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Cardiology · Perfusion SPECT

Myocardial Perfusion SPECT

Snapshot

Stress/rest myocardial perfusion SPECT (⁹⁹ᵐTc-sestamibi or tetrofosmin, or ²⁰¹Tl) detects flow-limiting coronary artery disease and is a powerful risk-stratifier: a normal study carries a low annual cardiac event rate. Reported sensitivity is ≈85–90% for obstructive CAD, with more variable specificity (≈61% pooled across older studies, ≈85% for contemporary gated, attenuation-corrected SPECT); gated acquisition adds ejection fraction and wall motion. Attenuation correction and prone/upright imaging mitigate artefacts.

A perfusion tracer is injected at peak stress (exercise or pharmacological vasodilator/inotrope) and at rest. Regions supplied by a stenosed artery show relatively reduced stress uptake that “fills in” at rest (reversible ischaemia); fixed defects usually reflect scar.

Se ≈85–90%Obstructive CAD
Normal = low riskStrong warranty period
GatedEF + wall motion
Simulated stress and rest myocardial perfusion SPECT slices and polar maps: an anterior, septal and apical defect at stress that fills in at rest, and an inferior defect present on both stress and rest images.
Figure. Simulated images of stress and rest ⁹⁹ᵐTc myocardial perfusion SPECT in short-axis, vertical long-axis and horizontal long-axis slices with polar maps (white lines mark the usual coronary territories). A: a stress defect in the LAD territory that fills in at rest is reversible and indicates ischaemia; B: an inferior (RCA territory) defect on both stress and rest images is fixed and usually reflects scar.
Diagram of the 17-segment polar map and of short-axis, vertical long-axis and horizontal long-axis slices coloured by the LAD, RCA and LCx territories.
Figure. The 17-segment model and the usual coronary territories on the polar map and on the three standard slice orientations (after the AHA standardised myocardial segmentation, Cerqueira et al., 2002). Assign a defect to an artery only after checking it in two views, remembering that territories vary with coronary dominance.

When to image

  • Symptomatic patients with intermediate pretest probability of CAD.
  • Risk stratification in known CAD and before major surgery in selected cases.
  • Assessing functional significance of known stenoses.
  • Evaluating chest pain when the ECG is uninterpretable or exercise ECG is equivocal.

Protocol

  • Stress with exercise or pharmacological agents (adenosine, regadenoson, dipyridamole; dobutamine if vasodilators contraindicated).
  • ⁹⁹ᵐTc agents (gated) or ²⁰¹Tl; one- or two-day protocols.
  • Attenuation correction and/or prone/upright imaging to reduce artefacts.
  • Gated SPECT for EF and regional wall motion.

How to read it

  • Reversible defect (stress-only) → ischaemia; fixed defect → scar; partial reversibility → mixed.
  • Assess extent/severity, transient ischaemic dilatation, and post-stress EF drop as high-risk markers.
  • Correlate with symptoms, ECG and coronary anatomy.

Diagnostic performance

Per-patient sensitivity for obstructive CAD is ≈85–90%; specificity varies widely (pooled ≈61% in a meta-analysis of 1990–2010 studies, ≈85% with contemporary gated, attenuation-corrected SPECT); a normal perfusion study confers a low annual rate of cardiac death/MI. PET generally out-performs SPECT (see Perfusion PET).

Pitfalls

  • Attenuation (breast, diaphragm) mimics defects — use correction/positioning.
  • Balanced multivessel disease can look near-normal on relative imaging.
  • Sub-maximal stress reduces sensitivity.
  • Left bundle branch block causes septal artefacts (prefer vasodilator stress).
Evidence & guidelines
  • ASNC imaging guidelines (e.g. Henzlova et al., 2016, on stress, protocols and tracers) cover acquisition, stress protocols and reporting.
  • Normal MPI carries a well-documented low-risk “warranty period”.
  • PET is preferred where available for accuracy and flow quantification.
In depth
  • ⁹⁹ᵐTc-sestamibi/tetrofosmin (140 keV, negligible redistribution): image delays sestamibi 15–20 min (exercise)/45–60 (rest)/60 (pharmacologic); tetrofosmin 10–15/30–45/45.
  • Adenosine and regadenoson cause coronary vasodilatation via A2A receptors, increasing myocardial blood flow 3.5–4-fold; side effects arise from A1 (AV block), A2B (peripheral vasodilatation) and A2B/A3 (bronchospasm) activation and can be reversed with IV aminophylline.
  • Adenosine effects: flushing 35–40%, chest pain 25–30%, dyspnoea 20%, AV block ~8% (mostly self-limiting).
  • Before vasodilator stress, withhold caffeine and other methylxanthines for at least 12 h and dipyridamole for at least 48 h, and fast for at least 3 h.
  • Vasodilator stress rather than exercise or dobutamine is preferred in LBBB, permanent ventricular pacing and ventricular pre-excitation (WPW), because rate-related septal perfusion artefacts can mimic ischaemia.
  • Absolute contraindications to exercise stress include severe symptomatic aortic stenosis, acute MI within 2–4 days, acute pulmonary embolism, aortic dissection or myo/pericarditis, and resting BP above 200/110 mmHg.
  • High-risk markers: transient ischaemic dilatation, post-stress EF drop, and multi-territory reversible defects.

Sources: ASNC SPECT stress, protocols and tracers guideline 2016 (PMID 26914678) · ACC/AHA/ASNC radionuclide imaging guideline · ACCF/AHA 2012 stable ischaemic heart disease guideline high-risk criteria

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