RESUMEN
OBJECTIVE: To test the hypothesis that negative perceptions about heart disease at the time of the myocardial infarction (MI) were associated with the onset of new episodes of depression following MI. METHOD: We recruited 269 subjects admitted following first MI and monitored their depression status over the subsequent 12 months. At baseline, we recorded demographic information, family and personal history of cardiac disease and severity of MI; subjective health beliefs were assessed using the Illness Perceptions Questionnaire (IPQ). We assessed depression at baseline, 6 and 12 months following MI using a standardised questionnaire, validated in this population against a semistructured research interview. RESULTS: In the days following MI, patients who subsequently developed depression were more likely to anticipate that their heart disease would last a long time (P=.012) and was unlikely to be cured (P=.038). Controlling for potential confounding variables, scores on the IPQ remained associated with subsequent depression (P = .036), with anticipation that heart disease would last a long time [odds ratio (OR)=2.7, P=.013] and that heart disease could be cured (OR=0.45, P=.048) showing strongest association. CONCLUSIONS: Negative perceptions about heart disease in the days following admission to hospital with first MI are associated with the development of subsequent new episodes of depression.
Asunto(s)
Trastorno Depresivo Mayor/diagnóstico , Conducta de Enfermedad , Infarto del Miocardio/psicología , Factores de Edad , Anciano , Trastornos de Ansiedad/diagnóstico , Trastornos de Ansiedad/psicología , Estudios de Cohortes , Cultura , Trastorno Depresivo Mayor/psicología , Femenino , Estudios de Seguimiento , Humanos , Control Interno-Externo , Masculino , Tamizaje Masivo , Persona de Mediana Edad , Estudios Prospectivos , Recurrencia , Factores de RiesgoRESUMEN
OBJECTIVE: Studies investigating the effects of depression on mortality following myocardial infarction (MI) have produced heterogeneous findings. We report on a study investigating whether the timing of the onset of depression, with regard to the MI, affected its impact on subsequent cardiac mortality. METHODS: Five hundred and eighty-eight subjects admitted following MI underwent assessments of cardiac status, cardiac risk factors, and noncardiac illness. We identified separately subjects who were depressed before their MI (pre-MI depression) and those who developed depression in the 12 months after MI (new-onset depression), using a standardized questionnaire and a research interview. Patients dying of cardiac cause were identified during 8-year follow-up using information from death certificates. RESULTS: Multivariate predictors of cardiac death during follow-up included: greater age (hazards ratio (HR) = 1.06, p = .007), previous angina (HR = 4.15, p < .0005), high Killip Class (HR = 2.21, p = .013), prescription of beta-blockers on discharge (HR = 0.37, p = .02), and new-onset depression (HR = 2.33, p = .038). Pre-MI depression did not convey any additional risk of cardiac mortality. CONCLUSION: We have shown increased cardiac mortality in patients who develop depression after suffering MI. Further observational studies need to separate pre- and post-MI depression if we are to determine underlying mechanisms by which depression is associated with mortality following MI.
Asunto(s)
Trastorno Depresivo/mortalidad , Trastorno Depresivo/psicología , Infarto del Miocardio/mortalidad , Infarto del Miocardio/psicología , Anciano , Trastornos de Ansiedad/diagnóstico , Trastornos de Ansiedad/mortalidad , Trastornos de Ansiedad/psicología , Estudios de Cohortes , Comorbilidad , Trastorno Depresivo/diagnóstico , Femenino , Estudios de Seguimiento , Humanos , Estimación de Kaplan-Meier , Masculino , Persona de Mediana Edad , Análisis Multivariante , Inventario de Personalidad/estadística & datos numéricos , Modelos de Riesgos Proporcionales , Estudios Prospectivos , Psicometría , Recurrencia , Factores de Riesgo , Rol del Enfermo , Apoyo SocialRESUMEN
OBJECTIVES: This study sought to investigate the long-term impact of depression on cardiac mortality after myocardial infarction (MI) and to assess whether the timing of depression influences the findings. BACKGROUND: Previous studies have shown that depression increases the risk of cardiac death after MI, although some studies with robust methodology have failed to show this effect. Clinical trials of depression treatments have failed to improve mortality. Until the relationship between depression and post-MI mortality is understood fully, clinical trials aimed at reducing mortality by treating depression remain premature. METHODS: We recruited 588 subjects after MI and followed up their cases for up to 8 years. Patients underwent detailed assessments of cardiac status, conventional cardiac risk factors, and noncardiac illness at baseline. Depression was assessed for the period immediately preceding MI and at 12 months after MI, using a standardized questionnaire and a research interview. At follow-up, the mortality status, cause, and date of death were recorded for 587 subjects using population records. RESULTS: Multivariate predictors of cardiac death included older age (hazard ratio [HR] = 1.04, p = 0.007), previous angina (HR = 1.8, p = 0.03), previous MIs (HR = 1.6, p = 0.004), Killip class (HR = 1.8, p = 0.005), beta-blockers (HR = 0.5, p = 0.023), and angiotensin-converting enzyme inhibitors (HR = 0.6, p = 0.047) prescribed on discharge. Depression was not associated with cardiac mortality, whether detected immediately before MI (p = 0.48), 12 months after MI (p = 0.27), or at both time points (p = 0.97). CONCLUSIONS: The association between depression and post-MI mortality is complex, possibly being limited to depression immediately after MI. Defining the window when intervention for depression might benefit survival is crucial for the design of future trials.
Asunto(s)
Depresión/epidemiología , Infarto del Miocardio/mortalidad , Anciano , Comorbilidad , Angiopatías Diabéticas/epidemiología , Femenino , Humanos , Hipertensión/epidemiología , Masculino , Persona de Mediana Edad , Análisis Multivariante , Infarto del Miocardio/epidemiología , Estudios Prospectivos , Recurrencia , Factores de Riesgo , Fumar/epidemiología , Análisis de Supervivencia , Factores de TiempoRESUMEN
Depression following myocardial infarction is associated with a higher mortality rate. The authors studied 314 patients admitted to the hospital with a first myocardial infarction to assess whether cardiac failure after the infarction, which is also linked to a higher mortality rate, was predicted by psychosocial characteristics present before the myocardial infarction. One-fifth (20.7%) of the subjects met the ICD-10 criteria for depressive episode in the 1 month before the attack. Variables independently associated with worse cardiac failure after the myocardial infarction were greater age, a history of angina preceding the infarction, and a previous depressive episode. The impact of depression on postinfarction outcome may result from the influence of preinfarction depression on the degree of cardiac failure.
Asunto(s)
Depresión/epidemiología , Insuficiencia Cardíaca/etiología , Insuficiencia Cardíaca/psicología , Infarto del Miocardio/epidemiología , Infarto del Miocardio/psicología , Depresión/diagnóstico , Femenino , Insuficiencia Cardíaca/diagnóstico , Insuficiencia Cardíaca/mortalidad , Humanos , Clasificación Internacional de Enfermedades , Masculino , Persona de Mediana Edad , Infarto del Miocardio/complicaciones , Infarto del Miocardio/diagnóstico , Prevalencia , Índice de Severidad de la Enfermedad , Tasa de SupervivenciaRESUMEN
OBJECTIVE: It is not known why acute pancreatitis in Soweto, South Africa, pursues an aggressive course. We sought clues from circulating trypsinogen load at admission as marker of initial acinar injury, trypsinogen activation using the carboxypeptidase B activation peptide as surrogate, proteinase inhibitors, the coagulation-fibrinolysis axis, indicators of inflammation, oxidative stress markers, and antioxidant status. This article reports on the first four aspects. METHODS: The study involved 24 consecutive patients with a first attack. All of them were admitted within 24 h, and 22 were alcoholic. Urine was analyzed for anionic trypsinogen and the carboxypeptidase B activation peptide. Serum was tested for anionic and cationic trypsinogen, alpha1 proteinase inhibitor and alpha2 macroglobulin. Plasma from a subset was assayed for soluble fibrin, cross-linked fibrin degradation products (surrogates for thrombin and plasmin activity, respectively), and tissue-type plasminogen activator and inhibitor. RESULTS: Soweto controls had higher serum anionic trypsinogen (p = 0.004) and plasminogen activator:inhibitor ratio (p = 0.047) than U.K. controls. The outcome of acute pancreatitis was mild in 17 but severe in seven with three deaths, two on day 2. In mild pancreatitis, intense plasmin activity (p < 0.001) accompanied the surge in trypsinogen, especially anionic (p < 0.001), but without increased thrombin activity and in five patients without trypsinogen activation. In severe pancreatitis, further significant increments in plasmin activity and trypsinogens were accompanied by increased thrombin activity (p = 0.013) and trypsinogen activation (p = 0.046). There was no correlation between surrogates of plasmin and thrombin activity, or between either and the carboxypeptidase B activation peptide, which showed a curvilinear relationship to total serum trypsinogen. CONCLUSIONS: The aggressive nature of alcoholic acute pancreatitis in Soweto seems to reflect early profound fibrinolysis, which precedes coagulation and is initially independent of trypsin. Subclinical acinar-cell injury and a profibrinolytic diathesis in outwardly healthy Sowetans may predispose to this problem.