The exact nature of the comorbidity between cardiovascular disease (CVD) and major depressive disorder (MDD) is poorly understood. The proposed mechanisms include various biochemical and molecular pathways as well as health behaviors such as physical inactivity. One possible link between MDD and CVD is increased platelet activity and blood viscosity. Recently, it was discovered that platelets express functional subtype of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors, for example, glutamate receptor 1 (GluR1). Here, I propose that this type of AMPA receptor could play a role in comorbid MDD and CVD, and antidepressants may interfere with platelet activation via direct or indirect effects on platelet GluR1 phosphorylation. Testing this hypothesis could provide a novel view on the pathobiological mechanisms of comorbid MDD and CVD. With respect to the recently discovered role of AMPA receptors in regulating platelet activation and thrombosis, it appears that the information about the putative effects of psychoactive AMPA-modifying drugs on platelet AMPA receptors would be critical in evaluating the putative effects of such drugs on CVD.

Hu Chen

Possible Role of Platelet GluR1 Receptors in Comorbid Depression and Cardiovascular Disease

<i  >Background.</i> Over-stimulation of the purinergic <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M2" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptor may bring about cellular dysfunction and injury in settings of neurodegeneration, chronic inflammation, as well as in psychiatric and cardiovascular diseases. Here we speculate how <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M3" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptor over-activation may lead to the co-occurrence of neurological and psychiatric disorders with cardiovascular disorders. <i  >Presentation.</i> We hypothesize that proinflammatory cytokines, in particular interleukin-1<svg style="vertical-align:-2.29482pt;width:8.8500004px;" id="M4" height="13.425" version="1.1" viewBox="0 0 8.8500004 13.425" width="8.8500004"  xmlns="http://www.w3.org/2000/svg">
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</svg>, are key players in the pathophysiology of neurological, psychiatric, and cardiovascular diseases. Critically, this premise is based on a role for the <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M5" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptor in triggering a rise in these cytokines. Given the broad distribution of <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M6" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptors in nervous, immune, and vascular tissue cells, this receptor is proposed as central in linking the nervous, immune, and cardiovascular systems. <i  >Testing.</i> Investigate, retrospectively, whether a bidirectional link can be established between illnesses with a proinflammatory component (e.g., inflammatory and chronic neuropathic pain) and cardiovascular disease, for example, hypertension, and whether patients treated with anti-inflammatory drugs have a lower incidence of disease complications. Positive outcome would indicate a prospective study to evaluate therapeutic efficacy of  <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M7" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptor antagonists. <i  >Implications.</i> It should be stressed that sufficient direct evidence does not exist at present supporting our hypothesis. However, a positive outcome would encourage the further development of <svg style="vertical-align:-3.20526pt;width:34.025002px;" id="M8" height="14.6875" version="1.1" viewBox="0 0 34.025002 14.6875" width="34.025002"  xmlns="http://www.w3.org/2000/svg">
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</svg> receptor antagonists and their application to limit the co-occurrence of neurological, psychiatric, and cardiovascular disorders.

Stephen D. Skaper

Pietro Giusti

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Neurons, glial, cells, and brain tumor cells tissues release small vesicles (secretory exosomes and microvesicles), which may represent a novel mechanism by which neuronal activity could influence angiogenesis within the embryonic and mature brain. If CNS-derived vesicles can enter the bloodstream as well, they may communicate with endothelial cells in the peripheral circulation and with cells concerned with immune surveillance.

Neil R. Smalheiser

Do Neural Cells Communicate with Endothelial Cells via Secretory Exosomes and Microvesicles?

The high comorbidity between psychiatric disorders and cardiovascular disease has received increasing attention, yet little is known about the processes linking the two. One plausible contributing mechanism is the tendency of those with psychiatric disorders to ruminate on stressful events. This phenomenon, sometimes called perseverative cognition, can extend the psychological and physiological effects of stress, which could contribute to cardiovascular disease etiology. In this paper, we discuss the potential role of perseverative cognition in mediating the relationship between psychiatric illness and cardiovascular disease. Rumination can delay physiological recovery from acute stress, which in turn has been found to predict future cardiovascular health. This delayed recovery could act as a mechanism in the longitudinal link between worry and cardiovascular health. The cognitive inflexibility that characterizes mood and anxiety disorders may then contribute to disease not by producing greater reactivity, but instead through extending activation, increasing the risks for cardiovascular damage.

Britta A. Larsen

Nicholas J. S. Christenfeld

Cardiovascular Disease and Psychiatric Comorbidity: The Potential Role of Perseverative Cognition

<i>Background</i>. Studies have implicated abnormalities in epigenetic gene regulation in schizophrenia. <i>Presentation</i>. We hypothesize that identifying abnormalities in chromatin structure and the epigenetic machinery in peripheral blood mononuclear cells (PBMC) from schizophrenia patients could (a) help characterize a subset of schizophrenia patients and (b) lead to targeted pharmacological interventions. <i>Testing</i>. Investigate the relationship between clinical symptoms, demographics, hormonal fluctuations, substance abuse, disease characteristics across the major mental illnesses, and epigenetic parameters in PBMC. In addition, examine the effects of individual antipsychotics, mood stabilizers, as well as experimental agents both as clinically prescribed as well as in cultured PBMC to understand the effects of these agents on chromatin. <i>Implications</i>. If PBMC could serve as a reliable model of overall epigenetic mechanisms then this could lead to a &#8220;biomarker&#8221; approach to revealing pathological chromatin state in schizophrenia. This approach may provide an informed method for selecting chromatin modifying agents for psychiatric disorders.

David P. Gavin

Rajiv P. Sharma

Chromatin from Peripheral Blood Mononuclear Cells as Biomarkers for Epigenetic Abnormalities in Schizophrenia

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Patrizia Debetto

P2<svg style="vertical-align:-3.39069pt" height="15.4" version="1.1" viewBox="0 0 17.575001 15.4" width="17.575001" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns="http://www.w3.org/2000/svg"><g transform="matrix(.017,-0,0,-.017,.062,11.112)"><path id="x58" d="M655 0h-263v28q46 5 55.5 14.5t-5.5 34.5l-132 214q-69 -104 -122 -202q-19 -32 -10.5 -43.5t58.5 -17.5v-28h-229v28q44 5 70 17t47 40q47 59 164 239l-134 214q-33 50 -54 64t-74 20v28h246v-28q-44 -5 -52 -14t5 -28q32 -55 114 -182q66 102 99 162q19 33 10.5 44.5&#xA;t-57.5 17.5v28h228v-28q-56 -6 -80 -19.5t-58 -57.5q-45 -62 -121 -179l157 -246q35 -53 60.5 -70t77.5 -22v-28z" /></g><g transform="matrix(.012,-0,0,-.012,11.175,15.187)"><path id="x37" d="M447 623l8 -12l-283 -613l-74 -10l-7 11q174 283 297 551h-216q-48 0 -62.5 -12t-33.5 -63h-29q10 60 18 148h382z" /></g></svg> Receptors in Neurological and Cardiovascular Disorders

Variant (Prinzmetal&#39;s) angina is an uncommon cause of precordial pain caused by coronary vasospasm and characterized by transient ST elevation and negative markers of myocardial necrosis. This is the case of a female patient with a prior history of depression and panic attacks who presented with recurrent symptoms including chest pain. A cardiac event monitor positively documented coronary vasospasm associated with anxiety-provoking chest pain, whereas the coronary arteries were angiographically normal. We noted that the frequency of angina attacks apparently increased during the period that coincided with the introduction of Bupropion SR for treatment of the patient&#39;s depression. Considering the possibility of bupropion-associated negative impact on coronary vasospasm, the antidepressant therapy was adjusted to exclude this drug. Although Prinzmetal&#39;s angina is relatively uncommon, we suspect that a routine use of cardiac event monitors in subjects with panic disorder might reveal a greater incidence of coronary vasospasm in this patient population.

Mladen I. Vidovich

Aneet Ahluwalia

Radmila Manev

Depression with Panic Episodes and Coronary Vasospasm

Epidemiological studies point to a strong and possibly causal association of psychiatric and neurological disorders with cardiovascular disease (CVD). Mechanistic links between these co-occurring illnesses are not well understood. Better insight into their relationship could help identify novel diagnostic markers and therapeutic targets. For successful translation of basic biomedical research into clinical practice, analyses 
                  of postmortem human tissues are essential. However, current tissue banks dedicated to psychiatric and neurological research collect only brain tissue samples 
                  deemed most important to the institution&#39;s participating investigators. While this practice is often dictated by budget constraints, restricted tissue storage space and other practical reasons, it limits the ability of the biological research community to access and study multiple organ systems relevant to cardiovascular and neuronal systems dysfunction. This problem is worsened when clinical records pertaining to coexistent systemic pathology are not available. To promote further understanding of co-occurring CVD and psychiatric/neurological disorders, efforts should be made to support tissue banks that harvest heart, coronary arteries, and aorta samples as well as brain tissue, from the same subjects.

Milos D. Ikonomovic

Heart and Brain Tissue Banks for Research on Co-Occurring Cardiovascular and Neurological/Psychiatric Disorders

Hari Manev

The Heart-Brain Connection Begets Cardiovascular Psychiatry and Neurology

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Cardiovascular Psychiatry and Neurology