{'fraction_non_alphanumeric': 0.06257668711656442, 'fraction_numerical': 0.06441717791411043, 'mean_word_length': 4.585616438356165, 'pattern_counts': {'":': 0, '<': 2, '<?xml version=': 0, '>': 1, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Effects of chronic kidney disease on platelet response to antiplatelet therapy in acute myocardial infarction patients].

OBJECTIVE
To elucidate the effects of dual antiplatelet therapy on platelet response in acute myocardial infarction patients with chronic kidney disease.


METHODS
From September 2011 to June 2012, a total of 195 acute myocardial infarction patients with drug eluting stent implanting were enrolled. Among them, 133 cases had normal renal function and 62 cases suffered chronic kidney disease (CKD). Platelet reactivity was examined after clopidogrel 300 mg and aspirin 300 mg treatment for 24 h. High on treatment platelet reactivity (HPR) was defined as>55% for light transmission aggreometry.


RESULTS
The CKD patients had a higher incidence of diabetes mellitus (43.5% (27/62) vs 24.8% (33/133), P = 0.01), anemia (16.1% (10/62) vs 5.3% (7/133), P = 0.03) and high on treatment platelet reactivity (45.2% (28/62) vs 28.6% (38/133), P = 0.03) than those with normal kidney function. Logistic regression analyses showed that CKD and diabetes mellitus were independent predictors of HPR. Prevalence of HPR was higher in CKD patients than normal kidney function patients (65.1% ± 10.2% vs 45.3% ± 7.8%, P < 0.01). In subgroup analysis, testing was done before and after antiplatelet treatment. At baseline, no differences existed in platelet aggregation. However, absolute decrease in reactivity after antiplatelet treatment was significantly less in CKD patients than those with normal kidney function (63.2% ± 8.6% vs 43.2% ± 5.2%, P < 0.01).


CONCLUSION
CKD is an important contributor to apparent HPR.