Biomedical subjects

Joost P van Melle

Publications and source records attributed to Joost P van Melle.

10 recordsLinked to original sources

PubMed2006

Beta-blockers and depression after myocardial infarction: a multicenter prospective study.

OBJECTIVES: The purpose of this research was to explore the prospective relationship between the use of beta-blockers and depression in myocardial infarction (MI) patients. BACKGROUND: Beta-blocker use has been reported to be associated with the development of depression, but the methodological quality of studies in this field is weak. METHODS: In a multicenter study, MI patients (n = 127 non-beta-blocker users and n = 254 beta-blocker users) were assessed for depressive symptoms (using the Beck Depression Inventory [BDI] at baseline and t = 3, 6, and 12 months post-MI) and International Classification of Diseases-10 depressive disorder (Composite International Diagnostic Interview). Patients were matched using the frequency matching procedure according to age, gender, hospital of admission, presence of baseline depressive symptoms, and left ventricular function. RESULTS: No significant differences were found between non-beta-blocker users and beta-blocker users on the presence of depressive symptoms (p > 0.10 at any of the time points) or depressive disorder (p = 0.86). Controlling for confounders did not alter these findings. A trend toward increasing BDI scores was seen in patients with long-term use of beta-blockers and patients with higher beta-blocker dose. CONCLUSIONS: In post-MI patients, prescription of beta-blockers is not associated with an increase in depressive symptoms or depressive disorders in the first year after MI. However, long-term and high-dosage effects cannot be ruled out.

Adrenergic beta-Antagonists↗

PubMed2006

Decreased impact of post-myocardial infarction depression on cardiac prognosis?

OBJECTIVE: A recent meta-analysis suggests that the impact of post-myocardial infarction (MI) depression on cardiac prognosis has decreased over the last decade. We tested whether depression still significantly affects prognosis in the present health care situation. METHODS: Four hundred ninety-four MI patients were screened for depression. Patients with depression were compared with patients without on cardiovascular events (fatal or nonfatal) during an average follow-up of 2.5 years. Demographic characteristics and cardiac risk factors were controlled for. RESULTS: We found that depression was associated with the occurrence of cardiovascular events in both univariate [hazard ratio (HR), 1.84; 95% confidence interval, 1.24-2.72] and multivariate analysis (HR, 1.56; 1.02-2.38). CONCLUSIONS: Depression still has an independent impact on cardiac prognosis after MI, but this influence is smaller than found in early studies. Improvements in general care for MI and better recognition and treatment of post-MI depression may have decreased the impact of depression on prognosis.

Major Depressive Disorder↗

PubMed2006

Symptom dimensions of depression following myocardial infarction and their relationship with somatic health status and cardiovascular prognosis.

OBJECTIVE: The reporting of depressive symptoms following myocardial infarction may be confounded by complaints originating from the myocardial infarction. Therefore, it is difficult to estimate the effects of post-myocardial infarction depression and its treatment on cardiovascular prognosis. The authors' goal was to study the relationship between depressive symptom dimensions following myocardial infarction and both somatic health status and prospective cardiovascular prognosis. METHOD: In two studies of myocardial infarction patients (N=494 and 1,972), the Beck Depression Inventory was used to determine the dimensional structure of depressive symptoms following myocardial infarction. Three symptom dimensions-somatic/affective, cognitive/affective, and appetitive-were compared with baseline left ventricular ejection fraction, Charlson comorbidity index, Killip class, and previous myocardial infarction. The relationship between depressive symptom dimensions and prospective cardiovascular mortality and cardiac-related readmissions was also examined (mean follow-up duration=2.5 years). RESULTS: Somatic/affective symptoms were associated with poor health status (left ventricular ejection fraction, Charlson comorbidity index, Killip class, and previous myocardial infarction) and predicted cardiovascular mortality and cardiac events. Cognitive/affective symptoms were only marginally associated with somatic health status and not with cardiovascular death and cardiac events. Appetitive symptoms were related to somatic health status but did not predict cardiovascular death or cardiac events. CONCLUSIONS: Somatic/affective depressive symptoms following myocardial infarction were confounded by somatic health status yet were prospectively associated with cardiac prognosis even after somatic health status was controlled. Cognitive/affective depressive symptoms were only marginally related to health status and not to cardiac prognosis. These findings suggest that treatment of depression following myocardial infarction might improve cardiovascular prognosis when it reduces somatic/affective symptoms.

Cause of Death↗

PubMed2006

Treatment of depression in acute coronary syndromes with selective serotonin reuptake inhibitors.

Depression in patients with acute coronary syndromes (ACS) is common and associated with impaired cardiovascular prognosis in terms of cardiac mortality and new cardiovascular events. It remains unclear whether antidepressant treatment may reverse these effects. In this review, the literature is evaluated on (i) the antidepressant efficacy of selective serotonin reuptake inhibitors (SSRIs) for depression in patients with ACS; (ii) the pleiomorphic effects of SSRIs that may be associated with cardiovascular prognosis; and (iii) the effects of SSRIs on cardiovascular prognosis.SSRIs provide modest relief of depressive symptoms in selected subgroups of depressed patients with ACS. With respect to the pleiomorphic effects of SSRIs, three mechanisms of how SSRIs may improve cardiovascular prognosis are discussed: via platelet function, via the autonomic nervous system (ANS) and via vasomotor tone. Some studies show that SSRIs may reduce platelet activity and sympathetic nervous system activation, but results are inconclusive. SSRIs are associated with vasodilation but this needs to be confirmed with in vivo experiments. Some non-experimental studies describe favourable effects of SSRIs on cardiovascular prognosis. Despite recent developments, much of the effect of SSRIs on cardiovascular prognosis remains unclear. Although some studies suggest effects of SSRIs on platelet function, ANS and vasomotor tone, which may lead to improved cardiovascular prognosis, results are largely inconclusive. More well designed studies addressing these questions are needed. Moreover, since the effects of SSRIs on depression itself are limited, efforts should be dedicated to study the diagnostic validity and homogeneity of depression in the context of ACS and the presence of clinically relevant subtypes.

Acute Disease↗

PubMed2005

Relationship between left ventricular dysfunction and depression following myocardial infarction: data from the MIND-IT.

AIMS: Depression in patients following myocardial infarction (MI) is associated with an increased risk of mortality, but this association may be confounded by cardiac disease severity. We explored the relationship between left ventricular ejection fraction (LVEF) and depression in MI patients. METHODS AND RESULTS: In the Myocardial Infarction and Depression-Intervention Trial (MIND-IT), 1989 MI patients were assessed for depressive symptoms [Beck Depression Inventory (BDI) t = 0, 3, 6, 9, and 12 months post-MI]. Patients with BDI score > or =10 were assessed for the presence of International Classification of Diseases, 10th revision (ICD-10) depressive disorder (t = 3, 6, 9, and 12 months post-MI). Patients were divided into categories according to their LVEF during hospitalization, i.e. LVEF <30%, LVEF 30-45%, LVEF 45-60%, and LVEF > or = 60%. During hospitalization, presence of depressive symptoms was higher in patients with LV dysfunction. A relationship was found between LVEF and ICD-10 depressive disorder, i.e. a lower LVEF was associated with a higher rate of depression from 3-12 months post-MI (P < 0.01). Levels of LVEF inversely correlated with the BDI score at 3 months post-MI. Associations persisted after adjustment for demographics, risk factors for coronary artery disease, co-morbidity, Killip class, and baseline BDI score. CONCLUSION: In MI patients, the rate of depression and the severity of depressive symptoms are significantly related to the severity of LV dysfunction. The association between depression and LV dysfunction must be acknowledged when evaluating the prognostic effects of depression in cardiac patients.

Depressive Disorder↗

PubMed2005

QT interval prolongation after sertraline overdose: a case report.

BACKGROUND: Selective serotonin reuptake inhibitors (SSRIs) are the most common antidepressants used in first-world countries and are generally well tolerated. Specifically, less cardiovascular toxicity has been reported in comparison with tricyclic antidepressants. Here we report QT interval prolongation after an overdose of the SSRI sertraline. CASE PRESENTATION: A previously healthy female patient presented with an attempted suicide with overdoses sertraline (2250 mg), diazepam (200 mg), and temazepam (400 mg). Routine laboratory studies were normal and her ECG upon admission showed a normal QT interval. The next day, her ECG showed prolongation of the QTc interval up to 525 ms. After discontinuation of sertraline the QT interval normalized. Echocardiography and exercise electrocardiography were normal. After hospitalization, the patient resumed sertraline in the normally recommended dose and QT interval remained within normal ranges. CONCLUSION: It seems that the SSRI sertraline in overdose may cause QT interval prolongation.

Journal Article↗

PubMed2005

Prediction of depressive disorder following myocardial infarction data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).

BACKGROUND: Depression following myocardial infarction (MI) is associated with complicated cardiac rehabilitation, non-compliance and poor prognosis. Whether depression following MI can be predicted from variables routinely assessed during hospitalization for MI is unknown. METHODS: Using data from the Myocardial INfarction and Depression-Intervention Trial (MIND-IT), we identified 2,177 MI patients (mean age 63 years; 23% female). Patients were randomly divided into a derivation and a validation sample. In the derivation sample, we analyzed variables potentially associated with the development of post-MI depressive disorder, which were tested in the validation sample. RESULTS: In the year following MI, 18.5% suffered from depressive disorder (ICD-10 criteria). In a multivariate model, factors associated with depression were younger age (OR 1.94; CI 1.38-2.74), hypercholesterolemia (OR 1.68; CI 1.08-2.61), the use of calcium channel blockers at discharge (OR 1.80; CI 1.20-2.71), and left ventricular ejection fraction (LVEF) (OR 4.14 for patients with LVEF <30%; CI (2.42-7.10). The derived predictors were tested in the validation sample. The final model yielded two clinical predictors, i.e., younger age and severe LV-dysfunction, which correctly predicted post-discharge depression status in 82.9% of the MI patients. The model yielded a high negative predictive value (89%). A positive depression questionnaire (BDI) during hospitalization increased the positive predictive value of 23% to 52%. CONCLUSIONS: During hospitalization for MI and using a two-step strategy with common clinical variables, i.e., younger age, severe LV-dysfunction and BDI score during hospitalization, it is possible to identify MI patients with a high risk for subsequent development of depression.

Adult↗

PubMed2004

Sertraline causes strong coronary vasodilation: possible relevance for cardioprotection by selective serotonin reuptake inhibitors.

OBJECTIVE: Although Selective Serotonin Reuptake Inhibitors (SSRIs) are important antidepressant drugs, knowledge of their vaso active effects is limited. Vaso active effects of the SSRI sertraline were studied in rings of rat aorta, human Internal Mammary Arteries (IMAs) and in Langendorff perfused rat hearts. METHODS: The effects of sertraline (0.1 to 300 micromol x L(-1)) on precontracted rat aortic and IMA rings were evaluated in organ bath chambers. Precontraction was elicited by serotonin (5-HT; 10 micromol x L(-1)), phenylephrine (PE; 10 micromol x L(-1)) and potassium chloride (KCl; 50 mmol x L(-1)). In addition, the effects of sertraline on PE induced contraction curves were established by subjecting vascular rings to increasing doses of PE (1 nmol x L(-1) to 10 (micro)mol x L(-1)) in the presence of sertraline or vehicle. Finally, the effects of sertraline on ex vivo coronary flow in rat hearts were examined using a retrograde Langendorff perfusion model. RESULTS: Sertraline elicited dose-dependent relaxation, independent of the substance used for precontraction (p < 0.025). Sertraline showed a rightward shift of dose-response curves to PE (p < 0.01). Vasodilatory effects of SSRIs were endothelium independent. In perfused rat hearts, sertraline (0.3 to 10 micromol x L(-1)), showed a concentration-dependent increase in coronary flow that returned to baseline levels after wash-out of the antidepressant (p = 0.005). CONCLUSIONS: One of the SSRIs, sertraline, showed marked vasodilatory effects in rat aorta and human IMAs. Sertraline elicited vasodilatation in coronary arteries during perfusion of rat hearts. These hemodynamic effects may explain

Animals↗

PubMed2002

Treatment of depression after myocardial infarction and the effects on cardiac prognosis and quality of life: rationale and outline of the Myocardial INfarction and Depression-Intervention Trial (MIND-IT).

BACKGROUND: Patients with a depressive disorder after myocardial infarction (MI) have a significantly increased risk of major cardiac events. The Myocardial INfarction and Depression-Intervention Trial (MIND-IT) investigates whether antidepressive treatment can improve the cardiac prognosis for these patients. The rationale and outline of the study are described. METHODS: In this multicenter randomized clinical trial, 2140 patients admitted for MI are screened for depressive symptoms with a questionnaire 0, 3, 6, 9, and 12 months after MI. Patients with symptoms undergo a standardized psychiatric interview. Those with a post-MI depressive episode are randomized to intervention (ie, antidepressive treatment; n = 190) or care-as-usual (CAU; n = 130). In the intervention arm, the research diagnosis is to be confirmed by a psychiatrist. First-choice treatment consists of placebo-controlled treatment with mirtazapine. In case of refusal or nonresponse, alternative open treatment with citalopram is offered. In the CAU arm, the patient is not informed about the research diagnosis. Psychiatric treatment outside the study is recorded, but no treatment is offered. Both arms are followed for end points (cardiac death or hospital admission for MI, unstable angina, heart failure, or ventricular tachyarrhythmia) during an average period of 27 months. Analysis is on an intention-to-treat basis. CONCLUSION: The MIND-IT study will show whether treatment of post-MI depression can improve cardiac prognosis.

Adult↗

PubMedDate not supplied

Prognostic association of depression following myocardial infarction with mortality and cardiovascular events: a meta-analysis.

OBJECTIVE: To assess the association of depression following myocardial infarction (MI) and cardiovascular prognosis. METHODS: The authors performed a meta-analysis of references derived from MEDLINE, EMBASE, and PSYCINFO (1975-2003) combined with crossreferencing without language restrictions. The authors selected prospective studies that determined the association of depression with the cardiovascular outcome of MI patients, defined as mortality and cardiovascular events within 2 years from index MI. Depression had to be assessed within 3 months after MI using established psychiatric instruments. A quality assessment was performed. RESULTS: Twenty-two papers met the selection criteria. These studies described follow up (on average, 13.7 months) of 6367 MI patients (16 cohorts). Post-MI depression was significantly associated with all-cause mortality (odds ratio [OR], fixed 2.38; 95% confidence interval [CI], 1.76-3.22; p <.00001) and cardiac mortality (OR fixed, 2.59; 95% CI, 1.77-3.77; p <.00001). Depressive MI patients were also at risk for new cardiovascular events (OR random, 1.95; 95% CI, 1.33-2.85; p = .0006). Secondary analyses showed no significant effects of follow-up duration (0-6 months or longer) or assessment of depression (self-report questionnaire vs. interview). However, the year of data collection (before or after 1992) tended to influence the effect of depression on mortality (p = .08), with stronger associations found in the earlier studies (OR, 3.22; 95% CI, 2.14-4.86) compared with the later studies (OR, 2.01; 95% CI, 1.45-2.78). CONCLUSIONS: Post-MI depression is associated with a 2- to 2.5-fold increased risk of impaired cardiovascular outcome. The association of depression with cardiac mortality or all-cause mortality was more pronounced in the older studies (OR, 3.22 before 1992) than in the more recent studies (OR, 2.01 after 1992).

Cardiovascular Diseases↗