Cilostazol reduced restenosis and repeat revascularization after EVT in patients with intermittent claudication due to femoropopliteal disease.

We compared the myocardial ischemic burden of provisional and routine final kissing-balloon inflation (FKI) with the 1-stent strategy using a second-generation drug-eluting stent for coronary bifurcation lesions (CBL). There are no established guidelines for side branch (SB) intervention after main vessel stenting. In total, 113 CBL patients were randomized to receive different SB intervention strategies: provisional-FKI group (n = 57; FKI only when SB flow was TIMI <3) and routine-FKI group (n = 56; mandatory FKI with aggressive treatment until SB-residual stenosis <50%). Dipyridamole-stress myocardial perfusion scintigraphy with Tc was performed after 8 months. The regional summed-difference score (r-SDS) was calculated according to the coronary territory. The primary endpoint included target vessel ischemia (TVI; r-SDS ≥ 2) at 8 months, whereas the clinical primary endpoint was major adverse cardiovascular events (MACE) at 3 years. The percent (%) myocardial ischemia (100 × SDS/68) was also calculated. At 8 months, TVI was identified in 11 and 4% in the provisional-FKI and routine-FKI groups, respectively (p = 0.226). SB-binary restenosis (48 vs. 4%, p< 0.001) and myocardial ischemia at the SB territory (11 vs. 0%, p = 0.030) were more common in the provisional-FKI group; however, in TVI patients, % myocardial ischemia (4.12 ± 1.23% vs. 3.68 ± 1.04%; p = 0.677) did not significantly differ. Moderate/severe ischemia (>10% myocardial ischemia) was not observed in the target vessel in either group. Long-term cumulative MACE were similar between the groups (9 vs. 14%; p = 0.358). Provisional-FKI according to TIMI-SB flow grade led to similar and acceptable myocardial ischemia, in comparison with routine-FKI, which may contribute to the identical long-term follow-up.

A woman was admitted due to dyspnea. She had familial pulmonary arterial hypertension and typical echocardiographic findings including early diastolic bulging of the interventricular septum toward the left ventricular cavity. Her symptoms improved with medication. Five months later, she was hospitalized again due to severe dyspnea. Echocardiography demonstrated aortic valve vegetation and its regurgitation. Echocardiography also showed attenuation of early diastolic compression of the interventricular septum, however, the peak tricuspid regurgitant flow velocity did not improve. It is likely that development of left-sided heart failure attenuated abnormal interventricular septal motion due to pulmonary hypertension.

Segmental left ventricular (LV) dysfunction associated with subarachnoid hemorrhage usually develops in the apex.

Reactive hyperemia following temporary coronary occlusion recreates local conditions associated with delayed resolution of myocardial ischemia following successful PTCA. Further, this phenomenon appears to be distinct from changes in coronary blood flow induced by dipyridamole.