Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0151744 (myocardial ischemia)
 31,282 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Progress in understanding the genetic basis of panic attacks may extend current knowledge on susceptibility to panic and pathogenesis of panic disorder. In the present study we applied the microarray Illumina platform for whole genome expression profiling in healthy subjects participating in the CCK-4-induced panic test. The study sample consisted of 31 male and female healthy volunteers, who were categorized according to predefined criteria as "panickers" or "non-panickers" to a CCK-4 challenge. The gene expression profiles were measured on peripheral blood cells at baseline and at 120 min post-CCK-4 injection using Illumina Human-6 v2 BeadChips. The fold change was used to demonstrate rate of changes in average gene expressions between studied groups. Statistical analyses were performed using the false discovery rate (FDR). Gene expression profiling 2 hr post-CCK-4 challenge showed changes in transcriptional levels of 226 genes. A total of 61 genes were differentially expressed between panickers and non-panickers with most of them related to immune, enzymatic or stress regulation systems. Other distinctive mRNA transcripts were from the genes known to be related to phenotypes associated with increased occurrence of panic attacks, such as asthma, diabetes, or myocardial ischemia. Our findings provide preliminary evidence for genetic substrates of panic attacks on the transcriptional level and indicate potential biological proximity between acute panicogenesis and several somatic conditions.
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PMID:Peripheral gene expression profiling of CCK-4-induced panic in healthy subjects. 1905 Dec 87

Comorbidities, are common in COPD, have been associated with poor outcomes and are thought to relate to systemic inflammation. To investigate comorbidities in relation to systemic inflammation and outcomes we recorded comorbidities in a well characterized cohort (ECLIPSE study) for 2164 clinically stable COPD subjects, 337 smokers and 245 non-smokers with normal lung function. COPD patients had a higher prevalence of osteoporosis, anxiety/panic attacks, heart trouble, heart attack, and heart failure, than smokers or nonsmokers. Heart failure (Hazard Ratio [HR] 1.9, 95% Confidence Interval [CI] 1.3-2.9), ischemic heart disease (HR 1.5, 95% CI 1.1-2.0), heart disease (HR 1.5, 95% CI 1.2-2.0), and diabetes (HR 1.7, 95% CI 1.2-2.4) had increased odds of mortality when coexistent with COPD. Multiple comorbidities had accumulative effect on mortality. COPD and cardiovascular disease was associated with poorer quality of life, higher MRC dyspnea scores, reduced 6MWD, higher BODE index scores. Osteoporosis, hypertension and diabetes were associated with higher MRC dyspnea scores and reduced 6MWD. Higher blood concentrations of fibrinogen, IL-6 and IL-8 levels occurred in those with heart disease. Comorbidity is associated with poor clinical outcomes in COPD. The comorbidities of heart disease, hypertension and diabetes are associated with increased systemic inflammation.
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PMID:Comorbidity, systemic inflammation and outcomes in the ECLIPSE cohort. 2379 63

Chest pain is often seen alongside with panic attacks. Moreover, panic disorder has been suggested as a risk factor for cardiovascular disease and even a trigger for acute coronary syndrome. Patients with coronary artery disease may have myocardial ischemia in response to mental stress, in which panic attack is a strong component, by an increase in coronary vasomotor tone or sympathetic hyperactivity setting off an increase in myocardial oxygen consumption. Indeed, coronary artery spasm was presumed to be present in cases of cardiac ischemia linked to panic disorder. These findings correlating panic disorder with coronary artery disease lead us to raise questions about the favorable prognosis of chest pain in panic attack. To investigate whether myocardial ischemia is the genesis of chest pain in panic attacks, we developed a myocardial perfusion study through research by myocardial scintigraphy in patients with panic attacks induced in the laboratory by inhalation of 35% carbon dioxide. In conclusion, from the data obtained, some hypotheses are discussed from the viewpoint of endothelial dysfunction and microvascular disease present in mental stress response.
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PMID:Myocardial perfusion imaging study of CO(2)-induced panic attack. 2418 91