scholarly journals Pathophysiological basis of cardiovascular disease and depression: a chicken-and-egg dilemma

2010 ◽  
Vol 32 (2) ◽  
pp. 181-191 ◽  
Author(s):  
Gilberto Paz-Filho ◽  
Julio Licinio ◽  
Ma-Li Wong

OBJECTIVE: To describe the pathophysiological basis linking cardiovascular disease (CVD) and depression; to discuss the causal relationship between them, and to review the effects of antidepressant treatment on cardiovascular disease. METHOD: A review of the literature based on the PubMed database. DISCUSSION: Depression and cardiovascular disease are both highly prevalent. Several studies have shown that the two are closely related. They share common pathophysiological etiologies or co-morbidities, such as alterations in the hypothalamic-pituitary axis, cardiac rhythm disturbances, and hemorheologic, inflammatory and serotoninergic changes. Furthermore, antidepressant treatment is associated with worse cardiac outcomes (in case of tricyclics), which are not observed with selective serotonin reuptake inhibitors. CONCLUSION: Although there is a strong association between depression and cardiovascular disease, it is still unclear whether depression is actually a causal factor for CVD, or is a mere consequence, or whether both conditions share a common pathophysiological etiology. Nevertheless, both conditions must be treated concomitantly. Drugs other than tricyclics must be used, when needed, to treat the underlying depression and not as mere prophylactic of cardiac outcomes.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4556-4556
Author(s):  
Omer Iqbal ◽  
Cafer Adiguzel ◽  
Jawed Fareed ◽  
Debra Hoppensteadt ◽  
Evangalos Litinas ◽  
...  

Abstract Selective serotonin reuptake inhibitors (SSRI) are a first-line treatment option for depressive illnesses, anxiety and obsessive-compulsive disorders with a favorable risk benefit ratio and side effects. They selectively inhibit neuronal reuptake of serotonin and result in depleted serotonin stores in the dense bodies of platelets. It is hypothesized that depressive illnesses cause platelet activation and endothelial dysfunction, which could be modulated by the use of SSRIs. In order to validate this hypothesis an institutional-based co morbidity of depression and cardiovascular study is undertaken. Patients with depression (n=25) and healthy control (n=25) are recruited in this study. Males and females between the ages of 20 and 65 years meeting the DSM-IV criteria for major depressive disorder served as the inclusion criteria for the study. The exclusion criteria included patients with heart disease, diabetes, lipid disorders, history of smoking, pregnant and lactating women, psychosis, schizoaffective illnesses and presence of other Axis I diagnosis with the exception of generalized anxiety disorder. Blood samples were collected at baseline and then 4 and 8 weeks following treatment with Escitaloprim, an SSRI. Preliminary results from the agonist-induced platelet aggregation showed varying degrees of inhibition of collagen, ADP, arachidonic acid and epinephrine-induced platelet aggregation as shown in the table below. Agonist induced platelet aggregation profile Averaged % aggregation Time Collagen AA ADP Epinephrine Saline Baseline 71.5± 22.4 64.1± 35.1 48.15± 30.9 55.65± 29.2 6.9± 4.5 Week 4 63.4± 19.5 67.1± 25.1 33± 26.7 37.375± 25.8 9.375± 7.8 Week 8 74.7± 21.3 55.71± 36.1 52.4± 31 50.4± 32.3 5± 3.9 While a number of patients showed an inhibition of ADP (2.5μM) and epinephrine (10μg/ml) and collagen (380μg/ml), however, other patients showed an inhibition of collagen-induced platelet aggregation. These results indicate that patients treated with SSRIs may have inhibition of platelet activation and aggregation, which may have an impact in the prevention of atherothrombotic cardiovascular disease. SSRIs might increase the bleeding tendency in some patients by inhibiting platelet aggregation. However, when the SSRIs are given in combination with other drugs patients may have a propensity for bleeding complications due to drug-drug interactions. Further large-scale trials are warranted to validate these results.


2004 ◽  
Vol 91 (01) ◽  
pp. 119-128 ◽  
Author(s):  
Cheryl Pittendreigh ◽  
Kevin Solomons ◽  
Elisabeth Maurer-Spurej

SummaryClinical depression has been proposed to be an independent risk factor for cardiovascular disease. While it is suggested that selective serotonin reuptake inhibitors (SSRIs) reduce the risk of acute cardiovascular problems of depressed patients, the effect of SSRIs on platelets, the only blood cells committed to serotonin (5-HT) transport, remains largely unknown. The goal of this pilot study was to measure the 5-HT levels in platelets of untreated and SSRI-treated depressed patients and normal subjects and to determine whether the interaction of SSRIs with platelets can explain their possible cardiovascular benefit in patients with depression. Platelet 5-HT was determined by an immunocytochemical assay and high-pressure liquid chromatography with electrochemical detection (HPLC-ECD). In normal control subjects without cardiovascular disease, 78 ± 8% of platelets were 5-HT-positive (n = 14). Depression caused a significant reduction in platelet 5-HT to 46 ± 21% in untreated patients (n = 13) and 22 ± 13% in SSRI-treated patients (n = 14). As a class, all selective serotonin reuptake inhibitors significantly reduced the 5-HT concentration in patient platelets. An inverse relationship of 5-HT level and dose of medication might be suggested. These results correlated well with 5-HT data from HPLC (r = 0.8509, p < 0.001). SSRIs did not affect platelet aggregation and dense granule release in response to thrombin, but significantly reduced ADP-induced platelet aggregation and dense granule release in both patient and normal control samples. The active inhibition of platelet aggregation by SSRIs might explain their cardiovascular benefit.


Author(s):  
Alfredo Bellon ◽  
Kieuhanh Nguyen

Patients with schizophrenia (SCZ) are at high risk of cardiovascular disease (CVD) due to an inherited predisposition, a sedentary life style and the use of antipsychotic medications. Several approaches have been taken to minimize this risk but results continue to be unsatisfactory. A potential alternative is prescribing Selective Serotonin Reuptake Inhibitors (SSRIs). SSRIs decrease platelet aggregation and reduce the risk of coronary heart disease in patients with depression. We therefore aim to investigate whether there is evidence that supports the use of SSRIs to reduce the risk for CVD in SCZ. A systematic review of the literature revealed five published reports relating to the impact of SSRIs on CV risk in SCZ. Three trials assessed the influence on metabolic parameters of fluvoxamine when combined with clozapine. Two of those studies found improvements with fluvoxamine. Of the other two reports, one indicates SSRIs as a group caused minimal but statistically significant increments in total cholesterol, LDL and triglyceride. The second report suggests that when SSRIs are combined with antipsychotics, the metabolic impact depends on the antipsychotic prescribed. While there are promising results, further studies are needed to establish the impact of SSRIs on CV risk in SCZ.


2018 ◽  
Vol 28 (2) ◽  
pp. 138-140 ◽  
Author(s):  
Tamara Pang ◽  
Alakananda Gudi

Selective serotonin reuptake inhibitors are considered to be the drug of choice in patients with major depression and cardiovascular disease. Fluvoxamine in particular has been shown to be safe for use in patients with cardiovascular disease. We report a case of chest pain precipitated by fluvoxamine in an elderly lady with a known history of cardiovascular disease. This highlights the need for psychiatrists to be aware of chest pain as a potential side effect of fluvoxamine in their patients.


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