PE was the underlying mechanism in one-fourth of STEMI. PE was characterized by eccentric fibrous plaque. CN was characterized by superficial large calcium and negative remodeling. PE was associated with less microvascular damage after PCI.

A series of 10 cases of posterior cerebral artery (PCA) aneurysms were retrospectively reviewed. There were five men and five women aged 38 to 68 years (mean 57.5 years). Seven patients presented with subarachnoid hemorrhage. Two aneurysms were found incidentally during clinical examination for stroke. One aneurysm was associated with moyamoya disease. All aneurysms were saccular. The aneurysms arose from the P 1 segment in three patients, the P 1 /P 2 junction in three patients, the P 2 segment in three patients, and the P 3 segment in one patient. Two patients died before operation and one patient refused surgery. Aneurysmal clipping was performed for seven patients. All aneurysms except the P 2 and the P 3 aneurysms were treated via the pterional approach. Four patients had excellent outcome, but one patient with a P 3 aneurysm developed homonymous hemianopsia due to thrombosis of the parent vessel and another patient with a P 2 aneurysm had moderate disability from the initial insult. Coil embolization has been indicated as the first choice of therapy, but PCA aneurysms are good candidates for direct clipping.

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STEMI patients with greater residual thrombus burden after aspiration thrombectomy had worse microvascular dysfunction and greater myocardial damage compared with those with smaller residual thrombus burden.

Background— Spotty superficial calcium deposits have been implicated in plaque vulnerability based on previous intravascular imaging studies. Biomechanical models suggest that microcalcifications between 5 and 65 µm in diameter can intensify fibrous cap stress, promoting plaque rupture. However, the 100- to 200-µm resolution of intravascular ultrasound limits its ability to discriminate single calcium deposits from clusters of smaller deposits, and a previous optical coherence tomographic investigation evaluated calcifications within a long segment of artery, which may not truly reflect the mechanics involved in potentiating focal plaque rupture. Methods and Results— Detailed optical coherence tomographic assessment of coronary calcification at the culprit plaque (10-mm length) was performed in 53 patients with acute ST-segment–elevation myocardial infarction mediated by plaque rupture and 55 patients with stable angina pectoris. The number and longitudinal length of individual calcium deposits were recorded. Cross-sectional images were analyzed every 1 mm for calcium arc and depth, and these quantitative parameters were used to define individual deposits as spotty, large, and superficial. There was no significant difference between ST-segment–elevation myocardial infarction mediated by plaque rupture and stable angina pectoris groups in the number of total ( P =0.58), spotty ( P =0.87), or large calcium deposits ( P =0.27). Minimum calcium depth was similar between groups ( P =0.27), as was the number of superficial deposits ( P =0.35 using a 65-µm depth threshold and P =0.84 using a 100-µm depth threshold). Conclusions— The number and pattern of culprit plaque calcifications did not differ between patients presenting with ST-segment–elevation myocardial infarction mediated by plaque rupture versus stable angina pectoris. The optical coherence tomographic assessment of coronary calcification may not be a useful marker of local plaque vulnerability as previously suspected. Registration Information— URL: http://www.clinicaltrials.gov . Unique identifier: NCT01110538.