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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a sample of 114 patients, 6 patients developed hypertension while taking tricyclic antidepressants. All these patients were diagnosed as having panic disorder, with or without major depression. Half of the 6 patients had a previous diagnosis of hypertension, which had been well controlled by antihypertensive drugs for years. A comparison group of patients with major depression, who had never had panic attacks, had no cases of hypertension induced by these antidepressants. These findings raise the possibility that patients who have panic disorder may experience cardiovascular disregulation that increases their risk for antidepressant-induced hypertension.
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PMID:Systemic hypertension associated with tricyclic antidepressant treatment in patients with panic disorder. 144 82

Few disorders of endocrine function are so sudden and dramatic in their presentation as those caused by a pheochromocytoma. This chromaffin cell tumor arises within the adrenal medulla or within the sympathetic nervous system and causes wide fluctuations in blood pressure, tachydysrhythmias, and manifestations of intense anxiety. The patient experiences explosive paroxysms of catecholamine overload. The diagnoses of accelerated hypertension or panic disorder often are prematurely adopted. The condition kills, with deaths primarily attributed to irreversible cardiovascular and end-organ damage caused by profound hypertension. For those with a pheochromocytoma, the disorder caused by the tumor is a terrifying constellation of symptoms. Although pheochromocytoma is rare, it must be considered in the treatment of any patient with sudden, extreme hypertension and accompanying hypermetabolism. A cure is possible, but only with early diagnosis and treatment.
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PMID:Pheochromocytoma: a clinical review. 157 30

In order to examine the validity of the distinction between generalized anxiety disorder (GAD) and panic disorder (PD) we compared 41 subjects with GAD and 71 subjects with PD. The GAD subjects had never had panic attacks. In contrast to the symptom profile in PD subjects suggestive of autonomic hyperactivity, GAD subjects had a symptom pattern indicative of central nervous system hyperarousal. Also, subjects with GAD had an earlier, more gradual onset of illness. In terms of coexisting syndromes, GAD subjects more often had simple phobias, whereas PD subjects more commonly reported depersonalization and agoraphobia. GAD subjects more frequently had first-degree relatives with GAD, whereas PD subjects more frequently had relatives with PD. A variety of measures indicated that our GAD subjects had a milder illness than those with PD. Also, fewer GAD subjects gave histories of major depression than did PD subjects. Among GAD subjects, coexisting major depression was associated with simple phobia and thyroid disorders and among PD subjects, comorbid depression was associated with social phobia and hypertension. Our findings indicate that the separation of GAD from PD is a valid one. They also indicate that, within disorders, unique patterns of comorbidity may exist that are important both clinically and theoretically.
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PMID:Generalized anxiety disorder vs. panic disorder. Distinguishing characteristics and patterns of comorbidity. 143 31

Increased coronary disease rates, as well as increased all-cause mortality, in persons with high levels of hostility/anger and in persons suffering from panic disorder or phobic anxiety suggest that biological concomitants of these traits/conditions lead to major medical illnesses. Benzodiazepines have effects, e.g. blunting of stress hormone responses, that could prevent disease in persons so predisposed. It will be necessary to identify subgroups with sufficiently high absolute rates of disease risk to justify pharmacological interventions, and then to carry out controlled prevention trials to document the benefits, before such approaches can be recommended for the general population. This approach (use of drugs when other measures fail) is now standard for more traditional risk factors, such as hyperlipidemia and hypertension. In contrast to primary prevention, a stronger case can be made for the use of benzodiazepines in secondary prevention. Research has shown benzodiazepine treatment to improve control of angina and to reduce "silent ischemia", directly suggesting clinical benefits to be gained from the effects of benzodiazepines to reduce stress hormone responses. While benzodiazepines have long been prescribed for the postmyocardial infarction patient, there are no controlled clinical trials documenting such benefits. These are now clearly in order so that the use of benzodiazepines in coronary patients can be advised on a rational basis.
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PMID:Do benzodiazepines have a role in the prevention or treatment of coronary heart disease and other major medical disorders? 198 Jun 99

A case of placental abruption is described in a nonmedicated pregnant woman with panic disorder who experienced panic symptoms and resultant hypertension. The authors suggest that sympathetic arousal associated with panic symptoms may have an adverse effect on the fetoplacental unit. The potential impact of untreated anxiety symptoms on fetal well-being must be considered when deciding whether pharmacotherapeutic intervention is appropriate for certain patients with anxiety disorders.
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PMID:Panic attack-associated placental abruption: a case report. 273 32

An hypothesis is proposed that there exists a subgroup of African-American hypertensive patients whose hypertension could have been prevented by the early detection and treatment of easily recognizable symptoms that signal the initiation of the pathophysiologic processes that lead to essential hypertension.A pilot study of 31 patients with elevated blood pressure revealed that 41.9 percent had isolated sleep paralysis, 35.5 percent had panic attacks, and 9.7 percent had panic disorder. These proposed hyperadrenergic phenomena may be related to the development of hypertension in certain individuals.
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PMID:The relationship of isolated sleep paralysis and panic disorder to hypertension. 335 70

Anxiety is the fifth most common clinical diagnosis in the primary care setting. Panic disorder, a severe episodic form of anxiety, has been found to occur in approximately 6% of primary care patients. These patients often selectively focus on one of the frightening autonomic symptoms and are frequently misdiagnosed. The three most common presentations of panic disorder in the medical setting are cardiac symptoms (chest pain, tachycardia), neurologic symptoms (headache, dizziness/vertigo, syncope), and gastrointestinal symptoms, especially epigastric distress. The presentation of cardiac symptoms by patients with panic disorder is especially likely to lead to expensive and potentially iatrogenic medical testing. Hypertension and peptic ulcer are the most commonly associated medical diagnoses in patients with panic disorder. Major depression, alcohol abuse, simple phobias, and posttraumatic stress disorder are the most frequently associated psychiatric diagnoses. Psychopharmacologic treatment of panic disorder has been demonstrated to be highly effective in double-blind, placebo-controlled studies. Effective psychopharmacologic agents include the tricyclic antidepressants (notably imipramine and desipramine), the monoamine oxidase inhibitors (phenelzine), and the high-potency benzodiazepines (alprazolam).
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PMID:Panic disorder: epidemiology, diagnosis, and treatment in primary care. 353 Nov 89

Episodic elevation of blood pressure was evaluated in two middle-aged men by assessing home, clinic, and 24-hour ambulatory values following exclusion of secondary forms of hypertension. Both individuals had normotensive home and clinic readings. The 24-hour blood pressure was 125/85 +/- 12/9 mm Hg in patient 1 and 119/84 +/- 13/13 mm Hg in patient 2; however, both patients experienced large, sustained rises in blood pressure associated with panic attacks that were not abolished with prophylactic benzodiazepine therapy. Episodic blood pressure elevations were not associated with concomitant increases in heart rate. Patient 1 underwent extensive psychological investigation that diagnosed a panic disorder, and he underwent therapy that reduced the frequency and intensity of his panic-related hypertensive episodes. Because patient 2 demonstrated hypertensive readings at work, he was given a beta-blocking agent that ultimately controlled his blood pressure during episodes of anxiety and panic. These findings suggest that patients with panic attacks may present with episodic hypertension and that ambulatory blood pressure monitoring is useful in the diagnosis of this disorder and in assessment of treatment outcome.
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PMID:Episodic hypertension secondary to panic disorder. 371

A retrospective study of 55 patients with panic disorder referred for psychiatric consultation by primary care physicians is presented. Eighty-nine percent of the patients initially presented with one or two somatic complaints, and misdiagnosis often continued for months or years. The three most common presentations were cardiac symptoms (chest pain, tachycardia, irregular heart beat), gastrointestinal symptoms (especially epigastric distress), and neurologic symptoms (headache, dizziness/vertigo, syncope, or paresthesias). Eighty-one percent of patients had a presenting pain complaint. Hypertension and peptic ulcer were the most common medical diagnoses, and depression and alcoholism the most frequently associated psychiatric diagnoses.
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PMID:Panic disorder and somatization. Review of 55 cases. 637 87

Hyperventilation is an important feature of panic disorder, and an association has been reported between panic disorder and hypertension. We have examined the effect of hyperventilation on the blood pressure (BP) of healthy subjects. Twenty six subjects were randomised in a balanced two-period cross-over study to compare the effects of hyperventilation with that of normal breathing on sitting BP, heart rate and the electrocardiogram. Each study phase lasted 40 min, with 15 min of baseline observation, 5 min of hyperventilation or normal breathing, and 20 min of continued observation. Hyperventilation significantly increased SBP by 8.9 mm Hg (95% CI 3.8-13.8, P < 0.01), diastolic blood pressure by 8.2 mm Hg (95% CI 1.7-14.7, P < 0.05), mean arterial pressure by 10.0 mm Hg (95% CI 3.3-16.7, P < 0.01) and heart rate by 36 beats/min (95% CI 31-44, P < 0.01). The changes in diastolic and mean arterial pressure correlated significantly with the total volume of air expired during hyperventilation (r = 0.57, p < 0.01 and r = 0.50 P < 0.01, respectively), but not with the change in expired carbon dioxide. In the electrocardiogram, T wave changes occurred in the inferior leads in 10 of 26 subjects, but there were no significant changes in other measurements. Hyperventilation significantly increased the BP of healthy subjects, and the role of hyperventilation in the link between panic disorder and hypertension deserves further study.
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PMID:Pressor effect of hyperventilation in healthy subjects. 775 73


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