More and more cardiac surgeons are realizing the gravity of visceral malperfusion in acute type A aortic dissection (ATAAD) and choose to treat the visceral malperfusion first when a patient has already developed malperfusion syndrome (MPS). [1][2][3] The difference between malperfusion and MPS is similar to the difference between bacteremia and sepsis, or between HIVand AIDS. End-organ malperfusion is inadequate blood flow to the end organs, which can be diagnosed by clinical exam (peripheral pulses) and computed tomography angiography. MPS is the consequence of prolonged malperfusion, including cell, tissue, and organ necrosis, dysfunction, and failure, which can be clinically diagnosed based on symptoms (eg, abdominal pain), physical exam (eg, peritoneal signs), and laboratory tests (eg, serum lactate, arterial blood gases). Just like sepsis, MPS is a process of development of end-organ damage. In the early stage, because of ischemia, patients start to have cell death, tissue death, and organ dysfunction, but no organ death and failure. For example, patients with superior mesenteric artery (SMA) malperfusion can have abdominal pain, mildly elevated lactate, and mild metabolic acidosis but no bloody stools, peritoneal signs, or transmural necrosis of intestine, as in the case described by Ni and colleagues. 2 We can define this stage of malperfusion syndrome as early-stage MPS, which also includes mildly increased liver enzymes, bilirubin, creatinine, and myoglobin in early MPS due to celiac artery, renal artery, and extremity malperfusion. If the malperfusion is not resolved, patients will continue to develop extensive organ