Treatment modalities of non-ST-elevation acute coronary syndromes in the real world. Results of the prospective R.OS.A.I.-2 registry.
BACKGROUND
Despite advances in the treatment of non-ST-elevation acute coronary syndromes (ACS) based on randomized studies and published guidelines, the extent to which such treatments are applied in daily clinical practice remains elusive. The R.OS.A.I.-2 registry was undertaken to assess the modalities of the treatment of non-ST-elevation ACS, both in terms of the use of drugs, with particular attention to glycoprotein IIb/IIIa inhibitors and clopidogrel, as well as type of strategy, aggressive versus conservative, in a consecutive series of patients admitted to 76 coronary care units (CCU) in Italy.


METHODS
The R.OS.A.I.-2 study group consisted of 76 hospitals in 7 regions of Northern and Central Italy: 38 centers had a CCU without cath lab facilities (type 1), whereas 38 type 2 centers had a CCU with an on-site interventional cath lab. Globally, 1581 patients with a diagnosis of non-ST-elevation ACS entered the registry during an 8-week period and had a 30-day follow-up. Patients were considered as being aggressively treated if they had coronary arteriography within 96 hours of admission, whereas all other patients were considered as being conservatively treated even if they underwent coronary arteriography after the first 96 hours of hospitalization.


RESULTS
An aggressive approach was employed in 789 patients (50%), whereas of the 792 (50%) conservatively treated patients 363 had a late coronary arteriography at a mean of 10.5 +/- 13 days after admission. Aggressively treated patients were younger (p < 0.0001), had less frequently ST-segment depression (p = 0.04), troponin positivity (p = 0.02), elevated creatine kinase (CK) and/or CK-MB levels within 24 hours of admission (p = 0.01), and had been more often admitted to type 2 hospitals (p < 0.0001) than those treated conservatively. Glycoprotein IIb/IIIa blockers (predominantly "small molecules") were more frequently used in younger patients (p = 0.04), in those treated aggressively (p < 0.0001), with ST-segment depression (p = 0.01), and in those with a high TIMI risk score (p = 0.001), whereas the use of clopidogrel did not differ in any patient subgroup except in patients < 70 years (p = 0.01) and in those treated aggressively (p < 0.0001). Percutaneous coronary interventions were performed in 656 patients (481 in the aggressively treated group and 175 in the conservatively treated group). At 30 days, the death rate was 3.4% and the myocardial infarction rate was 5.8%. Age, ST-segment depression, elevated CK and/or CK-MB levels within 24 hours of admission and a conservative approach were significant predictors of an unfavorable outcome.


CONCLUSIONS
The R.OS.A.I.-2 registry confirms that the population admitted to the CCU with non-ST-elevation ACS has a higher risk profile than that included in recent clinical trials. The aggressive approach is still more dependent on the cath lab availability than on a risk stratification process. Conservatively treated patients have worse clinical features and short-term prognosis. Applying an invasive approach to higher risk groups might further improve the global outcome of non-ST-elevation ACS.
D000208:Acute Disease; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D015906:Angioplasty, Balloon, Coronary; D015415:Biomarkers / Q000097:blood; D003131:Combined Modality Therapy; D017023:Coronary Angiography; D001026:Coronary Artery Bypass; D003325:Coronary Care Units; D003327:Coronary Disease / Q000097:blood / Q000000981:diagnostic imaging / Q000628:therapy*; D003402:Creatine Kinase / Q000097:blood; D052279:Creatine Kinase, MB Form; D004562:Electrocardiography; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007527:Isoenzymes / Q000097:blood; D007558:Italy / Q000453:epidemiology; D008297:Male; D008875:Middle Aged; D015999:Multivariate Analysis; D010343:Patient Admission; D010975:Platelet Aggregation Inhibitors / Q000627:therapeutic use; D019039:Platelet Glycoprotein GPIIb-IIIa Complex / Q000627:therapeutic use; D011237:Predictive Value of Tests; D011446:Prospective Studies; D012042:Registries; D013318:Stroke Volume / Q000502:physiology; D013577:Syndrome; D016896:Treatment Outcome; D019210:Troponin I / Q000097:blood; D020107:Troponin T / Q000097:blood
D015415:Biomarkers; D007527:Isoenzymes; D010975:Platelet Aggregation Inhibitors; D019039:Platelet Glycoprotein GPIIb-IIIa Complex; D019210:Troponin I; D020107:Troponin T; D003402:Creatine Kinase; D052279:Creatine Kinase, MB Form