[Acute coronary syndrome complicated by heart failure as predictor of long-term infarction]. / Insuficiencia cardiaca en el seno de un síndrome coronario agudo como predictor de infarto a largo plazo.

BACKGROUND: Heart failure (Killip>I) in patients with acute coronary syndrome (ACS) is a recognized risk factor for death. However, its relationship with the risk of new acute ischemic events has not been well established. OBJECTIVE: The aim of this study has been to evaluate the association between Killip>I on admission and the risk of a new acute myocardial infarction (AMI) during follow-up due to ACS. PATIENTS AND METHODS: A total of 972 and 426 survivors of an ACS with non-ST segment evaluation (Non-STE-ACS) and AMI with ST segment elevation (STEMI) were studied prospectively and consecutively. The presence of Killip>I was determined on admission together with the classical prognostic variables. The relationship between Killip>I and subsequent post-discharge AMI was established with the Cox regression adapted for competitive events. RESULTS: During a median follow-up of 3 years, 135 (13.9%) and 53 (12.4%) patients with Non-STE-ACS and STEMI presented a new AMI. Patients with Non-STE-ACS and STEMI with Killip>I (15.6% and 21.3% respectively) showed a higher incidence of AMI (28.3 vs 6.3 and 10.6 vs 3.3 per 100 patients-years of follow-up, p<0.001, respectively). In the multivariate analysis, adjusted for traditional risk factors and controlled for competitive events (death and revascularization), confirmed that Killip>I subjects with Non-STE-ACS and STEMI showed a significantly higher risk of AMI (HR: 1.76; CI 95%: 1.15-2.68; p=0.009 and HR: 1.90; 95% CI: 1.07-3.36; p=0.029 respectively). CONCLUSIONS: In patients with Non-STE-ACS and STEMI, the presence of Killip>I on admission is independently associated to an increased risk of long-term AMI.

Calcium inhibits colon carcinogenesis in an experimental model in the rat.

Different dietary factors can affect colorectal cancer incidence. However, the effect of increased levels of dietary calcium on neoplasms is unclear. The present study was designed to examine the effect of a low calcium supplement on experimental colon carcinogenesis induced by parenteral administration of dimethylhydrazine (DMH). One hundred and twenty 10-week-old Sprague-Dawley rats were divided into five groups of equal sex distribution. The 10 rats in group A (control group) received no treatment; the 30 rats in group B (DMH group) were injected subcutaneously with 18 weekly doses of 21 mg/kg DMH; the 20 rats in group C (EDTA control group) received EDTA solution only; the 30 rats in group D (calcium group) received calcium at 3.2 g/l by adding calcium lactate to the drinking water from the start until the conclusion of the experiment; and the 30 rats in group E (DMH + calcium group) received oral calcium supplements at the same dose as the rats in group D (calcium group) and the same DMH injections as the rats in group B (DMH group). The rats were sacrificed at 25-34 weeks. In group E, we observed a significant diminution in the number of tumours (P = 0.01); an increase in the number of tumour-free animals (P = 0.006); a change in tumour location towards the distal colon (P < 0.025); more adenomas (P = 0.02); and a diminution of adenocarcinomas and mucinous carcinomas, although this was not significant. We conclude that a low dietary calcium supplement in rats inhibits colon cancer carcinogenesis induced by DMH, and changes tumour location towards the distal colon.

Microvascular perfusion 1 week and 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging.

OBJECTIVE: To characterise the evolution of myocardial perfusion during the first 6 months after myocardial infarction by first-pass perfusion cardiovascular magnetic resonance imaging (CMR) and determine its significance. DESIGN: Prospective cohort design. SETTING: Single-centre study in a teaching hospital in Spain. PATIENTS: 40 patients with a first ST-elevation myocardial infarction, single-vessel disease and thrombolysis in myocardial infarction (TIMI) grade 3 flow (stent in 33 patients) underwent rest and low-dose dobutamine CMR 7 (SD 1) and 184 (SD 11) days after infarction. Microvascular perfusion was assessed at rest by visual assessment and quantitative analysis of first-pass perfusion CMR. Of the 640 segments, 290 segments subtended by the infarct-related artery (IRA) were focused on. RESULTS: Both 1 week and 6 months after infarction, segments with normal perfusion showed more wall thickening, contractile reserve and wall thickness, and less transmural necrosis, p <0.05 in all cases. Of 76 hypoperfused segments at the first week, 47 (62%) normalised perfusion at the sixth month. However, 42 segments (14% of the whole group) showed chronic abnormal perfusion; these segments showed worse CMR indices in the late phase (p<0.05 in all cases). CONCLUSIONS: In patients with an open IRA, more than half of the segments with abnormal perfusion at the first week are normally perfused after six months. First-pass perfusion CMR shows that in a small percentage of segments, abnormal perfusion may become a chronic phenomenon-these areas have a more severe deterioration of systolic function, wall thickness, contractile reserve and the transmural extent of necrosis.