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Query: UMLS:C0018799 (heart disease)
 34,133 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This article describes the long-term course of anxiety disorders based on the findings of the Harvard/Brown Anxiety Research Program (HARP) study--a prospective, naturalistic, longitudinal study of patients with anxiety disorders. Data from the HARP study emphasize both the chronicity of anxiety disorders and their frequent psychiatric comorbidity with other anxiety disorders and depression. Social phobia and generalized anxiety disorder are more chronic than panic disorder, although the latter has higher rates of relapse following recovery. Anxiety disorders have a major impact on the everyday lives of sufferers. The detrimental effects on social, psychological, and physical functioning are comparable with other chronic medical and psychiatric conditions, including diabetes, heart disease, and depression. Comorbidity with depression significantly increases the probability of suicide and is associated with poorer outcome. Findings from the HARP study have significant implications for treatment, which currently tends to focus on short-term outcomes. Future studies should emphasize the role of preventive pharmacotherapy to improve the long-term course of anxiety and to reduce its associated suffering, suicide, and occupational and social impairment.
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PMID:Raising the expectations of long-term treatment strategies in anxiety disorders. 1249 Aug 33

Panic disorder serves as a clinical model for testing whether mental stress can cause heart disease. Our own cardiologic management of panic disorder provides case material of recurrent emergency room attendances with angina and electrocardiogram ischemia, triggered arrhythmias (atrial fibrillation, ventricular fibrillation), and documented coronary artery spasm, in some cases with coronary spasm being complicated by coronary thrombosis. Application of radiotracer catecholamine kinetics and clinical microneurography methodology suggests there is a genetic predisposition to panic disorder that involves faulty neuronal norepinephrine uptake, possibly sensitizing the heart to symptom generation. During panic attacks there are large sympathetic bursts, recorded by clinical microneurography in the muscle sympathetic nerve neurogram, and large increases in cardiac norepinephrine spillover, accompanied by surges of adrenal medullary epinephrine secretion. In other conditions such as heart failure and presumably here also, a high level of sympathetic nervous activation can mediate increased cardiac risk. The sympathetic nerve cotransmitter, neuropeptide Y (NPY), is released from the cardiac sympathetics during panic attacks, an intriguing finding given that NPY can cause coronary artery spasm. There is ongoing, continuous release of epinephrine from the heart in panic sufferers, perhaps attributable to epinephrine loading of cardiac sympathetic nerves by uptake from plasma during panic attacks, or possibly to in situ synthesis of epinephrine through the action of intracardiac phenylethanolamine-N-methytransferase (PNMT) activated by repeated cortisol responses. We have used internal jugular venous sampling and measurement of overflowing lipophilic brain monoamine metabolites to quantify brain norepinephrine and serotonin turnover in untreated patients with panic disorder. We find normal norepinephrine turnover but a marked increase in brain serotonin turnover in patients with panic disorder, in the absence of a panic attack, which presumably represents an underlying neurotransmitter substrate for the condition.
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PMID:Cardiac sympathetic nerve biology and brain monoamine turnover in panic disorder. 1524 Apr 8

This cross-sectional psychiatric and cardiological study compared patients with and without coronary artery disease (CAD) with respect to psychiatric morbidity, psychological factors, pain characteristics, medical morbidity and the prevalence of coronary risk factors. The 199 participants had been referred to cardiological outpatient clinics for the investigation of chest pain and had no history of heart disease. Current panic disorder occurred significantly more often in non-CAD patients (41% vs. 22%). No significant differences were found for other psychiatric disorders and psychological variables. Non-CAD patients reported significantly longer histories of pain and a higher prevalence of atypical chest pain. In other respects, there were surprisingly few differences between the groups. High morbidity of both psychiatric disease (pain disorder, 19%; any current psychiatric disorder, 72%) and somatic conditions (musculoskeletal disease, 33%; dyspepsia, 23%) was found with no significant differences between the groups. In these patients, multifactorial complaints may explain chest pain in both patient groups. The physicians should attend to psychiatric disorders in non-CAD as well as in CAD patients.
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PMID:Psychological factors, pain attribution and medical morbidity in chest-pain patients with and without coronary artery disease. 1556 12

Panic disorder can serve as a clinical model for testing whether mental stress can cause heart disease. Potential neural mechanisms of cardiac risk are the sympathetic activation during panic attacks, continuing release of adrenaline as a co-transmitter in the cardiac sympathetic nerves, and impairment of noradrenaline neuronal reuptake, augmenting sympathetic neural respnses. The phenotype of impaired neuronal reuptake of noradrenaline: an epigenetic mechanism? We suspect that this phenotype, in sensitizing people to heart symptom development, is a cause of panic disorder, and by magnifying the sympathetic neural signal in the heart, underlies increased cardiac risk. No loss of function mutations of the coding region of the norepinephrine transporter (NET) are evident, but we do detect hypermethylation of CpG islands in the NET gene promoter region. Chromatin immunoprecipitation methodology demonstrates binding of the inhibitory transcription factor, MeCP2, to promoter region DNA in panic disorder patients. Cardiovascular illnesses co-morbid with panic disorder. Panic disorder commonly coexists with essential hypertension and the postural tachycardia syndrome. In both of these cardiovascular disorders the impaired neuronal noradrenaline reuptake phenotype is also present and, as with panic disorder, is associated with NET gene promoter region DNA hypermethylation. An epigenetic 'co-morbidity' perhaps underlies the clinical concordance. Brain neurotransmitters. Using internal jugular venous sampling, in the absence of a panic attack we find normal norepinephrine turnover, but based on measurements of the overflow of the serotonin metabolite, 5HIAA, a marked increase (six to sevenfold) in brain serotonin turnover in patients with panic disorder. This appears to represent the underlying neurotransmitter substrate for the disorder. Whether this brain serotonergic activation is a prime mover, or consequential on other primary causes of panic disorder, including cardiac sensitization by faulty neuronal noradrenaline reuptake leading to cardiac symptoms and the enhanced vigilance which accompanies them, is unclear at present.
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PMID:The neuronal noradrenaline transporter, anxiety and cardiovascular disease. 1678 72

A 10-year-old boy was admitted to the Pediatric Cardiology Unit with complaints of chest pain and dizziness. Physical examination did not show any pathologic signs. Family history revealed no heart disease and diagnosis of panic disorder (PD) in one of his family members. On follow-up, he was admitted to the pediatric emergency department several times with the same complaint. Organic etiologies of chest pain were excluded by extensive diagnostic work-up. He was referred to the Child and Adolescent Psychiatry Department for further work-up, and PD was diagnosed. A few weeks after starting paroxetine therapy, the frequency and the intensity of the chest pain attacks began to diminish. Early diagnosis of PD will avoid unnecessary investigations and prevent utilization of expensive health services, especially those performed in the emergency department. Physicians should consider that chest pain may be related to psychiatric disorders and refer their patient to mental health professionals for further management. Pharmacological therapy and cognitive-behavioral interventions are successfully used in the management of PD in children and adolescents.
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PMID:Panic disorder in a child with recurrent chest pain. 1747 56

Chest pain may be due benign diseases but often suggests an association with coronary artery disease, which justifies a quick search for medical care. However, some people have anxiety disorder with symptoms that resemble clearly an acute coronary syndrome. More specifically, during a panic attack an abrupt feeling of fear accompanied by symptoms such as breathlessness, palpitations and chest pain, makes patients believe they have a heart attack and confuse physicians about the diagnosis. The association between panic disorder and coronary artery disease has been extensively studied in recent years and, although some studies have shown anxiety disorders coexisting or increasing the risk of heart disease, one causal hypothesis is still missing. The aim of this systematic review is to present the various ways in which the scientific community has been investigating the relation between chest pain, panic disorder and coronary artery disease.
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PMID:Chest pain, panic disorder and coronary artery disease: a systematic review. 2492 48

The association between panic disorder (PD) and cardiovascular diseases (CVD) has been extensively studied in recent years and, although some studies have shown anxiety disorders co-existing or increasing the risk of heart disease, no causal hypothesis has been well established. Thus, a critical review was performed of the studies that evaluated the association between PD and cardiovascular diseases; synthesizing the evidence on the mechanisms mediators that theoretically would be the responsible for the causal pathway between PD and CVD, specifically. This overview shows epidemiological studies, and discusses biological mechanisms that could link PD to CVD, such as pleiotropy, heart rate variability, unhealthy lifestyle, atherosclerosis, mental stress, and myocardial perfusion defects. This study tried to provide a comprehensive narrative synthesis of previously published information regarding PD and CVD and open new possibilities of clinical management and pathophysiological understanding. Some epidemiological studies have indicated that PD could be a risk factor for CVD, raising morbidity and mortality in PD, suggesting an association between them. These studies argue that PD pathophysiology could cause or potentiate CVD. However, there is no evidence in favour of a causal relationship between PD and CVD. Therefore, PD patients with suspicions of cardiovascular symptoms need redoubled attention.
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PMID:Panic disorder and cardiovascular diseases: an overview. 2889 14


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