Creatinine clearance and adverse hospital outcomes in patients with acute coronary syndromes: findings from the global registry of acute coronary events (GRACE).

OBJECTIVE: To determine whether creatinine clearance at the time of hospital admission is an independent predictor of hospital mortality and adverse outcomes in patients with acute coronary syndromes (ACS). DESIGN: A prospective multicentre observational study, GRACE (global registry of acute coronary events), of patients with the full spectrum of ACS. SETTING: Ninety four hospitals of varying size and capability in 14 countries across four continents. PATIENTS: 11 774 patients hospitalised with ACS, including ST and non-ST segment elevation acute myocardial infarction and unstable angina. MAIN OUTCOME MEASURES: Demographic and clinical characteristics, medication use, and in-hospital outcomes were compared for patients with creatinine clearance rates of > 60 ml/min (normal and minimally impaired renal function), 30-60 ml/min (moderate renal dysfunction), and < 30 ml/min (severe renal dysfunction). RESULTS: Patients with moderate or severe renal dysfunction were older, were more likely to be women, and presented to participating hospitals with more comorbidities than those with normal or minimally impaired renal function. In comparison with patients with normal or minimally impaired renal function, patients with moderate renal dysfunction were twice as likely to die (odds ratio 2.09, 95% confidence interval 1.55 to 2.81) and those with severe renal dysfunction almost four times more likely to die (odds ratio 3.71, 95% confidence interval 2.57 to 5.37) after adjustment for other potentially confounding variables. The risk of major bleeding episodes increased as renal function worsened. CONCLUSION: In patients with ACS, creatinine clearance is an important independent predictor of hospital death and major bleeding. These data reinforce the importance of increased surveillance efforts and use of targeted intervention strategies in patients with acute coronary disease complicated by renal dysfunction.

Prior aspirin users with acute non-ST-elevation coronary syndromes are at increased risk of cardiac events and benefit from enoxaparin.

BACKGROUND: The aim of this article was to investigate whether prior aspirin use in patients with acute coronary syndromes affects clinical outcome. The Efficacy Safety Subcutaneous Enoxaparin in Non-Q-Wave Coronary Events Study (ESSENCE) and Thrombolysis in Myocardial Infarction (TIMI) 11B trials have shown superiority of enoxaparin over unfractionated heparin (UFH) in patients with unstable angina and non-ST-segment elevation myocardial infarction (UA/NSTEMI). However, the treatment effect of enoxaparin in the subset of patients reporting prior aspirin use has not been determined. METHODS: The rate of death, myocardial infarction, and urgent revascularization at days 8 and 43 after randomization was compared among patients who received aspirin within the week before randomization with those who did not receive aspirin in the TIMI 11B trial. A total of 3275 patients (84%) were prior aspirin users. RESULTS: The admission diagnosis was similar for prior and nonprior aspirin users. At both day 8 and day 43 the event rate was higher for prior aspirin users than for nonprior aspirin users (odds ratio 1.6 [1.24-2.08], P =.0004 at day 43), even after correction for baseline characteristics. Compared with those prior aspirin users taking UFH, enoxaparin-treated prior aspirin users had a reduced rate of the composite end point of death, myocardial infarction, and urgent revascularization at day 8 (odds ratio 0.82 [0.67-1.00], P =.046) and day 43 (odds ratio 0.83 [0.70-0.98], P =.032). CONCLUSION: Patients with UA/NSTEMI and prior aspirin use had a 60% higher risk of death and cardiac ischemic events compared with nonprior aspirin users. On the basis of this subanalysis, enoxaparin is superior to UFH in all patients. In prior aspirin users the benefit is more clearly demonstrated.

Low-molecular-weight heparin alone versus a combination of unfractionated heparin and low-molecular-weight heparin.

OBJECTIVES: We analyzed the effect of the pharmacologic combination of 2 indirect antithrombin drugs--enoxaparin (low-molecular-weight heparin) and unfractionated heparin--versus enoxaparin alone on the recurrence of ischemia. BACKGROUND: Blocking some key factors of the coagulation cascade supports the concept that an antithrombin effect is needed during the acute phase of ischemia. METHODS: This was a prospective, randomized, pilot trial in patients with an acute coronary ischemic event occurring within the previous 24 hours. A total of 126 patients were allocated to receive aspirin (200 mg/day orally) plus 1 mg/kg subcutaneous enoxaparin at 8 AM and 12.500 IU of subcutaneous unfractionated heparin at 8 PM (group A) or subcutaneous enoxaparin 1 mg/kg (group B). RESULTS: Severe recurrent ischemia provoking urgent coronary revascularization occurred in 12 patients (9.5%), 3 (5%) in group A and 9 (13%) in group B (P = .1). Refractory angina was present in 27 patients (21%), 10 (17%) in group A and 17 (25%) in group B (P = .45). The combination of severe recurrent ischemia and refractory angina occurred in 23% of group A, and 37% of group B (odds ratio 0.49; 95% confidence intervals, 0.21-1.15; P = .07). A total of 7 patients (5%) had acute nonfatal myocardial infarction develop, 3 (5%) in group A and 4 (6%) in group B. Two (1.6%) deaths were observed in the study, both in group B. The incidence of the double end point (death plus nonfatal myocardial infarction) was 5% in group A versus 9% in group B (P = .5) and the triple end point (death, nonfatal myocardial infarction, and severe recurrent ischemia) was 10.5% in group A vs 22% in group B (odds ratio 0.42, 95% confidence intervals, 0.13-1.29; P = .09). CONCLUSIONS: The combination of 2 indirect antithrombin drugs capable of intermittently blocking the coagulation system is not associated with a significant loss of safety.

Early treatment with low-dose enalapril after acute myocardial infarction: an equilibrium radionuclide angiographic study. Enalapril despues del Infarto (EDI) Trial Investigators.

BACKGROUND: To further elucidate the mechanisms involved in the treatment of acute myocardial infarction (AMI) with angiotensin-converting enzyme inhibitors, we compared the effects on left ventricular volumes of early (< 48 hours) versus late (45 days) administration of a fixed low dose of enalapril (10 mg) in patients with AMI. We also analyzed the changes of left ventricular volumes after withdrawal of the study drug. Reduced dilation of the left ventricle is one of the beneficial effects of angiotensin-converting enzyme inhibition after AMI. However, the nature of this effect is not completely understood. METHODS AND RESULTS: We included 89 patients within 48 hours after onset of a first AMI and radionuclide left ventricular ejection fraction less than 45%. The study was double-blind and compared enalapril and placebo with a crossover design. All patients were randomly assigned to a sequence A (enalapril, 45 days; placebo, 45 days) or B (placebo, 45 days; enalapril, 45 days). The end point was the change of left ventricular volume at 45 and 90 days. Thrombolysis was administered to 26 patients (70%) in group A and 25 (75%) in group B. All pretreatment clinical variables were similar in both groups. Median and 95% confidence intervals (CIs) of left ventricular diastolic volumes were 46.8 ml/m2 (39 to 61 ml/m2) and 46.6 ml/m2 (39 to 60 ml/m2) for groups A and B, respectively. Baseline end systolic volumes were 28.5 ml/m2 (20 to 36 ml/m2) and 28.9 ml/m2 (23 to 28 ml/m2) in the same groups. Placebo treatment during the initial 45 days was associated with an increase of left ventricular diastolic volume of 8.75 ml/m2 (95% CI, 3.25 to 17.1 ml/m2; p < 0.01) and end-systolic volume of 4.20 ml/m2 (95% CI, 0.00 to 10.1 ml/m2; p < 0.05). No significant changes during other phases of the study were observed. At 45 days left ventricular diastolic volume was 11.1 ml/m2 (95% CI, 0.5 to 2.2 ml/m2), greater in placebo-treated patients compared with patients receiving enalapril. CONCLUSIONS: In patients with a first Q wave AMI and left ventricular ejection fraction less than 45%, treatment with enalapril can prevent left ventricular dilation. This protective effect involves at least partially a structural modification of the left ventricle. Hence, maximal benefit can be obtained only with early initiation of treatment.

Derrame pleural quiloso bilateral asociado a tromboembolismo pulmonar / Bilateral chylothorax associated with pulmonary artery embolism

Se describe una paciente con quilotórax bilateral asociado a embolismo de la rama inferior de la arteria pulmonar derecha. Este derrame se desarrolló como resultado de incremento en las presiones venosas centrales. El tratamiento definitivo se logró con streptokinasa

Un caso atípico de abdomen agudo / Atipical case of acute abdomen

Introducción: El potasio es el ión más importante en el funcionamiento de las células excitables, la hiperkalemia se relaciona con efectos peligrosos sobre miocardio, músculo liso y nervios periféricos. A pesar de la clara asociación fisiopatológica entre el aumento del potasio y el íleo paralítico, no se han hallado casos que mencionen al abdomen agudo como forma de presentación en la búsqueda bibliográfica por Medline de los últimos diez años. Se presenta por tanto un caso en el cual el motivo de consulta fue dolor abdominal. Presentación: Paciente de sexo femenino, 83 años, consulta por dolor abdominal muy intenso asociado a náuseas y oliguria de 24 hs de evolución. Antecedentes: tromboembolismo de pulmón a repetición a pesar de estar anticoagulada de forma suficiente, hipertensión pulmonar, fibrilación auricular, medicada con furosemida, espironolactoma, digoxina, acenocumarol. Examen físico: desasosegada, taquipneica, soplo de regurgitación tricúspidea, abdomen doloroso, sin ruidos hidroaéreos. Urea: 108 mg por ciento, creatinina: 1,91 mg/dl, K: 6,8 meq, Ph: 7,52, Po2: 142, PCo2 35, COH3 29,9. ECG: ritmo nodal. Colon por enema: dolicocolon. Ecografía abdominal y endoscopía esófago-gástrica normales. Se trata con soluciones polarizantes, cediendo el dolor abdominal y retornando el ritmo cardíaco a fibrilación auricular, recupera el ritmo diurético y normaliza urea y creatinina. Conclusiones: 1) Esta hiperkalemia sin fallo renal crónico previo fue multifactorial. a- Uso prolongado de espironolactona en paciente deshidratada con escaso aporte de Na. b- Seudohipoaldosteronismo. c- Alcalosis mixta. 2) Debido a la acción del potasio sobre las células excitables, la hiperkalemia puede provocar íleo paralítico y presentarse como abdomen agudo sobre todo en pacientes polimedicados

Derrame pleural quiloso bilateral asociado a tromboembolismo pulmonar / Bilateral chylothorax associated with pulmonary artery embolism

Se describe una paciente con quilotórax bilateral asociado a embolismo de la rama inferior de la arteria pulmonar derecha. Este derrame se desarrolló como resultado de incremento en las presiones venosas centrales. El tratamiento definitivo se logró con streptokinasa (AU)

Un caso atípico de abdomen agudo / Atipical case of acute abdomen

Introducción: El potasio es el ión más importante en el funcionamiento de las células excitables, la hiperkalemia se relaciona con efectos peligrosos sobre miocardio, músculo liso y nervios periféricos. A pesar de la clara asociación fisiopatológica entre el aumento del potasio y el íleo paralítico, no se han hallado casos que mencionen al abdomen agudo como forma de presentación en la búsqueda bibliográfica por Medline de los últimos diez años. Se presenta por tanto un caso en el cual el motivo de consulta fue dolor abdominal. Presentación: Paciente de sexo femenino, 83 años, consulta por dolor abdominal muy intenso asociado a náuseas y oliguria de 24 hs de evolución. Antecedentes: tromboembolismo de pulmón a repetición a pesar de estar anticoagulada de forma suficiente, hipertensión pulmonar, fibrilación auricular, medicada con furosemida, espironolactoma, digoxina, acenocumarol. Examen físico: desasosegada, taquipneica, soplo de regurgitación tricúspidea, abdomen doloroso, sin ruidos hidroaéreos. Urea: 108 mg por ciento, creatinina: 1,91 mg/dl, K: 6,8 meq, Ph: 7,52, Po2: 142, PCo2 35, COH3 29,9. ECG: ritmo nodal. Colon por enema: dolicocolon. Ecografía abdominal y endoscopía esófago-gástrica normales. Se trata con soluciones polarizantes, cediendo el dolor abdominal y retornando el ritmo cardíaco a fibrilación auricular, recupera el ritmo diurético y normaliza urea y creatinina. Conclusiones: 1) Esta hiperkalemia sin fallo renal crónico previo fue multifactorial. a- Uso prolongado de espironolactona en paciente deshidratada con escaso aporte de Na. b- Seudohipoaldosteronismo. c- Alcalosis mixta. 2) Debido a la acción del potasio sobre las células excitables, la hiperkalemia puede provocar íleo paralítico y presentarse como abdomen agudo sobre todo en pacientes polimedicados (AU)