Nonatherosclerotic Ischemia: Cocaine, Vasospasm, SCAD & Type 2 MI
Ischemia without a ruptured plaque — where the usual ACS reflexes backfire
Overview: ischemia without a ruptured plaque
The exceptions to type 1 MI. Most acute MIs are type 1: a plaque ruptures or erodes and thrombus occludes the vessel. Cocaine toxicity, coronary vasospasm, spontaneous coronary artery dissection (SCAD), and supply–demand (type 2) infarction also raise troponin, but the reflexive ACS bundle — beta-blocker, heparin, dual antiplatelets, stent, fibrinolysis — may be useless or harmful.
Injury versus infarction. Myocardial injury is any troponin value above the 99th percentile upper reference limit; it is acute when serial values rise and/or fall and chronic when they stay flat. Infarction requires acute injury plus evidence of ischemia: ischemic symptoms, new ischemic ECG changes or pathologic Q waves, new loss of viable myocardium or a new regional wall-motion abnormality on imaging, or coronary thrombus at angiography or autopsy.
Universal definition types. 1 atherothrombotic; 2 supply–demand; 3 sudden death before biomarkers; 4 PCI-related (4a procedural, 4b stent thrombosis, 4c restenosis); 5 CABG-related. Vasospasm, coronary embolism, and SCAD count as type 2 mechanisms.
| Feature | Cocaine | Vasospasm | SCAD | Type 2 MI |
|---|---|---|---|---|
| Typical patient | Young, agitated, tachycardic user | Young smoker, early-morning rest pain | Woman in her 40s–50s, peripartum, FMD | Patient with another acute illness |
| Mechanism | Sympathetic surge, α1 spasm, thrombosis | Transient epicardial spasm | Intramural hematoma compresses true lumen | O2 supply–demand mismatch |
| First move | Benzodiazepine, aspirin, nitroglycerin | CCB ± long-acting nitrate | Aspirin, beta-blocker, monitoring | Correct the trigger |
| Avoid | Beta-blockers while intoxicated | Triptans, ergots, nonselective beta-blockers | Fibrinolysis, routine PCI | Reflex heparin, DAPT, angiography |
Cocaine-associated chest pain
Mechanism. Cocaine blocks presynaptic reuptake of norepinephrine and dopamine (and serotonin). The sympathetic surge raises heart rate, blood pressure, and contractility, increasing oxygen demand, while α1-mediated coronary vasoconstriction reduces supply. Cocaine also activates platelets, promotes thrombus, and accelerates atherosclerosis. MI risk peaks in the first hour after use, yet only a minority of users with chest pain are having an MI — each still needs an ECG and serial troponins. Methamphetamine produces the same picture.
Sodium-channel effect. Cocaine also blocks fast sodium channels like a class I antiarrhythmic; QRS widening or a wide-complex tachycardia is treated with IV sodium bicarbonate.
- BenzodiazepineIV lorazepam or diazepam first: lowers central sympathetic outflow, heart rate, blood pressure, and chest pain; also treats agitation, seizures, and hyperthermia.
- AspirinGive early unless tearing chest or back pain suggests aortic dissection, for which cocaine is a risk factor.
- NitroglycerinSublingual or IV for persistent pain and hypertension.
- CCB or phentolamineVerapamil or diltiazem to reverse persistent spasm; phentolamine (an α-blocker) for severe hypertension.
- Reperfusion if STEMIPersistent ST elevation despite the above → primary PCI, preferred over fibrinolysis.
Avoid beta-blockers while signs of intoxication persist (tachycardia, hypertension, agitation). Blocking β2-mediated vasodilation leaves α1 stimulation unopposed and worsens coronary spasm and hypertension. Labetalol is mostly a beta-blocker (β:α about 7:1 IV), so it is not a safe substitute on exams.
Vasospastic (Prinzmetal) angina
Presentation. Typically a younger patient, often a smoker, with chest pain at rest — classically between midnight and the early morning — lasting minutes. An ECG recorded during pain shows transient ST elevation that normalizes as the pain resolves; troponin is usually normal and exercise tolerance is often preserved. More common in East Asians; associated with Raynaud phenomenon and migraine.
Triggers. Smoking is the main modifiable risk factor. Other precipitants: cocaine and amphetamines, triptans (sumatriptan), ergot alkaloids (ergotamine), cold exposure, hyperventilation, nonselective beta-blockers, and the fluoropyrimidines 5-fluorouracil and capecitabine. Triptans and ergots are contraindicated with known vasospasm or CAD.
Diagnosis. Capture transient ST elevation on a 12-lead ECG during pain or on ambulatory Holter monitoring. Angiography excludes fixed obstructive disease, and intracoronary acetylcholine (or ergonovine) that reproduces spasm with symptoms and ischemic ECG changes confirms the diagnosis.
Treatment. Stop smoking and remove triggers. Long-acting calcium channel blockers (diltiazem, verapamil, amlodipine, nifedipine) are first-line; add a long-acting nitrate if attacks continue, and use sublingual nitroglycerin to abort episodes. Avoid nonselective beta-blockers such as propranolol, which can provoke spasm through unopposed α tone.
Prolonged spasm is not benign: it can cause MI, AV block, ventricular tachyarrhythmias, and sudden death.
Spontaneous coronary artery dissection
Mechanism. An intramural hematoma, with or without an intimal tear, separates the layers of the coronary wall; the blood-filled false lumen compresses the true lumen and causes ACS without atherosclerosis.
Who gets it. Typically women in their 40s–50s with few traditional risk factors. SCAD is the leading cause of pregnancy-associated MI, mostly in the early postpartum period. Precipitants include intense emotional stress, extreme or isometric exertion, Valsalva-type strain, and stimulant use.
Associated arteriopathies. Fibromuscular dysplasia (FMD) coexists in up to half or more of patients, so image the renal, iliac, and cerebrovascular arteries once (CTA or MRA from head to pelvis); FMD's extracoronary signature is the "string of beads" renal artery that causes renovascular hypertension in young women. Also consider inherited connective tissue disease: vascular Ehlers–Danlos, Marfan, and Loeys–Dietz syndromes.
Diagnosis. Coronary angiography most often shows a long, smooth, tapered narrowing, commonly in the mid-to-distal LAD; intravascular imaging (OCT or IVUS) confirms equivocal cases by showing the hematoma or false lumen.
Management. Most dissected segments heal spontaneously over weeks to months, whereas during PCI wires can enter the false lumen and stents can propagate the hematoma. Stable patients get aspirin and a beta-blocker (fewer recurrences) with prolonged inpatient monitoring. Revascularization (PCI or CABG) is reserved for ongoing ischemia, hemodynamic or electrical instability, or left main or proximal multivessel dissection. Afterward: blood-pressure control, cardiac rehabilitation, and counseling about recurrence, including with future pregnancy.
Avoid fibrinolysis when SCAD is suspected — it can extend the intramural hematoma.
Type 2 MI, nonischemic injury and MINOCA
Type 2 MI. Ischemic injury from an imbalance between oxygen supply and demand without acute atherothrombosis. Common drivers: sepsis, severe anemia or hemorrhage, tachyarrhythmias (e.g., AF with rapid ventricular response) or severe bradyarrhythmias, hypotension or shock, respiratory failure with hypoxemia, and severe hypertension.
Management. Treat the precipitant: transfusion for bleeding, fluids and antibiotics for sepsis, rate control, oxygen or ventilatory support. Do not reflexively start heparin, dual antiplatelet therapy, or urgent angiography — anticoagulating the GI bleed that caused the infarct is harmful. Evaluate for underlying CAD once the acute illness resolves. Type 2 MI carries high mortality, driven largely by the underlying disease.
Nonischemic myocardial injury. Troponin can rise without ischemia: chronic kidney disease, myocarditis, pulmonary embolism (RV strain), acute or chronic heart failure, sepsis, takotsubo syndrome, cardiac contusion, and stroke or subarachnoid hemorrhage. A dynamic rise and/or fall signals acute injury; a stable, flat elevation (typical of dialysis patients) signals chronic injury.
MINOCA. MI with no stenosis ≥50% in any major epicardial artery makes up about 5–6% of MIs and is more common in women. It is a working diagnosis: seek plaque disruption (IVUS or OCT), spasm (provocation testing), microvascular dysfunction, coronary embolism, or SCAD, and exclude nonischemic mimics. Therapy follows the mechanism, such as a CCB for proven spasm.
| Diagnosis | Late gadolinium enhancement | Other clue |
|---|---|---|
| Infarct (true MINOCA) | Subendocardial or transmural, in a coronary territory | Regional wall-motion abnormality |
| Myocarditis | Patchy midwall or subepicardial, non-coronary distribution | Viral prodrome, younger patient |
| Takotsubo | Usually absent | Apical ballooning after emotional or physical stress; recovers over weeks |