Contrast-induced acute kidney injury is associated with poor short- and long-term outcomes after primary percutaneous coronary intervention in STEMI.

STEMI patients with CKD have significantly higher rates of death and major bleeding compared with those without CKD. In patients with CKD, there appears to be no benefit of bivalirudin compared with heparin + GPI, or DES versus BMS during primary PCI in improving clinical outcomes.

BackgroundIndividuals referred for stress testing to identify coronary artery disease may have nonobstructive atherosclerosis, which is not detected by stress tests. Identification of increased risk despite a negative stress test could inform prevention efforts. Abnormal ankle‐brachial index (ABI) is associated with increased cardiovascular risk.HypothesisRoutine ABI testing in the stress laboratory will identify unrecognized peripheral arterial disease in some patients.MethodsParticipants referred for stress testing without known history of atherosclerotic disease underwent ABI testing (n = 451). Ankle‐brachial index was assessed via simultaneous arm and leg pressure using standard measurement, automated blood‐pressure cuffs at rest. Ankle‐brachial index was measured after exercise in 296 patients and 30 healthy controls. Abnormal postexercise ABI was defined as a >20% drop in ABI or fall in ankle pressure by >30 mm Hg.ResultsOverall, 2.0% of participants had resting ABI ≤0.90, 3.1% had ABI ≥1.40, and 5.5% had borderline ABI. No patient with abnormal or borderline ABI had an abnormal stress test. Participants who met peripheral arterial disease screening criteria (age ≥65 or 50–64 with diabetes or smoking) tended toward greater frequency of low ABI (2.9% vs 1.0%; P = 0.06) and were more likely to have borderline ABI (0.91 to 0.99; 7.8% vs 2.9%; P = 0.006). Postexercise ABI was abnormal in 29.4% of patients and 30.0% of controls (P not significant).ConclusionsAnkle‐brachial index screening at rest just before stress testing detected low ABI in 2.0% of participants, all of whom had negative stress tests.

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As a prelude to clinical trials with a bovine surfactant (surfactant TA), in human infants with hyaline membrane disease, pulmonary and hemodynamic changes following its instillation in premature baboons were investigated. Baboons, delivered by cesarean section at 141 ± 3.5 days (mean ± SD, 77% gestation), were provided with intensive care. At 2 hours of age in one group (n = 10), 100 mg/kg of surfactant TA (reconstituted bovine surfactant, Tokyo Tanabe Co., Tokyo) was instilled into the lungs. Sequential measurements and monitoring of pulmonary and hemodynamic variables were carried out in these ten baboons and in a control group of five baboons for 16 hours, at which time the experiments were electively terminated. At birth, the pulmonary compliance, findings of chest radiographs, ratio of arterial Po2 to alveolar Po2, and respirator variables needed to maintain normal blood gas and acid base status were identical in both groups and indicative of severe hyaline membrane disease. Following surfactant instillation, the treated group demonstrated a rapid increase in Po2 with significantly improved ratio of arterial Po2 to alveolar Po2 (from a mean ± SD pretreatment value of 0.21 ± 0.11 to 0.45 ± 0.11 by 16 hours). Pulmonary compliance improved similarly (from pretreatment value of 0.18 ± 0.06 mL/cm H2O/kg to 0.27 ± 0.09 mL/cm H2O/kg). Significant reduction in respirator support variables could be achieved in all treated animals; however, in the control animals, the pulmonary status worsened as evidenced by increasing mean airway pressure and respirator variables to keep normal blood gas and acid base status, thus worsening compliance. At autopsy, pulmonary pressure-volume curves were significantly different with large hysteresis obtained in the surfactant-treated group. Although no deleterious effect on hemodynamics was noted in surfactant TA-treated animals, a large patent ductus arteriosus was demonstrated by aortography. Increased lung blood flow, probably due to a large patent ductus arteriosus flow, was demonstrated by radiolabeled microsphere technique. The physiologic significance and clinical relevance of these findings in premature baboons treated with surfactant TA are discussed.

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( l 3 -19kg) were a n e s t h e t i z e d w i t h a l p h a -c h l o r a l o s e , volume v e n t i l a t e d , and a c u t e l y i n s t r u m e n t e d t o measure h e a r t r a t e ( H R ) , r i g h t a t r i a l (RAP), wedge(PAhT) , a o r t i c ( A o P ) , i n f e r i o r vena c a v a l (IVCP) , and abdominal p r e s s u r e s . AAD was accomplished by i n f l a t i n g t h e abdomen t o 20 mmHg w i t h n i t r o g e n . C a r d i a c index(C1) and BF t o h e a r t (H) , s k e l e t a l muscle(SM) , l i v e r ( L ) , and r e n a l cortex(RC) were measured by i n j e c t i n g 1 5 micron r a d i o a c t i v e m i c r o s p h e r e s i n t o t h e l e f t v e n t r i c l e .Measurements were made and u r i n e and blood c o ll e c t e d d u r i n g 30 min p r e -i n f l a t i o n and p o s t -d e f l a t i o n c o n t r o l p e r i o d s and d u r i n g 60 min of AAD. AAD markedly d e p r e s s e d C I ( 3 6 % ) * w i t h o u t a l t e r i n g HR o r AoP. RAP(43%)* and PAWP(27%)* r o s e , a s d i d pulmonary(63%)* and s y s t e m i c ( 6 6 % ) * v a s c u l a r r e s i s t a n c e s , b u t l e f t ( 2 7 % ) and r i g h t ( 2 2 % ) v e n t r i c u l a r stroke-work f e l l ; t h u s , dec r e a s e d CI d i d n o t r e s u l t from i n c r e a s e d a f t e r l o a d . CI d e c r e a s e d due t o impaired myocardial c o n t r a c t i l i t y o r , i f t r a n s m u r a l vent r i c u l a r f i l l i n g p r e s s u r e s f e l l w i t h AAD, t o d e c r e a s e d p r e l o a d . L(56%) and RC(32%)* BF f e l l more t h a n SM(3%) o r H(20%) BF. Redist r i b u t i o n of BF was n o t e x p l a i n e d by p e r f u s i o n p r e s s u r e changes. Decreased CrC1(84%) r e s u l t s , a t l e a s t i n p a r t , from d e c r e a s e d RC BE. (*p < 0.05 v s . p r e -i n f l a t i o n c o n t r o l ) ALTERATIONS IN REGIONAL BLOOD FLOW PRODUCED BY HIGH SALT DIET. A. P. Rocchlni K. P. Gallagher. (Spons. A. Rownthal). Univ. of M I C~: Ann Arbor. 200Previously we documented t h a t a hlgh salt diet (NaD) prevents f a t a l hemorrhagic shock (HS) by bluntlng the response of the renlnanglotensln-system (RAS). T o determine lf the improved survlval was associated wlth Improved tlssue perfusion, we examlned the abllity of a NaD (9 gms NaCl/day for 6 weeks) t o alter regional blood flow (BF) durlng HS. SIX dogs recelved the NaD for 6 weeks and 5 dogs recelved a normal (NO diet for 6 weeks. HS was lnduced by bleedlng Into an overhanging reservoir until the mean pressure was reduced t o 35 mmHg. Prlor t o and a t 0.5, 1.5 and 2.5 hrs of HS, BF was measured in the heart. aut (GI), and kldney uslng mlcrospheres. hrs t h e Na dogs experienced a slgniflcant and progressive IncreaseIn both GI and heart BF (~<.01). In a d d~t l o n , plasma renin activity ( 4 ) , i n 1 7 h e a l t h y t e r m and 3 p r e t e r m (30-33 wks) i n f a n t s , w i t h a PD d e v i c e (ATL, Mark IV). I n f a n t s w e r e p l a c e d on t h e i r s i d e s a n d a 7.5 MHZ t r a n sd u c e r was u s e d . The Doppler l i n e and c u r s o r w e r e...