much antithrombotic therapy, however, risks extending the false lumen hematoma; hence, only antiplatelet therapy is typically used, not anticoagulation.181,182
In patients with ongoing STEMI, total occlusion, or hemodynamic compromise, PCI is justified: low-pressure balloon dilatation may be tried as a stand-alone strategy to re-establish flow, avoiding long stenting in a pathology that will heal on its own. CABG is an option in left main or multivessel SCAD; CABG is hampered by distal vessel involvement and by a high rate of graft closure (70%) on long-term follow-up, as native disease regresses.183
Progression and follow-up:
SCAD almost always heals, yet acute extension may be seen in ~5-10% of cases in the first week, before eventual healing; thus, ECG signs of ongoing or recurrent ischemia may justify repeat coronary angiography or CT. Note that persistent pain, by itself, does not necessarily imply ischemia, as the dissection process may be painful by itself.Figure 1.10 NSTEMI in a healthy 47-year-old woman. Chest pain started during kick boxing. Several features suggest SCAD type 2 and argue against performing PCI: (1) long smooth disease >30 mm with no calcification (arrows), (2) tortuous, elongated coronary arteries, (3) distal disease, (4) woman <60 years. The flow was TIMI 2 and she was not having ongoing angina, so conservative management was adopted. Intravascular imaging was avoided.
Instead of repeating coronary angiography, coronary CT may be used to document SCAD healing 6 weeks later; it may also be used in patients with recurrent symptoms, to rule out proximal SCAD extension that would warrant intervention. CT is not a great initial diagnostic modality as it is insensitive for distal SCAD of small vessels <2.5 mm.
In-hospital and long-term survival is very favourable in non-pregnancy SCAD (0 to 2% in-hospital mortality, 0% mortality in the Canadian SCAD registry).183 Yet, one series suggests a high mortality, higher than traditional MI, mainly when PCI is attempted or in women older than 60.179 Also, there is a 10-30% risk of recurrence at 1-3 years, and 30% at 5 years. Recurrence is reduced with: β-blockers (2/3 reduction), avoidance of emotional and physical triggers, such as heavy lifting>30-50 pds, Valsalva, and hormonal therapy.
SCAD is associated with a high prevalence of peripheral fibromuscular dysplasia (renal ~70%, iliac ~50%, carotid ~50%), and intracranial aneurysms (~15-20%). Therefore, screening with abdominal CT and carotid-cerebral CT angiography is often warranted.
Peripartum SCAD is more severe clinically than non-pregnancy SCAD. SCAD, even non-pregnancy SCAD, generally contraindicates future pregnancies.
Appendix 7. Harmful effects of NSAIDs and cyclooxygenase-2 inhibitors in CAD
There are two types of cyclooxygenases (COX): COX-1 and COX-2. COX-1, found in the normal epithelium and in platelets, is responsible for the homeostatic prostaglandins but also for the generation of thromboxane A2 and platelet activation. Conversely, COX-2, found in inflammatory cells, generates inflammatory prostanoids but also the protective prostacyclin (vasodilatory and antiplatelet effects). The low aspirin dose predominantly inhibits COX-1 with less effect on COX-2.
NSAIDs are harmful in several ways: (i) NSAIDs bind to COX-1, the site of action of aspirin, yet, as opposed to aspirin, they bind in a reversible manner and do not have a sustained antiplatelet effect; (ii) NSAIDs inhibit COX-2 and thus, prostacyclin production. Predominant or selective COX- 2 inhibitors are potentially worse from a platelet standpoint, as they block prostacyclin without any reduction of COX-1’s thromboxane and are more detrimental to the prostacyclin–thromboxane balance.
Moreover, if aspirin is administered after NSAID, the COX-1 site will be blocked by the NSAID, which prevents aspirin from binding to it; since the plasma half-life of aspirin is only 20 minutes, aspirin will be eliminated before it gets an opportunity to act.
Appendix 8. Additional ideas on the physiology of hs-troponin-Role of hs-troponin in primary prevention
While troponin release above MI cutoff reflects myocardial cell necrosis, low but detectable hs-troponin typically represent physiological levels of troponin release, or ischemia without necrosis. This may be due to expulsion of the cytosolic pool of troponin without cell death (most of the troponin is in the myofibrils and degrades over 12-24 hours after cell death, but ~8% is cytosolic and may be released physiologically or pathologically without cell death). For example, myocardial stretching, ischemia, or fast heart rate may increase cell membrane permeability without necrosis.184 This may explain why, following rapid atrial pacing for a few minutes, hs-troponin levels rise, and sometimes double or triple (without exceeding MI cutoff) even in patients without CAD and sometimes even without ischemia (as evidenced by a lack of lactate release in the coronary sinus).184 This also explains why, after a positive stress test, hs-troponin slightly rises, even while remaining well below MI cutoff, and is associated, in this case, with the presence and severity of perfusion defects.185 As such, physiological demands or transient provoked ischemia can release troponin in the absence of necrosis. The change is so small that it cannot be detected with conventional troponin, and troponin level does not usually rise above MI cutoff even if stress-induced ischemia is severe. Ischemia or injury must be sustained to raise troponin above MI cutoff.
Hs-troponin is more likely to be chronically detectable in patients with underlying CAD and in patients with comorbidities such as hypertension or diabetes.184,186 In fact, even in the outpatient setting, an undetectable hs-troponin, or a detectable troponin that is in the lower tertile of detection, is associated with a very low risk of long-term events (even lower than that of a normal stress test), and a low probability of obstructive CAD.187,188 In another study that screened asymptomatic outpatients with a mean age of 62, an undetectable troponin (<0.003 ng/ml) predicated a very low risk of cardiac events, 0.5% per year, similar to the risk of patients with a calcium score of 0.189
The only circumstance wherein troponin may exceed MI cutoff physiologically, without necrosis, is marathon exercise among non-highly trained individuals. After marathon, ~50% of nonelite participants have a rise in troponin above MI cutoff (>0.03, up to 0.8 ng/ml), along with transient LV diastolic dysfunction and RV dilatation.190 Yet troponin rise is brief and normalizes within a few hours, and there is no evidence of late gadolinium enhancement on MRI (troponin leak from myocardial stretch rather than cell necrosis?).191
QUESTIONS AND ANSWERS
1 Question 1. A 72-year-old man is admitted with fever, severe bilateral pneumonia, and sepsis. His exam does not suggest volume overload. During his first hospitalization day, his ECG shows transient deep ST depression in the lateral leads. His troponin I peaks at 1.2 ng/ml, with a rise and fall pattern; BNP = 65. He has acute renal failure with creatinine of 1.7 mg/dl. He does not complain of chest pain. His echo shows a hyperdynamic LV. What is the next step?His troponin rise is due to ischemic imbalance. He does not fulfill the definition of MI. No need for further cardiac workupHis troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform stress testing before dischargeHis troponin is partly due to ischemic imbalance. He fulfills the definition of MI. Perform coronary angiography after stabilization of infectious state and renal function
2 Question 2. A 72-year-old man is admitted with fever, severe bilateral pneumonia, and sepsis. His exam does not suggest volume overload. His ECG shows mild lateral T inversion. His troponin I peaks at 0.8 ng/ml, with a rise and fall pattern; BNP = 65. He has acute renal failure with creatinine of 1.7 mg/dl. He does not complain of chest pain. His echo shows a hyperdynamic LV. What is the next step?His troponin rise is due to ischemic imbalance. He does not fulfill the definition of
