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Lou et al. Vessel Plus 2022;6:38 https://dx.doi.org/10.20517/2574-1209.2021.108 Page 3 of 9

In MMP, several factors further contribute to the poor outcomes in ATAAD. First, the insidious onset
makes it difficult to pinpoint the diagnosis leading to delays in treatment. Forty percent of patients
presenting with MMP do not present with abdominal pain, and 20% of patients with abdominal pain do not
[3,4]
have mesenteric malperfusion . Moreover, there are no definitive laboratory studies that accurately
identify visceral ischemia, which is often associated with other organ system malperfusion. Radiographic
findings can allude to MMP but cannot always distinguish between dynamic and static obstruction.

The pathogenesis of MMP creates an added layer of complexity. Intestinal ischemia disrupts the gut
mucosal barrier, which incites endotoxin release to the portal system and mediates reperfusion injury.
Perhaps the greatest contributor to the high mortality rate in MMP syndrome is the autoregulatory response
of the splanchnic vessels to ischemia, which occurs when there is a > 75% decrease in blood flow to the
[5]
celiac and superior mesenteric artery vascular beds . This leads to a compensatory arteriolar vasodilatory
response that converts to vasoconstriction when the ischemic period is prolonged. This vasoconstriction is
often irreversible even after restoring blood flow. Both of these mechanisms can be further compounded by
aortic surgery and likely account for the high incidence of necrotic bowel and persistent acidosis that may
be observed after central aortic repair.

MALPERFUSION SYNDROME BY ORGAN SYSTEM: AN OVERVIEW
Malperfusion complicates 20%-30% of all ATAAD cases with relative incidences as listed below :
[6]
• Coronary and acute myocardial infarction (MI): 1.7%-10%;
• Spinal cord: 0.3%-4.8%;
• Cerebral and associated stroke: 5.2%-13.1%;
• Visceral/extremity:
○ Mesenteric: 3.6%-14%
○ Renal: 2.3%-12%
○ Lower extremity: 2.3%-23%

Coronary malperfusion
Coronary malperfusion with acute MI is a rare but potentially fatal complication of ATAAD. The available
data and management of this condition remain scant, given difficulties with its diagnosis and the high-
associated mortality rate.

While acute aortic dissection often extends to the coronary ostia (particularly favoring involvement of the
right coronary artery), it does not always lead to myocardial ischemia. Other considerations such as the size
and location of the primary entry tear and false lumen flow pattern may impact the onset and severity of
coronary malperfusion. A thorough evaluation is not always possible under static conditions, and coronary
malperfusion may occasionally be diagnosed clinically when flow is resumed after aortic de-clamping.

[7]
According to the Neri definition of coronary malperfusion in acute aortic dissection , there are three types
of dissections based on operative findings: type A, ostial dissection with disruption of the inner layer but
limited to the coronary ostium; type B, dissection extending into the coronary artery; and type C, coronary
[8]
disruption (i.e., intimal detachment). While some groups advocate for CABG repair in all patients , others
including the Penn group have suggested a more tailored strategy based on the type of lesion involved. In
[9]
their analysis of 76 patients presenting with coronary artery malperfusion, Kreibich et al. reported
successful ostial repair in 88% of type A patients, 63% of type B patients and 0% of type C patients. They
therefore recommended CABG primarily for patients with type C lesions or in those with underlying
coronary artery disease for which optimal delivery of cardioplegia could not be achieved .
[9]