Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008031 (chest pain)
 17,248 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Panic disorder is a chronic illness that affects at least 3 percent of the population. Panic disorder is associated with significant morbidity and an increased risk of suicide. Patients generally present with multiple somatic and psychologic complaints, including heart palpitations, chest pain, tremor, shortness of breath, choking, nausea or abdominal distress, dizziness, derealization, fear of losing control or going crazy, fear of dying, paresthesias, chills or hot flushes, headache, diarrhea, insomnia, chronic fatigue, anxiety and depression. To make the correct diagnosis, these symptoms must be evaluated carefully since they also occur with serious cardiovascular, pulmonary, endocrinologic and neurologic disorders. Many effective treatments are available, including tricyclic antidepressants, selective serotonin reuptake inhibitors, monoamine oxidase inhibitors, benzodiazepines such as alprazolam and clonazepam, and psychotherapy.
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PMID:Panic disorder. 748 99

Panic attack symptomatology was investigated in 212 panic disorder patients (60 men, 152 women) using the Panic Attack Questionnaire, Feelings of helplessness and thoughts of escape had the highest mean severity ratings, but are not currently listed in the DSM-III-R. The DSM-III-R symptoms labeled choking or smothering sensations, paresthesias, nausea, and chest pain had low severity ratings. Evidence was obtained for a three-factor model of panic symptomatology consisting of dizziness-related symptoms, cardiorespiratory distress, and cognitive factors. These results provide only limited support for the current DSM-III-R symptom structure, and support the notion that panic disorder is a heterogeneous condition.
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PMID:The symptom structure of panic attacks. 799 26

Spinal cord stimulation (SCS) has routinely been used since the beginning of the 1970s. The initial indications for stimulation were the so-called deafferentation or neurogenic pain. Further work has confirmed that neurostimulation is useful in severe peripheral vascular disease in relieving pain and increasing capillary blood flow and oxygen tension. The effects are similar to those of sympathectomy. In 1964 Apthorp et al. discovered that sympathectomy relieved angina in about 75% of patients. The use of SCS to treat angina follows logically from its use in peripheral vascular disease. METHODS. The pain-relieving effect of SCS was investigated in two patients, 54 and 69 years old, who were hospitalised for 8 and 28 days. Both patients had severe angina pectoris (duration 2 and 15 years, New York Heart Association class III and II), related to three-vessel disease, and one of them had previously undergone his third bypass operation. The other patient was not considered suitable for surgery. The antianginal treatment (long-acting nitrates, beta-blockers, calcium antagonists) was regarded as optimal and was not changed during the observation period (Table 1). SURGICAL TECHNIQUE AND STIMULATION EQUIPMENT. We used the commercially available Medtronic SCS system. The operation was performed under local anaesthesia to allow the patient to answer questions during the intraoperative stimulation. The epidural space was punctured at the level of T7-T8 in one case and T11-T12 in the other. The electrode tip was positioned in the midline or a few millimetres to the left at the T1-T2 level (Figs. 1, 2), so that the patient felt a prickling sensation in the precordial area and into the arms. The distal end of the electrode was sutured to the fascia and connected via a tunnelled extension lead to the external pulse generator. The pulse width was 200 microseconds, frequency 80 Hz. An appropriate amplitude (usually 8-10 V) was used for comfortable paraesthesia. The study consisted of two parts: a run-in period (1 week) to standardise the stimulation when mobilisation was performed. A treatment period (18 months) to determine the patient's working capacity after continuous stimulation (Table 2). After a successful run-in period a Medtronic receiver was implanted, connected to the electrode and stimulated by external pulse generator. Different variables were used to assess the effect: pulse rate, blood pressure, the product of pulse rate and systolic blood pressure, estimated anginal pain, and ST changes in the electrocardiogram (ECG) before, during and after mobilisation. RESULTS. The stimulation was carried out for 30 min 10-12 times a day during the run-in period and five to six times a day during the treatment period. Altogether there was slight lowering of heart rate and systolic blood pressure. Consequently the product of heart rate and systolic blood pressure was diminished. In one case (NYHA II) the distinct disorder of repolarisation reverted to the normal condition as shown on ECG. In the other case (NYHA III) the ECG remained unchanged because of a severe aneurysm of the cardiac wall. Both patients experienced nearly complete pain relief after a few days for 6 and 12 months respectively. However, an increasing effort tolerance could be demonstrated in both patients by reducing the extent of the heart failure (NYHA II/III to NYHA I/II) (Table 2). DISCUSSION. Our two hospitalised patients had clinically intractable angina pectoris and severe manifestations of heart disease corresponding to at least NYHA functional class II-III. Both were unsuitable for operation and showed no improvement on individually titrated maximal oral antianginal drug treatment. During SCS treatment significant improvement was obvious: chest pain, ST-segment depression, and the extent of heart failure could be reduced. Both patients reached a better NYHA functional class, exhibited increased working capacity and reported reductions in anginal attacks and pain. Th
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PMID:[Epidural spinal cord stimulation in therapy-resistant angina pectoris]. 836 77

The patient was a 48-year-old man who was brought to our hospital complaining of chest pain, paresthesia of the lower extremities, and pain in the lumbar region. At first, acute myocardial infarction was diagnosed, but transthoracic echocardiogram revealed an intimal flap in the ascending aorta. The presence of an intimal tear below the left subclavian artery was confirmed by intraoperative transesophageal echocardiogram, and a diagnosis of myocardial infarction accompanying type IIIb aortic dissection with retrograde extension to the ascending aorta was made. Coronary artery bypass grafting to segment #2 using a section of saphenous vein and total aortic arch replacement with "elephant trunk" technique, which concurrently served as a means of amputated stump plasty, was performed. The cerebral circulation was preserved by retrograde cerebral circulation. The post operative progress was good, and thrombo-occlusion of the false lumens of the proximal descending aorta was verified. Type IIIb aortic dissection complicated with myocardial infarction is rare, but examination with both transthoracic and transesophageal echocardiograms were useful for the morphological diagnosis and for determining the surgical technique for the dissection.
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PMID:[Successful surgical treatment in a case of type IIIb acute aortic dissection complicated with acute myocardial infarction]. 855 Oct 82

Using cluster analysis of 207 patients with panic disorder (PD), we investigated the relationships between several panic symptoms at the time of panic attacks, which included anticipatory anxiety, agoraphobia, and 13 clinical symptoms based on the Diagnostic and Statistics Manual-III-Revised. Cluster analysis revealed three panic symptom clusters: cluster A (dyspnea, choking, sweating, nausea, flushes/chills); cluster B (dizziness, palpitations, trembling or shaking, depersonalization, agoraphobia, and anticipatory anxiety); and cluster C (fear of dying, fear of going crazy, paresthesias, and chest pain or discomfort). Generally, cluster A was comprised exclusively of physiological symptoms, among which respiratory symptoms were prominent, cluster B included both panic and non-panic symptoms such as agoraphobia and anticipatory anxiety, and cluster C was comprised chiefly of fear symptoms.
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PMID:The symptom structure of panic disorder: a trial using factor and cluster analysis. 868 87

We studied 23 consecutive patients with acute hyperventilation presenting to an inner-city emergency department, diagnosed on clinical grounds by the attending physician and confirmed by arterial blood gas values in 5 patients. An organic basis for the presenting complaints was excluded and chest radiograph, serum biochemistry, blood cell count, and thyroid function test results were normal. The male to female ratio was 12:11. Presenting complaints were dyspnea (61%), paresthesia (35%), chest pain or tightness (43%), muscle spasm (9%), dizziness (13%), palpitations (13%), and panic (30%). Similar previous episodes were reported in 74%. Misattribution of the presenting complaints to a cardiac or other life-threatening disorder was reported in 20 patients (87%) and was the main reason for their presentation to the hospital. Although no patients presented with clinical features of asthma, 7 (30%) were known asthmatics receiving treatment and another 10 (44%) had a history and investigation results suggestive of asthma. Only 2 had a history of anxiety or depression, but 17 (78%) patients exceeded the threshold for anxiety or panic on Clinical Interview Schedule (CIS-R) interview (score > or = 12). Marihuana or alcohol abuse were involved in 17% with a history of past abuse in 26%. When assessed 2 months after the attack, 13 (57%) had resting or stressor-induced hyperventilation with a significant (p < 0.05) association with asthma but not with a positive CIS-R score. These results illustrate the multifactorial basis of acute hyperventilation, the importance of misattribution, and the danger of using the term "hyperventilation syndrome" in the emergency department.
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PMID:Patients with acute hyperventilation presenting to an inner-city emergency department. 922 1

Panic disorder is a chronic and debilitating illness. In this article, we present an algorithm of the diagnosis and treatment of the illness. We place much importance upon the patient variables associated with the treatment decisions. We emphasize strong patient involvement in treatment as a way to become panic free and improve level of functioning. Panic disorder is defined in DSM-IV1 as "The presence of recurrent panic attacks followed by at least one month of persistent concern about having another panic attack, worry about the possible implications or consequences of the panic attack, or a significant behavioral change related to the attacks." A panic attack is defined as "a discrete period of intense fear or discomfort, in which four or more of the following symptoms developed abruptly and reached a peak within 10 minutes." 1) Palpitations, pounding heart or accelerated heart rate; 2) sweating; 3) trembling or shaking; 4) sensations of shortness of breath or smothering; 5) feeling of choking; 6) chest pain or discomfort; 7) nausea or abdominal distress; 8) feeling dizzy, unsteady, light-headed or faint; 9) derealization or depersonalization; 10) fear of losing control or going crazy; 11) fear of dying; 12) paresthesias; 13) chills or hot flashes. The following hypotheses have been used to conceptualize panic disorder from a psychiatrist's perspective.
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PMID:Panic disorder: a different perspective. 949 26

Allogeneic peripheral blood stem cell transplantation leads to an earlier engraftment compared to BMT. The feasibility, acceptance and long-term side-effects of G-CSF mobilisation of PBSC in unrelated healthy donors needs to be evaluated. Forty unrelated healthy donors received G-CSF in a dose of 10 microg/kg bodyweight for 5 days and two aphereses were performed. The donors were monitored prospectively. The data were compared to bone marrow harvests from unrelated donors. Almost all stem cell donors reported some side-effects due to Filgrastim application. Bone pain (32), headache (20), chest pain (two) and night sweats (one) were complained of. By taking analgesics, the pain was relieved in most cases. No donor discontinued the filgrastim application. Bone pain and headache resolved within 2-4 days after termination of Filgrastim application. There was, as expected, a seven-fold increase in the number of total WBCs. There were no significant changes of platelet counts during G-CSF application. After 4 weeks haemoglobin concentration and platelet counts showed no significant differences compared to baseline values. The aphereses were mostly tolerated very well. Eighteen donors reported paraesthesia, one donor developed dizziness, two complained of nausea and vomiting. There was a significant decrease in platelet count (242 before, 98 x 10(9)/l after aphereses). Autologous platelets were transfused after the second aphereses in four donors. These data were compared to data from 245 unrelated bone marrow donors, who had on average, 14 days bone pain and tiredness after donation. The G-CSF mobilisation and apheresis of peripheral blood stem cells is an alternative to traditional bone marrow harvesting in unrelated healthy donors. It is well tolerated and the duration of side-effects on average is shorter than after the surgical procedure. So far no long-term effects have been observed in the follow-up.
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PMID:Acceptance and feasibility of peripheral stem cell mobilisation compared to bone marrow collection from healthy unrelated donors. 971 88

DACA, also known as XR5000, is an acridine derivative active against both topoisomerase I and II. In this phase I study, DACA was given as a 3-h intravenous infusion on 3 successive days, repeated every 3 weeks. A total of 41 patients were treated at 11 dose levels between 9 mg m(-2) d(-1) and the maximum tolerated dose of 800 mg m(-2) day(-1). The commonest, and dose-limiting, toxicity was pain in the infusion arm. One patient given DACA through a central venous catheter experienced chest pain with transient electrocardiogram changes, but no evidence of myocardial infarction. At the highest dose levels, several patients also experienced flushing, pain and paraesthesia around the mouth, eyes and nose and a feeling of agitation. Other side-effects, such as nausea and vomiting, myelosuppression, stomatitis and alopecia, were uncommon. There was one minor response but no objective responses. DACA pharmacokinetics were linear and did not differ between days 1 and 3. The pattern of toxicity seen with DACA is unusual and appears related to the mode of delivery. It is possible that higher doses of DACA could be administered using a different schedule of administration.
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PMID:Phase I and pharmacokinetic study of DACA (XR5000): a novel inhibitor of topoisomerase I and II. CRC Phase I/II Committee. 1046 97

The emergency medical service was called to a 60-year-old woman with intensive chest pain, signs of shock, dyspnoea, intermittent paraesthesia of the right leg and disturbance of consciousness. With the diagnosis of an acute rupture of an aneurysm of the thoracic aorta, the patient was stabilised with volume, catecholamines, intubation and mechanical ventilation before being rushed to the preinformed department of cardiovascular surgery. The diagnosis was verified by transesophageal echocardiography immediately and the patient underwent surgery 2 h after onset of symptoms. Despite the rupture of the aorta and a short period of cardiac arrest, the patient recovered totally and could be discharged without any residual problems. This case shows that a ruptured thoracic aortic aneurysm can be survived although the overall mortality of this incident is more than 97%. The essentials of a good outcome are: 1. perfectly coordinated rescue operation which means an emergency medical service which includes the rupture of an aortic aneurysm in the differential diagnosis of acute chest pain, 2. an early verification of the diagnosis by means of transesophageal echocardiography which should also be carried out by anaesthesiologists due to its importance in the differential diagnosis in haemodynamic unstable patients.
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PMID:[Emergency management of an acute rupture of a perforated thoracic aortic aneurysm]. 1212 10


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