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.

[Pulmonary hypertension and early mortality after orthotopic heart transplantation]. / Hipertensión pulmonar y mortalidad precoz después del trasplante cardíaco ortotópico.

INTRODUCTION AND OBJECTIVES: To study the relationship between hemodynamic parameters before heart transplantation and the mortality rate at the first week posttransplant. METHODS: 85 patients had an orthotopic heart transplant. Before the operation we measured: vascular pulmonary resistance, index of vascular pulmonary resistance, pulmonary arterial pressure systolic and median and transpulmonary gradient. Ten patients with values of vascular pulmonary resistance higher than four Wood units and/or pulmonary artery systolic pressure higher than 60 mmHg, had a test of pulmonary vascular reactivity, the result of that test did not contraindicate the transplant. We used the Student's t test and chi 2 with continuity correction and the Fisher's exact test for the analysis of the data. RESULTS: During the study period eight patients were dead (9.4%). The causes of death were: acute disfunction of the graft, 5 patients; multiorgan failure, 2 patients and septic shock, 1 patient. We compared the parameters of both groups of patients live and dead and could find a significant difference between the data with higher values in the death group: pulmonary arterial systolic pressure (p < 0.01); pulmonary arterial median pressure (p < 0.03) and transpulmonary gradient (p < 0.02). We also saw that the relative risk of mortality was 10.4 when the pulmonary artery systolic pressure was > or = 50 mmHg and 5.7 when the pulmonary vascular resistance was > or = 5 Wood units. CONCLUSIONS: It is important a good evaluation of the pulmonary hemodynamic before the heart transplantation for a better selection of the receptor. The severe pulmonary hypertension (pulmonary vascular resistance > or = 5 Wood units or pulmonary artery systolic pressure > or = 50 mmHg) was associated with a higher rate of early death.

[The relationship between clinical events and the angiographic lesions in coronary atherosclerosis. Hypolipemic treatment and plaque stabilization]. / Relación entre eventos clínicos y lesiones angiográficas en la aterosclerosis coronaria. Tratamiento hipolipemiante y estabilización de placa.

Secondary prevention studies have shown that lipid-lowering therapy improve angiographic outcome and reduce mortality and incidence of ischemic clinical events in patients with coronary artery disease. The mechanism responsible for the improvement in prognosis seem to be subtle as this improvement cannot be explained by changes in the angiographic diameter of coronary arteries. Atherosclerotic plaque rupture and subsequent thrombosis are the central features in the pathogenesis of acute coronary events: unstable angina, myocardial infarction and sudden death. Cholesterol lowering might decrease the risk of plaque rupture and its thrombogenicity, as well as normalise the impaired endothelial function in hypercholesterolemic patients. In this report, the effects of lipid-lowering therapy on angiographic outcome and incidence of clinical events, in patients suffering from coronary artery disease, are reviewed, and the mechanisms that might explain these findings are discussed.

[Corticoid-resistant rejection and humoral rejection. The diagnostic criteria and therapeutic management]. / Rechazo corticorresistente y rechazo humoral. Criterios diagnósticos y manejo terapéutico.

The standard treatment of rejection episodes post-heart transplantation is based on high dose of steroids followed by monoclonal or policlonal antibodies directed against T lymphocytes like ATG or OKT3. When this treatment is insufficient it can be used other drugs like metothrexate, ciclofosfamide and another procedures such as total lymphoid irradiation, plasmapheresis or photopheresis. Cardiac allograft rejection is defined by histologic features that include the presence of lymphocytic infiltration of the myocardium with or without necrosis and this histologic pattern is termed cellular rejection. However there is a second form of acute rejection, associated with capillary injury, usually mediated by humoral immune response and without interstitial infiltrates which has been named vascular or humoral rejection. Vascular allograft rejection is commonly resistant to standards forms of immunosuppressive therapy and may result in irreversible allograft dysfunction and reduced patient survival.

Spontaneous coronary artery dissection.

Spontaneous coronary artery dissection is a rarely identified entity whose exact incidence, etiology, pathogenesis, medium-term evolution, and optimal treatment have not yet been firmly established. This article describes five new cases with additional specific characteristics. Five of 2,241 coronary arteriograms taken between September 1989 and November 1992 showed angiographic signs of coronary dissection. Three of the patients were treated pharmacologically, and two were operated on. All were evaluated angiographically 10-18 months after diagnosis and followed up clinically for > or = 20 months. Three patients exhibited acute myocardial infarction, one showed effort angina and the fifth unstable angina. In four cases, coronary dissection was associated with coronary atherosclerosis, but in the fifth the coronary tree was apparently healthy except for the dissection. Dissection affected the right coronary artery in three cases and the left in two. Angiographic evolution varied among the five and was uncorrelated with treatment. Dissection disappeared in three; it persisted, with total obstruction of the artery in the middle of the dissected segment in one case; and advanced to affect the whole left coronary tree in the fifth. After an 18-month follow-up, none of the five patients experienced symptoms. These cases provide a good illustration of the variability of spontaneous coronary dissection as regards etiology, clinical presentation, treatment, and evolution. Coronary dissection is always caused by hemorrhage in the media of the arterial wall; its variability in evolution and in optimal treatment may be derived from the cause of the hemorrage, which possibly was not the same in all cases.