Depression is an independent risk factor leading to a cardiac event, which has . with cardiac disease, with no difference in efficacy, but fluoxetine did not which looked at patients with depression and recent MI, the authors. Relationship between left ventricular dysfunction and depression following myocardial infarction: data from the MIND-IT European Heart Journal, Volume 26, Issue 24, 1 December , Pages –, vifleem.info eurheartj/. not simply “in the mind.” They are real illnesses, tion of a clear relationship between mental health and car- diovascular myocardial infarction, heart failure, and arrhythmias are depression and anxiety and cardiovascular disease is bidi -.
Alternative approaches, antidepressants, coronary artery disease, depression How to cite this article: Chang L, Liu N. The Safety, efficacy, and tolerability of pharmacological treatment of depression in patients with cardiovascular disease: A look at antidepressants and integrative approaches.
Patients with CVD are at an increased risk of developing psychiatric illnesses, particularly depression. Morbidity and mortality in CVD patients with untreated psychiatric illnesses significantly increase, with Chung et al.
Consequences of psychotropic intervention include adverse drug effects such as weight gain, hyperlipidemia or hypertension HTNdrug—drug interactions, and even direct cardiac effects such as delayed repolarization. In addition, an increasingly pertinent issue in psychiatry in recent years is that of the limitations of conventional antidepressants, with two-thirds of people treated with first-line antidepressants not achieving remission. A number of novel therapeutic approaches have been considered to ameliorate depressive symptoms, including changes in lifestyle and diet.
Developing treatments targeted toward the heterogeneity of depression is not only required for improved quality of life among individuals with major depressive disorder MDD but also remains an important aspect of translating more recent findings, produced from the brain—mind—body trichotomy, into clinical practice.
The focus of this article is to explore the pharmacological options for treating patients with comorbid depression and CVD.
- Depression and myocardial infarction: relationship between heart and mind.
- Heart–brain Interactions in Heart Failure
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The use of antidepressants and supplements in patients with CVD will be discussed. Of note, nonpharmacological interventions such as cognitive behavior therapy,  cardiac rehabilitation,  exercise training,  and psychosocial rehabilitation  also have significant evidence in decreasing psychiatric symptoms in this population. Antidepressants Monoamine oxidase inhibitors Due to the risk of hypertensive crisis and their tendency to elevate blood pressure, monoamine oxidase inhibitors MAOIs are typically avoided in patients with CVD.
If used, careful attention should be paid to dietary intake of tyramine-containing foods as well as avoiding the use of other sympathomimetic agents. Several studies  demonstrated that therapeutic doses of TCAs did not impair left ventricular function, even in patients with congestive heart failure.
TCAs prolong interventricular conduction secondary to sodium channel blockade, which results in a decrease in the frequency of premature ventricular contractions. This discovery led investigators to hypothesize that the antiarrhythmic effect of TCAs could be of particular benefit to depressed patients with preexisting arrhythmias.
However, results from the cardiac arrhythmia suppression trial CAST led to reconsideration of this theory.
Heart–Brain Interactions Heart Failure - cardiac failure review
The CAST trials sought to determine whether treatment of postmyocardial infarction MI ventricular irritability with an antiarrhythmic resulted in decreased mortality.
However, these studies were discontinued prematurely after it was demonstrated that treatment with a Type IC or IA antiarrhythmic in post-MI patients actually resulted in increased mortality, possibly secondary to an interaction between the antiarrhythmic drug and ischemic myocardium. Given that TCAs have a Class I antiarrhythmic action similar to the antiarrhythmics utilized in the CAST trials, it is not unreasonable to assume that TCAs might carry the same risk of increased mortality in this population.
Later research demonstrated that TCAs decrease all component measures of heart rate variability and increase QT variability, which are associated with ventricular fibrillation and sudden cardiac death.
However, even after using imipramine for 1 year, Shrivastava et al. However, if a TCA must be used, Mavrides and Nemeroff identify nortriptyline as the preferred medication due to its lower incidence of orthostatic hypotension. As such, unless there is convincing evidence to utilize a TCA in this population, they are best to be avoided. Selective serotonin reuptake inhibitors SSRIs as a class offer numerous advantages compared to the earlier antidepressants. However, in patients at risk for hemorrhage, such as those who are also taking an antiplatelet or anticoagulant, SSRIs could increase risk of bleeds.
As such, Teply et al. Specifically, there is an increased risk of bleeding when fluoxetine or fluvoxamine is combined with warfarin, even beyond the baseline combined antiplatelet activity, due to their inhibition of CYP2C9 and thus the potential for increased levels of warfarin. Finally, because of their CYP2C19 inhibition, fluoxetine and fluvoxamine should not be combined with clopidogrel, as this could reduce its antiplatelet effect.
Interestingly, paroxetine has also been studied for the treatment of atrial fibrillation due to its effects on vagal tone and ability to inhibit the vasovagal reflex. Although this study was small 9 male patients with paroxysmal atrial fibrillationresponse was favorable. There were no differences between citalopram and placebo when considering blood pressure changes or electrocardiography ECG measures, including QTc intervals.
Still, newer research done by Zivin et al. Both organs are linked by multiple feedback signals, and the discovery of bi-directional interactions of failing heart and neuronal signals has led to the concept of the cardio-cerebral syndrome in HF. Several risk factors for stroke in patients with HF have been established.
A hypercoagulable state, with activated coagulation and disturbances in proteolytic systems,13 reduced blood flow, inflammation and endothelial dysfunction, has been implicated in the development of systemic cardioembolic events in HF including stroke. Further factors such as low flow patterns due to an enlarged left atrium14 or reduced contractility of the left ventricle LV with apical akinesia or aneurysm represent additional risk factors of intracardiac thrombosis and, consequently, embolic stroke in patients with HF.
A borderline significant benefit of warfarin on the primary outcome ischaemic stroke, haemorrhagic stroke or death from any cause was observed only after 4 years. Open ppt While stroke represents an acute case of low cerebral perfusion, chronic low cerebral perfusion may manifest in a series of structural cerebral alterations of grey and white matter damage in HF patients.
Regional hypoperfusion may occur at low perfusion pressures, and chronic low perfusion may account for metabolic impairment, structural decrease and eventual functional decline of brain areas involved in autonomic, neuropsychological and cognitive control. The decreased regional perfusion may contribute to the autonomic, mood and cognitive regulatory deficits observed in HF.
Depression and myocardial infarction: relationship between heart and mind.
Further, impaired perfusion of multiple brain areas involved in the control of vision, language and speech have been observed that could explain the respective deficits in HF patients. I have no control over anything and on top of that there is this threat jumping inside my chest, I wake up at night and I can tell that the heart rate is not normal, is this living? But being able to listen to others here, brings me relief and comfort, we understand each other.
Friends of infarction and misfortune, let's unite here to accept this Hiroshima bomb in our lives referring to the MIit's no use pretending we'll rescue everything, we will not. Imagine my situation waiting for a heart transplantI still depend on someone's death, to have a heart, I have always made a lot of money, I did bank operations involving big sums, today I depend on someone to save me, I do not recognize myself anymore.
In the past I had pleasure in eating in good restaurants, drinking good wine, but today I remember the heart attack, and nothing is fun anymore. If I'm in a good restaurant, I order a tasty dish, but the negative and judgmental thought comes: I should not be eating this, there goes off the pleasure.
How can I get out of bed? I took this medicine for 1 week and I felt worse, so I stopped taking it. I take medicine for blood pressure, cholesterol and now another one? It is no good. You know what for?
For not killing ourselves, a heart attack is just like suicide Think that if our heart failed, an antidepressant should speed up our heart rate, and then we have a heart attack again I will have to force myself out of this sadness, you cannot count on more medicine. And how to do it if my wife cared for me throughout the hospital stay?
Mind and mood after a heart attack
However, has my life ended after this bomb here? Before that I liked sex, now it has become boring. I have desire, but I am in no mood for it. I am another person… a boring person, without a job and without a heart. In the study proposed by Kim et al. On the contrary, the antidepressant may be an important contributor to improve the patient's quality of life following MI if the patient understands the importance of it.