Presence of bacterial DNA in thrombotic material of patients with myocardial infarction.

Infectious agents have been suggested to be involved in etiopathogenesis of Acute Coronary Syndrome (ACS). However, the relationship between bacterial infection and acute myocardial infarction (AMI) has not yet been completely clarified. The objective of this study is to detect bacterial DNA in thrombotic material of patients with ACS with ST-segment elevation (STEMI) treated with Primary Percutaneous Coronary Intervention (PPCI). We studied 109 consecutive patients with STEMI, who underwent thrombus aspiration and arterial peripheral blood sampling. Testing for bacterial DNA was performed by probe-based real-time Polymerase Chain Reaction (PCR). 12 probes and primers were used for the detection of Aggregatibacter actinomycetemcomitans, Chlamydia pneumoniae, viridans group streptococci, Porphyromonas gingivalis, Fusobacterium nucleatum, Tannarella forsythia, Treponema denticola, Helycobacter pylori, Mycoplasma pneumoniae, Staphylococus aureus,  Prevotella intermedia and Streptococcus mutans. Thus, DNA of four species of bacteria was detected in 10 of the 109 patients studied. The most frequent species was viridans group streptococci (6 patients, 5.5%), followed by Staphylococus aureus (2 patients, 1.8%). Moreover, a patient had DNA of Porphyromonas gingivalis (0.9%); and another patient had DNA of Prevotella intermedia (0.9%). Bacterial DNA was not detected in peripheral blood of any of our patients. In conclusion, DNA of four species of endodontic and periodontal bacteria was detected in thrombotic material of 10 STEMI patients. Bacterial DNA was not detected in the peripheral blood of patients with bacterial DNA in their thrombotic material. Bacteria could be latently present in plaques and might play a role in plaque instability and thrombus formation leading to ACS.

Comparison of the performance of the CRUSADE, ACUITY-HORIZONS, and ACTION bleeding risk scores in STEMI undergoing primary PCI: insights from a cohort of 1391 patients.

AIMS: To compare the performance of the CRUSADE, ACUITY-HORIZONS, and ACTION risk models in the ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (PPCI). METHODS: We studied all consecutive patients with STEMI who underwent PPCI at our institution between 2006 and 2010 (n=1391). The CRUSADE, ACUITY-HORIZONS, and ACTION risk scores were calculated based on the patients' clinical characteristics. The occurrence of in-hospital major bleeding (defined as the composite of intracranial or intraocular bleeding, access site haemorrhage requiring intervention, reduction in haemoglobin ≥4 g/dl without or ≥3g/dl with overt bleeding source, reoperation for bleeding, or blood transfusion) reached 9.8%. Calibration and discrimination of the three risk models were evaluated by the Hosmer-Lemeshow test and the C-statistic, respectively. We compared the predictive accuracy of the risk scores by the DeLong non-parametric test. RESULTS: Calibration of the three risk scores was adequate, given the non-significant results of Hosmer-Lemeshow test for the three risk models. Discrimination of CRUSADE, ACUITY-HORIZONS, and ACTION models was good (C-statistic 0.77, 0.70, and 0.78, respectively). The CRUSADE and ACTION risk scores had a greater predictive accuracy than the ACUITY-HORIZONS risk model (z=3.89, p-value=0.0001 and z=3.51, p-value=0.0004, respectively). There was no significant difference between the CRUSADE and ACTION models (z=0.63, p=0.531). CONCLUSIONS: The CRUSADE, ACUITY-HORIZONS, and ACTION scores are useful tools for the risk stratification of bleeding in STEMI treated by PPCI. Our findings favour the CRUSADE and ACTION risk models over the ACUITY-HORIZONS risk score.

Prevalence of donor-transmitted coronary artery disease and its influence on heart transplant outcomes.

BACKGROUND: It is uncertain whether donor-transmitted coronary artery disease (DTCAD) affects heart transplant (HT) recipients. METHODS: This retrospective analysis includes records of all patients who underwent a HT at our center over an 8-year period, who survived for at least 1 month, and who were examined by coronary angiography within 2 months post-HT. We distinguished angiographically from keep ultrasonography (IVUS) detected DTCAD. Major adverse cardiovascular events (MACE) comprised death, myocardial infarction, unstable angina, coronary revascularization, and admission because of heart failure not due to an acute rejection episode. RESULTS: Among the 171 patients of mean age 53±13 years and including 83% men, 65 (38%) were evaluated by IVUS. Donors were aged 40±14 years (range=14-73). Angiographic DTCAD affected seven patients (4.1%), and IVUS-detected DTCAD, 35 (53.8% of those examined by IVUS). DTCAD donors were older than non-DTCAD donors, by an average of 13 years (P=.001) for angiographic DTCAD and 18 years (P<.0001) for IVUS-detected DTCAD. Two patients underwent percutaneous revascularization upon detection of angiographic DTCAD. The angiographic- and IVUS-detected DTCAD groups did not differ significantly from the corresponding non-DTCAD groups as regards MACE incidence during 54±41 and 38±20 months follow-up, respectively. Cox regression analysis with adjustment for relevant confounders confirmed that IVUS-detected DTCAD was not a predictor of MACE (hazard ratio 1.2, 95% confidence interval 0.2-8.1). CONCLUSIONS: Among HT patients surviving≥1 month, angiographic- and IVUS-detected DTCAD showed prevalences of <10% and >50%, respectively. Neither detection method was associated with a greater long-term incidence of MACE.

[Acute myocardial infarction after anaphylactic reaction to amoxicillin]. / Infarto agudo de miocardio tras reacción anafiláctica por amoxicilina.

A 62-year-old man was admitted to the hospital in a state of shock with electrocardiographic signs of inferior-wall acute myocardial infarction. He was initially diagnosed of cardiogenic shock. An urgent coronary angiography showed an irregular stenosis of 90% in the right coronary artery. Coronary angioplasty was performed, and a stent was placed in this lesion. In-depth questioning of the family revealed that the patient had taken an oral dose of amoxicillin 15 minutes before the onset of the symptoms. Further tests proved that he was allergic to amoxicillin, and was diagnosed of anaphylactic shock, complicated with acute myocardial infarction. There are several reports of myocardial infarction as a complication of anaphylactic reaction. We have found very few cases related to antibiotics, and none associated with amoxicillin. The most frequently quoted mechanism in these cases is coronary artery spasm due to the mediators of anaphylaxis. In the case reported herein, the irregular lesion suggests that disruption of an atherosclerotic plaque and platelet aggregation have occurred.