040), CK = 38 U/L

ECG: NSR, LVH with nonspecific ST-T abnormalities

Echocardiogram: moderate concentric LVH, no regional wall-motion abnormalities, EF = 50%

Referred for adenosine stress ^99mTc sestamibi SPECT MPI

5-Minute adenosine infusion without supplemental low-level treadmill exercise, peak HR = 91 beats/min, normal BP response

Baseline ECG

The baseline ECG demonstrates increased QRS voltage consistent with left ventricular hypertrophy (LVH), with nonspecific ST-T abnormalities possibly related to LVH.

4:50 Adenosine (Mild Chest Pain)

The patient complained of mild chest pain near the completion of the adenosine infusion. The ECG tracing obtained at 4 minutes, 50 seconds of the adenosine infusion demonstrated more prominent ST-T abnormalities with T-wave inversions suspicious for (but not diagnostic for) myocardial ischemia. This finding is common in patients with baseline LVH.

5:50 Recovery (Persistent Chest Pain)

The patient described persistent chest pain nearly 6 minutes after completion of the adenosine infusion. This is highly unusual; the side effects of adenosine are typically very short-lived, owing to the very short half-life of adenosine (<10 seconds). An ECG tracing was obtained and demonstrated persistent nonspecific ST-T abnormalities.

9:00 Recovery (Worsening Chest Pain)

The patient described worsening chest pain 9 minutes after completion of the adenosine infusion. A repeat ECG tracing was obtained and demonstrated ST-segment elevation in the inferior leads (II, III, and aVF) and ST depression in V2 (suggestive of inferior and posterior injury, respectively), associated with reciprocal ST depression in leads I and aVL.

14:50 Recovery (No Chest Pain)

Sublingual nitroglycerin was administered, and the patient’s chest pain resolved. An ECG tracing performed at 14 minutes, 50 seconds after the adenosine infusion demonstrated resolution of the inferior-posterior injury pattern, with mild residual nonspecific ST-T abnormalities.

Rotating Raw Planar Images

The rotating raw images demonstrate moderately severe subdiaphragmatic ^99mTc sestamibi activity on both the poststress and resting images. The finding of subdiaphragmatic tracer activity on poststress images is common when pharmacologic stress is employed without supplemental low-level exercise. Subtle localized tracer activity is also noted on the anterior chest wall on poststress images, likely due to a small amount of tracer contamination of the chest wall or the patient’s gown.

SPECT Images

The poststress SPECT images demonstrate a mild perfusion defect involving the inferior and inferoapical regions. Interpretation of perfusion in the inferior wall was complicated by adjacent GI tracer activity. There is minimal defect reversibility evident on resting images, which is equivocal for ischemia. Also note that the left ventricular cavity appears larger on poststress images, with a computed stress/rest LV cavity ratio (SRLVCR) of 1.64 (normal < 1.22 with the same-day, low-dose rest, high-dose stress ^99mTc sestamibi protocol).

Gated SPECT Images

The poststress gated SPECT images demonstrated mild global left ventricular hypokinesis, with a computed left ventricular ejection fraction (LVEF) of 47%. The left ventricular end-diastolic volume (LVEDV) and left ventricular end-systolic volume (LVESV) were borderline increased at 117 and 62 mL, respectively.

Patient Management

Though the stress perfusion abnormalities were subtle (and interpretation was complicated by GI tracer interference), the presence of the inferior-posterior injury pattern on ECG following adenosine stress raised suspicion for a high-grade coronary stenosis. The patient was therefore referred for urgent coronary angiography.

Coronary Angiography

• RCA: 60% distal

• LAD: mild diffuse

• LCX: 40% distal

Medical therapy was recommended by the interventional cardiologist.

Coronary Angiography

• RCA: 80% distal PCI (DES)

• LAD: mild diffuse

• LCX: 40% distal

After further consideration of the implications of the stress ECG findings, the angiogram was reviewed more closely, and the RCA lesion was felt to be more severe. A drug-eluting stent was placed.

Teaching Points: Stress-Induced ST-Segment Elevation

1. Exercise-induced ST-segment elevation (in absence of baseline Q waves) suggests transmural ischemia and predicts severe (usually > 95%) coronary stenosis in the artery supplying the region with ST elevation.

2. If ST elevation is detected, inject the isotope, terminate exercise, and have a low threshold to admit the patient to the hospital for urgent coronary angiography.

3. If the patient is not admitted, perform a recovery ECG to confirm resolution of ST elevation before permitting the patient to leave the nuclear laboratory.

4. There have been a few case reports of ST elevation during recovery after adenosine stress (as in the present case report). The mechanism of ST elevation following adenosine stress is not known. In the cases reported thus far, coronary angiography has not demonstrated severe coronary artery disease. Nonetheless, until much more experience has accumulated, coronary angiography is advisable.

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